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20 October 2018          Reflective Practice

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20 October 2018          Reflective Practice

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Tedious but necessary (that is what I wrote on 20/10/2018)   22 March 2019.  (D1, D2, D3, D4) Interestingly, the more I reflect, the easier it becomes and it becomes easier to treat my patients as I understand their conditions better.  I am becoming more reflective, although increasingly tired, I find it very helpful to review my patients' cases and see how I can improve my treatment for next time.  I am understanding the process better and I think it is becoming interesting, rather than tedious.  I wish there were more hours in the day so I have more time to reflect on how I have done with my patients.
https://www.brookes.ac.uk/students/upgrade/study-skills/reflective-writing-gibbs/
10 April 2019
I am finding it easier to reflect on patients and how I have been with them, especially when I give myself time and space to reflect on the process. (D1, D2, D3, D4)  Sometimes it helps having someone to listen to what I am saying, although I think I can also 'pretend' to have someone listening, as that also gives me an outlet as though there were someone listening to me. I think it is also hard finding the time to write reflective pieces all the time, I frequently reflect on my performance in clinic, good and bad, but sometimes I am in the car and don't have the ability to record what I am thinking or saying.

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Reflective writing: About Gibbs reflective cycle - Oxford Brookes University

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Upgrade study skills: Reflective writing: About Gibbs reflective cycle

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I originally posted this to see how easy it would be to upload coursework to the padlet as part of the reflective process.  I didn't really reflect on the exam initially, however I have written about this below.  I have also realised that uploading coursework to the padlet is a little slow and cumbersome but it will make assessing the portfolio much easier for my assessor, so from that point of view it is very useful having an online tool we can implement.
What I have learnt from the exams this year and what I can do to improve my knowledge (B2, B3, B4)
I find practical exams really hard.  No matter how much I revise, I still don't seem to get a good mark.  I get really nervous, and I was pleasantly surprised with the mark I received on the sheet below.  I didn't do as well on the subsequent exams.  I find I need to use these techniques in clinic on real patients (B2, B3, B4) who need these techniques performed, as it is much harder knowing whether you have been effective on fellow students, and if it is not relevant for me, my brain struggles to remember the technique.  Recently however, I was able to use an MET technique on a patient that clearly resonated with me; I had not had time to practise it but I had managed to visualise it when we learned it and I used it successfully.  It is has taken a long time for me for all the permutations of anatomy to be utilised in a practical way; I am finally beginning to be able to use techniques and occasionally improvise when I fully understand how the muscle's actions work.  We were taught anatomy in a very dry fashion over the first two years of the course, which I think did not really go in to my brain very well, so I have had to find ways to understand the anatomy and make it come to life in a 3D.  By doing more anatomy/prosection days (B2, B3, B4), like the one I went to in January is definitely the way forward for me.  Each time I do this, a little more sticks and I build on a firm base (see below).  I have also booked two more of these courses because it had such a profound effect on me (and I don't usually like getting up at 6 am on a saturday morning).

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I have recognised the need for empathy at the highest level here (C1, C2, C3, C4, C5, C6, C7, C8, D1, D4, D6, D7, D14, D17).  There is an issue of sensitivity here that needs to be met at both clinical and ethical levels.  I can help, through talking to the patient's mother (and treatment too, if she is open to that) and I can help remove the restrictions in the baby that are causing the problems; however with this patient the problem lies deeper within the mother and what happened before this baby was conceived, and how her body responded to the stressful event and the new, exciting but still stressful event afterwards.  These issues need to be reconciled with the mother in order to help her baby; (A1, A2, A3, A4, A5, A6, B1, B2, B3, B4) however I think we can do a lot to reduce the problems that the mother is dealing with and allow her to come to terms with her grief and possible guilt at becoming pregnant so quickly.  (A1, A2, A3, A4, A5, A6, B1, B2, B3, B4, C1, C2, C3, C4, C5, C6, C7, C8, D1, D2, D3, D6, D8, D14, D17)

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A lot of the 'D' Osteopathic Practice Standards were difficult to write about initially; I wasn't sure how many of them I would meet through patients; so I decided that it would be easier to write about these as individual pieces; as I wrote about them I was able to see how I had actually met these standards, without actually realising I had met them!  It was good to reflect on the process of how I had met these standards, almost incidentally, by being who I am, by being polite, caring and aware of issues such as health and safety, as well as the need to clean my hands between patients.
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23 august 2018 learning more about Multiple Sclerosis and how relapses affect the patient

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23 august 2018 learning more about Multiple Sclerosis and how relapses affect the patient

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Increasing my learning; follow up from the previous post (B2, B3, B4)

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In relapsing remitting MS, people have distinct attacks of symptoms which then fade away either partially or completely. Around 85% of people with MS are diagnosed with this type.

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https://www.medscape.com/viewarticle/760191

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There are many different medications on the market, however one that is frequently in use for many patients is omeprazole.  I have learned more about this medication so that I am better informed.  It is not a very nice drug: it inhibits gastric acids and means that calcium, magnesium and vitamin B12 are not absorbed by the body (A3, A5, A6, B2, B3, B4, C3, C5, C7, D1). Not good.  However for many of these patients it gives them relief.  It is important though to understand the mechanism of these medications so that I can help my patients make an informed choice.  However, omeprazole  has also been shown to offer protection to the small intestine against gastric and duodenal ulcers in those people taking high quantities of NSAIDs (A3, A5, B2, B3, B4, C3, C5, C7, D1) It may also protect the small intestine from damage induced by the use of indomethacin. This may work by the anti-inflammatory and anti-oxidant properties of this medication. It may be that this is a benefit that can be utilised for people with iintestinal inflammatory diseases (A3, A5, A6, B2, B3, B4, C3, C5, C7, C8).Omeprazole works by reducing the production of acid by the stomach; by irreversibly blocking an enzyme called H+/K+ ATPase which controls acid production. This enzyme is also known as the proton pump and is found in the parietal cells of the stomach wall.

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Clinic 23 may 2018
Reflective practice  - realised GOT is as effective as BMT for my patient today. I need to revise PMR.

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Ulnar Nerve neuropathy/T1 radiculopathy - what is the difference?

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Ulnar Nerve neuropathy/T1 radiculopathy - what is the difference?

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20 October 2018
I had a patient who told me he had pain which was in the ulnar border area; I thought I should revise the difference between an ulnar nerve neuropathy and a T1 radiculopathy to make it easier to diagnose this.  In fact, I had already had some feedback in year 3 that I should revise the ulnar nerve, so I was a little late doing this, however this patient and this revision helped my knoweldge.
As you will see below, I did quite a lot to increase my knowledge.

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Cranial techniques
I love using these techniques.  I am good at them but I need to understand them better, so I can explain to my patient how they work and they can give me consent for the treatment.

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Cranial techniques
I love using these techniques.  I am good at them but I need to understand them better, so I can explain to my patient how they work and they can give me consent for the treatment.

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20 October 2018

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symptoms of lower back problems and spine conditions

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Learn about the function of ulnar nerve roots, along with the conditions and treatment options associated with this branch of the medial cord.

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The C7-T1 spinal segment, sometimes referred to as the cervicothoracic junction, is located at the very bottom of the neck.

More specifically, this is where the neck ( cervical spine) connects with the upper back ( thoracic spine).

See Spinal Anatomy and Back Pain

This spinal segment is unique because it is the point of transition from the highly flexible neck to the nearly completely inflexible upper back. It is also the point where the lordosis, or backward curvature of the cervical spine, reverses into kyphosis, or forward curvature, of the upper back.

Watch Cervical Spine Anatomy Video

C8 Radiculopathy

The C8 nerve root exits the spinal cord at the C7-T1 spinal segment. If the C8 nerve becomes compressed or irritated for any reason, then C8 radiculopathy will occur. Symptoms can include pain, weakness, numbness, or tingling radiating down the lower shoulder and back of the arm and forearm, going into the pinky and ring finger. Cervical radiculopathy is usually only on one side of the body, but if both C8 nerve roots are involved, then it can be felt on both sides.

Watch Cervical Radiculopathy Interactive Video

Compared to the spinal segments directly above it at C6-C7 and C5-C6, radiculopathy is less common at the C7-T1 level. One reason is because at the cervical spinal levels of C5-C6 and C6-C7, the disc is located at about the same height as the nerve roots; but at C7-T1, the C8 nerve roots are located higher than the disc. ¹ So there is less chance for the disc to compress the C8 nerve root.

See Diagnosing Cervical Radiculopathy

Common Causes of C7-T1 pain

Some of the conditions that can cause symptoms at the C7-T1 level include the following:

C7-T1 degenerative disc disease
If the disc between the C7 and T1 vertebrae degenerates enough it can become a source of pain. The pain can be from the disc itself or perhaps from irritation and/or inflammation associated from the collapsing disc.

See Cervical Degenerative Disc Disease

C7-T1 disc herniation
While disc herniation at the C7-T1 level is not that common, it is possible for the disc to herniate if a tear in its fibrous outer layer occurs, allowing a portion of the gelatinous inner layer to leak out of the disc. This inner substance of the disc contains proteins that cause inflammation when they come into contact with nerves and soft tissues.

See Cervical Herniated Disc Symptoms and Treatment Options

C7-T1 osteoarthritis
With less bending and fewer joints than the cervical spinal segments directly above it, the C7-T1 spinal segment is less likely to be affected by osteoarthritis. However, it can still happen through natural wear and tear of the facet joints or be accelerated by an injury.

See Cervical Osteoarthritis (Neck Arthritis)

C7-T1 spinal stenosis with myelopathy
Spinal stenosis at this level is possible if the spinal canal narrows. If this narrowing causes the spinal cord to become affected, then myelopathy and its neurological symptoms may be diagnosed.

See Cervical Stenosis with Myelopathy

Myelopathy indicates that the spinal cord's health is in jeopardy. Without treatment, a permanent spinal cord injury could develop. If a spinal cord injury happens at the C7-T1 spinal segment, then some or most of the ability to feel sensations beneath the neck could be lost; and it is possible for full or partial paralysis of the legs, core muscles (trunk), and fingers to develop.

See Spinal Stenosis Treatment

C7-T1 foraminal stenosis
The C8 nerve can become compressed at the foramen-a bony hole where the nerve root branches off from the spinal cord and exits the spinal canal-if the foramen narrows enough due to bone overgrowth.

See Treatment for Cervical Stenosis with Myelopathy

Less Common Causes of C7-T1 Pain

Spondylolisthesis
This rare condition is more likely to occur in the lower back than the neck. However, it can still happen at the C7-T1 spinal segment if the C7 vertebra slips forward over the T1 vertebra. Some people are more genetically predisposed to having spondylolisthesis, but it can also happen due to trauma, such as from a sports injury that affects the neck and/or upper back.

See Degenerative Spondylolisthesis

Infection
An infection in a cervical spinal segment is rare. It is also possible for the C7-T1 level to become infected secondary to a lung infection.

See Osteomyelitis, a Spinal Infection

Tumor
A tumor growing at the C7-T1 level is rare, but when it happens, it can be painful and might cause cervical radiculopathy by pressing against the C8 nerve.

See Treatments for Spinal Tumors

Fracture
A broken bone at the C7-T1 level can cause pain and other symptoms, especially if the C8 nerve root becomes irritated and/or if the spinal cord is affected by the fracture.

See Vertebral Fracture Symptoms

C7-T1 Treatment

Most types of pain that originate at the C7-T1 level can be treated with nonsurgical methods. As a general rule, if nonsurgical methods prove to be insufficient after 3 to 6 months and the pain is severe, then surgery can be recommended.

See Treatment for Neck Pain

The C7 and T1 vertebrae have different shapes compared to the cervical vertebrae above it, making this spinal segment more difficult for surgeons to access through the front for the following reasons:

Deeper in the body

Surrounded by more bone

Near critical neurovascular bundles²

As such, the surgical options at C7-T1 tend to be fewer and more complex compared to surgical options typically commonly done higher in the neck, such as an ACDF.

See ACDF Surgery Procedure

References:

1. Cramer GD, Darby SA. The cervical region. Clinical Anatomy of the Spine, Spinal Cord, and ANS. 3rd ed. 2014:151.

2. Scheer JK, Deviren V, Lee SH, Ames C. Posterior cervicothoracic osteotomy. In: Vaccaro A, Eck JC. Surgical Atlas of Spinal Operations. 1st ed. New Dehli, India. Jaypee Brothers Medical Publishers. 2013:211-21.

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All About the C7-T1 Spinal Segment (Cervicothoracic Junction)

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The C7-T1 spinal segment, sometimes referred to as the cervicothoracic junction, is located at the very bottom of the neck. More specifically, this is where the neck ( cervical spine) connects with the upper back ( thoracic spine).

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Ulnar nerve neuropathy

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Ulnar neuropathy is a disorder involving the ulnar nerve. Ulnar neuropathy may be caused by entrapment of the ulnar nerve with resultant numbness and tingling.

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What did I learn?
what is it?
An auto-immune disorder, it affects men and women equally.
I have two patients with it, so I thought really I should know more about the condition.
It can affect any area of the body although different types of psoriasis tend to occur on different areas of the body.
There is a link with coeliac disease; these people tend to have a genetic component with the HLA-B27 marker frequently present.

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Psoriasis is more than just a skin condition, and it can affect people physically and psychologically. Although there is no cure for psoriasis, it is important to remember that it can be managed. With the right treatment and advice, many people live well with psoriasis.

We're committed to producing good quality information, and we've used our experience and best practice to pull together as much information as possible on treating and living with psoriasis and psoriatic arthritis. Please use the links below and on the left to learn more!

It's important to remember that the information on this website is not a replacement for advice from a qualified health professional. Please also remember that posts on the forums and social media can come from a variety of sources and may not always be factually correct. You can learn more about our information by reading our Good Quality Information Policy.

What is psoriasis?

Psoriasis is an immune condition, which causes symptoms on the skin and sometimes the joints.

When a person has psoriasis, their skin replacement process speeds up, taking just a few days to replace skin cells that usually take 21-28 days.

This accumulation of skin cells builds up to form raised 'plaques' on the skin, which can also be flaky, scaly, red on caucasian skin, darker patches on darker skin tones, and itchy.

Psoriasis can occur on any area of the body, including the scalp, hands, feet and genitals, although different types tend to occur on different areas.

Who gets psoriasis?

The current thinking is that psoriasis affects between 2% and 3% of the UK population- up to 1.8 million people - although this is an estimate.

It affects males and females equally.

Psoriasis can occur at any age, although there seem to be two 'peaks'; from the late teens to early thirties, and between the ages of around 50 and 60.

Some people with psoriasis may also get psoriatic arthritis - a type of arthritis associated with the skin condition. However, just having psoriasis doesn't mean you will get psoriatic arthritis, and not everybody who goes on to develop psoriatic arthritis necessarily has psoriasis of the skin, either.

What causes psoriasis?

Recent research has found that the psoriasis-causing changes in the skin begin in the immune system when certain immune cells (T cells) are triggered and become overactive.

The T cells act as if they were fighting an infection or healing a wound, which leads to them producing inflammatory chemicals, again leading to the rapid growth of skin cells causing psoriatic plaques to form. You may therefore hear psoriasis being described as an "auto-immune disease" or "immune-mediated condition". It is not yet clear what initially triggers the immune system to act in this way.

Some people will have a family history of the condition, but others may not. A flare-up of psoriasis can be triggered by a number of factors, such as stress or anxiety, injury to skin, hormonal changes, or certain infections or medications.

How will psoriasis affect me?

Psoriasis is a complicated condition that is very unique to each individual. Everyone has different ways in which they cope with their psoriasis, and the amount of skin affected by psoriasis can differ greatly from person to person.

It is important that both the physical signs of psoriasis (how much of your skin is affected by it) and the psychological aspects of psoriasis (how you cope with the condition) are assessed together, and regularly, so that the most appropriate treatment can be prescribed. The psychological impact is not always related to the clinical severity of psoriasis, so do not worry about telling healthcare professionals how you are feeling.

If you are finding it difficult to cope with your psoriasis, please visit your GP, or get in touch with the Psoriasis Association for information and advice.

If you'd like to speak with others who have psoriasis, and share personal experiences and advice, feel free to register for our forums.

For more information, or for a list of resources used in the production of this information, please contact the Psoriasis Association.

November 2017 (Review Date: March 2019)

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psoriasis cure curable treatment psoriatic arthritis diet topical cream moisturiser uv light sun systemic tablets biologic injections doctor gp dermatologist uk

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Psoriasis & Treatments - Psoriasis Association

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Psoriasis is more than just a skin condition, and it can affect people physically and psychologically. Although there is no cure for psoriasis, it is important to remember that it can be managed. With the right treatment and advice, many people live well with psoriasis.

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How can I best help my patient with spinal stenosis?

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In the medical field, stenosis means the abnormal narrowing of a body channel. When combined with the word spinal, it defines a narrowing of the bone channel occupied by the spinal nerves or the spinal cord.

Some people are born with a congenital form, but most develop spinal stenosis as part of the degenerative cascade. A few do not feel any effects of the narrowing, but as part of the aging process, most people will eventually notice radiating pain, weakness, and/or numbness secondary to the compression of the nerves or spinal cord.

See Radiculopathy, Radiculitis and Radicular Pain

While the narrowing may occur at different parts of the spine, the symptoms of nerve compression are often similar. That is why specialists often will perform testing to determine the cause and location of the narrowing.

Lumbar vs. Cervical Stenosis

The lower back develops lumbar stenosis, while the neck develops cervical stenosis.

Lumbar Spinal Stenosis
In lumbar stenosis, the spinal nerve roots in the lower back become compressed and this can producesymptoms of sciatica-tingling, weakness or numbness that radiates from the low back and into the buttocks and legs-especially with activity.

Lumbar spinal stenosis often mimics symptoms of vascular insufficiency. Both conditions can cause claudication, which means leg pain with walking. If vascular studies identify normal blood flow, and there is confirmation of spinal stenosis on diagnostic testing, the symptoms are then called neurogenic claudication. In the classic description, people with spinal stenosis will describe an onset of leg pain, or weakness with walking, but with relief of symptoms with sitting. Many will also describe increased tolerance to walking when flexed forward, such as when walking while leaning forward on a shopping cart.

While lumbar spinal stenosis most often occurs at the L4-L5 and L3-L4 levels, it can occur any level in the spine. The degenerative cascade may eventually effect most of the vertebral segments of the lumbar spine.

See Lumbar Spinal Stenosis: A Definitive Guide

Cervical Stenosis
Spinal stenosis pain in the neck is called cervical spinal stenosis. This condition means that there is potential compression of the spinal cord. Unfortunately, the spinal cord compression can lead to serious problems such as extreme weakness, or even paralysis. With cervical stenosis, anyone who develops signs of spinal cord compression (myelopathy) may need more invasive treatment, such as surgery.

See Cervical Stenosis with Myelopathy

Thoracic stenosis can also occur, but is less common. The thoracic part of the spine is the middle/upper portion of the spine, and mainly consists of the vertebrae that are attached to the rib cage. This stable and strong part of the spine allows for minimal movement, which is why degenerative conditions such as spinal stenosis are less likely to develop.

Spinal Stenosis and the Aging Spine

Spinal stenosis is related to degeneration in the spine and usually will become significant in the 5th decade of life and extend throughout every subsequent age group. As it is a gradual process and rarely causes immediate symptoms, the subtle changes of spinal stenosis often result in a gradual decrease in physical activity, and a development of a more kyphotic or forward flexed posture.

See All About Thoracic Kyphosis: Forward Curvature of the Upper Back

This gradual accommodation may be evident when looking at a series of oneself in pictures-over the course of several years-after around age 50. It is typical to start stooping forward more and become less active as effects of spinal stenosis increase.

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Learn about the types of spinal stenosis, including lumbar stenosis and cervical stenosis, and associated pain and symptoms.

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Signs and symptoms

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There are a number of potential symptoms of spinal stenosis, and one's specific symptoms are mainly determined by the location and severity of the stenosis in the spine.

See The Major Types of Spinal Stenosis

Common Spinal Stenosis Symptoms

Overall, spinal stenosis symptoms are often characterized as:

Developing slowly over time, or slow onset

Coming and going, as opposed to continuous pain

Occurring during certain activities (such as walking for lumbar stenosis, or biking while holding the head upright) and/or positions (such as standing upright for lumbar stenosis)

Feeling relieved by rest (sitting or lying down) and/or any flexed forward position.

Lumbar Stenosis Symptoms

When stenosis has developed in the lower back (lumbar spine), leg pain with walking may develop.

See Lumbar Spinal Stenosis: A Definitive Guide

Leg pain with walking is medically known as claudication, and it can be caused by either arterial circulatory insufficiency (vascular claudication) or from spinal stenosis (neurogenic or pseudo-claudication). Leg pain from either condition will go away with rest, but with spinal stenosis the patient usually has to sit down for a few minutes to ease the leg and often low back pain, whereas leg pain from vascular claudication will go away if the patient simply stops walking.

For lumbar stenosis, flexing forward or sitting will open up the spinal canal by stretching the ligamentum flavum and will relieve the leg pain and other symptoms, but the symptoms will recur if the patient gets back into an upright posture. Numbness and tingling can accompany the pain, but true weakness is a rare symptom of spinal stenosis.

See Leg Pain and Numbness: What Might These Symptoms Mean?

Spinal Stenosis Diagnosis

Diagnostic imaging studies for patients with any type of spinal stenosis include either an MRI scan or a CT scan with myelogram (using an X-ray dye in the spinal sac fluid), and sometimes both. Plain CT scans can better identify bony causes of spinal stenosis, but cannot give the same detail for soft tissue causes of stenosis such as disc bulges, disc herniations, and ligament hypertrophy. Due to this changing compression, spinal stenosis symptoms vary from time to time and the physical examination generally will not show any neurological deficits or motor weakness. Certain activities and body position may trigger the symptoms.

In some medical centers, upright MRIs, flexion extension MRIs, and spine load-bearing MRIs have been used to identify the dynamic changes on the spine, and the canal dimensions. The efficacy of these tests are still being studied, but there may be additional information provided by such tests.

See MRI Scan of the Spine

Cervical foraminal stenosis can be pinpointed not only by the CT and MRI scans, but by injecting the suspicious nerve with a small volume of local anesthetic. This procedure is called a selective nerve root block.

See Selective Nerve Root Blocks (SNRB) and Facet Joint Injections

After the injection a remission of the patient's symptoms along with true temporary weakness of the limb is clinically diagnostic and can help the surgeon determine the source of symptoms, and potentially reduce the size and complexity of the surgery.

Rarely, a surgeon will use electrodiagnostic studies to determine the type of surgery. Those studies can be helpful in trying to determine if a symptom is caused by a neuropathy, rather than a radiculopathy. But few surgeons are confident of the specificity provided by these studies. The results will not help plan a surgical procedure, but may help decide to cancel one-for example, if it is a global neuropathic problem, surgery may not be beneficial.

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Spinal stenosis symptoms, including symptoms of lumbar spinal stenosis, and diagnosis with a MRI scan or CT scan with myelogram.

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Leg pain can range from a mild nuisance that comes and goes, to debilitating pain that makes it difficult to sleep, walk, or engage in simple everyday activities.

Leg pain and numbness can be experienced in many forms-some patients describe the pain as aching, searing, throbbing, or burning, or like standing in a bucket of ice water.

See Accurately Diagnosing Leg Pain

The pain can also be accompanied by neurological symptoms, such as a pins-and-needles sensation, numbness, or weakness. The weakness may be persistent, or it may come on suddenly or unpredictably, often described as the leg "giving out."

Leg pain may be caused by a problem in the leg, but often the root cause of the problem starts in the lower back, where the sciatic nerve originates, and then travels along the path of the nerve (called sciatica).

See What You Need to Know About Sciatica

Or it could start at the L3-L4 level, where a nerve branches off from the lumbar spine and travels through the front of the thigh.

The medical term for leg pain that is caused by irritation of a lumbar nerve root is lumbar radiculopathy.

Read about Lumbar Radiculopathy

Because the lumbar nerves travel through various parts of the leg and foot, a diagnosis of anyone with leg pain, foot pain, and/or leg or ankle or foot weakness or numbness, should include an examination of the lower back.

See Lumbar Spine Anatomy and Pain

Leg Pain Symptoms and Descriptions

Not all leg pain derived from low back problems presents the same way. Some typical descriptions of leg pain and accompanying symptoms include:

Leg numbness or tingling. Anyone who has had a leg or foot "fall asleep" and then gradually return to normal can imagine what numbness in a leg would feel like. Not being able to feel pressure, or hot or cold, is unnerving. Unlike the short-lived numbness of an asleep limb, numbness coming from a low back problem can be nearly continuous and can severely affect a person's quality of life. For example, it can be difficult or almost impossible to walk or drive a car if one's leg or foot is numb. Typical symptoms can range from a slight tingling sensation to complete numbness down the leg and into the foot.

For most leg pain symptoms, an accurate diagnosis of the underlying cause of problems is an important first step in getting effective treatment.

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Leg Pain and Numbness: What Might These Symptoms Mean?

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Leg pain and foot pain is often caused by a condition in the lower back. Learn about the various leg pain symptoms and what they may mean.

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Video: Is Spinal Stenosis Causing My Leg Pain?

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Dr. Stephen Hochsculer speaks about Spinal Stenosis. He explains the spinal canal, how one can get Spondylothesis, and the treatment options.

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Laminectomy back surgery in the lumbar spine helps relieve spinal stenosis related pain. Animated video explains the surgical procedure and how it works.

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How I HEALED from STENOSIS - Naturally! - part 2

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How I have achieved these standards.

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D4:  make sure your beliefs and values do not prejudice your patients' care

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D4:  make sure your beliefs and values do not prejudice your patients' care

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I love using 'cranial' techniques: I am good at this and it helps improve my patients health.  However I have realised it is not always easy to explain to my patients what I am doing or why I am doing it (C7, D4).  This article has helped increase my knowledge of BLT and BMT.  It is essential so that I can share the decision making process with them and enable them to give me full consent.

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I need to improve my knowledge of medications.

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Statins are a group of medicines that can help lower the level of low-density lipoprotein (LDL) cholesterol in the blood.
LDL cholesterol is often referred to as "bad cholesterol", and statins reduce the production of it inside the liver.

Why have I been offered statins?

Having a high level of LDL cholesterol is potentially dangerous, as it can lead to a hardening and narrowing of the arteries (atherosclerosis) and cardiovascular disease (CVD).

CVD is a general term that describes a disease of the heart or blood vessels. It's the most common cause of death in the UK.

The main types of CVD are:

coronary heart disease - when the blood supply to the heart becomes restricted

angina - chest pain caused by reduced blood flow to the heart muscles

heart attacks - when the supply of blood to the heart is suddenly blocked

stroke - when the supply of blood to the brain becomes blocked

A doctor may recommend taking statins if either:

you have been diagnosed with a form of CVD

your personal and family medical history suggests you're likely to develop CVD at some point over the next 10 years and lifestyle measures have not reduced this risk

Find out more about when statins may be recommended.

Taking statins

Statins come as tablets that are taken once a day.

For some types of statin it does not matter what time of day you take it, as long as you stick to the same time.

Some types of statin should be taken in the evening.

Check with your doctor whether there's a particular time of day you should take your statin.

You usually have to continue taking statins for life because if you stop taking them, your cholesterol will return to a high level within a few weeks.

If you forget to take your dose, do not take an extra one to make up for it. Just take your next dose as usual the following day.

If you accidentally take too many statin tablets (more than your usual daily dose), contact a doctor or pharmacist for advice or call NHS 111.

Cautions and interactions

Statins can sometimes interact with other medicines, increasing the risk of unpleasant side effects, such as muscle damage.

Some types of statin can also interact with grapefruit juice.

It's very important to read the information leaflet that comes with your medicine to check if there are any interactions you should be aware of.

If in doubt, contact a GP or pharmacist for advice.

Find out more things to consider when taking statins.

Side effects of statins

Many people who take statins experience no or very few side effects.

Others experience some troublesome, but usually minor, side effects, such as diarrhoea, a headache or feeling sick.

Your doctor should discuss the risks and benefits of taking statins if they're offered to you.

The risks of any side effects also have to be balanced against the benefits of preventing serious problems.

A review of scientific studies into the effectiveness of statins found around 1 in every 50 people who take the medicine for 5 years will avoid a serious event, such as a heart attack or stroke, as a result.

Find out more about the side effects of statins.

Alternatives to statins

If you're at risk of developing CVD in the near future, your doctor will usually recommend lifestyle changes to reduce this risk before they suggest that you take statins.

Lifestyle changes that can reduce your cholesterol level and CVD risk include:

Statins may be recommended if these measures do not help.

Read more about treating high cholesterol and preventing CVD.

Types of statin

There are 5 types of statin available on prescription in the UK:

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Statins are a group of medicines that can help lower the level of low-density lipoprotein (LDL) cholesterol in the blood. LDL cholesterol is often referred to as "bad cholesterol", and statins reduce the production of it inside the liver.

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My patient came to the Clinic today after being let down by the Osteopath at the YMCA. Networking does work, a friend of her's recommended she come to the Clinic, when the YMCA muddled up her time, she phoned the Clinic and made an appointment!

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Find out about vitiligo, which is a long-term condition that causes pale, white patches to develop on the skin.

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What happened? VITILIGO, THYROID DISEASE AND AUTOIMMUNITY W. J. CUNLIFFER. HALLD. J. NEWELLC. J. STEVENSONFirst published: March 1968https://doi.org/10.1111/j.1365-2133.1968.tb12282.xCited by: 165ePDFPDFToolsShareAbstractSUMMARY. There is a significant association between vitiligo and thyroid disease. Thyroglobulin antibodies are significantly associated with vitiligo, whether patients with psoriasis or a general practice population are taken as controls. Similarly complement‐fixing antibodies are significantly associated with vitiligo as compared with psoriasis. There is no evidence that thyroid autoimmunity is associated positively or negatively with psoriasis. Alopecia areata, pernicious anaemia and diabetes mellitus are also significantly associated with vitiligo.

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What happened? VITILIGO, THYROID DISEASE AND AUTOIMMUNITY W. J. CUNLIFFER. HALLD. J. NEWELLC. J. STEVENSONFirst published: March 1968https://doi.org/10.1111/j.1365-2133.1968.tb12282.xCited by: 165ePDFPDFToolsShareAbstractSUMMARY. There is a significant association between vitiligo and thyroid disease. Thyroglobulin antibodies are significantly associated with vitiligo, whether patients with psoriasis or a general practice population are taken as controls. Similarly complement‐fixing antibodies are significantly associated with vitiligo as compared with psoriasis. There is no evidence that thyroid autoimmunity is associated positively or negatively with psoriasis. Alopecia areata, pernicious anaemia and diabetes mellitus are also significantly associated with vitiligo.

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I had a patient who had various auto immune disorders, including thyroid dysfunction.
I looked up the significance of this and realised that there is a connection between thyroid dysfunction and vitiligo. This has increased my understanding of auto-immune disease.

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Migraine - with and without aura

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This was discussed in the team room and I decided to investigate this further (B2, B3, B4, C7)
Bladder Pain syndrome
Chronic bladder health issue
- pain and pressure in the bladder area
symptoms:
lasting more than six weeks - without having an infection or other clear causes
Age: 30s and 40s
Women > men
Conventional treatment:
NSAIDs and naproxen
tricyclic antidepressants eg amitriptyline or imipramine
antihistamines eg loratadine
Potassium sensitivity test may help to diagnose interstitial cystitis.

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In this article

Polymyalgia rheumatica is an inflammatory condition that causes a particular pattern of joint pain and stiffness, most commonly in older people. It is a rheumatic disorder closely associated, and often co-existing, with giant cell arteritis. Diagnosis is based on the patient's clinical features, supported by laboratory investigations. Before making a diagnosis, other conditions which can mimic polymyalgia rheumatica should be ruled out, and most importantly, the patient should be assessed for co-existing giant cell arteritis. Treatment of polymyalgia rheumatica, with long-term oral prednisone, can usually be managed in primary care, but referral to a Rheumatologist may be necessary if the diagnosis is unclear, the response to treatment is poor or multiple relapses of symptoms occur during tapering.

What is polymyalgia rheumatica?

Polymyalgia rheumatica is an inflammatory rheumatological syndrome that causes pain and stiffness, most commonly in the neck, shoulders and pelvic girdle. The pain and stiffness is worse in the morning, usually lasts for one hour or more and may be accompanied by systemic features, such as fever, fatigue and anorexia. 1 The onset of symptoms is typically between two weeks and two months. 2

The incidence of polymyalgia rheumatica increases with age, with an average age of onset of approximately 70 years, and it rarely occurs in people aged under 50 years. 3 The incidence of polymyalgia rheumatica is highest in people of Scandinavian or Northern-European descent, although it does occur in people of other ethnicities. 3 Polymyalgia rheumatica is twice as common in females. 3 In total, the yearly incidence is approximately 50 per 100 000 people aged over 50 years. 4

It is not known what causes polymyalgia rheumatica. It is closely associated with giant cell arteritis, although it is two to three times more common. 2 Like giant cell arteritis, both genetic and external factors, e.g. infection, are thought to be involved in the development of the condition. 3

Polymyalgia rheumatica is managed with corticosteroids and significant remission of symptoms can be expected within one week of starting treatment. 5 The prognosis is usually good and complications, such as recurrent relapse of symptoms, are limited. 3

Never trust a diagnosis of polymyalgia rheumatica

As polymyalgia rheumatica has a non-specific clinical presentation and few significant sequelae, it should be diagnosed with caution. Ruling out other illnesses, such as cancers or insidious-onset rheumatoid arthritis, is more important than immediately treating polymyalgia rheumatica, if it is present. Unlike giant cell arteritis, a delay in treatment will not significantly endanger a patient. Conversely, long-term corticosteroid treatment can have significant adverse effects and a daily treatment course of up to three years will be a burden for many people. In addition, an initial or partial response to corticosteroids may be seen in people with other conditions who present with similar features to polymyalgia rheumatica, such as rheumatoid arthritis, and this may provide false reassurance that the correct diagnosis has been identified. Therefore, even if a patient presents with clinical features typical of polymyalgia rheumatica, and a working diagnosis is made, they should be regularly reviewed and other possible causes always considered, particularly if the patient does not respond to treatment.

For further information, see: " Giant cell arteritis".

Making a diagnosis

The British Society for Rheumatology has developed a set of inclusion and exclusion criteria for diagnosing polymyalgia rheumatica. 6 These criteria were derived by consensus and represent a clinically typical patient with polymyalgia rheumatica. They are most useful for "ruling in", i.e. a patient who meets the criteria is likely to have polymyalgia rheumatica, rather than "ruling out", as people with polymyalgia rheumatica can present atypically, such as with a shorter duration of symptoms or found to have a normal acute phase response.

The core inclusion criteria are: 6

Age > 50 years

Symptom duration > two weeks

Bilateral shoulder or pelvic girdle aching, or both

Morning stiffness duration of > 45 minutes

Evidence of an acute-phase response, e.g. raised CRP

The core exclusion diagnoses are: 6

Patient presentation, history and examination

Shoulder, neck, hip and pelvic pain

Shoulder pain occurs in 70 - 95% of people with polymyalgia rheumatica. 2 Between 50 - 70% of people report hip and neck pain. 2 Upper arm pain is also common. Pain is usually bilateral and symmetrical, although it may be worse on one side early in the course of the condition. 3 Pain will usually worsen with movement of the affected area. Pain may radiate to the elbows and knees. 3 There may be tenderness on examination, most commonly in the upper arms, neck and shoulders, usually related to synovial or bursal inflammation. Muscle weakness is not a feature of polymyalgia rheumatica, although this may be difficult to assess due to muscle pain. 5

Stiffness

Marked morning stiffness that persists for at least 45 minutes is typical for people with polymyalgia rheumatica. 6 The patient may describe difficulties with daily activities, such as brushing their hair or getting out of bed. In some patients the stiffness will be so severe that rising from a chair or turning over in bed are difficult. Asking the patient about the severity of stiffness in the morning compared to the evening may be helpful. Stiffness and pain that lessens over the course of the day can be important in differentiating polymyalgia rheumatica from other forms of degenerative arthritis, which usually cause pain or stiffness that is worse with activity and worse later in the day. 1

Systemic symptoms and signs

Systemic features may be present in approximately one-third of patients and include low grade fever, malaise, anorexia and weight loss. 2 A brief general examination, including assessment of temperature, pulse and blood pressure, is recommended.

Peripheral symptoms

Symptoms, such as pain or stiffness in the joints of the hands and feet, are present in approximately half of people with polymyalgia rheumatica, however, peripheral symptoms are also common in other, similar conditions, such as rheumatoid arthritis and other inflammatory arthritides. 2 A predominance of peripheral symptoms may suggest an alternative diagnosis, such as rheumatoid arthritis. 3 It is important to also examine the hands, feet, knees and elbows for signs of joint inflammation.

Giant cell arteritis symptoms

Always specifically enquire about symptoms that may suggest giant cell arteritis, such as unilateral temporal headaches, scalp tenderness, jaw claudication or visual symptoms. 3

For further information, see: " Giant cell arteritis".

Differential diagnosis

The differential diagnosis of polymyalgia rheumatica is critically important, particularly for atypical cases, or where inflammatory markers are normal. Incorrectly diagnosing polymyalgia rheumatica and missing a diagnosis such as cancer or an occult infection can have significant consequences. Conversely, a patient with polymyalgia rheumatica who remains untreated in the short term is unlikely to have any significant adverse effects. The aim should be to rigorously exclude all other possibilities rather than quickly diagnosing polymyalgia rheumatica. Atypical clinical features such as age < 60 years, chronic onset (longer than two months), lack of shoulder involvement, muscle weakness, peripheral joint disease, predominance of pain with little or no stiffness, prominent systemic features, a very high or normal CRP (see " Laboratory investigations") or lack of response to a trial dose of prednisone (see " Treatment of polymyalgia rheumatica") should lead to consideration of alternative diagnoses and consultation with a Rheumatologist where necessary.

Conditions that should be considered include: 3, 6

Giant cell arteritis

Malignancy

Rheumatoid arthritis and other arthritides

Endocrine and iatrogenic causes of proximal myopathy, e.g. hypothyroidism, Cushing's disease, statin-induced myopathy/myalgia

Osteoarthritis and other degenerative musculoskeletal conditions, e.g. rotator cuff tendinopathy

Systematic lupus erythematous or polymyositis

Fibromyalgia and localised causes of pain

Occult infection, e.g. sub-acute bacterial endocarditis

Laboratory investigations

If the patient's presentation suggests polymyalgia rheumatica is likely, the following tests should be requested: 4-6

C-reactive protein (CRP)

Full blood count (FBC)

Liver function tests (LFTs)

Creatinine and electrolytes - as a baseline prior to initiation of corticosteroid treatment

An elevated CRP level in a patient with symptoms of polymyalgia rheumatica should increase suspicion of the condition. 6 However, a normal acute phase response does not rule out polymyalgia rheumatica. ESR is sometimes recommended in the literature, however, CRP alone is likely to be sufficient to aid the diagnosis of polymyalgia rheumatica in most people. In addition, some laboratories will no longer accept requests for ESR outside of a limited range of conditions. If the initial CRP is normal, and the patient's symptoms strongly suggest polymyalgia rheumatica, it may be appropriate to then request an ESR at follow-up.

Most patients with polymyalgia rheumatica have mild-to-moderate anaemia, and may have elevated white blood cell and platelet levels. 2 Approximately one-third of patients will have mildly abnormal liver function tests, particularly alkaline phosphatase. 2

Depending on the patients symptoms and signs, additional tests may need to be added to rule out other potential diagnoses, including: 6

Thyroid stimulating hormone (TSH)

Rheumatoid factor and, potentially, anticyclic citrullinated peptide (anti-CCP) antibodies

Serum protein electrophoresis (consider serum free light chain assay if electrophoresis is negative)

Creatine kinase

Antinuclear antibodies

Imaging is not essential for diagnosis

If ultrasound is accessible, assessment of the shoulder and hip joints can be considered. 6 Bursitis and synovitis are common manifestations of polymyalgia rheumatica. 2 Plain x-rays of affected joints will usually be normal and therefore are not required for investigating polymyalgia rheumatica.

Additional investigations such as CT scanning, and MRI imaging may be used in a secondary care setting to help identify bursitis, synovitis or tenosynovitis in the shoulders and hips in atypical cases, and for ruling out other potential diagnoses.

Distinguishing polymyalgia rheumatica from rheumatoid arthritis

Rheumatoid arthritis can be a challenging condition to differentiate from polymyalgia rheumatica, particularly in patients who are subsequently found to have seronegative or late-onset rheumatoid arthritis. 3 Although the initial clinical presentation can be very similar with many overlapping symptoms and signs, the following features may help distinguish between the two conditions:

Polymyalgia rheumatica is rare in people aged < 50 years, therefore rheumatoid arthritis is a much more likely diagnosis in this age group5

The onset of symptoms tends to be more gradual in people with rheumatoid arthritis

Typically, symptoms of pain and swelling in the smaller distal joints are more common in people with rheumatoid arthritis, however, approximately half of people with polymyalgia rheumatica will also have involvement of the peripheral joints3

Characteristically the wrist and metacarpophalangeal (MCP) joints are affected in people with rheumatoid arthritis, therefore a patient presenting with myalgia and clinical evidence of symmetric synovitis in the wrists or MCP joints is more likely to have a diagnosis of rheumatoid arthritis than polymyalgia rheumatica3

A family history may increase the individual risk of rheumatoid arthritis, and should be considered7

If the clinical diagnosis remains uncertain:

Rheumatoid factor should be requested, however, a negative test does not rule out the condition as some patients will have seronegative rheumatoid arthritis. If there is still doubt about the diagnosis, anti-CCP antibodies may be useful.2

X-rays of affected joints may show erosive changes consistent with rheumatoid arthritis

A trial of treatment with corticosteroids can be considered in patients who are seronegative for rheumatoid factor and have symptoms and signs that could be indicative of either condition. In a patient with polymyalgia rheumatica there is likely to be a rapid, strong clinical response to low dose prednisone (15 mg). If the patient has rheumatoid arthritis, the response to low dose prednisone is likely to be less pronounced. 3,8 In some patients, clinical features more characteristic of rheumatoid arthritis may evolve during the trial of corticosteroid.

Treatment of polymyalgia rheumatica

Corticosteroids are the first-line treatment for polymyalgia rheumatica. Corticosteroid treatment is predominantly for symptom control, and there is no clear evidence that it will alter the natural history of the condition, which is largely self-limiting.

Once all other differential diagnoses have been considered, the patient should be assessed for response to an initial dose of prednisone, 15 mg, daily. 6 The dose should be taken in the morning, with food.

If the patient reports a significant improvement in their symptoms within one week, this is consistent with polymyalgia rheumatica, and treatment can continue. 6 Alternative diagnoses should be considered if there is a minimal response to corticosteroid treatment.

The patient's acute phase response, measured with CRP, should normalise within four weeks. 6

The British Society for Rheumatology guidelines suggests the following method for titrating the dose of prednisone in people with polymyalgia rheumatica: 6

Initial dose - 15 mg, once daily, for three weeks, followed by;

12.5 mg, once daily, for three weeks, followed by;

10 mg, once daily, for four to six weeks, followed by;

A reduction of 1 mg from the daily dose, every four to eight weeks

In practice, Rheumatologists may use a faster tapering regimen to lessen exposure to prednisone, such as reducing the dose every two weeks, down to 10 mg, followed by reductions of 1 mg per month, depending on the patient's symptoms. If the patient is at higher risk of adverse effects from long-term steroid use, e.g. is elderly or has co-morbidities, discuss an appropriate dosing regimen with a Rheumatologist.

If symptoms of polymyalgia rheumatica reoccur during the dose tapering period, return the patient to their previous steroid dose and then re-start the taper again from that point. The low dose "tail" of the taper will need to be very gradual in some people to prevent symptom recurrence. Some patients will require treatment with low-dose corticosteroids for two to three years due to recurrent relapses.

Vitamin D supplements should be prescribed alongside long-term corticosteroid treatment for all people with polymyalgia rheumatica. Adequate dietary calcium, or supplementation if this is not possible, is also necessary.

Bisphosphonates should be considered in patients with a previous history of fragility fractures or reduced bone-mineral density. 6

A proton pump inhibitor (PPI), such as omeprazole may be considered for people who experience adverse gastrointestinal affects when taking prednisone. 6

For further information, see " Practical consideration when prescribing long-term corticosteroids".

Follow-up of people with polymyalgia rheumatica

Early follow-up to assess the response to treatment is recommended. A follow-up consultation should be scheduled within a few days after starting corticosteroid treatment, and then further follow up appointments scheduled one, two, three and six weeks later, where possible. Follow-up should then occur once every three months for the duration of corticosteroid treatment.

A history and clinical examination including an assessment for symptoms and signs of giant cell arteritis, such as scalp tenderness, temporal artery tenderness and new-onset or new type of headache, should be included in each follow-up. If symptoms of giant cell arteritis arise, the patient should be presumed to have the condition, and referred to secondary care for temporal artery biopsy. 6 Also assess for symptoms and signs of corticosteroid adverse effects (see: " Practical considerations when prescribing long-term corticosteroids " for further information).

Clinical signs and symptoms are the primary marker for relapse, with laboratory tests providing supporting information only. 1 CRP, FBC, creatinine, electrolytes and HbA 1ctests* (due to the increased risk of diabetes in people taking long-term steroids) are recommended at each follow-up consultation, 6 however, in practice, not all tests would be necessary in each follow up appointment and this is based on clinical judgement.

Relapses of polymyalgia rheumatica symptoms should be treated with a return to the higher, previous dose of prednisone. 6 After two relapses, consideration should be given to a trial of disease-modifying anti-rheumatic drugs (DMARDs), usually methotrexate. 6 This will require consultation with a Rheumatologist, and if a DMARD is prescribed, regular monitoring is necessary. The dosing and monitoring regimen should be decided upon in consultation with the Rheumatologist. Methotrexate is usually continued until the corticosteroids can be tapered without the recurrence of polymyalgia rheumatica symptoms. 4 Once the steroids have been successfully tapered, methotrexate can usually be tapered over approximately three months. 4

* A fasting glucose test should be used for monitoring in the first two months of steroid treatment, as serum glucose will rise too rapidly to be accurately captured by HbA 1c. After two months, an HbA 1c test can be used.

Practical considerations when prescribing long-term corticosteroids

Corticosteroids are associated with significant adverse effects and they must be slowly tapered rather than stopped abruptly. The lowest effective dose should be used, then tapered and stopped as soon as possible.

The following practice points should be considered whenever a patient is prescribed corticosteroids long-term: 9

The patient's co-morbidities and risk factors for adverse effects should be evaluated and managed where indicated, these include; hypertension, diabetes, peptic ulcer, recent fractures, cataract/glaucoma, chronic infection, dyslipidaemia and concurrent NSAID use

During the course of treatment, monitor body weight and blood pressure, assess for peripheral oedema and heart failure and test serum lipids, HbA1c (or fasting glucose in the first two months) depending on the individual patient's risk of adverse effects, dose and duration

If the patient's dose is ≥7.5 mg, daily, for more than three months, vitamin D supplementation is necessary, along with adequate dietary calcium

Bisphosphonates should be prescribed to patients with risk-factors for osteoporosis

Patients treated with corticosteroids and NSAIDS should be given appropriate gastro-protective medicines, usually a proton pump inhibitor

Patients taking corticosteroid treatment for longer than one month, who need to undergo surgery, will require perioperative management with adequate glucocorticoid replacement to overcome potential adrenal insufficiency

Tapering the dose

Tapering must be done carefully to avoid relapses of the condition and potential adrenal deficiency resulting from hypothalamic-pituitary-adrenal axis (HPA) suppression. Higher doses of corticosteroid, e.g. 20 mg daily, for more than three weeks, or bedtime dosing increase the likelihood of HPA axis suppression. Higher doses also increase the likelihood of adverse affects. The taper is usually started as soon as symptoms are under control. The dose is reduced by 10% every two to four weeks depending on the severity of symptoms, response to prednisone and the starting dose. The individual condition being treated will alter the length of the taper, e.g. in a person with polymyalgia rheumatica, the course of treatment is usually two to three years, with a gradual taper period. The dose of prednisone should be titrated against the patient's symptoms, not their acute phase response, i.e. the dose may not need to be increased when the CRP rises if the patient remains asymptomatic.

The adverse effects of corticosteroid treatment

Adverse effects of corticosteroids include: 10

Skin changes and disorders, e.g. thinning and bruising, striae, acne, alopecia and hirsuitism

Body composition changes, e.g. weight gain, Cushingoid features

Ocular disorders, e.g. glaucoma and cataracts

Cardiovascular disease

Gastrointestinal disorders, e.g. dyspepsia, oesophagitis, gastritis, ulcers, bleeding

Osteoporosis

Central nervous system changes, e.g. mood changes, restlessness, depression, psychosis

Diabetes

Renal changes, e.g. hypertension and fluid retention

Older age, higher cumulative doses of corticosteroids and female sex increase the risk of adverse effects occurring. 11

Preventing the adverse effects of corticosteroids

Vitamin D supplements should be prescribed alongside long-term corticosteroid treatment, in patients taking doses of ≥7.5 mg, daily, for more than three months. 9 Colecalciferol* 1.25 mg, once monthly, is recommended for vitamin D supplementation. 10 Patients do not need their vitamin D levels to be tested, but if they have been, and severe deficiency has been detected, a loading dose of one 1.25 mg tablet, daily for ten days is recommended. 10 Calcitriol, 500 - 750 nanograms, daily, can be used instead of colecalciferol for patients with severe renal impairment. 10

* Recommended International Non-proprietary Names (RINN or INN) spelling

Calcium supplementation is also recommended, but there have been concerns that calcium supplementation may increase cardiovascular risk, particularly in older people. 12, 13 General dietary advice may be more appropriate for most people, and supplementation reserved for people in whom dietary calcium intake alone is insufficient. If calcium supplementation is required, oral calcium carbonate 1.5 g, daily, can be considered. 10

Ideally a bone-mineral density (BMD) scan of the lumbar spine and hip should be requested for patients when starting long-term corticosteroids, however, this depends on the availability and funding of the local service, e.g. some services require that patients have been taking corticosteroid treatment for three months before a scan is prioritised. 2

Bisphosphonates should be considered in patients with a previous history of fragility fractures or reduced bone-mineral density. 6 Alendronate or zoledronic acid are recommended for most people who require a bisphosphonate for corticosteroid-related osteoporosis prevention, based on patient preference and the expected length of corticosteroid treatment.

Alendronate, 70 mg, once weekly, should be taken first thing in the morning, on an empty stomach, with a full glass of water to ensure adequate absorption. 10 The patient should then refrain from eating or taking other medicines and remain upright (i.e. sitting or standing) for thirty minutes to minimise the risk of oesophageal irritation or erosion.

Zoledronic acid, 5 mg IV infusion over 15 minutes, once per year is an alternative. 10 The patient should be well hydrated prior to starting the infusion. The patient should have their renal function assessed prior to starting, and be informed that dizziness and influenza-like symptoms are common after infusion.

The Special Authority requirements for the initial application for either alendronate or zoledronic acid require that:

The patient is receiving systemic glucocorticosteroid treatment (≥5 mg per day prednisone equivalent) and has already received or is expected to receive treatment for at least three months, and;

The patient has documented BMD ≥1.5 standard deviations below the mean normal values in young adults (i.e. T-Score ≤1.5), or;

The patient has a history of one significant osteoporotic fracture demonstrated radiologically, or;

The patient has had a Special Authority approval for alendronic or zoledronic acid* (underlying cause - glucocorticosteroid therapy) or raloxifene

* If either alendronate or zoledronic acid has been approved, and the other bisphosphonate is to be trialled, then the patient is considered to have already meet the requirements for the new medicine.

If a funded bisphosphonate is required, but the patient does not meet the Special Authority requirements of alendronate or zoledronic acid, etidronate disodium may be used, however, etidronate is significantly weaker than either alendronate or zoledronic acid.

Etidronate disodium is prescribed at 400 mg, daily on and empty stomach, for 14 days, repeated every three months.

Risedronate, an alternative to alendronate, is to be listed on the Pharmaceutical Schedule, without restrictions, from 1 September, 2013.

Acknowledgement

Thank you to Associate Professor Andrew Harrison, Rheumatologist, Clinical Head of Department, Wellington Regional Rheumatology Unit and Wellington School of Medicine, University of Otago, Wellington for expert review of this article.

References

1. Mackie S, Pease C. Diagnosis and management of giant cell arteritis and polymyalgia rheumatica: Challenges, controversies and practical tips. Postgrad Med J. 2013;89:284-92.

2. Salvarani C, Cantini F, Hunder G. Polymyalgia rheumatica and giant-cell arteritis. Lancet. 2008;9634:234-45.

3. Kermani T, Warrington K. Polymyalgia rheumatica. Lancet. 2013;381(9860):5-11.

4. BMJ Best Practice. Polymyalgia rheumatica. BMJ; 2012. Available from: http://bestpractice.bmj.com/best-practice/monograph/153.html (Accessed May, 2013).

5. Mitchet C, Matteson E. Polymyalgia rheumatica. BMJ. 2008;336:765.

6. Dasgupta B, Borg F, Hassan N, et al. BSR and BHPR guidelines for the management of polymyalgia rheumatica. Rheumatology. 2010;49(1):186-90.

7. Larkin J. Family history of rheumatoid arthritis - a non-predictor of inflammatory disease? Rheumatology. 2010;49(3):608-9.

8. Pease C, Haugeberg G, Montague B, et al. Polymyalgia rheumatica can be distinguished from late onset rheumatoid arthritis at baseline: results of a 50yr prospective study. Rheumatology. 2009;48(2):123-7.

9. Hoes J, Jacobs J, Boers M, et al. EULAR evidence-based recommendations on the management of systemic glucocorticoid therapy in rheumatic diseases. Ann Rheum Dis. 2007;66(12):1560-7.

10. New Zealand Formulary (NZF). NZF v12. NZF; 2013. Available from: www.nzf.org.nz (Accessed Jun, 2013).

11. Fardet L, Flahault A, Kettaheh A, et al. Corticosteroid-induced clinical adverse events: frequency, risk factors and patient's opinion. Brit J Dermatol. 2007;157(1):142-8.

12. Bolland MJ, Avenell A, Baron JA, et al. Effect of calcium supplements on risk of myocardial infarction and cardiovascular events: meta-analysis. BMJ. 2010;341:c3691.

13. Bolland MJ, Avenell A, Gamble G, Reid I. Calcium supplements with or without vitamin D and risk of cardiovascular events: reanalysis of the Women's Health Initiative limited access dataset and meta-analysis. BMJ. 2011;342:D2040.

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Polymyalgia rheumatica: Look before you leap

# data[].attributes.attachment_link.description
In this article Polymyalgia rheumatica is an inflammatory condition that causes a particular pattern of joint pain and stiffness, most commonly in older people. It is a rheumatic disorder closely associated, and often co-existing, with giant cell arteritis. Diagnosis is based on the patient's clinical features, supported by laboratory investigations.

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Adhesive capsulitis - link between AC and hypo/hyper thyroidism

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Adhesive capsulitis - link between AC and hypo/hyper thyroidism

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I looked up the link between hypo/hyper thyroidism to understand the link between adhesive capsulitis and auto-immune dysfunction.  This has increased my understanding of this and other similar dysfunctions (B2, B3, B4)

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Hyperthyroidism is a Risk Factor for Developing Adhesive Capsulitis of the Shoulder: A Nationwide Longitudinal Population-Based Study

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The purpose of this study was to investigate the prevalence and risk of adhesive capsulitis among hyperthyroidism patients. The data were obtained from the Longitudinal Health Insurance Database 2005 (LHID 2005) in Taiwan, using 1 million participants and a prospective population-based 7-year cohort study of survival analysis.

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Auto-immune diseases.

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Autoimmune thyroid disease and the polymyalgia rheumatica-giant cell arteritis syndrome. - PubMed - NCBI

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Clin Endocrinol (Oxf). 1978 Sep;9(3):215-9. Case Reports; Comparative Study

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Recently I have had quite a few patients with interesting pathology! My understanding of PMR (B2, B3, B4) is greater and I understand now how an underlying systemic disease can create 'better' conditions for things such as adhesive capsulitis to occur.

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JavaScript is disabled on your browser. Please enable JavaScript to use all the features on this page.

Abstract

1.

(1) Epidemiologic, clinical, radiologic and serologic evidence suggests that psoriatic arthritis is a specific entity and not the coincidental occurrence of two common diseases, psoriasis and rheumatoid arthritis.

2.

(2) Psoriatic arthritis may be defined as psoriasis associated with inflammatory arthritis (peripheral arthritis and/or spondylitis) and usually a negative serologie test for rheumatoid factor.

3.

(3) Epidemiologic evidence for psoriatic arthritis is based on the finding of a significantly higher prevalence of psoriasis in arthritic populations and, conversely, a significantly higher prevalence of arthritis in psoriatic populations compared with controls.

4.

(4) Clinical characteristics of the disease include: almost equal distribution between males and females; peripheral arthritis involving few small joints in asymmetrical fashion; involvement of DIP joints; sausage digits; arthritis mutilans; ankylosing spondylitis; gout-like onset; higher incidence of nail involvement than occurs in uncomplicated psoriasis. The rash may present with arthritis, or, equally, may precede or succeed joint involvement.

5.

(5) Radiologic characteristics of the disease include: erosion of terminal phalangeal tufts (acro-osteolysis); whittling of phalanges, metacarpals, and metatarsals; cupping of proximal ends of phalanges, metacarpals, and metatarsals; ankylosis of IP and MP joints; lack of symmetry; severe destruction of isolated small joints: predilection for DIP and PIP joints with relative sparing of MP joints; sacro-iliitis or ankylosing spondylitis.

6.

(6) Laboratory characteristics are: negative serologic tests for rheumatoid factor; hyperuricemia; various changes of doubtful specificity in blood proteins and enzymes.

7.

(7) Morbid anatomical findings include excessive fibrous tissue in affected joints and abnormal nailfold capillaries in both normal and psoriatic skin.

8.

(8) Family studies have shown that psoriatic arthritis is probably determined genetically in a multifactorial manner. Environmental factors such as trauma may be important in triggering arthritis in the genetically predisposed.

9.

(9) Familial and clinical interrelationships exist between psoriatic arthritis and other seronegative arthritides, particularly Reiter's disease, idiopathic ankylosing spondylitis, and the intestinal arthritides.

10.

(10) Treatment of psoriatic arthritis is the same as the routine treatment of the individual components of the disease (psoriasis, peripheral arthritis, and spondylitis). However, antimalarials should be avoided as they exacerbate the rash. Folate antagonists (e.g., methotrexate) may be tried in severe cases not responding to traditional and less potentially harmful treatment.

11.

(11) With regard to pain and disability, the prognosis in psoriatic arthritis is better than in rheumatoid arthritis.

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JavaScript is disabled on your browser. Please enable JavaScript to use all the features on this page. 1. (1) Epidemiologic, clinical, radiologic and serologic evidence suggests that psoriatic arthritis is a specific entity and not the coincidental occurrence of two common diseases, psoriasis and rheumatoid arthritis. 2.

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The study appeared last month in the Journal of Dermatology.

Among the patients involved in the study, the risk of osteopenia and osteoporosis increased the longer someone had psoriatic disease, going up 5 percent for every year since diagnosis, the researchers report.

In addition, even though bone loss is generally considered to affect women more than men, the researchers actually identified more men than women with osteopenia or osteoporosis.

"Patients with psoriasis seem to be at high risk for developing osteopenia, especially if suffering from psoriasis for a long time," said Sara D'Epiro, a co-author of the study. "These findings place attention on under-recognized and often untreated osteopenia and osteoporosis in both female and male psoriasis patients."

D'Epriro recommended that psoriatic disease patients, especially those with a long history of the disease, should get screened for bone loss.

Osteoporosis and osteopenia cause bones to become thin and weak, resulting in a loss of bone density. According to the National Osteoporosis Foundation, approximately 54 million Americans have osteoporosis or some form of low bone mass.

The inflammation caused by psoriatic disease could be one reason patients are more at risk for bone loss, the researchers noted. As they reported in the study, several cytokines, or pro-inflammatory proteins, involved in psoriatic disease are also involved in osteoporosis.

The researchers thought that bone density loss would occur more often in people with psoriatic arthritis than psoriasis alone, due to increased joint pain and inflammation, D'Epiro said. Although their results did not identify a higher prevalence in the 19 psoriatic arthritis patients included in the study, she recommended that future research examine a possible connection.

Because this study involved a fairly small number of patients, D'Epiro also noted that larger studies are needed to corroborate these findings.

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Link found between osteoporosis and psoriasis, psoriatic arthritis

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If you have psoriasis or psoriatic arthritis, here's something else for your to-do list: get checked for osteoporosis. A recent study has found a high prevalence of osteopenia, an early form of the bone disease osteoporosis, in people with psoriatic disease.

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Since the function of the liver is so very complex, it should not come as a surprise that it can play a role in a vast array of diseases. Like so many problems, psoriasis has been treated symptomatically as a skin problem but research is now coming along which links it to more profound causes and suggests that addressing liver damage may be the best way to treat psoriasis.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5209456/pdf/PG-11-25606.pdf
Psoriasis is a chronic inflammatory disease that affects the skin. Studies have shown that psoriasis is not merely a skin problem; psoriasis is linked with various comorbid conditions, especially obesity and metabolic syndrome [1-5], which are known risk factors for non-alcoholic fatty liver disease (NAFLD).
In the past decade, many studies have drawn attention to comorbid conditions in psoriasis, and preliminary epidemiological data suggest that psoriasis could be associated with the development of NAFLD. Non-alcoholic fatty liver disease includes a spectrum of conditions that range from simple fatty liver, which is relatively benign, to non-alcoholic steatohepatitis (NASH), which can give rise to fibrosis, cirrhosis, and end-stage liver disease [6]. Moderate or severe conditions of psoriasis have a high prevalence of chronic liver disease [7]. It is hypothesised that components of metabolic syndrome as the most likely pathogenic basis may play a role in the manifestation of NAFLD and psoriasis. You might want to consider the liver fibrosis diet as it may help your psoriasis click here for info Uncontrolled studies have suggested that individuals with psoriasis or psoriatic arthritis may benefit from a diet supplemented with fish oil rich in eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA).[86] Diet recommendations include consumption of cold water fish (preferably wild fish, not farmed) such as salmon, herring, and mackerel; extra virgin olive oil; legumes; vegetables; fruits; and whole grains; and avoid consumption of alcohol, red meat, and dairy products. The effect of consumption of caffeine (including coffee, black tea, mate, and dark chocolate) remains to be determined.[87] There is a higher rate of celiac disease among people with psoriasis.[87][88] Disease severity generally decreases in people with celiac disease and those with anti-gliadin antibodies after the adoption of a gluten-free diet.[86][89][90]https://psoriasisnewstoday.com/2017/01/12/psoriasis-may-be-linked-to-liver-disease/
Previous studies have suggested links between psoriasis and health conditions such as obesity and metabolic syndrome that can lead to NAFLD, which can cause liver fibrosis and cirrhosis, and end-stage liver disease.

Metabolic syndrome can lead to heart problems and stroke. Its manifestations include high blood pressure, high cholesterol, excess abdominal fat, and other factors.

Many of those with moderate-to-severe psoriasis also have chronic liver disease, supporting the notion of a link between NAFLD and psoriasis.

To find evidence of a link, researchers studied 250 psoriasis patients. Their mean age was 44 and most were overweight, with an average body-mass index of 24.7 kg/m2).

Patients told the researchers how long they had had psoriasis and whether they had hypertension, dyslipidemia - increased cholesterol - and diabetes. Patients' height, weight, and waistlines also were measured.

Doctors gave all the patients skin evaluations to confirm psoriasis, and a liver ultrasound to detect signs of NAFLD.

Forty-eight percent of the patients were found to have excess abdominal fat, 96% had high cholesterol, 52.8% hyperglycemia, or high blood sugar, 53.6% hypertension, and 44% elevated levels of ALT, an enzyme measure of liver damage.

Almost half the patients, 45.2%, had NAFLD. Those with NAFLD were younger and more obese than those with psoriasis alone. The NAFLD patients, mostly men, also had higher body-mass levels and more metabolic syndrome.

In addition, NAFLD patients had higher fibrosis scores than non-NAFLD patients. None of the NAFLD patients had cirrhosis of the liver, however.

"[NAFLD] is highly prevalent among our cohort of patients with psoriasis, occurring in 45.2% of patients," the researchers wrote. "Comorbidity of NAFLD is highly associated with psoriasis, which emphasizes that both diseases may develop simultaneously. Healthcare providers should be mindful of this association since early evaluation and diagnosis of NAFLD in patients with psoriasis may play a vital role in alleviating the progression of liver disease."

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Psoriasis and fatty liver are frequent companians - If you have psoriasis consider the NAFLD diet

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Studies have suggested links between psoriasis and health conditions such as obesity and metabolic syndrome that can lead to NAFLD, which can cause liver fibrosis and cirrhosis, and end-stage liver disease. Metabolic syndrome can lead to heart problems and stroke. Its manifestations include high blood pressure, high cholesterol, excess abdominal fat, and other factors.

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Polymyalgia rheumatica and giant cell arteritis | GPonline

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Diagnosis and management of polymyalgia rheumatica and giant cell arteritis, including American College of Rheumatology criteria for a diagnosis, recommended corticosteroid therapy and potential side-effects of treatment.

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Herbal teas for detoxification 28 Jan 2019

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Herbal teas for detoxification 28 Jan 2019

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My patient's liver needs detoxification. I looked up suitable herbs that could help him.

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NaturalON - Natural Health News and Discoveries

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Everyone knows how important a regular detox is when it comes to helping your body remove toxins and get some rest but did you know that you can detox a bit every single day? Eating foods that are organic and avoiding pesticide and chemically laden foods is one way but another great way to help to detox your body bit by bit is by drinking certain teas. Drinking detoxifying teas can help remove the buildup of those harmful substances.

Many of the teas listed below are high in antioxidant cleansing power. Rotating these teas can help you gain even more detox power. Who would have thought that something as simple as tea could help your body so much?! No hassle, low price, and very little time required. Take a look at our list of the top 10 best teas for daily detoxing and get started today. Ask RoyalEssays to write essays online and get any paper from scratch across 20+ disciplines.

1. Red Clover Tea

Red clovers ability to detox comes from its high antioxidant compounds. Antioxidants give your body some serious backup when it comes to killing off those free radicals that cause us so much damage to our bodies. Getting a daily boost of antioxidants is important because if there is no defense against them, free radicals can do a real number on our health.

Red clover grows just about everywhere so chances are good that you can find some close to where you live. The flowers are the part of the plant that most people use for medicinal, cleansing purposes. When dried, these flowers can last for a year or more. Traditional Chinese medicine uses red clover to remove toxins from the blood and liver. This flower is also an excellent expectorant, which means it can also clear the lungs of toxins and phlegm. Red clover is also highly nutritious as it contains vitamin C and many of the B vitamins.

Buying organic red clover tea is simple, tasty, and a guaranteed winning way to fight free radicals and cleanse the blood.

2. Burdock Tea

This is not as well-known as other teas or herbs but it has powerful detoxifying benefits. This herb has been used for hundreds of year for blood purification purposes. This root is a powerful diuretic so it helps the body purge toxins through the urine.

This herb contains a compound called polyacetylene, an organic compound that has high electrical conductivity, antibacterial, and antifungal properties. This compound not only cleans the blood, but has been used by herbalists to treat acne and abscesses as it increases circulation to the skin and helps detoxify the epidermal tissues of the body.

Burdock root strengthens the body's immune system while it purifies the blood. It also improves liver function and the digestion process, which helps your body become more efficient at ridding itself of toxins each day. Just one cup of burdock tea every day will keep you cleansed and feeling better than ever.

3. Milk Thistle Tea

Milk thistle has many benefits to the liver that make this one a real winner! Your liver is what does a great deal of the detoxing in your body and when your liver isn't in top notch condition, this can affect the whole body.

Any detox plan you undertake should always have your liver in mind. Milk thistle is also great for your digestive system, so you can help your liver remove toxins from within your body, and then allow your digestive system to kick them out of your body! The active compound in milk thistle is called silymarin, Mother Nature's own liver protector and supporter. Who doesn't need some of that in their life?! The seeds of this plant have been used for at least 2,000 years to help protect health cells in the body, encourage the production of new cells, and stop inflammation in the body, especially of the liver.

Milk thistle extract is so powerful; it can actually help those with liver diseases. Be sure to choose a tea or extract that has at least 80 percent silymarin.

4. Cayenne Pepper Tea

As word gets around, more and more people are adding a bit of cayenne pepper to their diets for its health benefits. You can always add this spice directly to your food dishes but when brewed as a tea, its benefits go directly towards cleansing the body and boosting your energy levels throughout the day!

Cayenne pepper stimulates your circulatory system by opening up the capillaries, regulates your blood sugar, and helps with your digestion. It's also a great way to kick start your metabolism, that's the energy you are going to be feeling all day long. Cayenne pepper might make your nose run but that's not a bad thing. It will help your body detox by removing more toxins through your phlegm and mucus.

Also, It's a natural antiviral and antifungal food that should help keep you healthy and prevent from getting that nasty stuffy nose and colds during the flu season. Try drinking some hot water with lemon juice and a 1/8 of a teaspoon of cayenne pepper to do a little detox every morning.

5. Garlic Tea

OK, so this won't make you the most kissable person in town but everyone knows garlic has terrific medicinal properties. Read more about garlic tonic benefits.

Garlic is very effective at cleansing the body and giving it vital nutrients while supporting the liver function so that your body can naturally detox itself more efficiently.

6. Ginger Tea

Ginger tea is a superior cleansing root and when brewed up as a tea, it's a tart little pleasure. Even though ginger might be a bit strong to your taste buds, it's actually very gentle on the body, so you can feel comfortable about drinking it several times per day or long term.

This is a great detox tea you can make each morning, as a pick me up in the afternoon, or as a warm up after dinner. This healing spice has been used for thousands of years both as medicine and as a food enhancer. Ginger is perhaps one of the world's best detoxifying herbs, hands down. Ginger has anti-inflammatory, antioxidant, and anti-ulcer compounds.

Ginger helps to cleanse the body by stimulation digestion, improved circulation, and sweating out toxins. It's also great at removing a buildup of toxins and waste in the colon and liver. This is a great tea that you can add to any detox program.
(By the way, if you're enjoying this article, you may want to subscribe to the Naturalon's free newsletter; get breaking news alerts on GMO's, fluoride, superfoods, natural cures and more... You privacy is protected. Unsubscribe at any time.)
7. Cilantro Tea

This herb is for a lot more than just Pico de Gallo or guacamole! Cilantro makes a great tasting as well. It detoxes the body by working on your digestive system so it can remove those toxins through your urine and bowel movements.

Cilantro is so cleansing, you can use it to purify water so imagine what it can do for your body! Cilantro is rich in phytonutrients, flavonoids, as well as active phenolic compounds, The two main compounds in cilantro are linoleic acid and cineole, both of which contain powerful anti-arthritic and anti-rheumatic compound ds, as well as another compound called dodecenal, which is twice as strong as most antibiotics at fighting infections and removing dangerous microbes from the body.

Cilantro is well known for removing heavy metals from the body as well (find out how to use cilantro to remove heavy metals from tap water). Try some cilantro tea on a daily basis and notice how quickly you start to feel better and have more energy.

8. Chicory Tea

Like cilantro, chicory tea helps your digestive system remove toxins in the body by increasing the amount of gastric juices and revving up your entire digestive system.

Sometimes called wild succor, cornflower, endive, blue dandelion, and blue sailors, this herb is found all across America, Europe and Asia. It can help regulate your metabolism, and fight gall bladder disorders. It's long been used to treat liver dysfunction and is often recommended for those suffering from jaundice. It has powerful detoxifying agents and has a decongestive effect on the sinuses. It's also excellent at removing toxins through an increased urine output as it is a natural diuretic. Chicory also stimulates the bowels so you will remove even more toxins and excess waste in the body.

Chicory tea is also great for those suffering from anemia. Many people think chicory tastes an awful lot like coffee, so if you are a coffee lover, you can detox and still get that coffee flavor at the same time.

9. Dandelion Tea

Dandelion raises the amounts of enzymes that are known to help detox the body. It can even help remove carcinogens, which are substances known to cause cancers, so this tea is definitely one you should consider adding to your daily diet!
SEE ALSO: Top 20 Reasons to do a Detox Today
Many people think of dandelion tea as the perfect way to do a "spring cleaning" of the body. It stimulates and supports liver function and helps improve gallbladder function. Dandelion tea is also another tea that is a great diuretic, so it will help your body eliminate toxins through your urine. This "weed" is perfect for cleansing the digestive tract. Drinking dandelion tea every morning on an empty stomach cleanses the alimentary canal, treats different types of digestive problems, and is known well among home remedies for constipation.

This herb is known for preventing stones in the gallbladder and kidneys, so think of this tea as a whole body cleanser. Dandelion tea can also cleanse the skin from the inside out as it hinders the growth of bacteria.

10. Fenugreek Tea

Although this herb isn't well known in America, it's quite common in Europe. If you suffer from indigestion or bloating, you will find this tea really helps the efficiency of your digestive tract.

Not only will it relive those irritating problems but it helps to reduce inflammation, lowers blood pressure, and supports your livers ability to remove toxins from the body. This herb has potent antioxidants that have very positive effects on the liver. It's been used traditionally to support the health of the digestive system. In many other countries, such as the Mediterranean, this herb is relied upon as a powerful ally in liver detox and purification routines. The tea is made from the seeds of the fenugreek plant and it is also known for regulating blood sugar levels by slowing the rate at which sugar enters the blood stream.

Fenugreek tea is also a powerful laxative, so while it's great at removing excess waste and toxins through the bowels, you might not want to drink several cups of this before you have a big meeting or go to meet your mother-in-law.

Drinking any of the above detox tea on a daily basis is a great way to help keep your body in tip top shape. Doing detox programs two or three times per year is still recommended but these will help you with day to day maintenance, so toxins do not build up in your body and get so out of hand that they cause you problems.

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Everyone knows how important a regular detox is when it comes to helping your body remove toxins and get some rest but did you know that you can detox a bit every single day?

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I have been looking up more about psoriatic arthritis, as I have a patient tomorrow who has it.  Best to be more informed, so I know what questions to ask her (B2, B3, B4)

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Psoriatic Arthritis | National Psoriasis Foundation

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Psoriatic arthritis (PsA) is a form of arthritis that may result in swelling, stiffness, and pain in and around the joints. Psoriatic arthritis may also cause nail changes and fatigue. Early diagnosis and treatment can prevent lasting joint damage.

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something that patients with psoriatic arthritis may develop (B2, B3, B4)

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Dactylitis is swelling of the fingers and toes that can cause them to have a sausage-like appearance. Sometimes called sausage digit, dactylitis can be a symptom of several different medical conditions.

In this article, we look at the most common causes of dactylitis, as well as how it is diagnosed and treated.

What is dactylitis?

Dactylitis causes the fingers and hand to be become bloated and swollen.

One of the ways the body's immune system responds to illnesses and injuries is through a process called inflammation. Inflammation causes swelling, pain, and other physical changes while the body is fighting an infection.

Dactylitis is a form of inflammation in the fingers or toes. Symptoms include swelling in one or more fingers or toes, and often in the entire hand or foot. The swelling gives the fingers a bloated, sausage-like appearance. The swelling may be painful and can make it difficult to move the affected area.

Dactylitis can be due to an infection or because of a change in the immune system. It is often the result of an autoimmune disorder. Autoimmune diseases cause the immune system to attack healthy tissues.

Six common causes of dactylitis

Any disease or infection that causes inflammation has the potential to cause dactylitis. The most common causes of swollen fingers or toes include:

1. Sickle cell disease

Sickle cell disease is a group of genetic disorders of the red blood cells. Normally, red blood cells are shaped like discs. In people with sickle cell disease, changes in hemoglobin can alter the shape of blood cells to a sickle or curved shape.

Hemoglobin carries oxygen around the body, so changes in hemoglobin proteins can affect the body's ability to get enough oxygen. The lack of oxygen in the tissues causes sudden, severe pain and a person may need to go to the hospital for treatment.

Dactylitis may be the first symptom in people with sickle cell disease, especially in children. It can appear in infants as young as 6 months old.

When dactylitis occurs as a side effect of sickle cell disease, it can be accompanied by a fever, pain, and an increase in white blood cells. Children with swollen fingers should be evaluated by a doctor for sickle cell and other diseases.

2. Tuberculosis

Dactylitis is a rare complication of tuberculosis. Tuberculosis is an infectious bacterial disease that can cause inflammation in the lungs. In rare cases, it can cause bone inflammation.

This bone inflammation causes the bones of the hands or feet to swell, producing pain and changes in the shape of the fingers or toes. In most cases, only one side of the body is affected. Leprosy is another disease that can cause similar changes in the fingers.

3. Sarcoidosis

Sarcoidosis is an inflammatory autoimmune disease that can affect the heart, liver, kidneys, lungs, and other organs. It causes severe problems in the organs and can even be fatal.

Very rarely, sarcoidosis can affect the bones and muscles of the hands, causing painful swelling. People with this symptom may also develop lupus pernio, which causes lesions and plaques on the face, ears, and fingers.

4. Syphilis

Syphilitic dactylitis may be caused by congenital syphilis.
Image credit: Internet Archive Book Images, (2015, September 17)

Syphilis is a sexually transmitted infection (STI). Pregnant women with syphilis can pass the disease on to their babies, resulting in congenital syphilis.

In rare cases, babies born with congenital syphilis can develop dactylitis of the fingers or toes. This is due to inflammation in the bone and tissue, and usually, affects both sides of the body.

5. Spondyloarthritis

Spondyloarthritis refers to types of arthritis that affect the joints and the entheses, which are the tissues where tendons and ligaments attach to bones. One of the most common forms of spondyloarthritis is psoriatic arthritis. Dactylitis can sometimes be a sign of advanced psoriatic arthritis.

Dactylitis is common in spondyloarthritis, affecting about a third of people with the condition. Researchers do not yet have a clear understanding of why so many people with spondyloarthritis get dactylitis, but they know it is due to swelling in the joints and surrounding tissues.

People with rheumatoid arthritis do not get dactylitis, so some doctors use the presence of dactylitis to help diagnose the form of arthritis a person has.

6. Infection

Some infections can cause swelling of the tissue deep below the skin or even in the bone. This swelling can cause symptoms of dactylitis.

A form of dactylitis called blistering distal dactylitis is due to an infection of the fatty pad of a single finger or toe. Commonly caused by skin infections, such as Streptococcus or Staphylococcus, this form of dactylitis occurs due to problems with circulation.

Blistering distal dactylitis can be extremely painful and may produce lesions or blisters on or near the affected area. The condition is more common in children than in adults.

Symptoms and diagnosis

Dactylitis will be diagnosed with various tests, rather than just a visual assessment.
Image credit: Internet Archive Book Images, (2015, September 17)

The symptoms of dactylitis vary depending on the cause. For example, infections tend to affect only one finger, while dactylitis due to syphilis affects multiple fingers.

The appearance of dactylitis alone cannot accurately diagnose the cause. Instead, a doctor may perform X-rays or take blood tests to help determine the cause. They will also ask about the person's medical history.

The doctor may ask when the swelling appeared, whether it is accompanied by other symptoms, and whether the person has been previously diagnosed with an autoimmune disorder, inflammatory condition, or infection.

Treatment and management

Treatment for dactylitis primarily involves addressing the underlying cause of the swelling.

People with arthritis may need to take arthritis medications, while infections may require antibiotics. If the swelling is painful, a doctor may prescribe pain medications or recommend the use of non-steroidal anti-inflammatory drugs (NSAID), such as ibuprofen.

A person with tuberculosis or sickle cell disease may be very ill and require hospitalization. This is especially true for children.

Outlook

With prompt treatment, the outlook for dactylitis is good. The pain and swelling typically go away when the underlying condition is treated. In the case of sickle cell-related dactylitis, the swelling usually goes away on its own.

Many causes of dactylitis, however, are incurable chronic illnesses. These diseases may require ongoing treatment and management. If treatment stops working, dactylitis can reoccur.

People with psoriatic arthritis may have multiple dactylitis flare-ups as the disease progresses. Careful management and monitoring can reduce the severity of dactylitis, and may prevent it from returning.

Because many of the conditions that cause dactylitis are serious, it is vital that a person sees a doctor as soon as possible for swollen fingers.

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Six causes of dactylitis (sausage fingers)

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Many conditions cause the body to respond by swelling in certain areas due to inflammation. Dactylitis is when such swelling occurs in the fingers and causes a sausage-like appearance. This MNT Knowledge Center article explores causes of dactylitis, including syphilis and sickle cell disease.

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(28 jan)
What happened?
My patient had had a headache since the previous wednesday. My tutor proceded to ask me about nerve entrapment for the headache - was it root or peripheral entrapment.  I did eventually come up with greater occipital (peripheral nerve) due to the location of the area of pain (sub-occiptal muscles) but I realised that I need to do more revision of this area.

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For decades, HLA-C*06 has been accepted as the main descriptor of the two main phenotypes of skin psoriasis. There is now compelling evidence to suggest that HLA-C*06 is only a genetic biomarker for skin involvement and not for joint involvement in psoriatic disease. (B2, B3, B4)

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Abstract

Psoriasis and PsA are the main phenotypes of psoriatic disease. Both conditions are highly polygenic diseases in which stochastic and environmental factors are crucial in the pathogenic process. Although the MHC region is a highly dense genetic area, most of the genetic basis of psoriatic disease within it resides in the HLA region. For decades, HLA-C*06 has been accepted as the main descriptor of the two main phenotypes of skin psoriasis. There is now compelling evidence to suggest that HLA-C*06 is only a genetic biomarker for skin involvement and not for joint involvement in psoriatic disease. The role of HLA-B*27 in the genetic aetiology of PsA has been recognized since the 1970s. Recent population case-control studies with adequate patient groups and replication cohorts, as well as confirmation studies in family pedigrees through the use of modern molecular typing methods, have reinforced the aetiological role of this allele in PsA. These studies have offered a new vision of the role of this allele in disease expression. This review contextualizes the latest findings on the role of HLA-B27 in psoriatic disease, emphasizing those aspects of particular interest for clinical practice.

HLA-C*06 is a biomarker of skin involvement in psoriatic disease; it has little or no influence in the development of joint disease.

HLA-B*27 is a genetic biomarker of joint disease in psoriasis patients.

HLA-B*27 is also a marker of disease expression in PsA.

Psoriatic disease: the importance of the HLA region

Psoriasis and PsA are immune-mediated diseases in which the combination of multiple genetic risk factors, environmental noxae and stochastic factors are hypothesized to be responsible for the conditions [ 1, 2]. Recent genome-wide association studies have markedly expanded the group of genomic loci that are associated with the susceptibility of developing both conditions [ 3-12].

The strong familial aggregation, as demonstrated by a high occurrence rate of PsA and psoriasis in relatives, supports the theory of a genetic basis of these diseases [ 13]. Candidate gene and genome-wide studies have shown a strong association between psoriasis and the MHC region, particularly with a 300 kb segment in the MHC class I region on chromosome 6p21.3, known as PSORS1. The largest and most consistently reported association is with the HLA-C*06 allele within this region [ 3-12].

The role of the HLA genes in the susceptibility to PsA was demonstrated when increased sharing of the HLA haplotypes was documented among sibling pairs concordant for PsA; concordance for psoriasis only was not found [ 14]. Case-control studies have identified the HLA region as containing potential susceptibility loci for PsA. Whereas HLA-C*06 is increased in PsA patients when compared with the general population, compelling evidence suggests that this association is stronger with psoriasis than with PsA [ 15-26]. HLA B*27, B*39 and B*07 have been specifically associated with PsA in case-control studies that compared PsA patients with psoriasis patients [ 15-26]. Several HLA antigens have been related to specific manifestations of PsA. Thus HLA-B*27 is more common among PsA patients with axial disease, whereas B*38 and B*39 are increased among those with peripheral polyarthritis [ 15-26].

The following two susceptibility loci have been hypothesized to be associated with PsA in the HLA region: one located telomeric to HLA-C, which is associated with psoriatic skin lesions (present in the extended haplotypes EH13.1, EH37.1 and EH57.1), and another, MICAA9, that is associated with susceptibility to arthritis and is present in EH38.1, EH39.1 and EH57.1. [ 27, 28]. Most MICA allele associations with psoriasis and PsA are dependent on linkage disequilibrium with HLA-B and HLA-C risk alleles. Independent of HLA, only MICA*016 influences the risk of developing psoriasis without arthritis, and homozygosity for MICA*00801 increases the risk of developing PsA in patients with psoriasis [ 29].

In population- and family-based analyses, HLA-B*27 has been shown to be a stronger genetic marker for PsA than for psoriasis. In these studies, the absence of a detectable association between HLA-B*27 and psoriasis compared with an association with healthy individuals suggests that B*27 is not a marker for skin disease [ 15-26]. Analyses of the relationship between psoriatic disease and HLA-B*27 in different ethnic groups have consistently shown that HLA-B*27 is an independent risk allele for PsA that is unrelated to skin disease [ 30-35]. The prevalence of HLA-B*27 in PsA patients ranged from 20 to 35% in such studies, which is clearly much lower than its prevalence in AS (80-95% of the patients). Therefore this allele could only account for a small proportion of the total genetic risk for PsA. The HLA-B*27 allele might merely be a risk allele for AS that coexists with psoriasis, given the relatively high prevalence of psoriasis in the general population. However, because the frequency of HLA-B*27 is increased as well in PsA patients with peripheral joint involvement, HLA-B*27 could be an independent risk allele for PsA [ 23, 35]. Therefore HLA-B*27 could be considered as one of the strongest HLA risk alleles for PsA in patients with psoriasis and might help to differentiate the two conditions [ 35]. Herein we will review the reasons why this allele is important in disease susceptibility and its clinical phenotyping.

HLA-B27: disease pathogenic mechanisms

There are several theories regarding the pathogenic role of HLA-B*27: the arthritogenic peptide hypothesis; the HLA-B*27 misfolding hypothesis, which is linked to autophagy and/or the unfolded protein response (UPR); and the HLA-B*27-free heavy chain (HC) and homodimer hypothesis [36-38].

The arthritogenic peptide theory suggests that disease results from the ability of B*27 to bind and present unique arthritogenic peptides to CD8⁺ cytotoxic T lymphocytes (CTLs). Thus a B*27-restricted CTL response, triggered by peptides shared by disease-triggering pathogens, could cross-recognize a self-peptide or peptides bound to HLA-B*27. Further support for this model was presented in T cell studies in which B*27-restricted CTLs that could recognize bacterially infected and uninfected target cells were detected in the joints and peripheral blood of patients with reactive arthritis and AS [ 39]. However, the inability to identify suitable arthritogenic peptide candidates from joints and to demonstrate CTLs specific for these B*27-restricted epitopes, as well as the findings in animal models of SpA that indicate the disease appears not to require CD8⁺ T cells, have limited the acceptance of this theory [ 40].

The misfolding theory postulates that accumulation of B*27 HCs in the endoplasmic reticulum (ER) provides potent and chronic stimulation of ER stress response pathways culminating in the release of pro-inflammatory cytokines that contribute to disease pathogenesis [ 36-38]. Support for this model resulted from B*27 transgenic animal models that were shown to have an accumulation of misfolded B*27 HCs in their splenocytes and macrophages [ 41]. It is possible that misfolding provides one of several signals necessary for the activation of an inflammatory response, and it has been postulated that the misfolding might trigger or augment an innate immune response. This misfolding theory has been recently challenged by transgenic rat studies in which the accumulation of misfolded HCs could be reversed by the overexpression of human b2m without alleviating the disease phenotype [ 42].

IL-23 might play a key role in the pathogenesis of SpA, including PsA. The exact mechanism of how and where IL-23 production is induced and how it further contributes to disease processes is not yet known. Different hypotheses have been proposed, such as HLA-B*27 misfolding, with activation of the UPR as molecular drivers of IL-23 production [ 43, 44]. Strong evidence of misfolding and UPR activation in patient samples is lacking. It has been recently demonstrated that HLA-B*27 misfolding occurs in the gut of AS and Crohn's disease patients and is accompanied by activation of autophagy rather than a UPR. Autophagy appears to be associated with intestinal modulation of IL-23 in AS [ 45]. Other authors have failed to demonstrate autophagy as the main source of IL-23 overexpression in synovial tissue from patients with SpA [ 46]. A link between autophagy and B*27 misfolding in the pathogenesis of PsA has not been formally shown. In support of this view, in ileocolonoscopic studies of PsA, intestinal inflammation was more frequently seen in the oligoarticular and axial forms of the disease, as well as in patients with HLA-B*27 [ 47].

The B*27-free HC and homodimer hypothesis proposes that disease results from the immune recognition of aberrantly folded surface B*27 molecules [ 36-38]. These molecules include b2m-free and peptide-free B*27 HCs that could be monomeric (B27 HC) or dimeric (B27 ₂). A trigger, such as a bacterial infection, hypoxia or a stress-related signal, is proposed to promote the formation of cell surface B27 HCs and B27 ₂ from unstable B27-folded precursors, which are then recognized by innate immunoregulatory receptors on leucocytes including NK cells, T cells and other antigen-presenting cells [ 36-38]. The demonstration of cell surface expression of B27 ₂ led to the proposal that these immunoregulatory receptors might specifically recognize B27 ₂, which could modulate the immune response towards inflammatory disease [ 36, 48-52]. A variety of immunoregulatory receptors could recognize different forms of HLA-B*27 molecules. These molecules include the killer immunoglobulin-like receptors (KIRs) and leucocyte immunoglobulin-like receptors (LILRs), which are expressed on many types of leucocytes, including NK cells, NK T cells, monocytes, macrophages, dendritic cells and T cells [ 36, 48-52]. The manner in which the interaction of B27 ₂ with immunoregulatory receptors leads to disease remains undetermined; however, given the role that these receptors play in maintaining immune homeostasis, it is plausible that ligation by aberrant forms of B*27 might upset this balance in favour of a pro-inflammatory response [ 36, 48-52]. B27 ₂ is a ligand for a number of NK receptors, including KIR3DL1, KIR3DL2, LILRB2 and LILRA1. This pattern of recognition is distinct from that of B27 heterodimers, which are bound by KIR3DL1, LILRB1, LILRB2 and LILRA1 but not by KIR3DL2. One possibility is that the interaction of B27 ₂ with NK cells and T cells expressing KIR3DL2 results in altered cell signalling to promote the survival of pro-inflammatory cell subsets that participate in and exacerbate a pro-inflammatory response [ 50]. Thus the KIR3DL2⁺ NK cells were protected from apoptosis in the presence of B27 ₂-expressing AP cells, whereas the KIR3DL2⁺ CD4 T cells demonstrated enhanced survival and proliferation [ 51]. The KIR3DL2⁺ CD4 T cells produced IL-17 after B27 ₂ stimulation, and these IL-17-producing KIR3DL2⁺ CD4 T cells were enriched in the peripheral blood and SF of SpA patients [ 52]. These data support the hypothesis that aberrant forms of B27 promote the survival of KIR3DL2⁺ T and NK cells, which go on to participate in the inflammatory response through IL-17 overexpression.

It is unclear whether the disease pathogenesis linked to the presence of HLA-B*27 is the same in AS and PsA. The ER aminopeptidase 1 gene ( ERAP1) codes for a trimming aminopeptidase located in the ER, which has a function in the MHC class 1 peptide presentation [ 53]. The ERAP1-ERAP2 haplotype is hypothesized to influence the HLA-B*27-restricted peptide repertoire, folding mechanisms and HC dimer formation, and polymorphisms of these genes have clear implications in disease pathogenesis [ 53, 54]. The ERAP1 gene locus polymorphisms have shown a robust association with AS and psoriasis and several genome-wide association studies (GWASs) have identified ERAP1 as a candidate gene for AS, with an estimated population-attributable risk of 26% [ 37, 54]. The association of ERAP1 with AS or psoriasis has been shown to be highly dependent on the presence of HLA-B*27 and C*06, respectively (the association is only seen in subjects carrying B*27 or C*06) [ 54, 55]. A similar dependency of ERAP1 could not be demonstrated in PsA, irrespective of the HLA-B*27 or C*06 status [ 56].

HLA-B27 and psoriatic disease: a role in the disease aetiology

The aetiological role of HLA-B*27 in susceptibility to AS has been accepted for decades [ 57, 58]. In addition, a similar link has been implied regarding the susceptibility to PsA [ 59], with variability regarding the frequency of this allele in PsA populations. In some studies, the frequencies of HLA-B*27 are within the range of the control values, whereas frequencies as high as 39% have been found in other studies [ 23, 35, 60].

Recent population case-control studies with adequate patient groups and replication cohorts, as well as confirmation studies in family pedigrees using modern molecular typing methods, have reinforced the aetiological role of HLA-B*27 in PsA. In the largest study that has been performed of the association of HLA with PsA, which involved 678 cases and 688 controls as well as 283 families with 1000 individuals, HLA-B*27 was present in ∼20% of the cases [odds ratio (OR) 3.03 (95% CI 2.14, 4.28)]; in the multiple regression analysis, the association was independent of HLA-C*12 and B*38, two alleles that are associated with PsA as well. In addition, the HLA-B*27 haplotypes with HLA-C*01 and HLA-C*02 were found to be associated with PsA (B*27/C*01: OR 2.58; B*27/C*02: OR 2.92). In the family-based validation substudy, the haplotype transmission analysis showed that A*02 C*06 B*57 DRB1*07 DQB1*0303 formed an extended haplotype with excess transmission in PsA. In this substudy, HLA-B*27 was independently associated with risk, showing a Z value of 3.745 (Z values >0 indicate overtransmission of the allele) [61].

The previous study only included PsA patients, and the comparisons of the allele frequencies were performed using a healthy control population. It is essential to investigate the HLA genes that differentiate the patients with PsA from those with psoriasis alone, because this determination might enable the discovery of markers for the development of PsA in psoriasis patient populations. The work by Eder et al. [ 62] addressed this subject. In this population-based case-control study that included >700 PsA patients and 335 psoriasis patients, there was no difference in the frequency of HLA-B*27 between the psoriasis patients and the healthy controls (4.5% vs 7.2%), whereas the association between HLA-C*06 and psoriasis was stronger in the psoriasis-alone group than in the controls (44.2% vs 18.1%, P = 3 × 10 −¹⁹). In the multivariate analysis, the following three alleles were found to be associated with psoriatic disease (PsA + psoriasis alone): HLA-B*27 (OR 2.36, P < 0.0001), HLA-B*38 (OR 6.01, P < 0.0001) and HLA-C*06 (OR 2.23, P < 0.0001). The following markers were found to be overexpressed in PsA compared with their expression in psoriasis: HLA-B*27 (OR 5.07, P = 2 × 10 −¹⁰), HLA-C*01 (OR 2.55, P = 0.0009) and HLA-C*02 (OR 2.41, P = 0.0005). In a multivariate regression analysis, the following alleles were more frequent in PsA than in psoriasis: HLA-B*27 (OR 5.17, P < 0.0001), HLA-B*08 (OR 1.61, P = 0.009) and HLA-B*38 (OR 1.65, P = 0.026); HLA-C*06 was less frequent in the PsA group than in the psoriasis group (OR 0.58, P = 0.0002) and more frequent in the PsA group than in the healthy controls (OR 1.71, P = 2 × 10 −⁵). The following haplotypes remained significantly associated with PsA compared with psoriasis after the multivariate analysis: HLA-B*18-C*07 (OR 10.1, P = 0.004), HLA-B*27-C*01 (OR 41.1, P < 0.0001), HLA-B*27-C*02 (OR 19.9, P < 0.0001), HLA-B*38-C*12 (OR 2.9, P = 0.01), HLA-B*08-C*07 (OR 2.6, P = 0.004) and HLA-B*57-C*06 (OR 0.5, P = 0.03) [ 62].

To validate the previous results, the HLA alleles that were identified in the population-based study were further assessed in a family-based association study. In total, 178 PsA probands, 30 psoriasis probands and 561 first-degree family members belonging to 208 families were analysed. The alleles that were found to be overtransmitted in PsA when compared with psoriasis were HLA-B*27 (Z = 3.0, P = 0.002), C*12 (Z = 2.8, P = 0.005), B*38 (Z = 2.0, P = 0.04) and B*39 (Z = 2.0, P = 0.045) [ 63].

Finally, an important practical issue in this study was assessment of the utility of HLA risk alleles in identifying the PsA patients among the patients with psoriasis in terms of positive predictive values (PPVs). Assuming a PsA prevalence of 30% in those with psoriasis, the PPV of each of the identified HLA risk alleles was calculated as follows: HLAB*08 PPV = 42%, HLA-B*27 PPV = 64%, HLA-B*38 PPV = 43%, HLA-C*06 PPV = 35%. Therefore HLA-B*27 could be considered to be the strongest HLA risk allele for PsA among the patients with psoriasis, and it differentiates the conditions [62].

Winchester et al. [ 64] conducted a population-based case-control study in an Irish population to test the role of the HLA alleles in psoriatic disease risk. In the patients with PsA presenting to a rheumatology unit, the frequency of C*06 was significantly lower than that in the psoriasis cohort (28.7 vs 57.5%; P = 9.9 × 10 −¹²). In the combined discovery and validation cohort of the PsA patients, the frequency of B*27:05:02 (B*27) increased to 15.6% [OR 3.2 (95% CI 2.1, 4.7)]. The two haplotypes of HLA-B*27, EH27.1 and EH27.2, were significantly increased in frequency, accounting for 8.1% and 7.0%, respectively, of the combined cohort. To address the question of the possibility of epistatic interactions between C*06 and other MHC susceptibility alleles, the investigators conducted separate analyses in which all of the C*06-positive patients were excluded; the exclusion did not decrease the intensity of the association of PsA with EH27.1, EH27.2 or EH39.1, indicating that these haplotypes operate in a manner independent of the presence of C*06 in PsA susceptibility. The authors stated that because the EH27.1 and EH27.2 haplotypes associated with PsA susceptibility share the same B*27 allele and differ in their HLA-C alleles, this finding strongly suggests that this susceptibility maps to the HLA-B locus [ 64].

HLA-B27 and psoriatic disease: the role in disease expression

The relationships between the HLA genes and psoriatic disease are relevant in exploring disease susceptibility and understanding its several phenotypes. Chandran [ 65] found B*27 (OR 2.90, P < 0.0001) to be associated with PsA in type II psoriasis patients (psoriasis beginning at >40 years of age), which reinforces the role of this allele in determining musculoskeletal disease rather than skin disease in the psoriatic phenotype. In this cohort, comparing PsA with dactylitis to PsA without dactylitis showed, in the univariate analyses, that only the HLA-C*02 and B*27 frequencies were higher in dactylitis and, in the multivariate analysis, that HLA-C*02 (OR 1.85, P = 0.046) and HLA-B*27 (OR 1.74, P = 0.029) were independently associated.

Genetic factors have been shown to influence joint damage progression in PsA. Gladman et al. [ 66] showed that HLA-B27 in the presence of HLA-DR7, HLA-B39 and HLA-DQw3 in the absence of HLA-DR7 are each associated with progression of clinical damage, whereas HLA-DR7 and B22 antigens are 'protective'. In one study, the principal outcome was the change in the number of clinically damaged joints between visits, with patients having between 1 and 53 assessments of change between successive repeated visits. Using the data from a large well-defined prospective cohort of PsA patients followed for a median duration of 6 years, the HLA alleles B*39 (OR 1.87, P < 0.005), B*27 (OR 1.51, P = 0.003) and A*02 ( P = 0.026) were independently associated with the risk of peripheral joint damage progression between clinic visits, whereas the alleles DQB1*0604, C*04 and B*50 were associated with a lower risk [ 65]. These findings are in conflict because the B*27-negative patients developed more peripheral erosions than did the B*27-positive patients in a previous study [ 67]. A potential explanation for this discrepancy is found in a very recent study by Haroon et al. [ 68], in which the highest propensity score for severe PsA was with the B*27:05:02-C*02:02:02, B*08:01:01-C*07:01:01 and B*37:01:01-C*06:02:01 haplotypes and not the B*27:05:02-C*01:01:01 or B*57:01:01-C*06:02:01 haplotypes. Therefore the haplotype containing B*27-C*02 is linked to severe disease, whereas that containing B*27-C*01 is not.

Two small studies using serological HLA antigen testing showed that B27 and Cw2 were associated with axial disease in PsA [ 23]. This finding has been recently confirmed in a well-powered study using molecular HLA typing. The study showed that C*02 and B*27 are not independent of each other and detected their association with sacroiliitis and syndesmophytes [ 65]. Because HLA-B*27 is associated with peripheral joint damage progression as well, these findings indicate that HLA-B*27 with or without HLA-C*02 is a marker of disease progression and poor prognosis in PsA.

HLA-B*27 has been associated with axial PsA in several serological HLA studies [ 23]. Thus, in a Spanish series of axial PsA, 57% of the patients included under the label of isolated axial disease had this allele, compared with 19% in the polyarthritis plus axial group and 29% in the oligoaxial disease group ( P = 0.016). The authors found that patients with isolated axial disease were more often men, with more clinical (inflammatory back pain), radiological (bilateral sacroiliitis and marginal syndesmophytes), immunogenetic (HLA-B27) and extra-articular (uveitis) features, which strongly correlated this group with AS [ 69]. More recently, this finding has been validated by Chandran et al. [ 65], who investigated 633 Caucasian subjects with PsA satisfying the Classification Criteria for Psoriatic Arthritis (CASPAR) criteria and obtained the data on the time when at least unilateral grade 2 or greater sacroiliitis and the first syndesmophyte were observed on plain radiographs of the pelvis and spine. The authors conducted two separate analyses. The principal outcome for the first analysis was the time to development of radiographic sacroiliitis after the diagnosis of PsA, and the principal outcome for the second analysis was the time to the development of syndesmophytes after the diagnosis of PsA. The association between sacroiliitis and PsA was corroborated in the univariate analysis. In the multivariate analysis, HLA-B*27 [hazard ratio (HR) 1.66 (95% CI 1.21, 2.29), P = 0.002] was independently associated with a higher risk of developing syndesmophytes, whereas the allele HLA-A*29 [HR 0.39 (95% CI 0.18, 0.85), P = 0.018] was associated with a lower risk.

Eder et al. [ 62] found that the HLA-C*06 allele was associated with a prolonged interval of time from the onset of psoriasis to that of PsA, which supports its protective effect. The HLA-C*06 carriers had more than double the time interval from the onset of psoriasis to PsA. These results were in accordance with a previous study of Queiro et al. [ 70], who reported that HLA-C*06-positive PsA patients have longer psoriasis-arthritis latency periods (9 vs 5 years; P = 0.03). Winchester et al. [ 64] found, in addition to the susceptibility conferred by particular MHC alleles and haplotypes, preliminary evidence to suggest that the susceptibility genotype influences the timing of the onset of musculoskeletal features in PsA in relationship to the onset of psoriasis. Analysis of the data by quartiles based on the median value of the time interval between the onset of psoriasis and the onset of PsA showed that in the first quartile, arthritis developed before psoriasis, whereas arthritis followed the onset of psoriasis by>14.75 years in the last quartile. The B*27-positive cases accounted for 26.3% of those in the first time interval quartile, and this quartile included 58.8% of all of the B*27-positive individuals. The frequency of B*27 progressively declined through each of the quartiles of lengthening time intervals, accounting for only 5.1% of those in the fourth quartile, which included 7.8% of all of the B*27-positive cases. The individuals who were positive for C*06 accounted for 24.6% of those in the first time-interval quartile, and this proportion increased to 38.5% in the fourth quartile. Reflecting the progressive enrichment of C*06 in the cases with a long interval between the development of skin manifestations and the development of arthritic manifestations, the ratio of the C*06-positive cases to B*27-positive cases was 0.93 in the first quartile, increasing to a ratio of 7.5 in the fourth quartile. In a much smaller study conducted in PsA patients with axial disease, B*27 was found to be associated with the overall risk of disease (OR 6.4, P < 0.0004); however, this association was stronger in the patients with early onset compared with late-onset cases (51% vs 13%; P = 0.001) [ 71].

The previously cited data suggest that two separate principal patterns of the MHC effect would result in the psoriasis phenotype ( Fig. 1). The first pattern involves the classic psoriasis susceptibility gene C*06, and is characterized by more penetrant skin disease with less prevalent and more time-dependent development of musculoskeletal manifestations. The second pattern appears to be mediated by alleles of the HLA-B locus, including B*27 and B*39. This latter pattern includes a musculoskeletal phenotype nearly equivalent in penetrance to that of the skin disease and, in the case of B*27, occurs much more temporally coincident with the musculoskeletal involvement [ 35, 64]. In addition, it is plausible that, beyond the HLA-B locus, and because of the high linkage disequilibrium between the genes centromeric to HLA-C, other genes might contribute to the overall disease risk and define different subphenotypes of PsA [ 72].

HLA-B*27 has a striking relationship with AS and is associated with the severity of MRI-evident bone marrow osteitis in the axial and peripheral skeleton [ 73, 74]. Castillo-Gallego et al. [ 75] compared the total MRI scores of different groups of patients (PsA, axial SpA and AS) and patients with and without HLAB*27. When the groups were subanalysed according to the HLA-B*27 status, the disease severity in terms of the total MRI scores was found to be related to the presence of HLA-B*27. The HLA-B*27-negative PsA patients had lower MRI scores than the HLA-B*27-positive PsA and AS patients, whereas the B*27-positive PsA patients had similar scores to the AS patients. In addition, the overall number of bone marrow osteitis lesions was related to the presence of HLA-B*27 because the HLA-B*27-negative PsA patients had a lower number of lumbar spine lesions than the AS and HLA-B*27-positive PsA patients, whereas there were no differences between the AS patients and the HLA-B*27-positive PsA group. Collectively these findings support the concept of the key role of the HLA-B27 gene as a determinant of the osteitis extent in SpA, including PsA. These findings are in contrast with those of a previous small cross-sectional study in axial PsA, in which the univariate analysis could not demonstrate correlations between B*27 and clinical symptoms such as back involvement, syndesmophytes or functional impairment [ 67].

The prevalence and incidence of PsA has been increasing in the last decades in men and women, but this increase has been seen more markedly in men than in women [ 76]. The reason for this gender difference is not fully understood; however, one explanation might be a differential expression of the risk genes between the sexes. Queiro et al. [ 77] recently compared the MHC gene profile between men and women with PsA, and HLA-B*27 was found in 36% of the men (OR 7.3) and 27% of the women (OR 4.8); the comparison included healthy controls matched by sex. This differential expression of B*27 between the sexes was even more pronounced when the study population was stratified by the age at disease onset. Of the patients with onset of disease before 40 years of age, 42% of the men and 30% of the women had this allele. A declining effect of HLA-B*27 was seen in parallel with increasing age at disease onset, and this effect was more clearly found in men than in women [ 77]. In some studies of axial disease, the attributable risk of B*27 was restricted only to the male population [ 78]. Therefore B*27 might help explain the risk of disease because it appears to be related to the early onset of PsA, and may help to explain the higher incidence and prevalence of PsA among males, as highlighted in recent epidemiological studies.

Conclusion

Although the aetiological role of B*27 in psoriatic disease has been recognized for decades and corroborated in the most recent GWAS [ 12], its additional role in determining specific traits of the disease has been highlighted only recently. Thus PsA patients expressing this allele tend to have a shorter interval of time between onset of the skin disease and that of the musculoskeletal symptoms. They are more prone to developing enthesitis, dactylitis and uveitis and they tend to develop peripheral and axial joint damage more frequently over time. At present, HLA-C*06 and B*27 are the most important genetic biomarkers in psoriatic disease because they establish marked traits that in turn allow phenotypic differentiations in both populations [ 35, 79].

Funding: No specific funding was received from any funding bodies in the public, commercial or not-for-profit sectors to carry out the work described in this article.

Disclosure statement: The authors have declared no conflicts of interest.

References

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HLA-B27 and psoriatic disease: a modern view of an old relationship

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Psoriasis and PsA are the main phenotypes of psoriatic disease. Both conditions are highly polygenic diseases in which stochastic and environmental factors are crucial in the pathogenic process. Although the MHC region is a highly dense genetic area, most of the genetic basis of psoriatic disease within it resides in the HLA region.

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I felt today that some major revision of TOS is required as I have had a few patients recently who have presented with TOS like symptoms (B2, B3, B4).

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If you suspect thoracic outlet syndrome, you may consider cervical spine X-rays to evaluate for the presence of a cervical rib, or prominent C7 transverse process that may be contributing to the symptoms. Additional tests (e.g., MRI, EMG) can be used to rule out other causes.

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Ulcerative Colitis /Crohns Disease 8 Feb 2019

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Ulcerative Colitis /Crohns Disease 8 Feb 2019

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One of my patients suffers with this so I thought I should look up the medication associated with it and the symptoms too.

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IBD is also known as Inflammatory Bowel Disease. It is an auto-immune disease, in which the immune system of the body attacks or strikes on the parts of it's own digestive system. It affects both the small and the large intestine.

Based on the affected part and severity of the inflammatory conditions, IBD is classified into two types:

Crohn's Disease and Ulcerative Colitis:

It is a severe digestive disorder that affects the interior parts of the digestive tract. Crohn's disease mostly attacks the tips of the intestines. There is no absolute cure for Crohn's disease but they are various treatments available to oversee and manage the symptoms.Crohn's disease is an auto-immune disease.The inflammation can occur in any part of the digestive tract.

Ulcerative Colitis: It is a persistent disease that causes inflammation in the digestive tract, but this is not as severe as Crohn's disease.This mainly attacks the large intestine.

Diagnosis: Crohn's and Ulcerative Colitis conditions are usually diagnosed with investigations such as Colonoscopy, Enteroscopy etc. Blood screenings and Fecal calprotectin may also help in the diagnosis for IBD.

No. of people suffering with Crohn's?

There are more than 2 million people in the world suffering from Crohn's disease. It is more common in developed countries as compared to the developing ones and is equally common among Men and Women. The disease is common in the USA , Europe and now a days it is becoming prevalent in India too.

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IBD is also known as Inflammatory Bowel Disease. It is an auto-immune disease, in which the immune system of the body attacks or strikes on the parts of it's own digestive system. It affects both the small and the large intestine.

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Today I had a patient with ankylosing spondylitis (B2, B3, B4). I have been having hypnotherapy to try to be more calm in the room and I certainly didn't feel like the usual blank screen had entered my head.

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There is no cure for ankylosing spondylitis (AS), but treatment is available to help relieve the symptoms.

Treatment can also help delay or prevent the process of the spine fusing (joining up) and stiffening.

In most cases, treatment will involve a combination of exercise, physiotherapy and medication, which are described below.

Physiotherapy and exercise

Keeping active can improve your posture and range of spinal movement, along with preventing your spine from becoming stiff and painful.

As well as keeping active, physiotherapy is a key part of treating AS. A physiotherapist (a healthcare professional trained in using physical methods of treatment) can advise about the most effective exercises and draw up an exercise programme that suits you.

Types of physiotherapy recommended for AS include:

a group exercise programme - where you exercise with others

an individual exercise programme - you are given exercises to do by yourself

massage - your muscles and other soft tissues are manipulated to relieve pain and improve movement (the bones of the spine should never be manipulated as this can cause injury in people with AS)

hydrotherapy - exercise in water (usually a warm, shallow swimming pool or a special hydrotherapy bath); the buoyancy of the water helps make movement easier by supporting you, and the warmth can relax your muscles

Some people prefer to swim or play sport to keep flexible. This is usually fine, although some daily stretching and exercise is also important.

If you're ever in doubt, speak to your physiotherapist or rheumatologist before taking up a new form of sport or exercise.

The National Ankylosing Spondylitis Society (NASS) provides detailed information about different types of exercise to help you manage your condition.

Painkillers

You may need painkillers to manage your condition while you are being referred to a rheumatologist. The rheumatologist may continue prescribing painkillers, although not everyone needs them all the time.

Non-steroidal anti-inflammatory drugs (NSAIDs)

The first type of painkiller usually prescribed is a non-steroidal anti-inflammatory drug (NSAID). As well as helping to ease pain, NSAIDs can help relieve swelling (inflammation) in your joints.

Examples of NSAIDs include ibuprofen, naproxen and diclofenac.

When prescribing NSAIDs, your GP or rheumatologist will try to find the one that suits you, and the lowest possible dose that relieves your symptoms. Your dose will be monitored and reviewed as necessary.

Paracetamol

If NSAIDs are unsuitable for you, an alternative painkiller, such as paracetamol, may be recommended.

Paracetamol rarely causes side effects and can be used in women who are pregnant or breastfeeding. However, paracetamol may not be suitable for people with liver problems or those dependent on alcohol.

Codeine

If necessary, as well as paracetamol, you may also be prescribed a stronger type of painkiller called codeine.

Codeine can cause side effects including feeling sick, vomiting, constipation and drowsiness.

Anti-TNF medication

If your symptoms cannot be controlled using painkillers or exercising and stretching, anti-TNF (tumour necrosis factor) medication may be recommended. TNF is a chemical produced by cells when tissue is inflamed.

Anti-TNF medications are given by injection and work by preventing the effects of TNF, as well as reducing inflammation in your joints caused by ankylosing spondylitis.

Examples of anti-TNF medication include adalimumab, etanercept and golimumab.

These are relatively new treatments for AS, and their long-term effects are unknown.

However, they have been used for longer in people with rheumatoid arthritis, and this is providing clearer information about their long-term safety.

If your rheumatologist recommends using anti-TNF medication, the decision about whether they are right for you must be discussed carefully and your progress will be closely monitored. This is because anti-TNF medication can interfere with the immune system (the body's natural defence system), increasing your risk of developing potentially serious infections.

NICE guidelines

The National Institute for Health and Care Excellence (NICE) has produced guidance about the use of anti-TNF medication for AS. NICE states that adalimumab, etanercept and golimumab may only be used if:

your diagnosis of ankylosing spondylitis has been confirmed

your level of pain is assessed twice (using a simple scale that you fill in) 12 weeks apart and confirms your condition has not improved

your Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) is tested twice, 12 weeks apart, and confirms your condition has not improved - BASDAI is a set of measures devised by experts to evaluate your condition, by asking a number of questions about your symptoms

treatment with two or more NSAIDs for four weeks at the highest possible dose has not controlled your symptoms

After 12 weeks of treatment with anti-TNF medication, your pain score and BASDAI will be tested again to see whether they have improved enough to make continuing treatment worthwhile. If they have, treatment will continue and you will be tested every 12 weeks.

If there is not enough improvement after 12 weeks, you will be tested again at a later date or the treatment will be stopped.

Corticosteroids

Corticosteroids have a powerful anti-inflammatory effect and can be taken as tablets or injections by people with AS.

If a particular joint is inflamed, corticosteroids can be injected directly into the joint. After the injection, you will need to rest the joint for up to 48 hours.

It is usually considered wise to have a corticosteroid injection up to three times in one year, with at least three months between injections in the same joint. This is because corticosteroids injections can cause a number of side effects, such as:

infection in response to the injection

the skin around the injection may change colour (depigmentation)

the surrounding tissue may waste away

a tendon (cord of tissue that connects muscles to bones) near the joint may rupture (burst)

Corticosteroids may also calm down painful swollen joints when taken as tablets.

Disease-modifying anti-rheumatic drugs (DMARDs)

Disease-modifying anti-rheumatic drugs (DMARDs) are an alternative type of medication often used to treat other types of arthritis.

DMARDs may be prescribed for AS, although they are only beneficial in treating pain and inflammation in joints in areas of the body other than the spine.

Two DMARDs sometimes used to treat inflammation of joints other than the spine include sulfasalazine and methotrexate.

Surgery

Most people with AS will not need surgery.

However, in cases where a joint has become severely damaged, joint replacement surgery may be recommended to improve pain and movement in the affect joint. For example, if the hip joints are affected, a hip replacement may be carried out.

In rare cases, corrective surgery may be needed if the spine becomes badly bent.

Follow-up

As the symptoms of AS develop slowly and tend to come and go, you will need to see your rheumatologist or GP for regular check-ups.

They will make sure your treatment is working properly and may carry out physical assessments to assess how your condition is progressing. This may involve further sets of the same blood tests or X-rays you had at the time of your diagnosis.

Any complications of ankylosing spondylitis that arise will be treated as they develop.

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Ankylosing spondylitis symptoms and treatments

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There is no cure for ankylosing spondylitis (AS), but treatment is available to help relieve the symptoms. Treatment can also help delay or prevent the process of the spine fusing (joining up) and stiffening. In most cases, treatment will involve a combination of exercise, physiotherapy and medication, which are described below.

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Cranium/children's clinic 22 february 2019

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Cranium/children's clinic 22 february 2019

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I have been learning more about plagiocephaly and brachiocephaly as well as the more serious craniosynostosis (B2, B3, B4, C3, C5, C7, C8)

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Abstract

Craniosynostosis, defined as the premature fusion of the cranial sutures, presents many challenges in classification and treatment. At least 20% of cases are caused by specific single gene mutations or chromosome abnormalities. This article maps out approaches to clinical assessment of a child presenting with an unusual head shape, and illustrates how genetic analysis can contribute to diagnosis and management.

In brief

Craniosynostosis is best managed in a multispecialty tertiary referral unit.

Single suture synostosis affects the sagittal suture most commonly, followed by the coronal, metopic and lambdoid sutures.

Both environmental factors (especially intrauterine fetal head constraint) and genes (single gene mutations, chromosome abnormalities and polygenic background) predispose to craniosynostosis.

Most genetically determined craniosynostosis is characterised by autosomal dominant inheritance, but around half of cases are accounted for by new mutations.

Apart from the genetic implications, it is important to recognise cases with a genetic cause because they are more likely to be associated with multiple suture synostosis and extracranial complications.

Genes most commonly mutated in craniosynostosis are FGFR2, FGFR3, TWIST1 and EFNB1.

As well as being associated with syndromes, some clinically non-syndromic synostosis (usually affecting the coronal suture) can be caused by single gene mutations, particularly the Pro250Arg mutation in FGFR3.

In severe cases, initial care should be directed towards maintenance of the airway, support of feeding, eye protection and treatment of raised intracranial pressure.

Introduction

During infancy and childhood, the skull vault (calvaria) expands to accommodate the growing brain. This growth occurs predominantly at the narrow seams of undifferentiated mesenchyme, termed cranial sutures, which lie between different bones. The paired frontal and parietal bones are separated in the midline by the metopic and sagittal sutures, respectively; the frontal and parietal bones are separated by coronal sutures; and the parietal bones are separated from the single occipital bone by lambdoid sutures ( Figure 1a and b). Craniosynostosis describes the premature fusion of one or more of the cranial sutures: secondary distortion of skull shape occurs because of a combination of lack of growth perpendicular to the fused suture, and compensatory overgrowth at the non-fused sutures. The overall prevalence of craniosynostosis has been estimated at between 1 in 2100 and 1 in 2500 births.1, 2 Craniosynostosis is important to recognise and treat because it can be associated with many complications affecting sensory, respiratory and neurological function.

Figure 1

Diagnostic features of craniosynostosis. ( a) Schematic diagram showing positions of the major cranial sutures. ( b) CT scan (vertex view of skull) showing major sutures; anterior is at top. ( c,d) Sagittal synostosis: note long, narrow head. ( e,f) Metopic synostosis: note hypotelorism and triangular profile of forehead. ( g,h) Bicoronal synostosis: broad, flattened head. ( i,j) Right unicoronal synostosis: note flattened brow and anterior position of ear on affected side, deviation of nasal tip and prominent brow on unaffected side. ( k-m), Congenital anomalies of feet or hands characteristic of Pfeiffer syndrome ( k), Apert syndrome ( l) and craniofrontonasal syndrome ( m). ( n) Crouzonoid facial appearance. ( o) Severe hypertelorism, grooved nasal tip and left unicoronal synostosis in craniofrontonasal syndrome. ( p) Ptosis and left unicoronal synostosis in Saethre-Chotzen syndrome. ( q) Positional plagiocephaly: prominence on right anteriorly and left posteriorly, with right ear anterior and parallelogram shape to skull. ( r) CT reconstruction showing left unicoronal synostosis. ( s) CT reconstruction showing cloverleaf skull. ( t) CT venogram showing abnormal venous drainage in multisuture syndromic craniosynostosis. See text for further details.

Clinical overview

The aims of clinical assessment are to determine: (1) whether craniosynostosis is present; (2) whether there are additional features suggesting an associated syndrome and (3) to assess whether urgent or elective management is required. Craniosynostosis is very heterogeneous in its causes and presentation, and correspondingly in its management. Most isolated non-syndromic cases present electively, but a minority of syndromic cases present acutely and require immediate intervention. Classifications of craniosynostosis based on the combination of sutures closed, associated features suggesting a syndrome, and identifiable aetiological factors (for example, intrauterine constraint,3, 4 teratogenic exposure and genetic abnormalities) all have validity, and should be considered in combination.

The most common presentation is with an unusual head shape in the first year of life; the head may be long and narrow (scaphocephaly, dolichocephaly; Figure 1c and d), triangular at the front (trigonocephaly; Figure 1e and f), broad and flattened (brachycephaly; Figure 1g and h) or skewed (plagiocephaly Figure 1i and j). To seek aetiological clues, the history should focus on any family history of unusual head shapes, prenatal exposures (for example, valproate ingestion for maternal epilepsy), evidence of fetal intrauterine constraint (primiparity, multiple pregnancy, abnormal lie and oligohydramnios) and birth history. Obstructed labour and assisted delivery or caesarean sections are frequent, but more likely to be the consequence, rather than the cause of craniosynostosis. In assessing the functional consequences of the condition, the most important clinical information pertains to the airway, feeding, eye protection and raised intracranial pressure (ICP). It is essential to elicit any evidence of breathing difficulty, choking or vomiting on feeds, failure of eyelids to cover eyes during sleep, or irritability, as these may be indications for acute intervention.

The clinical examination should follow a set pattern to avoid overlooking clues. Our own routine is to start with the hands and feet looking for congenital anomalies, for example, a broad radially deviated thumb or big toe in Pfeiffer syndrome ( Figure 1k), more extensive syndactyly in Apert syndrome ( Figure 1l) and longitudinally split nails in craniofrontonasal syndrome ( Figure 1m). Examine the face for dysmorphic features, including hyper- or hypotelorism, exorbitism, midface hypoplasia, asymmetry and ear size, position and shape. The combination of exorbitism, flattened malar region and beaked nose signals a 'crouzonoid' appearance ( Figure 1n), likely to be associated with FGFR2 mutation. If there is hypertelorism, view the nose from above looking for a shallow groove, which suggests craniofrontonasal syndrome ( Figure 1o). Ptosis, low frontal hairline and small ears with prominent horizontal crura are features of Saethre-Chotzen syndrome ( Figure 1p). Look at the skull shape from front, back, sides and top, feel the sutures for ridging (associated with suture fusion), assess the size, shape and tension in the fontanelles, and measure the head circumference. The cephalic index (ratio of maximum breadth to maximum length of skull, normally between 0.76 and 0.83 (in boys) or 0.84 (in girls))5 provides an objective measure of its overall proportions, but requires calipers for accurate measurement. Finally look in the mouth for a cleft palate and complete the general physical examination. The parents should be assessed similarly for signs suggestive of a carrier state.

It is important, but not always easy, to distinguish synostotic plagiocephaly (caused by unicoronal or, less commonly unilambdoid synostosis) from non-synostotic plagiocephaly. The latter is a very common condition related to deformation and shear stress on the skull during late pregnancy and delivery, and frequently increases in severity before the acquisition of head control, because infants tend to be nursed in a supine position. Clues may be obtained by viewing the head, and particularly the position of the ears, from above (compare Figure 1i, j with q). In synostotic plagiocephaly caused by unicoronal synostosis, the ear on the affected side is shifted forward, and the distance to the flattened brow contour is reduced. The skull when viewed from above is a rhomboid shape. In non-synostotic anterior plagiocephaly, the ear on the flattened side is more posterior (parallelogram shape when viewed from above). If doubt remains, referral to a specialist unit is recommended.

Diagnostic approaches

Computed tomography (CT) scanning and three dimensional reconstruction using both bone and soft tissue windows is the investigation of choice.6 This should clearly reveal the patency, or closure, of each individual suture ( Figure 1b, r and s). CT of the brain should also be performed seeking associated anatomical abnormalities (for example, ventriculomegaly and agenesis of corpus callosum) and to check the fluid spaces for evidence of craniocerebral disproportion. CT venography is required in complex cases where abnormal venous drainage is suspected ( Figure 1t). Skull radiographs are of limited use as their sensitivity for detecting sutural patency is significantly less than CT. They are most useful when screening cases of plagiocephaly when the clinical findings are not conclusive. Magnetic resonance imaging (MRI), although ideal for the brain, is less good at visualising the cranial sutures.

Craniosynostosis should ideally be managed in a multidisciplinary setting. Full workup should also include baseline psychological, speech/language, hearing and orthoptic assessments. Neurosurgical review with ICP monitoring may be required, although this is more commonly used later in childhood to assess symptoms suggestive of raised ICP.

Molecular and genetic basis of disease

In a recent analysis of a 10-year prospective cohort of craniosynostosis presenting to our unit, a genetic diagnosis was achieved in 21% of cases, comprising 86% single gene disorders and 15% chromosome abnormalities (one patient had both).7 The genes most frequently mutated were FGFR2 (32% of all genetic cases), FGFR3 (25%), TWIST1 (19%) and EFNB1 (7%). Figure 2 illustrates the domain structures of proteins encoded by these four genes, together with the clinical presentation and molecular distribution of mutations in the cohort survey, illustrating the relative prevalence of the major mutations causing craniosynostosis. Much rarer, but well established associations of gene mutations and craniosynostosis are for FGFR1 (mild Pfeiffer syndrome), POR (Antley-Bixler syndrome) and RAB23 (Carpenter syndrome); further information about these genes is provided below. Single-gene mutation associations that are based on only a handful of cases are not further discussed; these include mutations in EFNA4 (non-syndromic coronal synostosis),8 ESCO2 (Roberts syndrome), GLI3 (Greig syndrome), JAG1 (Alagille syndrome), KRAS (Noonan syndrome), RECQL4 (Baller Gerold syndrome) and TGFBR1 or TGFBR2 (Loeys-Dietz syndrome). Mutation in MSX2, the first genetic cause of craniosynostosis to be molecularly determined,9 is exceptionally rare, having been reported to date only in the original family, but several duplications including MSX2 have been associated with craniosynostosis.10

Figure 2

Distribution and types of mutation that commonly cause craniosynostosis. The major domains of the proteins encoded by the FGFR2 ( a), FGFR3 ( b), TWIST1 ( c) and EFNB1 ( d) genes are shown to scale, together with the position and types of mutation identified, and their associated phenotypes. Dashed line before EPH domain encoded by EFNB1 indicates 5′ untranslated region. The data, which were obtained from the Oxford cohort study,7 convey the relative prevalence of the most common mutations, but many rare mutations were absent in this survey. Asterisk indicates position of Ala391Glu mutation of FGFR3. crs, craniosynostosis. See text for information on protein domains.

FGFR2 (fibroblast growth factor receptor type 2)

The FGFR2 gene encodes a transmembrane receptor tyrosine kinase ( Figure 2a) comprising an extracellular ligand-binding region (immunoglobulin-like domains IgI, IgII and IgIII), a single pass transmembrane region (TM) and split tyrosine kinase domain (TK1 and TK2). Heterozygous mutations of FGFR2 cause three classical craniosynostosis syndromes, those of Apert, Crouzon and Pfeiffer. All exhibit a characteristic crouzonoid facial appearance ( Figure 1n). Less commonly, mutations may present with non-syndromic synostosis,7 or Beare-Stevenson syndrome (multisuture synostosis associated with cutis gyrata). Mutations in FGFR2 and FGFR3 tend to encode highly localised, recurrent missense substitutions encoding proteins with gain-of-function properties. The cellular consequences of mutation are complex, including enhancement of proliferation, differentiation and apoptosis of osteoblasts bordering the cranial suture mesenchyme; premature differentiation is probably the most important factor leading to craniosynostosis.11, 12

Apert syndrome is characterised by bicoronal synostosis and bilateral symmetrical complex syndactyly of the hands and feet ( Figure 1l). Other frequent complications include cleft palate (44%) and learning disability, requiring special needs education (44%).13 Over 98% of cases are caused by specific missense mutations of FGFR2, either Ser252Trp (66%) or Pro253Arg (32%), in the linker between the IgII and IgIII domains ( Figure 2a); the former substitution is associated with a higher frequency of cleft palate, but milder syndactyly.13 These substitutions specifically increase the affinity and broaden the specificity of FGF-ligand binding, explaining the exquisite genotype-phenotype correlation.14 Nearly all Apert syndrome mutations arise de novo, and have been shown to originate exclusively from the father. These mutations provide a paradigm for paternal age effect mutations that are enriched in sperm owing to a paradoxical selective advantage to mutant spermatogonial cells in the testis.15, 16

Pfeiffer syndrome is usually characterised by broad, radially deviated thumbs and/or big toes ( Figure 1k), sometimes with cutaneous syndactyly, and includes individuals previously classified with a 'Jackson-Weiss' phenotype. The craniofacial severity is variable, an important subgroup presenting with severe multisuture synostosis ('Kleeblatschädel') ( Figure 1s), which is very challenging to manage and associated with significant mortality. FGFR2 mutations in Pfeiffer syndrome overlap those in Crouzon syndrome ( Figure 2a), but the majority of severe cases are caused by a small subset of substitutions encoding Trp290Cys, Tyr340Cys, Cys342Arg or Ser351Cys.17

Crouzon syndrome is usually the mildest of the FGFR2-associated disorders and the clinical diagnosis is suggested by the combination of crouzonoid facies ( Figure 1n) and absence of major abnormalities of the hands and feet. Although bicoronal synostosis is most common, Crouzon syndrome can present with late-onset pansynostosis.18, 19 It is important to be aware of this possibility in a child with a crouzonoid appearance, because apparently mild distortion of the skull shape may mask the presence of raised ICP. The association of crouzonoid facies with acanthosis nigricans is caused by a specific FGFR3 mutation (see below).

The distribution of mutations causing Pfeiffer and Crouzon syndromes in FGFR2 overlaps considerably. Most mutations (94%) occur in the third extracellular immunoglobulin-like domain encoded by exons IIIa or IIIc, where they cause constitutive activation by covalent cross-linking of receptor monomers. The remainder of the mutations are scattered in seven other exons of the gene, including several mutations in the tyrosine kinase domain.20 Abnormal splicing of the IIIc exon tends to be associated with more severe limb abnormalities, so these mutations generally present with Pfeiffer or occasionally even Apert syndrome ( Alu element insertions).21

FGFR3 (fibroblast growth factor receptor type 3)

FGFR3 encodes a protein that has a domain structure closely resembling its paralogue FGFR2 ( Figure 2b). Although FGFR3 mutations are commonly associated with bone dysplasia (hypochondroplasia-achondroplasia-thanatophoric dysplasia series), two heterozygous mutations cause specific craniosynostosis syndromes, Muenke syndrome and Crouzon syndrome with acanthosis nigricans ( Figure 2b).

Muenke syndrome, defined by identification of the Pro250Arg substitution, is individually the most common genetic abnormality found in craniosynostosis, comprising ∼ 5% of all cases.7 The associated phenotype is not distinctive and was not properly delineated until the mutation was described in 1996 (ref. 22). Patients usually present with either unicoronal or bicoronal synostosis, but at least 20% of mutation carriers do not have clinically significant craniosynostosis. The facial appearance ranges from normal to a dysmorphic appearance easily mistakable for Saethre-Chotzen syndrome. Minor digital abnormalities (especially brachydactyly) are not characteristic and there should be a low threshold for requesting the genetic test to establish the diagnosis. An important complication is low frequency hearing loss, requiring the fitting of hearing aids in ∼ 20% of patients.23 The Pro250Arg substitution is the exact equivalent to the Apert Pro253Arg substitution in FGFR2, and also causes ligand-dependent gain-of-function.24 However the reasons for the specific association of this mutation with craniosynostosis are not fully understood.

Crouzon syndrome with acanthosis nigricans is characterised by the Ala391Glu substitution. The acanthosis nigricans, which develops during childhood, is usually not apparent at presentation, so specific testing should be requested in the diagnostic workup of Crouzon syndrome. A positive result should prompt a careful neurosurgical assessment as hydrocephalus is a frequent association.25

TWIST1 (twist homologue 1)

Saethre-Chotzen syndrome is characterised by heterozygous mutations of TWIST1, which encodes a transcription factor belonging to the basic helix-loop-helix family (BHLH motif, Figure 2c). The facial appearance is fairly characteristic, but experience is required in its recognition ( Figure 1p). Affected individuals usually present with unicoronal or bicoronal synostosis, but non-penetrance for craniosynostosis occurs. Abnormal extremities (broad, laterally deviated first digits, 2/3 cutaneous syndactyly and brachydactyly) are variable and only occasionally diagnostic. Saethre-Chotzen syndrome results from haploinsufficiency of TWIST1, which may be the consequence of many different mutations, including whole gene deletions, intragenic nonsense and frameshifting mutations, and missense substitutions; note that the last category is largely confined to the highly conserved BHLH motif required for DNA binding and dimerisation ( Figure 2c) (ref. 26). No genotype-phenotype correlation is described, except that large deletions are associated with learning disability (not generally a feature of Saethre-Chotzen syndrome),26, 27 and occasional missense mutations in the C-terminal Twist box apparently confer increased risk of a more non-specific synostosis phenotype (with unknown penetrance).28 Rearrangements of a polyglycine-rich tract (amino acids 82-92), which turn up occasionally during mutation screening, seem to be harmless in the heterozygous state.29 Twist1 has a key role in maintaining the boundary between neural crest and cephalic mesoderm at the site of the developing coronal suture.8

EFNB1 (ephrin-B1)

Craniofrontonasal syndrome is an X-linked disorder that presents paradoxically with heterozygous females more severely affected than hemizygous males. Females have severe hypertelorism, unicoronal or bicoronal synostosis, bifid nasal tip, characteristic longitudinal nail splits ( Figure 1m and o) and, at lower frequency, sloping shoulders, asymmetric nipples, bifid digits and agenesis of the corpus callosum.30

The identification of causative mutations in EFNB1, which confer loss of function and are correspondingly diverse (whole gene deletions, intragenic nonsense and frameshifting and splice site mutations, and missense substitutions; Figure 2d) (refs. 31, 32), has provided an explanation for the paradoxical inheritance pattern. The encoded protein ephrin-B1 (which comprises an EPH domain that interacts with Eph receptor tyrosine kinases, single pass transmembrane (TM) sequence and intracellular PDZ (protein interaction) domain) is involved in cell recognition, so that cells expressing the molecule tend to group together (homophilic sorting). In the female, random X-inactivation generates groups of cells that either express, or do not express ephrin-B1, and the homophilic sorting process increases the patch size of these cells, causing abnormal tissue boundaries (for example, in the coronal sutures and limbs).33 This process has been termed cellular interference.31 In males this cannot occur, and it is presumed that functional redundancy between different ephrin family members mitigates the consequences of complete lack of ephrin-B1.

Other genes

The heterozygous FGFR1 mutation encoding Pro252Arg occurs at the equivalent position in FGFR1 to the Apert (FGFR2) and Muenke (FGFR3) mutations. However it is an unusual cause of Pfeiffer syndrome accounting for fewer than 10% of cases. Syndactyly of the feet, characteristically affecting digits 2-5 with a wide sandal gap with digit 1, seems to be the most characteristic feature.34

Whereas most genetically determined craniosynostosis is characterised by dominant inheritance, Antley-Bixler syndrome (features include disordered sex development and radio-humeral synostosis; mutation in POR encoding cytochrome P450 oxidoreductase)35 and Carpenter syndrome (with polysyndactyly; mutation in RAB23 encoding RAB23, member of RAS oncogene family)36 are recessive disorders. These mutations demonstrate pathogenic roles for steroid metabolism and hedgehog (or possibly Wnt) signalling in cranial suture development, both of which are at present poorly understood.

Chromosome abnormalities

A wide variety of chromosome abnormalities have been associated with craniosynostosis, many in single cases only. The clearest causal link is with deletions of 7p21.1, which includes the TWIST1 gene.26, 27 Other non-random associations that do not show complete penetrance are with deletions of 9p22 and 11q23.3-qter (metopic synostosis).37 Craniosynostosis is recognised as a low frequency association of the 22q11.21 microdeletion. Published studies of the prevalence of submicroscopic chromosomal abnormalities in syndromic craniosynostosis have ranged widely, from 6.7%7 to 28% (ref. 38). The Oxford study7 showed a predominance (85%) of metopic or sagittal synostosis in patients with chromosome abnormalities. Compared with single gene disorders, which often required reoperation (58% of cases), patients with chromosome abnormalities followed a less aggressive course (reoperation rate 17%) suggesting a different, secondary origin of the associated craniosynostosis.

Management

Genetic testing strategy

Although targeted genetic testing is appropriate for patients in whom a specific diagnosis is suspected, the general issue arises whether those with non-syndromic synostosis should be offered genetic testing. In the Oxford study, causative mutations were present in 11% multisuture, 37.5% bicoronal and 17.5% unicoronal synostosis, but were absent in all sagittal, metopic and lambdoid synostosis cases tested. Although the numbers of patients tested in some groups were relatively small, the low success rate of molecular diagnosis in sagittal synostosis has been independently confirmed.39 The numbers of mutations found in the non-syndromic patients were seven in FGFR3, three in the IIIa or IIIc exons of FGFR2 and one in TWIST1. On the basis of these data, we recommend that as a minimum, genetic testing of FGFR3 (for the Pro250Arg mutation) and FGFR2 (mutation hotspots in exons IIIa and IIIc), should be offered for all patients presenting with coronal or multisuture synostosis. The higher genetic load associated with coronal synostosis is likely to reflect the distinct embryological origin of the coronal suture, at the boundary between the developing frontal bone (neural crest origin) and parietal bone (cephalic mesoderm).8, 40

A flow diagram to aid prioritisation of genetic testing is shown in Figure 3.

Figure 3

Flow diagram for molecular genetic diagnosis of craniosynostosis, showing the minimum tests recommended for each clinical presentation. In practice, the Oxford laboratory bundles sequencing of the FGFR1, FGFR2 (exons IIIa and IIIc), FGFR3 and TWIST1 genes together into a single 'level 1' screen to simplify the workflow.41 If the suggested tests are negative, the diagnosis should be reviewed.

Genetic counselling/risk assessment

Where no molecular or cytogenetic diagnosis is made and the family history is negative, we suggest a sibling recurrence risk of 2% for sagittal and metopic synostosis, 5% for unicoronal synostosis and 10% for bicoronal and multisuture synostosis. These figures are informed by older epidemiological studies,1, 42, 43, 44 but do involve some guesswork, because these studies included patients in whom mutations could now be identified. Offspring risks are not well documented; they are probably low (∼ 5%) in the case of non-syndromic sagittal, metopic and unicoronal synostosis, but likely to be substantially higher (30-50%) in bicoronal and possibly multisuture synostosis.

For individuals with identified single gene disorders, the main issue surrounds the recurrence risk that should be given for apparently de novo mutations. In the case of FGF receptor mutations, provided that the blood of both parents is negative for the mutation, the recurrence risk is very low (well under 1%). This is because the vast majority of cases arise from mutations occurring in adult spermatogonia, which although subject to strong positive selection never populate large proportions of the sperm.15, 16 However, a single case of true mosaicism for FGFR2 mutation was recently described.45 At the opposite end of the spectrum, mosaicism was present in 19% of first affected individuals in pedigrees with EFNB1 mutations, so the mutation must be looked for very carefully in the parents (for example, by heteroduplex analysis in addition to DNA sequencing).32 A recurrence risk of 10% for the siblings of sporadic females with CFNS is appropriate. Mosaicism for TWIST1 mutations, although theoretically possible, has not been reported; however, the sample size of de novo TWIST1 mutations is relatively small, so a cautiously low (2%) sibling recurrence risk is appropriate.

Prenatal diagnosis

Where a molecular abnormality has been identified in the family, the issues regarding prenatal or preimplantation diagnosis do not differ substantially from those in other genetic disorders. More problematic is the question whether it is feasible to diagnose craniosynostosis prenatally by ultrasound or other imaging techniques. Cranial sutures form very late (∼ 16 weeks gestation)46 compared with most other embryonic structures, therefore at the time when most routine ultrasound diagnosis is being undertaken (∼ 20 weeks), insufficient time has elapsed for growth distortion of the skull to have occurred, except in the most severe cases. Although there have been a few reports of ultrasound diagnosis of craniosynostosis around this time,47 the majority of even syndromic craniosynostosis is not detected during the pregnancy. When the issue is to screen for recurrence of craniosynostosis present in an older sibling, evidence of Apert syndrome can be sought by careful examination of the limbs for syndactyly. In most other situations, a late ultrasound is recommended to check for cephalopelvic disproportion, but caution should be exercised in providing any confident opinion in the prenatal period that craniosynostosis, except for the most severe forms, has been excluded.

Treatment and care

Acute management

Care of neonates and infants with severe multisuture synostosis is directed towards maintenance of the airway, support of feeding, eye protection, and treatment of raised ICP. Respiratory difficulty may require urgent sleep study assessment by specialist paediatric respiratory physicians and ear, nose and throat (ENT) surgeons, necessitating either continuous positive airway pressure support, nasal stenting, tonsillectomy/adenoidectomy, choanal dilatation, early midface advancement or tracheostomy, depending on the anatomical cause. Exposure keratitis occurs if the eyelids are unable to close and an urgent ophthalmology opinion should be sought, with consideration given to tarsorraphies or early midface advancement to provide eye protection.

Raised ICP associated with craniosynostosis has several different causes, which require different treatments. Hydrocephalus needs a shunt; obstructive sleep apnoea is treated by improving the airway (see above). Craniocerebral disproportion (the consequence of craniostenosis) requires calvarial expansion. Foramen magnum decompression might be required if there is tonsillar herniation. In multisuture synostosis, abnormal venous drainage poses a significant hazard when operating on the back of the skull ( Figure 1t).

Elective management

Elective surgical management of craniosynostosis has three major objectives, which are to correct the skull deformity, prevent its progression and reduce the future risk of raised ICP. At the Oxford unit, the majority (∼ 60%) of primary surgical procedures are performed between the ages of 6 months and 2 years. Attention must be given to secondary sensory deficits, for example, resulting from ptosis (Saethre-Chotzen syndrome), strabismus (unicoronal synostosis and craniofrontonasal syndrome), hearing loss (conductive in the case of FGFR2 mutations and sensorineural in the case of Muenke syndrome) and dental malocclusion (especially FGFR2 mutations). Associated malformations, such as syndactyly and cleft palate (Apert syndrome) also require surgery.

Regular follow-up throughout childhood is advisable, particularly to monitor for symptoms of raised ICP, such as headaches, behaviour change, or decline in school performance. Information on the presence of specific mutations is of prognostic value: for example, coronal synostosis has a worse prognosis (higher risk of repeat surgery and persistent deformity) in the presence of the Muenke syndrome mutation;48, 49 subjects with TWIST1 mutations are at higher risk for secondary development of raised ICP;50 large TWIST1 deletions are associated with a higher risk of learning disability.26, 27

Conclusions

Genetic workup should be an integral part of the management of craniosynostosis as it contributes both to risk assessment for the family and prognostic information for the patient. Although the molecular bases of the common craniosynostosis syndromes have been defined, it is likely that a single molecular aetiology remains to be identified in a further 10-15% of individuals. Whole genome assessment of copy number changes and DNA sequencing are likely to identify further predisposing loci, and consideration should be given to other mechanisms of disease such as mosaicism and imprinting defects. Although surgery is expected to remain the mainstay of management for the foreseeable future, the identification of signalling pathways pathologically activated in the cranial suture (such as the RAS-ERK pathway activated by Apert syndrome mutations)51 raises the possibility of the use of adjuvant medical therapies in the future.

References

1. 2.
Boulet SL , Rasmussen SA , Honein MA : A population-based study of craniosynostosis in metropolitan Atlanta, 1989-2003. Am J Med Genet 2008; 146A: 984-991.

2. 5.
Haas LL : Roentgenological skull measurements and their diagnostic applications. Am J Roentgenol Radium Ther Nucl Med 1952; 67: 197-209.

3. 11.
Iseki S , Wilkie AOM , Morriss-Kay GM : Fgfr1 and Fgfr2 have distinct differentiation and proliferation-related roles in the developing mouse skull vault. Development 1999; 126: 5611-5620.

4. 12.

5. 16.
Goriely A , Hansen RMS , Taylor IB et al: Activating mutations in FGFR3 and HRAS reveal a shared genetic origin for congenital disorders and testicular tumors. Nat Genet 2009; 41: 1247-1252.

6. 18.
Hoefkens MF , Vermeij-Keers C , Vaandrager JM : Crouzon syndrome: phenotypic signs and symptoms of the postnatally expressed subtype. J Craniofac Surg 2004; 15: 233-240.

7. 21.
Bochukova EG , Roscioli T , Hedges DJ et al: Rare mutations of FGFR2 causing Apert syndrome: identification of the first partial gene deletion, and an Alu element insertion from a new subfamily. Hum Mutat 2009; 30: 204-211.

8. 23.

9. 30.

10. 31.

11. 39.
Boyadjiev SA : International craniosynostosis consortium: genetic analysis of non-syndromic craniosynostosis. Orthod Craniofacial Res 2007; 10: 129-137.

12. 40.

13. 49.

Download references
Further Reading

1. Jabs EW : TWIST1 and the Saethre-Chotzen syndrome; in Epstein CJ, Erickson RP, Wynshaw-Boris A (eds): Inborn Errors of Development. Oxford: Oxford University Press , 2008, pp 474-481.

2. Twigg SRF , Wilkie AOM : EFNB1 and EFNA4 in craniofrontonasal syndrome and craniosynostosis; in Epstein CJ, Erickson RP, Wynshaw-Boris A (eds): Inborn Errors of Development. Oxford: Oxford University Press , 2008, pp 1476-1482.

3. Wilkie AOM : Bad bones, absent smell, selfish testes: the pleiotropic consequences of human FGF receptor mutations. Cytokine Growth Factor Rev 2005; 16: 187-203.

4. Wilkie AOM : FGF receptor mutations: bone dysplasia, craniosynostosis, and other syndromes; in Epstein CJ, Erickson RP, Wynshaw-Boris A (eds): Inborn Errors of Development. Oxford: Oxford University Press , 2008, pp 461-470.

Acknowledgements

Research into craniosynostosis in AOMW's laboratory has been supported by the Wellcome Trust, Medical Research Council, EPA Cephalosporin Fund and Oxford Partnership Comprehensive Biomedical Research Centre with funding from the Department of Health's NIHR Biomedical Research Centres funding scheme. The views expressed in this publication are those of the authors and not necessarily those of the Department of Health. We thank all members of the craniofacial unit in Oxford for supporting the work on which this article is based.

Author information

Affiliations

1. Oxford Craniofacial Unit, Oxford Radcliffe Hospitals NHS Trust, John Radcliffe Hospital, Oxford, UK

David Johnson

& Andrew O M Wilkie

2. Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, UK

Authors

1. Search for David Johnson in:

2. Search for Andrew O M Wilkie in:

Competing interests

The authors declare no conflict of interest.

Corresponding author

Correspondence to Andrew O M Wilkie.

To obtain permission to re-use content from this article visit RightsLink.

Further reading

Weicai Wang

, Chen Zhou

, Zhicai Feng

, Hongyu Li

, Yadong Zhang

, Baicheng Bao

, Bin Cai

, Mu Chen

& Hongzhang Huang

Applied Microbiology and Biotechnology (2019)

Eric Lee

, Trang Le

, Ying Zhu

, George Elakis

, Anne Turner

, William Lo

, Hanka Venselaar

, Carol-Ann Verrenkamp

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, Maya Chopra

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, Tiong Yang Tan

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, David John Amor

, Wanda Lattanzi

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Journal of Applied Genetics (2018)

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Journal of Applied Genetics (2017)

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Craniosynostosis, defined as the premature fusion of the cranial sutures, presents many challenges in classification and treatment. At least 20% of cases are caused by specific single gene mutations or chromosome abnormalities. This article maps out approaches to clinical assessment of a child presenting with an unusual head shape, and illustrates how genetic analysis can contribute to diagnosis and management.

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another article about craniosynostosis (B2, B3, B4, C9, D1

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another article about craniosynostosis (B2, B3, B4, C9, D1

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It is important to know about this condition as this is a red flag, as we are trained to treat all ages and I am especially interested in treatment of babies (B2, B3, B4, C9, D1).

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Abstract

Positional skull deformities may be present at birth or may develop during the first few months of life. Since the early 1990s, US pediatricians have seen an increase in the number of children with cranial asymmetry, particularly unilateral flattening of the occiput, likely attributable to parents following the American Academy of Pediatrics "Back to Sleep" positioning recommendations aimed at decreasing the risk of sudden infant death syndrome. Positional skull deformities are generally benign, reversible head-shape anomalies that do not require surgical intervention, as opposed to craniosynostosis, which can result in neurologic damage and progressive craniofacial distortion. Although associated with some risk of positional skull deformity, healthy young infants should be placed down for sleep on their backs. The practice of putting infants to sleep on their backs has been associated with a drastic decrease in the incidence of sudden infant death syndrome. Pediatricians need to be able to properly differentiate infants with benign skull deformities from those with craniosynostosis, educate parents on methods of proactively decreasing the likelihood of the development of occipital flattening, initiate appropriate management, and make referrals when necessary. This report provides guidance for the prevention, diagnosis, and management of positional skull deformity in an otherwise normal infant without evidence of associated anomalies, syndromes, or spinal disease.

INTRODUCTION

Flattening of the occiput and asymmetrical skull molding may be caused by mechanical factors that act on the head in utero or during early infancy. This common condition has been referred to by many names such as benign positional molding, posterior plagiocephaly, occipital plagiocephaly, plagiocephaly without synostosis, and deformational plagiocephaly. Ancient civilizations recognized the malleability of the rapidly growing newborn skull and intentionally deformed skulls by selective positioning and using external constraints to achieve cultural distinction. The term "plagiocephaly" is a Greek derivative that means "oblique head." Most skull deformities present at birth are the result of in utero or intrapartum molding. Associated conditions involve uterine constraint, especially in cases of multiple-birth infants, and forces exerted on the skull during complex delivery associated with forceps or vacuum-assisted delivery. Infants born prematurely also have a greater incidence of skull deformity attributable to molding after birth. Most of these deformities improve spontaneously during the first few months of life if the infant does not rest his or her head predominantly on the flattened area of the skull. If the infant continues to rest his or her head on the flattened side of the occiput, an initially occipital plagiocephalic deformity may be perpetuated or worsened by gravitational forces and will be referred to in the remainder of this report as positional skull deformity as it relates to otherwise normal infants. Plagiocephaly is less commonly caused by unilateral lambdoidal or unilateral coronal craniosynostosis, which is a progressive and potentially devastating condition that requires early detection and surgical management. The clinical differentiation of benign positional skull deformity from craniosynostosis is well documented in the literature. A long narrow head, known as dolichocephaly, can be positional from breech presentation, familial, or caused by sagittal craniosynostosis. Occipital flattening and atypical shape also may be caused by craniosynostosis, particularly bilateral lambdoid craniosynostosis. However, the incidence of isolated lambdoid craniosynostosis is quite rare, estimated to be approximately 3 in 100 000 births (0.003%).

If the positional skull deformity develops postnatally, an initially typical, rounded skull shape may become flattened occipitally as a result of static supine positioning. Associated torticollis or "wryneck" may occur as a consequence of hemorrhage (within the sternocleidomastoid muscle) and/or subsequent scarring within the sternocleidomastoid muscle or muscle shortening caused by persistent, unidirectional positioning and limited neck motion resulting in plagiocephaly.

The incidence of positional skull deformity has been estimated to be as low as 1 in 300 live births to as high as 48% of typical healthy infants younger than 1 year, depending on the sensitivity of the criteria used to make the diagnosis. Since the American Academy of Pediatrics Task Force on Infant Positioning and Sudden Infant Death Syndrome (SIDS) in 1992 recommended that healthy infants be positioned supine for sleeping, the incidence of SIDS has decreased from 1.2 per 1000 live births in 1992 to 0.56 per 1000 live births in 2001. Coincident with this decrease in SIDS has been a drastic increase in positional skull deformity, estimated at approximately 13% in healthy singleton infants, which makes this a relatively common issue to be faced by the pediatrician caring for infants and their families.

Mild positional skull deformity may persist in some children into adolescence. Minor craniofacial asymmetry can be detected in a significant number of adults; however, there are few current cases of positional skull deformity serious enough to be acknowledged by patients.

Families are often concerned that positional skull deformity may cause developmental delays. Although there have been no rigorous prospective studies to address this concern, there is currently no evidence to suggest that positional skull deformity causes developmental delays. There has been some early motor skill developmental delay of all infants placed supine related to upper body strength and rolling over, which resolves over time. Long-term follow-up studies have primarily been retrospective and questionnaire in nature and have not noted delays in cognitive or neurologic function. As might be suspected, conditions that cause delayed or abnormal development may predispose to positional skull deformity (eg, infants with hypotonia or hypertonia).

Concerns have been raised over vision development and mandibular asymmetry, but a causal link to positional skull deformity has not been established. Likewise, there has been no credible medical evidence to support concerns brought up in lay literature associating positional skull deformity to otitis media, temporomandibular joint (TMJ) syndrome, scoliosis, or hip dislocation.

PREVENTION

The pediatrician or other primary care clinician should educate parents as well as other health care professionals, such as those in newborn care units, on methods for decreasing the risk of development of positional skull deformity and its treatment. A certain amount of prone positioning, or "tummy time," while the infant is awake and being observed is recommended to help prevent the development of flattening of the occiput and to facilitate development of the upper shoulder girdle strength necessary for timely attainment of certain motor milestones. Beginning at birth, most positional skull deformity also can be prevented by nightly alternating the supine head position (ie, left and right occiputs) during sleep and periodically changing the orientation of the infant to outside activity, such as is likely to occur at the door of the room. Avoidance of prolonged placement indoors in car safety seats and swings should be discouraged. Documentation of these educational discussions and notation of infants' positive physical findings longitudinally are important.

DIAGNOSIS

Positional skull deformity risk factors (multiple births, large for gestational age, oligohydramnios, breech or transverse position, etc) should be noted at birth, and positional skull deformity should be screened for at each health supervision visit up to 1 year of age to detect deformities that occur after birth as delineated in Bright Futures. Transient molding (caput, cephalhematoma) may be present at birth and obscure the true head shape. The diagnosis of positional skull deformity in infancy is made primarily on the basis of history and is confirmed by the physical examination. It is important for the pediatrician or other examiner to look down at the top of the head, view the position of the ears, and note the position of the cheekbones (maxilla). By doing this, the typical plagiocephalic positional skull deformity, which forms a parallelogram, will be observed. In addition to the usually unilateral flattening of the occipital area, there may be ipsilateral frontal (forehead) and parietal bossing, cheekbone prominence, and anterior ear displacement ipsilateral to the flattened occiput ( Fig 1).

In contrast to deformational plagiocephaly, true craniosynostosis (either unilateral coronal or, much less commonly, lambdoid) most commonly yields a trapezoidal head shape in which there is flattening of both the occipital and frontal regions on the affected side. Uncommonly, lambdoid craniosynostosis can produce a parallelogram head shape, although the affected ear is displaced posteriorly and inferiorly in contrast to deformational plagiocephaly, with which it is displaced anteriorly. There is also tilting of the posterior skull base with prominence of the mastoid. Facial deformities are minimal if present at all. Normal and abnormal physical findings should be documented.

Examination of the face also may lead to detection of abnormalities such as head tilt and contralateral facial flattening. An assessment of neck movements also should be made to confirm or rule out the presence of torticollis. Infants with torticollis have some limitation of active rotation of their heads away from the flattened side of the occiput. The rotating-chair or stool test is a procedure that assists in the diagnosis of torticollis associated with positional skull deformity. The examiner sits on a rotating chair or stool and holds the infant facing the parent: the parent attempts to keep the infant interested in maintaining eye contact while the examiner rotates with the infant on the chair or stool and observes the infant's head movements. The difference between movement toward and away from the flattened side is helpful in making the diagnosis of torticollis associated with positional skull deformity.

SKULL RADIOGRAPHS AND CRANIAL COMPUTED TOMOGRAPHY SCANS

Because the diagnosis of positional skull deformity is made on the basis of history, findings on physical examination, and resolution over time with positional intervention, imaging studies are unnecessary in most situations. In addition, if obtained, their interpretations may be misleading to clinicians, particularly in the case of computed tomography (CT) scans. For the infant born with a normal head shape that progressively changes during the first weeks postnatally, no studies should be performed. Imaging studies should be reserved for infants born with deformities or those that do not improve over the first several weeks with repositioning. To minimize the risk of radiation exposure and the possible need for sedation, it is recommended that imaging studies be ordered by the specialist, because most craniofacial surgeons reserve radiographic imaging or CT scans for those patients who are suspected of having craniosynostosis and/or require surgical intervention. Radiographs and other imaging studies are also rarely indicated for infants with torticollis unless it is progressive or associated with other clinical findings.

MANAGEMENT

Management of positional skull deformity involves preventive counseling for parents, mechanical adjustments, and exercises. Parental compliance with the management plan is pivotal in lessening the likelihood and severity of positional skull deformity. Skull-molding helmets are an option for patients with severe deformity or skull shape that is refractory to therapeutic physical adjustments and position changes. Surgery is rarely necessary but may be indicated in severe refractory cases of positional skull deformity. However, infants with craniosynostosis typically require surgical correction and skull reconstruction. Early surgical intervention results in less invasive procedures because an infant's normal brain growth assists in remodeling the skull postoperatively. Minimally invasive surgery is now available to some infants identified with craniosynostosis in the first months of life.

SUMMARY

In most cases, the diagnosis and successful management of positional skull deformity can be assumed by the pediatrician or other primary health care clinician. This management includes examination for and counseling regarding positional skull deformity in the newborn period and at health supervision visits during infancy, as well as monitoring for improvement or progression. For the mild-to-moderate deformity, positioning and observation is the recommended treatment. Both positional changes and molding helmets are options for the infant with severe deformity. Cranial orthoses should be reserved for severe cases of deformity or for the infant whose deformity does not improve after 6 months of age. Referral to a pediatric neurosurgeon with expertise in craniofacial malformations, a craniofacial surgeon, or a craniofacial team should be considered if there is progression or lack of improvement after a trial of mechanical adjustments or suspicion of craniosynostosis.

Lead Authors

James Laughlin, MD

Thomas G. Luerssen, MD

Mark S. Dias, MD

Committee on Practice and Ambulatory Medicine, 2009-2010

Lawrence Hammer, MD, Chairperson

Oscar Brown, MD

Edward Curry, MD

James Laughlin, MD

Herschel Lessin, MD

Chadwick Rodgers, MD

Geoffrey Simon, MD

Liaisons

Xylina Bean, MD

National Medical Association

Staff

Elizabeth Sobczyk, MSW, MPH

Section on Neurological Surgery Executive Committee, 2009-2010

Mark S. Dias, MD, Chairperson

Joseph Piatt, MD, Immediate Past Chairperson

Philipp Aldana, MD

John Ragheb, MD

Michael Partington, MD

David Gruber, MD

Past Executive Committee Member

Thomas G. Luerssen, MD

Staff

Aleksandra Stolic, MPH

Footnotes

This document is copyrighted and is property of the American Academy of Pediatrics and its Board of Directors. All authors have filed conflict of interest statements with the American Academy of Pediatrics. Any conflicts have been resolved through a process approved by the Board of Directors. The American Academy of Pediatrics has neither solicited nor accepted any commercial involvement in the development of the content of this publication.

The guidance in this report does not indicate an exclusive course of treatment or serve as a standard of medical care. Variations, taking into account individual circumstances, may be appropriate.

All clinical reports from the American Academy of Pediatrics automatically expire 5 years after publication unless reaffirmed, revised, or retired at or before that time.

View Abstract

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Prevention and Management of Positional Skull Deformities in Infants

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Positional skull deformities may be present at birth or may develop during the first few months of life. Since the early 1990s, US pediatricians have seen an increase in the number of children with cranial asymmetry, particularly unilateral flattening of the occiput, likely attributable to parents following the American Academy of Pediatrics "Back to Sleep" positioning recommendations aimed at decreasing the risk of sudden infant death syndrome.

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Anatomy of the adductor tubercle

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adductor tubercle
I palpated this tubercle on my patient today and realised that that is what it was!  I was fairly confident that the adductor magnus inserted into it, but thought I should do my homework later and check (B2, B3, B4, C3, C7)
Well I was right, but I was also able to confirm the innervation, which was the obturator nerve, whose nerve roots are the L3, L4, where my patient's back pain starts.  Is this co-incidence or is her pain to do with the surgery for her meniscus and recently diagnosed OA of her right knee?
I find it very helpful looking at pictures of the adductor magnus as well as observing pictures for adductor longus and brevis and seeing how/where they attach onto the pubic symphysis.

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(Last Updated On: February 4, 2019)

Origin: Anterior: Inferior pubic ramus and the ramus of the ischium
Posterior: Inferolateral aspect of the ischial tuberosity
Insertion: Anterior: Medial margin of the gluteal tuberosity of the femur, medial to gluteus maximus.
Posterior: By a broad attachment into the linea aspera and the proximal part of the medial supracondylar line and by a small tendon to the adductor tubercle.
Actions: Adduction of the thigh at the hip, extension of the thigh at the hip
Innervation: Anterior: Posterior division of the obturator nerve (L2, L4)
Posterior: Tibial portion of the sciatic nerve (L4, L5, S1, S2, S3)
Blood Supply: Femoral artery

Adductor Magnus Actions With Agonist and Antagonists

Primary Actions of the Adductor Magnus
1. Adduction of the thigh at the hip
Antagonists:

Gluteus maximus (upper fibers)

Gluteus medius

Gluteus minimus

2. Extension of the thigh at the hip

Gluteus Maximus

Semitendinosus

Semimembranosus

Biceps Femoris (long head)

Antagonists: 3. Anterior Part - Assists with internal rotation of the thigh at the hip

Tensor Fasciae Latae

Gluteus Minimus (anterior fibers)

Gluteus Medius (anterior fibers)

Antagonists:

Obturator Internus

Obturator Externus

Gemellus Superior

Gemellus Inferior

Quadratus Femoris

Information about the cause and effect of Adductor Magnus pain: Adductor Magnus Muscle: Groin, Pelvic and Thigh Pain
Recommended Anatomy Books:

Massage Therapist

Owner: thewellnessdigest.com

Twelve years of experience working with clients with chronic pain, post injury pain, and post surgery pain. Muscle dysfunction is often overlooked but can hold the key to many pain conditions.

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(Last Updated On: February 4, 2019) Origin: Anterior: Inferior pubic ramus and the ramus of the ischium Posterior: Inferolateral aspect of the ischial tuberosity Insertion: Anterior: Medial margin of the gluteal tuberosity of the femur, medial to gluteus maximus.

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this makes so much sense.  Now I just need to see what if anything goes through the adductor hiatus.

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this makes so much sense.  Now I just need to see what if anything goes through the adductor hiatus.

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Oh yes, allows the passage of the femoral vessels.  this makes even more sense now. (B2, B3, B4)

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Also found in: Wikipedia.

ad·duc·tor hi·a·tus
[TA]

the aperture in the aponeurotic insertion of the adductor magnus that transmits the femoral artery and vein from the adductor canal to the popliteal space.

adductor hiatus

the opening in the tendon of insertion of the adductor magnus through which the femoral artery and vein pass into the popliteal space.

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Also found in: Wikipedia. [TA] the aperture in the aponeurotic insertion of the adductor magnus that transmits the femoral artery and vein from the adductor canal to the popliteal space. the opening in the tendon of insertion of the adductor magnus through which the femoral artery and vein pass into the popliteal space.

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revision of the Adductor Canal (B2, B3, B4)

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revision of the Adductor Canal (B2, B3, B4)

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The adductor canal (Hunter's canal, subsartorial canal) is a narrow conical tunnel located in the thigh.

It is 15cm long, extending from the apex of the femoral triangle to the adductor hiatus of the adductor magnus. The canal serves as a passageway from structures moving between the anterior thigh and posterior leg.

In this article, we shall look at the anatomy of the adductor canal - its borders, contents and clinical relevance.

The adductor canal is bordered by muscular structures:

Lateral: Vastus medialis.

Posterior: Adductor longus and adductor magnus.

The apex of the adductor canal is marked by the adductor hiatus - a gap between the adductor and hamstring attachments of the adductor magnus.

The adductor canal serves as a passageway for structures moving between the anterior thigh and posterior leg. It contains the femoral artery, femoral vein, nerve to the vastus medialis and the saphenous nerve (the largest cutaneous branch of the femoral nerve).

As the femoral artery and vein exit the canal, they become the popliteal artery and vein respectively.

Clinical Relevance - Adductor Canal Block

In the adductor canal block, local anaesthetic is administered in the adductor canal to block the saphenous nerve in isolation, or together with the nerve to the vastus medialis.

The block can be used to provide sensory anaesthesia for procedures involving the distal thigh and femur, knee and lower leg on the medial side. The sartorius and femoral artery are used as anatomical landmarks to locate the saphenous nerve.

Clinical Relevance - Adductor Canal Compression Syndrome

Adductor canal compression syndrome describes entrapment of the neurovascular bundle within the adductor canal. A rare condition, it is usually caused by hypertrophy of adjacent muscles such as vastus medialis.

It is most common in young males, who may present with claudication symptoms due to femoral artery occlusion (more common) or neurological symptoms due to entrapment of the saphenous nerve.

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The adductor canal (Hunter's canal, subsartorial canal) is a narrow conical tunnel located in the thigh. It is 15cm long, extending from the apex of the femoral triangle to the adductor hiatus of the adductor magnus. The canal serves as a passageway from structures moving between the anterior thigh and posterior leg.

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Revision of the Cranium- falx cerebriI have been revising the falx cerebri to enhance my cranial skills in clinic.  It's beginning to make more sense and I think I am beginning to remember a lot more each time I revisit different areas of the brain (B2, B3, B4)

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Revision of the Cranium- falx cerebriI have been revising the falx cerebri to enhance my cranial skills in clinic.  It's beginning to make more sense and I think I am beginning to remember a lot more each time I revisit different areas of the brain (B2, B3, B4)

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What questions should I ask if my patient says they bruise easily?
I decided to investigate more fully and reflect on the fact that for a whole year and a half in clinic I have allowed myself to be ignorant of the answers (B2, B3, B4).  However now I know and am now more knowledgeable and safer in clinic as a result.  I love learning more too I should have looked up the question at the beginning of Year 3 but at least now is better than never.

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What happened?
I had a patient who had MS.  I was challenged by my tutor to look up the ccomplications of Multiple Sclerosis (B2, B3, B4).
She also suffers from asthma; and has a cough that doesn't go away.  I realised that I didn't understand the link between multiple sclerosis, so I thought it would be good for my learning and knowledge to learn more about how multiple sclerosis sufferers suffer from asthma, and what it does to the lungs. (C3, C5, C7, D1, D14 )
What did I gain from this? This improved my knowledge of this condition and showed me how important it is to be inquisitive about my patients' conditions.  This link showed me that it is as important to address the underlying problems, not just the 'superficial' problem on top; as I had no idea how the MS would affect the patient's lungs (although if I had thought more carefully, it is fairly obvious) that lung function would be affected due to the demyelination of the nerves which occurs in MS. Although I attempted to treat the diaphragm and the sternum with some success, I think I might have had more success if I could have got the patient 'more on board' to come for more regular treatment, rather than once a month. (A3, A5, A6, B2, B3, B4, C3, C5, C7, D1) However, although I used techniques which involved the IVM; I think now I would use techniques which mobilised the tissues more, to shift any build up of fluid on the lungs and encourage nutrition, drainage and waste removal. She brushes off the asthma (which is underlying rather than a big factor in her life) as 'less important' and I think as I reflect on this patient, my inexperience as I took over her treatment just before the beginning of summer clinic, begins to me to feel more relevant with this patient.  What would I do differently now?  I would try to get her really engaged with the treatment process (which I know has helped her) in an active way rather than a passive way (A3, A5, A6).  It is difficult to know whether someone can only afford one treatment per month, or whether they think that is all that necessary; there is the moral dilemma of how far you go to convince the patient that you can help them more if they visit you more frequently.

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Among the many possible complications of multiple sclerosis (MS) is a reduction in your ability to exhale fully and to cough effectively enough to clear secretions or food from your airway. A serious consequence of these changes is a higher risk of respiratory infections like pneumonia.

Changes in lung function can also cause fatigue, as you work harder to breathe and supply your body with the oxygen it needs.

How MS Affects the Lungs

There are a number of ways that MS can lead to breathing problems, including the following:

Lesions in the Brain As multiple sclerosis progresses, lesions in your brain and spine can affect almost every aspect of your physical functioning. It's possible that brain lesions could change your lung function, says Zulma Hernandez-Peraza, MD, neurologist at the University of Illinois Hospital and Health Sciences System in Chicago.

Lesions that disrupt the signals from the brain to the lungs can result in a condition known as central sleep apnea, in which breathing stops and restarts repeatedly during sleep. Symptoms of central sleep apnea include waking up abruptly with shortness of breath, having shortness of breath that improves with sitting up, insomnia, daytime sleepiness, and chest pain at night.

A more common form of sleep apnea, where the upper airway becomes intermittently obstructed, can also occur in people with MS if the muscles that normally keep the airway open become slack due to lesions in the brain. Obstructive sleep apnea is associated with snoring.

Spinal Lesions These can also restrict your ability to get air in and out of the lungs, says neurologist Staley Brod, MD, professor of neurology at the Medical College of Wisconsin in Milwaukee.

"A lesion in the cervical spine creates the 'MS hug' sensation, which can cause the feeling of shortness of breath," adds Dr. Hernandez-Peraza. "This is usually just an unpleasant perception. When tested, the oxygen levels in your blood should be normal."

The MS hug is caused by spasms in the intercostal muscles, the small muscles between the ribs.

Muscle Weakness and Spasticity "Weakness can affect breathing," says Dr. Brod. When the muscles that help with inhaling and exhaling are weak, you may not be able to breathe deeply enough to bring in the oxygen you need. Spasticity in those muscles contributes to the problem.

Medication One of the side effects of the MS disease-modifying drug Gilenya (fingolimod) is a reduction in some measures of lung function. Some types of medication, such as tranquilizers, muscle relaxants, and opioids, can also slow or reduce breathing.

What You Can Do

If you're unable to cough normally or you're feeling short of breath, dizzy, or even faint, don't just write off these symptoms as an expected part of life with MS. Take the following steps to manage the problem and prevent it from getting worse:

See your doctor. Your doctor will ask you about your symptoms and do a physical exam to look for the cause of the problem. He may conduct tests of your lung function or refer you to a pulmonologist for pulmonary function tests.

Lung function tests are painless and noninvasive, and they allow your doctor to see how much air is moving in and out of your lungs, how forcefully you can exhale after inhaling, and how quickly you can force air out of your lungs.

Go to pulmonary rehabilitation. Depending on the cause of your breathing problems, your doctor may refer you for pulmonary rehabilitation, where you'll learn exercises and techniques to improve your breathing. You may be instructed to spend several minutes a day using a handheld device to build your breathing muscles and increase your lung volume. You may also work with a physical therapist or pulmonary rehabilitation specialist on exercises to strengthen your upper body.

Aim for a healthy weight. Being overweight and having a thick neck can lead to sleep apnea, says Brod.

Stop smoking. "It is known that smoking is bad for a person with MS," points out Brod. It's also bad for your lungs. If you smoke and have multiple sclerosis, you're increasing the burden on your lungs.

Use oxygen if it's prescribed. Supplemental oxygen is rarely needed for MS unless you have another medical condition that affects your lungs, such as chronic obstructive pulmonary disease (COPD). But if oxygen is prescribed, it can help you feel better and function better.

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Gasping for Breath: When MS Attacks Your Lungs

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Among the many possible complications of multiple sclerosis (MS) is a reduction in your ability to exhale fully and to cough effectively enough to clear secretions or food from your airway. A serious consequence of these changes is a higher risk of respiratory infections like pneumonia.

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C8: ensure your patient records are full, accurate and completed promp

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C8: ensure your patient records are full, accurate and completed promp

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Ensure that your patient records are full, accurate and completed promptly.
Today I was again pulled up for inaccurate wording in my notes. I am trying harder to make sure I describe muscles accurately, if they are hyper contracted, or hyper tonic, or even hyper mobile. I will be hyper vigilant to make sure I don't do this again.

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I decided to revisit the anatomy of the larynx (B2, B3, B4) due to its pertinence to my own personal experience.

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I have revised the procedure for knee arthroscopy/meniscus repair. I understand this procedure much better now; it has increased my knowledge and how I should advise future patients who have this procedure t

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https://www.ted.com/talks/tom_thum_and_matthew_broadhurst_what_a_beatboxer_s_vocal_cords_look_like_in_action?utm_campaign=tedspread&utm_medium=referral&utm_source=tedcomshare

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https://pin.it/zpk6pm4rbzjdwm

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Mock exam January 2019  I found this a nerve-wracking experience. Interestingly, actually the real CCA1 was I think less bad, but maybe because I had the previous experience which had not gone well.  I really don't want to be incompetent so I am doing my best to make sure that I am knowledgeable.

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Mock exam January 2019  I found this a nerve-wracking experience. Interestingly, actually the real CCA1 was I think less bad, but maybe because I had the previous experience which had not gone well.  I really don't want to be incompetent so I am doing my best to make sure that I am knowledgeable.

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Feedback from my mock CCA.  I was asked how I felt this exam went, and I told the examiner that I felt my brain was whirring and that I got completely side tracked as well as feeling very stressed.  Autonomy definitely did not feel good on that day.

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Feedback from my mock CCA.  I was asked how I felt this exam went, and I told the examiner that I felt my brain was whirring and that I got completely side tracked as well as feeling very stressed.  Autonomy definitely did not feel good on that day.

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I had a patient in the summer clinic with cervical spondylosis; my tutor told me to look this up as I wasn't completely sure of demographics etc (B2, B3, B4,, C3, C7)

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I actually wrote this in 2018.  It is clear to me that I need to keep on revising this condition so I can help my patients more, as the more I understand it, the quicker my patients will get better (B2, B3, B4, C3, C5, C7)

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D2: you must respond effectively to requirements for the production of high-quality written material and data

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D2: you must respond effectively to requirements for the production of high-quality written material and data

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A short piece I wrote about meeting D2

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D3: you must be capable of retrieving, processing and analysing information as necessary

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D3: you must be capable of retrieving, processing and analysing information as necessary

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Safety: very important to be safe and knowledgable.

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Safety: very important to be safe and knowledgable.

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I have recently been revising the questions for Benign Prostatic Hyperplasia (B2, B3, B4, C1, C2, C3, C5, C7,  C8

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Reflection about a less-than good day in clinic

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Reflection about a less-than good day in clinic

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I am still going through my clinic diary; seeing what I wrote down from last summer.  Although I know I have revised these things, it takes a while for it to stick properly.  So writing this serves as useful learning and revision.

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I am still going through my clinic diary; seeing what I wrote down from last summer.  Although I know I have revised these things, it takes a while for it to stick properly.  So writing this serves as useful learning and revision.

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Psoriatic disease.  I was very interested by this disease.
What happened? A whole family, one by one, came to see me in clinic and I have seen first hand the different symptoms they have. What did I learn? How this disease affects peoples lives; it makes their skin very itchy and they tend to be inflamed and on quite nasty medications to reduce the symptoms of this disease.  In fact although the grandmother of the family doesn't have psoriatic arthritis, she has nodular prurigo and is currently using methotrexate to calm the symptoms. She knows that methotrexate has very nasty side effects but it makes her life considerably easier and less painful. I think I will find it quite easy to spot people with these diseases now, so this is what I have taken away from this experience.  I am beginning to become more 'investigative' (B2, B3, B4, C3, C7, D1) and see links with other inflammatory conditions.
What can I do for this patient of mine? I can support her in her decisions, and try to educate her so that she knows and understands the damage she does when she scratches her legs, which she does frequently.  She is also beginning to understand the consequences of eating food that been defrosted and sits around, 'growing' histamines which then make her legs hot, inflamed and itchy (C3, C7,  C8, A5). A truly horrible condition, but I am sure this is another auto-immune condition at least partially brought on because of stressful events in her life, some of which she has told me about.
What next? Since I have started seeing this patient, I have recently spoken to Howard Beardmore of the British Institute of Osteopathy about my mother's eczema (and I am thinking about doing his postgraduate course (B2, B3, B4) and I am going to investigate to see whether this patient's pelvis feels 'congested' as the nodular prurigo is on the L4/L5 dermatome, more so on the left leg than the right (C3, C5, C7, C8)

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Abstract

Psoriasis and PsA are the main phenotypes of psoriatic disease. Both conditions are highly polygenic diseases in which stochastic and environmental factors are crucial in the pathogenic process. Although the MHC region is a highly dense genetic area, most of the genetic basis of psoriatic disease within it resides in the HLA region. For decades, HLA-C*06 has been accepted as the main descriptor of the two main phenotypes of skin psoriasis. There is now compelling evidence to suggest that HLA-C*06 is only a genetic biomarker for skin involvement and not for joint involvement in psoriatic disease. The role of HLA-B*27 in the genetic aetiology of PsA has been recognized since the 1970s. Recent population case-control studies with adequate patient groups and replication cohorts, as well as confirmation studies in family pedigrees through the use of modern molecular typing methods, have reinforced the aetiological role of this allele in PsA. These studies have offered a new vision of the role of this allele in disease expression. This review contextualizes the latest findings on the role of HLA-B27 in psoriatic disease, emphasizing those aspects of particular interest for clinical practice.

HLA-C*06 is a biomarker of skin involvement in psoriatic disease; it has little or no influence in the development of joint disease.

HLA-B*27 is a genetic biomarker of joint disease in psoriasis patients.

HLA-B*27 is also a marker of disease expression in PsA.

Psoriatic disease: the importance of the HLA region

Psoriasis and PsA are immune-mediated diseases in which the combination of multiple genetic risk factors, environmental noxae and stochastic factors are hypothesized to be responsible for the conditions [ 1, 2]. Recent genome-wide association studies have markedly expanded the group of genomic loci that are associated with the susceptibility of developing both conditions [ 3-12].

The strong familial aggregation, as demonstrated by a high occurrence rate of PsA and psoriasis in relatives, supports the theory of a genetic basis of these diseases [ 13]. Candidate gene and genome-wide studies have shown a strong association between psoriasis and the MHC region, particularly with a 300 kb segment in the MHC class I region on chromosome 6p21.3, known as PSORS1. The largest and most consistently reported association is with the HLA-C*06 allele within this region [ 3-12].

The role of the HLA genes in the susceptibility to PsA was demonstrated when increased sharing of the HLA haplotypes was documented among sibling pairs concordant for PsA; concordance for psoriasis only was not found [ 14]. Case-control studies have identified the HLA region as containing potential susceptibility loci for PsA. Whereas HLA-C*06 is increased in PsA patients when compared with the general population, compelling evidence suggests that this association is stronger with psoriasis than with PsA [ 15-26]. HLA B*27, B*39 and B*07 have been specifically associated with PsA in case-control studies that compared PsA patients with psoriasis patients [ 15-26]. Several HLA antigens have been related to specific manifestations of PsA. Thus HLA-B*27 is more common among PsA patients with axial disease, whereas B*38 and B*39 are increased among those with peripheral polyarthritis [ 15-26].

The following two susceptibility loci have been hypothesized to be associated with PsA in the HLA region: one located telomeric to HLA-C, which is associated with psoriatic skin lesions (present in the extended haplotypes EH13.1, EH37.1 and EH57.1), and another, MICAA9, that is associated with susceptibility to arthritis and is present in EH38.1, EH39.1 and EH57.1. [ 27, 28]. Most MICA allele associations with psoriasis and PsA are dependent on linkage disequilibrium with HLA-B and HLA-C risk alleles. Independent of HLA, only MICA*016 influences the risk of developing psoriasis without arthritis, and homozygosity for MICA*00801 increases the risk of developing PsA in patients with psoriasis [ 29].

In population- and family-based analyses, HLA-B*27 has been shown to be a stronger genetic marker for PsA than for psoriasis. In these studies, the absence of a detectable association between HLA-B*27 and psoriasis compared with an association with healthy individuals suggests that B*27 is not a marker for skin disease [ 15-26]. Analyses of the relationship between psoriatic disease and HLA-B*27 in different ethnic groups have consistently shown that HLA-B*27 is an independent risk allele for PsA that is unrelated to skin disease [ 30-35]. The prevalence of HLA-B*27 in PsA patients ranged from 20 to 35% in such studies, which is clearly much lower than its prevalence in AS (80-95% of the patients). Therefore this allele could only account for a small proportion of the total genetic risk for PsA. The HLA-B*27 allele might merely be a risk allele for AS that coexists with psoriasis, given the relatively high prevalence of psoriasis in the general population. However, because the frequency of HLA-B*27 is increased as well in PsA patients with peripheral joint involvement, HLA-B*27 could be an independent risk allele for PsA [ 23, 35]. Therefore HLA-B*27 could be considered as one of the strongest HLA risk alleles for PsA in patients with psoriasis and might help to differentiate the two conditions [ 35]. Herein we will review the reasons why this allele is important in disease susceptibility and its clinical phenotyping.

HLA-B27: disease pathogenic mechanisms

There are several theories regarding the pathogenic role of HLA-B*27: the arthritogenic peptide hypothesis; the HLA-B*27 misfolding hypothesis, which is linked to autophagy and/or the unfolded protein response (UPR); and the HLA-B*27-free heavy chain (HC) and homodimer hypothesis [36-38].

The arthritogenic peptide theory suggests that disease results from the ability of B*27 to bind and present unique arthritogenic peptides to CD8⁺ cytotoxic T lymphocytes (CTLs). Thus a B*27-restricted CTL response, triggered by peptides shared by disease-triggering pathogens, could cross-recognize a self-peptide or peptides bound to HLA-B*27. Further support for this model was presented in T cell studies in which B*27-restricted CTLs that could recognize bacterially infected and uninfected target cells were detected in the joints and peripheral blood of patients with reactive arthritis and AS [ 39]. However, the inability to identify suitable arthritogenic peptide candidates from joints and to demonstrate CTLs specific for these B*27-restricted epitopes, as well as the findings in animal models of SpA that indicate the disease appears not to require CD8⁺ T cells, have limited the acceptance of this theory [ 40].

The misfolding theory postulates that accumulation of B*27 HCs in the endoplasmic reticulum (ER) provides potent and chronic stimulation of ER stress response pathways culminating in the release of pro-inflammatory cytokines that contribute to disease pathogenesis [ 36-38]. Support for this model resulted from B*27 transgenic animal models that were shown to have an accumulation of misfolded B*27 HCs in their splenocytes and macrophages [ 41]. It is possible that misfolding provides one of several signals necessary for the activation of an inflammatory response, and it has been postulated that the misfolding might trigger or augment an innate immune response. This misfolding theory has been recently challenged by transgenic rat studies in which the accumulation of misfolded HCs could be reversed by the overexpression of human b2m without alleviating the disease phenotype [ 42].

IL-23 might play a key role in the pathogenesis of SpA, including PsA. The exact mechanism of how and where IL-23 production is induced and how it further contributes to disease processes is not yet known. Different hypotheses have been proposed, such as HLA-B*27 misfolding, with activation of the UPR as molecular drivers of IL-23 production [ 43, 44]. Strong evidence of misfolding and UPR activation in patient samples is lacking. It has been recently demonstrated that HLA-B*27 misfolding occurs in the gut of AS and Crohn's disease patients and is accompanied by activation of autophagy rather than a UPR. Autophagy appears to be associated with intestinal modulation of IL-23 in AS [ 45]. Other authors have failed to demonstrate autophagy as the main source of IL-23 overexpression in synovial tissue from patients with SpA [ 46]. A link between autophagy and B*27 misfolding in the pathogenesis of PsA has not been formally shown. In support of this view, in ileocolonoscopic studies of PsA, intestinal inflammation was more frequently seen in the oligoarticular and axial forms of the disease, as well as in patients with HLA-B*27 [ 47].

The B*27-free HC and homodimer hypothesis proposes that disease results from the immune recognition of aberrantly folded surface B*27 molecules [ 36-38]. These molecules include b2m-free and peptide-free B*27 HCs that could be monomeric (B27 HC) or dimeric (B27 ₂). A trigger, such as a bacterial infection, hypoxia or a stress-related signal, is proposed to promote the formation of cell surface B27 HCs and B27 ₂ from unstable B27-folded precursors, which are then recognized by innate immunoregulatory receptors on leucocytes including NK cells, T cells and other antigen-presenting cells [ 36-38]. The demonstration of cell surface expression of B27 ₂ led to the proposal that these immunoregulatory receptors might specifically recognize B27 ₂, which could modulate the immune response towards inflammatory disease [ 36, 48-52]. A variety of immunoregulatory receptors could recognize different forms of HLA-B*27 molecules. These molecules include the killer immunoglobulin-like receptors (KIRs) and leucocyte immunoglobulin-like receptors (LILRs), which are expressed on many types of leucocytes, including NK cells, NK T cells, monocytes, macrophages, dendritic cells and T cells [ 36, 48-52]. The manner in which the interaction of B27 ₂ with immunoregulatory receptors leads to disease remains undetermined; however, given the role that these receptors play in maintaining immune homeostasis, it is plausible that ligation by aberrant forms of B*27 might upset this balance in favour of a pro-inflammatory response [ 36, 48-52]. B27 ₂ is a ligand for a number of NK receptors, including KIR3DL1, KIR3DL2, LILRB2 and LILRA1. This pattern of recognition is distinct from that of B27 heterodimers, which are bound by KIR3DL1, LILRB1, LILRB2 and LILRA1 but not by KIR3DL2. One possibility is that the interaction of B27 ₂ with NK cells and T cells expressing KIR3DL2 results in altered cell signalling to promote the survival of pro-inflammatory cell subsets that participate in and exacerbate a pro-inflammatory response [ 50]. Thus the KIR3DL2⁺ NK cells were protected from apoptosis in the presence of B27 ₂-expressing AP cells, whereas the KIR3DL2⁺ CD4 T cells demonstrated enhanced survival and proliferation [ 51]. The KIR3DL2⁺ CD4 T cells produced IL-17 after B27 ₂ stimulation, and these IL-17-producing KIR3DL2⁺ CD4 T cells were enriched in the peripheral blood and SF of SpA patients [ 52]. These data support the hypothesis that aberrant forms of B27 promote the survival of KIR3DL2⁺ T and NK cells, which go on to participate in the inflammatory response through IL-17 overexpression.

It is unclear whether the disease pathogenesis linked to the presence of HLA-B*27 is the same in AS and PsA. The ER aminopeptidase 1 gene ( ERAP1) codes for a trimming aminopeptidase located in the ER, which has a function in the MHC class 1 peptide presentation [ 53]. The ERAP1-ERAP2 haplotype is hypothesized to influence the HLA-B*27-restricted peptide repertoire, folding mechanisms and HC dimer formation, and polymorphisms of these genes have clear implications in disease pathogenesis [ 53, 54]. The ERAP1 gene locus polymorphisms have shown a robust association with AS and psoriasis and several genome-wide association studies (GWASs) have identified ERAP1 as a candidate gene for AS, with an estimated population-attributable risk of 26% [ 37, 54]. The association of ERAP1 with AS or psoriasis has been shown to be highly dependent on the presence of HLA-B*27 and C*06, respectively (the association is only seen in subjects carrying B*27 or C*06) [ 54, 55]. A similar dependency of ERAP1 could not be demonstrated in PsA, irrespective of the HLA-B*27 or C*06 status [ 56].

HLA-B27 and psoriatic disease: a role in the disease aetiology

The aetiological role of HLA-B*27 in susceptibility to AS has been accepted for decades [ 57, 58]. In addition, a similar link has been implied regarding the susceptibility to PsA [ 59], with variability regarding the frequency of this allele in PsA populations. In some studies, the frequencies of HLA-B*27 are within the range of the control values, whereas frequencies as high as 39% have been found in other studies [ 23, 35, 60].

Recent population case-control studies with adequate patient groups and replication cohorts, as well as confirmation studies in family pedigrees using modern molecular typing methods, have reinforced the aetiological role of HLA-B*27 in PsA. In the largest study that has been performed of the association of HLA with PsA, which involved 678 cases and 688 controls as well as 283 families with 1000 individuals, HLA-B*27 was present in ∼20% of the cases [odds ratio (OR) 3.03 (95% CI 2.14, 4.28)]; in the multiple regression analysis, the association was independent of HLA-C*12 and B*38, two alleles that are associated with PsA as well. In addition, the HLA-B*27 haplotypes with HLA-C*01 and HLA-C*02 were found to be associated with PsA (B*27/C*01: OR 2.58; B*27/C*02: OR 2.92). In the family-based validation substudy, the haplotype transmission analysis showed that A*02 C*06 B*57 DRB1*07 DQB1*0303 formed an extended haplotype with excess transmission in PsA. In this substudy, HLA-B*27 was independently associated with risk, showing a Z value of 3.745 (Z values >0 indicate overtransmission of the allele) [61].

The previous study only included PsA patients, and the comparisons of the allele frequencies were performed using a healthy control population. It is essential to investigate the HLA genes that differentiate the patients with PsA from those with psoriasis alone, because this determination might enable the discovery of markers for the development of PsA in psoriasis patient populations. The work by Eder et al. [ 62] addressed this subject. In this population-based case-control study that included >700 PsA patients and 335 psoriasis patients, there was no difference in the frequency of HLA-B*27 between the psoriasis patients and the healthy controls (4.5% vs 7.2%), whereas the association between HLA-C*06 and psoriasis was stronger in the psoriasis-alone group than in the controls (44.2% vs 18.1%, P = 3 × 10 −¹⁹). In the multivariate analysis, the following three alleles were found to be associated with psoriatic disease (PsA + psoriasis alone): HLA-B*27 (OR 2.36, P < 0.0001), HLA-B*38 (OR 6.01, P < 0.0001) and HLA-C*06 (OR 2.23, P < 0.0001). The following markers were found to be overexpressed in PsA compared with their expression in psoriasis: HLA-B*27 (OR 5.07, P = 2 × 10 −¹⁰), HLA-C*01 (OR 2.55, P = 0.0009) and HLA-C*02 (OR 2.41, P = 0.0005). In a multivariate regression analysis, the following alleles were more frequent in PsA than in psoriasis: HLA-B*27 (OR 5.17, P < 0.0001), HLA-B*08 (OR 1.61, P = 0.009) and HLA-B*38 (OR 1.65, P = 0.026); HLA-C*06 was less frequent in the PsA group than in the psoriasis group (OR 0.58, P = 0.0002) and more frequent in the PsA group than in the healthy controls (OR 1.71, P = 2 × 10 −⁵). The following haplotypes remained significantly associated with PsA compared with psoriasis after the multivariate analysis: HLA-B*18-C*07 (OR 10.1, P = 0.004), HLA-B*27-C*01 (OR 41.1, P < 0.0001), HLA-B*27-C*02 (OR 19.9, P < 0.0001), HLA-B*38-C*12 (OR 2.9, P = 0.01), HLA-B*08-C*07 (OR 2.6, P = 0.004) and HLA-B*57-C*06 (OR 0.5, P = 0.03) [ 62].

To validate the previous results, the HLA alleles that were identified in the population-based study were further assessed in a family-based association study. In total, 178 PsA probands, 30 psoriasis probands and 561 first-degree family members belonging to 208 families were analysed. The alleles that were found to be overtransmitted in PsA when compared with psoriasis were HLA-B*27 (Z = 3.0, P = 0.002), C*12 (Z = 2.8, P = 0.005), B*38 (Z = 2.0, P = 0.04) and B*39 (Z = 2.0, P = 0.045) [ 63].

Finally, an important practical issue in this study was assessment of the utility of HLA risk alleles in identifying the PsA patients among the patients with psoriasis in terms of positive predictive values (PPVs). Assuming a PsA prevalence of 30% in those with psoriasis, the PPV of each of the identified HLA risk alleles was calculated as follows: HLAB*08 PPV = 42%, HLA-B*27 PPV = 64%, HLA-B*38 PPV = 43%, HLA-C*06 PPV = 35%. Therefore HLA-B*27 could be considered to be the strongest HLA risk allele for PsA among the patients with psoriasis, and it differentiates the conditions [62].

Winchester et al. [ 64] conducted a population-based case-control study in an Irish population to test the role of the HLA alleles in psoriatic disease risk. In the patients with PsA presenting to a rheumatology unit, the frequency of C*06 was significantly lower than that in the psoriasis cohort (28.7 vs 57.5%; P = 9.9 × 10 −¹²). In the combined discovery and validation cohort of the PsA patients, the frequency of B*27:05:02 (B*27) increased to 15.6% [OR 3.2 (95% CI 2.1, 4.7)]. The two haplotypes of HLA-B*27, EH27.1 and EH27.2, were significantly increased in frequency, accounting for 8.1% and 7.0%, respectively, of the combined cohort. To address the question of the possibility of epistatic interactions between C*06 and other MHC susceptibility alleles, the investigators conducted separate analyses in which all of the C*06-positive patients were excluded; the exclusion did not decrease the intensity of the association of PsA with EH27.1, EH27.2 or EH39.1, indicating that these haplotypes operate in a manner independent of the presence of C*06 in PsA susceptibility. The authors stated that because the EH27.1 and EH27.2 haplotypes associated with PsA susceptibility share the same B*27 allele and differ in their HLA-C alleles, this finding strongly suggests that this susceptibility maps to the HLA-B locus [ 64].

HLA-B27 and psoriatic disease: the role in disease expression

The relationships between the HLA genes and psoriatic disease are relevant in exploring disease susceptibility and understanding its several phenotypes. Chandran [ 65] found B*27 (OR 2.90, P < 0.0001) to be associated with PsA in type II psoriasis patients (psoriasis beginning at >40 years of age), which reinforces the role of this allele in determining musculoskeletal disease rather than skin disease in the psoriatic phenotype. In this cohort, comparing PsA with dactylitis to PsA without dactylitis showed, in the univariate analyses, that only the HLA-C*02 and B*27 frequencies were higher in dactylitis and, in the multivariate analysis, that HLA-C*02 (OR 1.85, P = 0.046) and HLA-B*27 (OR 1.74, P = 0.029) were independently associated.

Genetic factors have been shown to influence joint damage progression in PsA. Gladman et al. [ 66] showed that HLA-B27 in the presence of HLA-DR7, HLA-B39 and HLA-DQw3 in the absence of HLA-DR7 are each associated with progression of clinical damage, whereas HLA-DR7 and B22 antigens are 'protective'. In one study, the principal outcome was the change in the number of clinically damaged joints between visits, with patients having between 1 and 53 assessments of change between successive repeated visits. Using the data from a large well-defined prospective cohort of PsA patients followed for a median duration of 6 years, the HLA alleles B*39 (OR 1.87, P < 0.005), B*27 (OR 1.51, P = 0.003) and A*02 ( P = 0.026) were independently associated with the risk of peripheral joint damage progression between clinic visits, whereas the alleles DQB1*0604, C*04 and B*50 were associated with a lower risk [ 65]. These findings are in conflict because the B*27-negative patients developed more peripheral erosions than did the B*27-positive patients in a previous study [ 67]. A potential explanation for this discrepancy is found in a very recent study by Haroon et al. [ 68], in which the highest propensity score for severe PsA was with the B*27:05:02-C*02:02:02, B*08:01:01-C*07:01:01 and B*37:01:01-C*06:02:01 haplotypes and not the B*27:05:02-C*01:01:01 or B*57:01:01-C*06:02:01 haplotypes. Therefore the haplotype containing B*27-C*02 is linked to severe disease, whereas that containing B*27-C*01 is not.

Two small studies using serological HLA antigen testing showed that B27 and Cw2 were associated with axial disease in PsA [ 23]. This finding has been recently confirmed in a well-powered study using molecular HLA typing. The study showed that C*02 and B*27 are not independent of each other and detected their association with sacroiliitis and syndesmophytes [ 65]. Because HLA-B*27 is associated with peripheral joint damage progression as well, these findings indicate that HLA-B*27 with or without HLA-C*02 is a marker of disease progression and poor prognosis in PsA.

HLA-B*27 has been associated with axial PsA in several serological HLA studies [ 23]. Thus, in a Spanish series of axial PsA, 57% of the patients included under the label of isolated axial disease had this allele, compared with 19% in the polyarthritis plus axial group and 29% in the oligoaxial disease group ( P = 0.016). The authors found that patients with isolated axial disease were more often men, with more clinical (inflammatory back pain), radiological (bilateral sacroiliitis and marginal syndesmophytes), immunogenetic (HLA-B27) and extra-articular (uveitis) features, which strongly correlated this group with AS [ 69]. More recently, this finding has been validated by Chandran et al. [ 65], who investigated 633 Caucasian subjects with PsA satisfying the Classification Criteria for Psoriatic Arthritis (CASPAR) criteria and obtained the data on the time when at least unilateral grade 2 or greater sacroiliitis and the first syndesmophyte were observed on plain radiographs of the pelvis and spine. The authors conducted two separate analyses. The principal outcome for the first analysis was the time to development of radiographic sacroiliitis after the diagnosis of PsA, and the principal outcome for the second analysis was the time to the development of syndesmophytes after the diagnosis of PsA. The association between sacroiliitis and PsA was corroborated in the univariate analysis. In the multivariate analysis, HLA-B*27 [hazard ratio (HR) 1.66 (95% CI 1.21, 2.29), P = 0.002] was independently associated with a higher risk of developing syndesmophytes, whereas the allele HLA-A*29 [HR 0.39 (95% CI 0.18, 0.85), P = 0.018] was associated with a lower risk.

Eder et al. [ 62] found that the HLA-C*06 allele was associated with a prolonged interval of time from the onset of psoriasis to that of PsA, which supports its protective effect. The HLA-C*06 carriers had more than double the time interval from the onset of psoriasis to PsA. These results were in accordance with a previous study of Queiro et al. [ 70], who reported that HLA-C*06-positive PsA patients have longer psoriasis-arthritis latency periods (9 vs 5 years; P = 0.03). Winchester et al. [ 64] found, in addition to the susceptibility conferred by particular MHC alleles and haplotypes, preliminary evidence to suggest that the susceptibility genotype influences the timing of the onset of musculoskeletal features in PsA in relationship to the onset of psoriasis. Analysis of the data by quartiles based on the median value of the time interval between the onset of psoriasis and the onset of PsA showed that in the first quartile, arthritis developed before psoriasis, whereas arthritis followed the onset of psoriasis by>14.75 years in the last quartile. The B*27-positive cases accounted for 26.3% of those in the first time interval quartile, and this quartile included 58.8% of all of the B*27-positive individuals. The frequency of B*27 progressively declined through each of the quartiles of lengthening time intervals, accounting for only 5.1% of those in the fourth quartile, which included 7.8% of all of the B*27-positive cases. The individuals who were positive for C*06 accounted for 24.6% of those in the first time-interval quartile, and this proportion increased to 38.5% in the fourth quartile. Reflecting the progressive enrichment of C*06 in the cases with a long interval between the development of skin manifestations and the development of arthritic manifestations, the ratio of the C*06-positive cases to B*27-positive cases was 0.93 in the first quartile, increasing to a ratio of 7.5 in the fourth quartile. In a much smaller study conducted in PsA patients with axial disease, B*27 was found to be associated with the overall risk of disease (OR 6.4, P < 0.0004); however, this association was stronger in the patients with early onset compared with late-onset cases (51% vs 13%; P = 0.001) [ 71].

The previously cited data suggest that two separate principal patterns of the MHC effect would result in the psoriasis phenotype ( Fig. 1). The first pattern involves the classic psoriasis susceptibility gene C*06, and is characterized by more penetrant skin disease with less prevalent and more time-dependent development of musculoskeletal manifestations. The second pattern appears to be mediated by alleles of the HLA-B locus, including B*27 and B*39. This latter pattern includes a musculoskeletal phenotype nearly equivalent in penetrance to that of the skin disease and, in the case of B*27, occurs much more temporally coincident with the musculoskeletal involvement [ 35, 64]. In addition, it is plausible that, beyond the HLA-B locus, and because of the high linkage disequilibrium between the genes centromeric to HLA-C, other genes might contribute to the overall disease risk and define different subphenotypes of PsA [ 72].

HLA-B*27 has a striking relationship with AS and is associated with the severity of MRI-evident bone marrow osteitis in the axial and peripheral skeleton [ 73, 74]. Castillo-Gallego et al. [ 75] compared the total MRI scores of different groups of patients (PsA, axial SpA and AS) and patients with and without HLAB*27. When the groups were subanalysed according to the HLA-B*27 status, the disease severity in terms of the total MRI scores was found to be related to the presence of HLA-B*27. The HLA-B*27-negative PsA patients had lower MRI scores than the HLA-B*27-positive PsA and AS patients, whereas the B*27-positive PsA patients had similar scores to the AS patients. In addition, the overall number of bone marrow osteitis lesions was related to the presence of HLA-B*27 because the HLA-B*27-negative PsA patients had a lower number of lumbar spine lesions than the AS and HLA-B*27-positive PsA patients, whereas there were no differences between the AS patients and the HLA-B*27-positive PsA group. Collectively these findings support the concept of the key role of the HLA-B27 gene as a determinant of the osteitis extent in SpA, including PsA. These findings are in contrast with those of a previous small cross-sectional study in axial PsA, in which the univariate analysis could not demonstrate correlations between B*27 and clinical symptoms such as back involvement, syndesmophytes or functional impairment [ 67].

The prevalence and incidence of PsA has been increasing in the last decades in men and women, but this increase has been seen more markedly in men than in women [ 76]. The reason for this gender difference is not fully understood; however, one explanation might be a differential expression of the risk genes between the sexes. Queiro et al. [ 77] recently compared the MHC gene profile between men and women with PsA, and HLA-B*27 was found in 36% of the men (OR 7.3) and 27% of the women (OR 4.8); the comparison included healthy controls matched by sex. This differential expression of B*27 between the sexes was even more pronounced when the study population was stratified by the age at disease onset. Of the patients with onset of disease before 40 years of age, 42% of the men and 30% of the women had this allele. A declining effect of HLA-B*27 was seen in parallel with increasing age at disease onset, and this effect was more clearly found in men than in women [ 77]. In some studies of axial disease, the attributable risk of B*27 was restricted only to the male population [ 78]. Therefore B*27 might help explain the risk of disease because it appears to be related to the early onset of PsA, and may help to explain the higher incidence and prevalence of PsA among males, as highlighted in recent epidemiological studies.

Conclusion

Although the aetiological role of B*27 in psoriatic disease has been recognized for decades and corroborated in the most recent GWAS [ 12], its additional role in determining specific traits of the disease has been highlighted only recently. Thus PsA patients expressing this allele tend to have a shorter interval of time between onset of the skin disease and that of the musculoskeletal symptoms. They are more prone to developing enthesitis, dactylitis and uveitis and they tend to develop peripheral and axial joint damage more frequently over time. At present, HLA-C*06 and B*27 are the most important genetic biomarkers in psoriatic disease because they establish marked traits that in turn allow phenotypic differentiations in both populations [ 35, 79].

Funding: No specific funding was received from any funding bodies in the public, commercial or not-for-profit sectors to carry out the work described in this article.

Disclosure statement: The authors have declared no conflicts of interest.

References

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HLA-B27 and psoriatic disease: a modern view of an old relationship

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Psoriasis and PsA are the main phenotypes of psoriatic disease. Both conditions are highly polygenic diseases in which stochastic and environmental factors are crucial in the pathogenic process. Although the MHC region is a highly dense genetic area, most of the genetic basis of psoriatic disease within it resides in the HLA region.

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picture of psoriasis (B2, B3, B4)

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HLA-B27 Syndromes: Overview, Pathophysiology, Clinical Features of HLA-B27 Syndromes - Acute Anterior Uveitis

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The first human leukocyte antigen (HLA) haplotype association with inflammatory disease was discovered in 1972, correlating HLA-B27 with ankylosing spondylitis. This remains one of the strongest known associations of disease with HLA-B27.

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picture of psoriasis (B2, B3, B4)

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Psoriasis is a common skin disease affecting 1 in 50 people. It occurs equally in men and women. It can appear at any age. Psoriasis is a long-term condition which may come and go throughout your lifetime. It is not infectious; therefore you cannot catch psoriasis from someone else. It does not scar the skin although sometimes it can cause a temporary increase or reduction in skin colour. Although psoriasis is a long-term condition there are many effective treatments available to keep it under good control.

Psoriasis can affect the nails and the joints as well as the skin. Psoriatic arthritis produces swelling and stiffness in the joints or stiffness in the lower back and should be managed by a rheumatologist who works closely with your dermatologist and/or your GP.

Psoriasis, particularly moderate to severe psoriasis, is associated with an increased risk of anxiety, depression and harmful use of alcohol. Moderate to severe psoriasis increases the risk of heart disease and stroke and treatment of psoriasis may reduce this risk. Psoriasis can also be associated with diabetes, obesity, venous thromboembolism, high cholesterol and high blood pressure. Psoriasis is also associated with inflammatory bowel disease and there is a small increased risk of skin cancer.

What causes psoriasis?

Both inherited and environmental factors play a role in the development of psoriasis

Skin affected by psoriasis is red and scaly. The outer layer of skin (the epidermis) contains skin cells which are continuously being replaced. This process normally takes between three and four weeks. In psoriasis, skin cells divide more quickly so that cells are both formed and shed in as little as three to four days.

Infections, stress, damage to the skin, alcohol, and sometimes intense sunlight may trigger flares of psoriasis. Certain medications such as beta blockers (used to treat high blood pressure and angina), lithium and some tablets used to treat malaria can also trigger flare-ups of psoriasis. Suddenly stopping some steroid tablets can also trigger or worsen psoriasis. Obesity and smoking are associated with a poor response to psoriasis treatments so exercise and being the correct weight can be beneficial.

Is psoriasis hereditary?

Yes, if you have a family member affected by psoriasis you are more likely to suffer from psoriasis. The way psoriasis is inherited is complex and not completely understood involving many genes.

What are the symptoms of psoriasis?

Psoriasis may not have any associated symptoms, but it can be itchy and painful. Certain sites such as the scalp, lower legs and groin can be particularly itchy. If psoriasis affects the hands and feet, painful fissures (cracks) can develop and these can affect use of the hands and walking. Severe psoriasis on the body can also develop cracks which are painful and can bleed.

Psoriasis can affect the nails and lifting away of the nail from the finger can be painful.

Psoriatic arthritis produces pain, swelling and stiffness in one or more joints, particularly in the morning.

What does psoriasis look like?

The skin changes of psoriasis (often known as plaques) are well defined and slightly raised pink or red (can differ in colour depending on your skin colour) areas with silvery-white scales. Many people have just a few plaques but some individuals with moderate to severe psoriasis may have several plaques covering large areas of their body.

Several patterns of psoriasis are recognised:

Chronic plaque psoriasis is the most common type of psoriasis. Plaques of psoriasis are usually present on the knees, elbows, trunk, scalp, behind ears and between the buttocks although other areas can be involved too.

Guttate psoriasis consists of small plaques of psoriasis scattered over the trunk and limbs. It can be caused by a bacteria called Streptococcus which can cause throat infections.

Palmoplantar psoriasis is psoriasis affecting the palms and soles. Psoriasis may appear at other sites too.

Pustular psoriasis is rare type of psoriasis where the plaques on the trunk and limbs are studded with tiny yellow pus filled spots. It can be localised or generalised and can flare rapidly necessitating hospital admission for treatment.

Erythrodermic psoriasis is an aggressive rare form of psoriasis which affects nearly all of the skin and can sometimes require hospital admission for treatment.

Nail psoriasis is present in about half of people with psoriasis. The features of nail psoriasis are:

Pitting (indentations) and ridging of the surface of the nail;

Salmon pink areas of discolouration under the nail;

Separation of the nail plate from the nail bed; and

Thickening and yellowing of the nails.

Complete nail destruction.

How will psoriasis be diagnosed?

Psoriasis is usually diagnosed on the appearance and distribution of the plaques. Skin biopsy is rarely used.

Psoriatic arthritis is usually diagnosed by a rheumatologist, but your dermatologist or GP may ask you if you have any joint symptoms or ask you to complete a screening questionnaire.

How is psoriasis assessed?

Psoriasis should be assessed at diagnosis, before your first referral to a specialist, every time you see a specialist and to assess your response to treatment. Psoriasis may be assessed by your doctors using a variety of scores which measure the severity in your skin and joints, how psoriasis is affecting your mood and your activities of daily living and whether you are at risk of heart disease.

These scores include the PASI (Psoriatic Arthritis Severity Index - a score that measures the severity of joint symptoms in psoriasis) and DLQI (Dermatology Life Quality Index - a score that measures the impact of psoriasis on your daily activities)

Can psoriasis be cured?

There is no cure for psoriasis and complete clearance of skin lesions may not always be possible. There are several effective treatments available to control your psoriasis. Spontaneous clearance of psoriasis may occur in some people.

How can psoriasis be treated?

Treatment of psoriasis depends upon your individual circumstances. Treatment applied to the surface of your skin (topical treatment) is sufficient alone in most patients. For people with more extensive or difficult to treat psoriasis, ultraviolet light treatment (phototherapy), tablet treatment or injection treatment may be required.

1. Topical treatments:

These include creams, ointments, gels, pastes and lotions. Topical treatments are dealt with in more detail in another of our leaflets (Topical treatments for psoriasis).

2. Phototherapy:

Phototherapy is ultraviolet light delivered in a controlled way to treat psoriasis. A course of treatment usually takes about 8-10 weeks and will require treatment sessions two to three times a week. This usually means attending a Phototherapy Unit in a hospital.

Two types of light are used: narrowband ultraviolet B light (nbUVB/TLO1) and ultraviolet A light (PUVA). The latter requires a sensitiser, known as a psoralen that can be taken as a tablet or added to a bath prior to treatment.

Further information on phototherapy is available in the following information leaflets: Treatments for moderate and severe psoriasis and Phototherapy).

3. Internal (systemic) treatments

Tablet options include acitretin (related to vitamin A), ciclosporin (suppresses the immune system), methotrexate (slows down the rate at which cells are dividing in psoriasis), and in some hospitals fumaric acid esters and apremilast.

Injectable treatments for psoriasis include etanercept, adalimumab, infliximab, ustekinumab, secukinumab, ixekizumab and guselkumab. Other new tablet and injected treatments are being developed in clinical studies at present.

Blood tests may be recommended by your GP or dermatologist. If you are considering tablet or injection treatment for your psoriasis, then blood tests will be needed before and during treatment.

Further details of these treatments can be found in the Treatments for moderate and severe psoriasis and individual drug patient information leaflets.

What can I do to help?

Discuss your psoriasis and how it affects your life with your GP or dermatologist and identify treatment goals.

Manage your risk factors for heart disease and stroke with your GP.

Adopt a healthy lifestyle: eat a balanced diet, try to lose weight if you are overweight and exercise regularly.

Stop smoking if you smoke.

If you drink excessive alcohol, reducing your intake might be helpful.

Reduce stress, where possible.

Take your medications as recommended by your GP or dermatologist.

If you have pain in your joints discuss with your GP or dermatologist.

This information is provided by the British Association of Dermatologists.

Gemma's story Marcus' story

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Psoriasis is a common inflammatory skin disease affecting 2% of the population. It occurs equally in men and women, can appear at any age, and tends to come and go unpredictably. It is not infectious, therefore you cannot catch psoriasis from someone else.

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I felt very disappointed after I received the results for this exam. Was I really this bad? Well I think they were fair with their assessment although I think a little of it is down to exam technique, which is something I am not good at, especially for practical exams. I have been investigating the things I fell down on such as the lack of reasoning as to why QL was in dysfunction.

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What is the Quadratus Lumborum (QL)?

The Quadratus Lumborum is a quadrangular shaped muscle which attaches to the bottom rib, the verterbrae in your lower back and the top of your pelvis. It acts as a stabiliser of the lower back and can laterally flex the spine. It extends your lower back when working with the other side and it aids forced exhalation, for example when coughing.

Why is it relevant?

Myofascial trigger points in the QL muscle often mimic symptoms of discogenic low back pain i.e. back and leg pain caused by a problem such as a 'slipped disc'. However 32% of such presentations have been shown to have QL muscle myofascial dysfunction as their primary issue, rather than a disc problem.

image courtesy of Wikipedia

What are Myofascial Trigger Points?

The most common cause of muscle pain is a phenomenon called 'Myofascial Trigger Points'. These are points of exquisite tenderness within a taut band of tight muscle which causes pain to refer in a particular pattern (Gerwin,1984). Myofascial trigger points often develop following overload of a particular muscle.

How do I activate Myofascial Trigger Points in the Quadratus Lumborum?

As mentioned above, QL trigger points can be activated by overload of the muscle. Bending and reaching movements (especially if holding something heavy) as well as other awkward movements is the most common method of injury. Other triggers include:

Major body trauma like car/motorbike accidents

Repetitive activities

Having a genetically short leg that causes a lateral tilt in pelvis

Walking or running on a sloping surface (side of the road)

A soft bed

What are the signs and symptoms of a Quadratus Lumborum muscle problem?

The QL muscle refers pain to a variety of areas about the lower back, abdomen and hip. These areas of pain include:

The sacroiliac joint (junction between the lower back and the pelvis)

The lower buttock

The front of the hip

The lower quadrant of the abdomen or groin

Over the outside of the hip i.e. over the greater trochanter

Aside from pain in these areas, you may be unable to turn in bed, stand or walk. Lying down will likely ease the pain. Coughing and sneezing may also be painful. Your pain may feel intense, or have a deep achy quality to it. It may also have a sharp, knifelike quality at times, particularly during movement.

Another possible consequence of Quadratus Lumborum muscle pain and trigger points is the development of 'Satellite Trigger Points'. As pain referring from the QL muscle projects over the gluteal muscles, secondary or satellite trigger points can therefore be activated within the gluteal region. In other words, pain that travels over a muscle can cause trigger points to develop within that muscle. This often results in pain referring down the leg, mimicking a 'sciatica' type presentation.

What treatment options are available for Quadratus Lumborum dysfunctions?

Our management of a Quadratus Lumborum issue would include the use of medical acupuncture, also referred to as dry needling (sometimes with neuro-electrical stimulation) to deactivate the trigger points in the QL itself, and in the surrounding musculature. We would also use soft tissue release techniques and manual therapy as an adjunct. Once the main pain driving trigger points have been largely deactivated, treatment would focus on exercise rehabilitation to improve the strength and function of the musculature in the lower back region to reduce the likelihood of a recurrence. Physio Pilates is an excellent way to aid a full return to function following an acute episode of back pain involving the Quadratus Lumborum muscle, or indeed many other lower back structures.

Article by Rachel Neary.

References:
Travell JG, Simons DG, Myofascial Pain and Dysfunction The Trigger Point Manual; The Lower Extremities. Vol 2, 1993.

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Quadratus Lumborum (QL) - 'The Joker of low back pain'

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What is the Quadratus Lumborum (QL)? The Quadratus Lumborum is a quadrangular shaped muscle which attaches to the bottom rib, the verterbrae in your lower back and the top of your pelvis. It acts as a stabiliser of the lower back and can laterally f

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Understanding the Quadratus Lumborum muscle better

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Understanding the Quadratus Lumborum muscle better

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Understanding what happens when QL is in dysfunction.

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Understanding what happens when QL is in dysfunction.

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I have reviewed the feedback from my CCA1 and have done digging into where / what I did wrong, not well enough etc.
By understanding the role that QL plays, I can better explain to the examiners what is happening to the patient's body and why. I have gone back to basics and checked the origins and insertions as well as nerve and action of this muscle. Although I knew this muscle's origins and insertions, I did not tell the examiners all I knew and maybe I had not quite processed its action on side bending of the spine. Well I definitely know now.

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Learning more about the QL and how it attaches, this was important to understand and process the actions of QL. I hadn't appreciated what makes the spine side bend. However, now I have definitely learned from my mistakes and will be able to apply this better in future.

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Ah, the fascia, full of sensory nerves connected to our movement brain, and an inter connected full body system. Enjoy this well written article.
http://www.ijtmb.org/index.php/ijtmb/article/view/62/82

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And its role in relationship to QL. I didn't understand the role of the iliolumbar ligament in relationship to the QL muscle, now however, I have researched it and my understanding of the lumbar spine and pelvis has improved by looking up this ligament and its involvement with the QL. It will be more in my fore thoughts when i am investigating back pain.

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The iliolumbar ligament, which has five bands, is one of three vertebra-pelvic ligaments responsible for stabilizing the spine where its lumbar section meets the sacral section in the pelvis. It does this along with the sacrospinous and sacrotuberous ligaments. This ligament is essential to restraining movement of the lumbosacral junction in the lower back.

The iliolumbar ligament passes through the transverse process at the side of the fifth lumbar vertebra and down to the iliac crest's inner lip on the posterior (back) side. The iliac crest is the top, outer portion of the ilium, the largest of the pelvic bones. The iliolumbar ligament forms a thickened, lower border for two thoracolumbar fascia (connective tissue) layers.

There are six ligaments in the lumbar spine region. Assisted by the lateral lumbosacral ligament, the iliolumbar ligament strengthens the lumbosacral joint, which connects the end of the lumbar spine with the beginning of the sacral section of the spine. Supraspinous, interspinous, ligamentum flavum, anterior longitudinal, and posterior longitudinal ligaments also play a role in strengthening vertebral joints.

This ligament stabilizes the connection between the pelvis and lower back, limiting trunk side-flexion. When this ligament becomes injured, bending to one side becomes painful in the sacroiliac joint area, though injuries to this ligament are rare. The sacroiliac joint area can be approximately located in some people by dimples in their lower back.

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Iliolumbar Ligament Anatomy, Function & Diagram | Body Maps

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The iliolumbar ligament, which has five bands, is one of three vertebra-pelvic ligaments responsible for stabilizing the spine where its lumbar section meets the sacral section in the pelvis. It does this along with the sacrospinous and sacrotuberous ligaments. This ligament is essential to restraining movement of the lumbosacral junction in the lower back.

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What hapened? CCA1 exam.
I failed to understand the implications of QL hypercontracture and possibly the involvement of the Ilio llumbar ligament as well.
What did i do next?
The ilio lumbar ligament has both horizontal and diagonal properties which enables it to stabilise both side bending and rotational movements.  Now, i have thoroughly investigated and I am better informed too.  Dysfunctions of this ligament contribute to lower back pain.
This better understanding of this ligament will allow me to have a greater understanding of low back pain when a patient rotates or side bends.

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The iliolumbar ligament connects the ilium to L5 and L4. It can often be source of lower back pain. Until we are about 18 it is contiguous with the quadratus lumborum, then they "separate". This ligament is involved in dysfunctions of side bending and rotation, as the L4 portion is diagonally oriented.

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I have revised my knowledge of PMR as I realised it needs frequent refreshment.

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Abstract

Polymyalgia rheumatica (PMR) is a unique disease of elderly people, traditionally diagnosed based on a clinical picture. A typical case is a combination of severe musculoskeletal symptoms and systemic inflammatory response with spectacular response to corticosteroids treatment. The severity of symptoms may be surprising in older patients where immunosenescence is normally expected. However, PMR may be diagnosed in haste if there is a temptation to use this diagnosis as a shortcut to achieve rapid therapeutic success. Overdiagnosis of PMR may cause more problems compared to underdiagnosis. The 2012 PMR criteria proposed by European League against Rheumatism/American College of Rheumatology aim to minimize the role of clinical intuition and build on more objective features. However, questions arise if this is possible in PMR. This has been discussed in this review.

Key words: Classification criteria, corticosteroids, diagnosis, musculoskeletal, polymyalgia rheumatica

Introduction

Polymyalgia rheumatica (PMR) is an auto-inflammatory rheumatic disease of people over 50 years, presenting with pain and stiffness in the neck, shoulder and hip girdles. The term PMR was first used to underline that it seemed substantially milder from rheumatoid arthritis (RA) as no joint damage had been observed. However, this name may be misleading as PMR is a disease but not a non-specific myalgic or paraneoplastic syndrome. Secondary PMR does not exist. The short definition of PMR may be also misunderstood as it does not suggest how unique the clinical picture of 'musculoskeletal pain and stiffness' might be. What makes PMR so special is a sudden onset of severe musculoskeletal symptoms that strongly reduce daily performance and quality of life, together with systemic inflammatory reaction in elderly but usually generally healthy patient, frequently accompanied by depressive reaction, lack of pathognomonic laboratory or radiologic findings, and splendid reaction to low-dose corticosteroids (CSs). Strong auto-inflammatory response is normally unexpected in an elderly patient, but immunosenescence seems not to apply in PMR. Good prognosis is also surprising as there is no good explanation to the fact that PMR patients apparently live longer than matched controls. However, PMR is frequently accompanied by giant cell arteritis (GCA). Therefore, there is an increased probability of all the ischaemic complications related to GCA in PMR. Further, generally favourable outcome of PMR may be easily wasted in case of excessive CSs treatment, resulting in side effect that eventually worsens patient's quality of life.

The aim of this review article is to discuss about correct diagnosis of PMR.

Epidemiology

Annual incidence of PMR is up to 50/100,000 population over 50 yr. It is uncommon in India. The highest prevalence is found in Caucasians, in Northern European countries, especially in Scandinavia. Vikings' ancestry is associated with increased risk of PMR (marked by migration from Scandinavia, in Western European lands invaded by Normands or Eastern European settled by Varangians). The incidence grows with age, starting from 50 yr, with peak above 70 yr. It is easier to find a report of wrong diagnosis of PMR in patients under 50 yr, than an undoubtful case report of PMR or GCA in young.

Polymyalgia Rheumatica Versus Giant Cell Arteritis

PMR and GCA are closely related. These have similar genetic background and epidemiology, and frequently overlap. However, PMR represents a non-specific immune-mediated inflammatory reaction triggered by innate immunity activation. GCA is manifested by vascular inflammation caused by faulty adaptive immune reaction that is mainly T cell dependent. The clinical outcome is so different that it is continuously debated why some patients express only one pathway. Evidence of vascular inflammation in needed to diagnose GCA. It is usually recorded in about 10 per cent of PMR patients, but detailed vascular examination may substantially increase that percentage. The historical term polymyalgia arteritica might still be accurate because it underlines suspected vascular pathogenesis of PMR. Silent vasculitis has been demonstrated in some of PMR patients. Regardless of PMR and GCA pathophysiologic relations, from a practical point of view, it must not be forgotten that patients diagnosed with PMR are also at an increased risk of GCA-associated complications. The concomitant GCA implies the need for more aggressive treatment strategy (). PMR symptoms can dominate over the clinical picture of GCA. Small CSs doses used for PMR do not suppress concomitant GCA (although this is more generally accepted than proved opinion) that may progress to cause blindness.

Table I

When Should Polymyalgia Rheumatica Be Suspected?

Proximal, musculoskeletal pain and stiffness are the leading manifestations and these raise little doubts about the diagnosis in a typical PMR case. However, PMR pivotal manifestations may be less specific: fewer or raised C-reactive protein (CRP) of unknown origin, general weakness, weight loss, depressive reaction, decompensation of chronic diseases (e.g. chronic heart failure) due to increased metabolism.

How to Diagnose Polymyalgia Rheumatica?

There is no universal answer to this question. Although clinical presentation is typical, in some cases, the disease may be surprising. The best strategy is a combination of different approaches (based on clinical picture, classification criteria, exclusions and ex juvantibus diagnosing), together with extensive diagnostics and follow up observation of atypical cases. Ninety per cent of rheumatologists in the United Kingdom (UK) declare the use of the classification criteria for PMR diagnosis although they admit not to adhere to the guidelines to exclude other diseases. This approach may be accepted only in countries with high incidence of PMR resulting in relatively low number of PMR mimics.

Diagnosis Based on Clinical Picture

Clinical assessment is most important for PMR diagnosis. There are no specific antibodies (PMR and GCA are T cell-dependent diseases) or additional testing to confirm PMR. Clinical manifestations come from a combination of musculoskeletal pain and stiffness and acute inflammatory response, which is quite different in elderly compared to young patients.

Musculoskeletal manifestations

It is difficult to find PMR case without bilateral pain and stiffness of muscles and joints of neck, shoulder and hip girdles. Generalized musculoskeletal pain is not a PMR manifestation. Small joints involvement is also not typical but may be rarely found. Shoulder girdle involvement usually appears first and may gradually extend to the area of neck and hip girdle. Symmetrical involvement is typical. The pain worsens during the night, typically waking the patient from sleep between 0400 and 0600 h in the morning. Morning stiffness of more than one hour is more specific for PMR than the pain, but the pain is more commonly reported. Pain may overwhelm the symptoms of stiffness. Limitations of upper limbs elevation make it difficult for the patient to comb his/her hair or pray in the morning. It is illustrated by the way patients get up out of bed: large joints stiffness makes them to rock the whole body to slip out beyond the edge of bed. However, after overcoming morning stiffness, patients can usually perform their daily activities fairly well. The feeling of stiffness can also reoccur during the day, after a period of immobility. In extreme cases, musculoskeletal stiffness may cause even a daylong immobilization. However, the course may also be self-limiting. Patients report limb weakness by which they understand the limitation of motion due to stiffness and pain. In contrast with polymyositis, PMR does not cause actual muscle weakness. Bilateral tenderness of proximal muscles is a valuable sign both for the diagnosis and treatment monitoring.

Manifestations associated with inflammatory response or deterioration of general state

It is surprising in PMR patient as to how intense inflammatory reaction in elderly may manifest. However, it is also possible to cause anergy-like state with depressive reaction and cachexia. In both situations, PMR may be confused with symptoms of premature ageing both by patients and their physicians. Acute or sub-acute onset of the disease (up to 2 wk) is characteristic, which means a sudden deterioration of daily performance and reduced quality of life. It may appear striking in an older patient who was previously coping well with his/her daily activities. Depressive reaction may be the first or the leading manifestation. Inflammatory reaction in elderly can manifest atypically, by reduction of psychomotor activity and decreased appetite. They can be difficult to differentiate from the endogenous depression. Pro-depressive characteristics of interleukin-6 (IL-6), which plays substantial role in PMR pathogenesis, should be taken into account for a better explanation of this phenomenon. Another reason for behavioural change in PMR patients may be an adaptive response associated with rapid deterioration of physical performance, causing anxiety of getting old and loosing self-reliance. Weight loss is a common manifestation and may progress severely. Low-grade fever and night sweats may persist for months. Patients describe it as 'a flu that does not go away'.

Atypical presentations

These are possible but frequently remain controversial. These include atypical musculoskeletal manifestations (distal or asymmetrical joints involvement, sternoclavicular joints involvement, lack of shoulder girdle involvement, lack of morning stiffness), younger age at the disease onset, normal erythrocyte sedimentation rate (ESR) and CRP serum levels, lack of good response to CSs treatment.

Diagnosis Based on the Classification Criteria

Classification criteria are not developed for diagnosing but are generally used for this purpose. Systems of classification of the diseases are demanded by clinical trials, public health and insurance systems. These criteria define most typical manifestation of the disease and provide an organized summary of its main manifestations. That is why the 'old' criteria such as formulated by Bird et al or Jones and Hazleman are still valid as these were formulated based on clinical observation (). Yet, PMR is not a disease diagnosed by simple ticking signs and symptoms on a checklist. If it were so, a coincidence of depression and shoulder joints osteoarthritis (OA) in an elderly patient would be misclassified as PMR according to Bird's criteria. The interpretation of the importance of complaints and findings in an individual patient by an expert remains fundamental for PMR diagnosis. Shoulder girdle pain must have inflammatory character and depression cannot be endogenous to be accounted in Bird's criteria. Jones and Hazleman's criteria have a potential superiority in countries with low PMR prevalence as they have a higher specificity and include a list of most important exclusions.

Table II

In 2012, European League against Rheumatism (EULAR) and American College of Rheumatology (ACR) formulated new classification criteria for PMR (). These may only be applied in patients meeting preliminary criteria: age over 50 yr, bilateral shoulder aching, elevated CRP or ESR. These are a good example of classification philosophy to reduce heterogeneity of positively classified cases by selecting the subset of the most typical manifestations. Therefore, these criteria are not to be met in atypical cases of PMR. On the other hand, these have a potential to reduce the rate of false positive diagnosis.

Ultrasound

Musculoskeletal ultrasound gains importance in rheumatology. PMR criteria integrated ultrasonographic evaluation into classification process for the first time in rheumatology. Ultrasound criterion requires examining both shoulders (for glenohumeral synovitis, bursitis or biceps tenosynovitis) and hips (for joint synovitis or trochanteric bursitis). The intention for this is assessment of the symmetry of changes between inflammatory changes in both shoulders and between upper and lower limbs involvement. Each of these will score an additional point to the scoring algorithm. Final sum of five out of eight (6 from algorithm without ultrasound plus 2 from ultrasound examination) points enables to classify a patient as PMR with 66 per cent sensitivity and 81 per cent specificity. Ultrasound evaluation is relatively simple to perform as the findings of merely the presence of joint effusion, tenosynovitis or bursitis are sufficient. However, these abnormalities are hardly specific for PMR. A short ultrasound examination of proximal joints usually fails to demonstrate differences between inflammatory joint diseases. The differentiation between PMR and RA is a common dilemma. A more detailed ultrasound assessment can demonstrate joints' erosions and extensive synovial proliferation of both small and large joints that are more typical for RA. Ultrasound can demonstrate degenerative or post-traumatic joint lesions as well as detect GCA overlap ().

Additional tests to help with the diagnosis

There are no pathognomonic antibodies or other PMR-specific markers discovered. Although ESR and CRP serum levels are not specific, it is hard to find PMR with normal inflammatory parameters. Other acute phase markers (fibrinogenemia, thrombocythemia and elevated IL-6, the latter correlates best with the disease activity) are also present. Anaemia of chronic disease type is common and is reversed shortly after CSs treatment initiation. Sometimes, slightly increased transaminases and alkaline phosphatase levels are present. Sparse studies indicated a significantly higher occurrence of anti-phospholipid antibodies, but these have not been proved to be associated with ischaemic or thromboembolic complications.

The benefits and drawbacks of classification criteria sets must be duly considered before applying them for diagnosis. The 2012 proposed EULAR/ACR PMR criteria (opposed to the previous sets) aim to minimize the role of clinical intuition and build on more objective features and additional tests. However, ESR, rheumatoid factor and ultrasound changes still have only limited specificity. The drawbacks of all of the PMR criteria sets are their unsatisfactory sensitivity and specificity. They were also formulated in populations with a high PMR prevalence. If classification criteria are not met (which usually takes place in atypical PMR), the disease should not be diagnosed hastly but only after excluding other causes of similar symptoms.

Diagnosis by Excluding Other Causes of Similar Symptoms

The need for considering PMR exclusions was underlined in the previous criteria and is also found in the current guidelines. The typical clinical picture of PMR requires only basic differential diagnostics. The more atypical the clinical picture, the wider differential diagnostics is required. The differential diagnostics in countries with low PMR incidence requires considering the relatively higher number of PMR mimics. It was illustrated in a study from Turkey that 30 per cent of patients with final PMR diagnosis were hospitalized, 30 per cent were treated with antibiotics, and in 29, 22 and 19 per cent abdominal, chest and brain computed tomography (CT), respectively, were performed. This approach seemed reasonable; however, there were still 13±13 months delay from onset of symptoms to diagnosis.

Why do PMR-like manifestations mask the symptoms of other diseases? PMR pathogenesis is mediated by innate immunity. It triggers non-specific inflammatory reaction which is not unique for PMR. Acute inflammatory response can mask more characteristic symptoms of a disease that are not reported by patients. For example, elderly onset RA may go with systemic inflammatory manifestations and large joint involvement that cause patient immobilization. Therefore, small joints inflammation is not reported by a patient whose main complaint is inability to get out of bed. Further, serious, GCA-associated ischaemic manifestations (such as double vision or jaw claudication that are typical prodromal symptoms of vision loss) can be unreported by patients seeking medical advice because of much more disturbing manifestations of overlapping PMR. Paraneoplastic syndromes that can be manifested long before an appearance of symptoms associated with tumour growth may also be misclassified as PMR.

Differential diagnosis of conditions associated with musculoskeletal symptoms

Differentiation between PMR and seronegative, elderly onset RA affecting proximal joints is actually a common reason for diagnostic uncertainty. It may also be a case if bilateral painful shoulder syndrome coexists with depression and elevated ESR. Ultrasound examination of the shoulder joints may be helpful in determining the cause of the pain. Diagnosing the sources of inflammatory reaction and mood disorders in the elderly may be demanding, requiring knowledge on geriatrics. Musculoskeletal symptoms resembling PMR may originate from myopathy due to hypo- or hyperthyroidism, CSs or statins use, amyloidosis; Addison's disease (also adynamia suggesting depression and a good response to CSs).

Differential diagnosis of conditions associated with inflammatory response or deterioration of general state

Typical PMR age group is associated with a high risk of cancer. Manifestations of PMR may also resemble paraneoplastic syndromes. However, PMR frequently starts suddenly and manifests more dynamically. Spontaneous remission, which can occur in PMR, is unusual for cancer. A 1.7-fold increase in the rate of cancer diagnoses was noted in the first six months of PMR observation in the UK, compared to age- and sex-matched patients with no PMR. Attempts should be made to minimize this period by differential diagnostics and careful observation of atypical PMR cases. Some of the PMR symptoms (fever, night sweats and joint pain) may suggest systemic lupus erythematosus or other autoimmune diseases and infectious diseases, including endocarditis or tuberculosis. Focus on musculoskeletal pain can mask the endogenous or reactive depression being the real cause of deterioration of patient's state.

Due to PMR and GCA overlap, physical examination of PMR patients should encompass temporal arteries (for tenderness, loss of pulsation) and large arteries analogically to Takayasu arteritis (upper and lower limbs intermittent claudication, differences in blood pressure between both limbs, presence of vascular bruits). Treatment-resistant PMR indicates a special need for imaging of large arteries for overlapping vasculitis. It may include ultrasound examination of temporal and large (axillary, sub-clavian, common carotid) arteries by a specialist experienced in differentiating vascular wall inflammation from arteriosclerosis, as well as assessment of the aorta and its branches with contrasted computed tomography (CT), magnetic resonance imaging (MRI) or positron emission tomography (PET) with CT. Lack of GCA manifestations at the time of PMR diagnosis should not stop the awareness of developing vasculitis during follow up. Small CSs doses used for PMR do not protect against the progression of arterial inflammation. PMR patients should be educated to immediately seek medical advice in case of vision disturbance (double vision, transient ischaemic attacks), jaw claudication or scalp tenderness.

Diagnosis ex juvantibus

Rapid and spectacular improvement shortly after CSs introduction enables concluding on a cause based on an observed response to the treatment. Therefore, PMR patients are much pleased shortly after treatment initiation and grateful to their doctors. Lack of improvement within five days suggest a need to verify the PMR diagnosis (to some different disease or GCA). Diagnosis ex juvantibus was included in Jones and Hazleman's criteria. New, 2012 PMR classification criteria do not include a good response to CSs in the diagnostic process. It raised some discussion as this criterion is widely used in a daily practice. It was argued that treatment response was non-specific and difficult to define feature. Indeed, elderly onset RA or other inflammatory conditions also respond well to CSs. However, this response would be weak in OA and transient if applied in infection or neoplasm. In these cases review of the initial PMR diagnosis is needed. It is not a mistake to reassess the initial diagnosis and change it accordingly. About 10 per cent of patients initially diagnosed with PMR are later reclassified as having elderly onset RA. For that purpose, careful monitoring of patients is needed. PMR patients require regular medical check-ups.

Diagnosing ex juvantibus may also be made eagerly because it does not require an effort of time-consuming and expensive procedures. Spectacular efficacy of CSs in PMR may cause a temptation to overuse them. There has been increased interest in GCA and PMR evoked by modern treatment possibilities and fast track GCA clinics. Based on our own experience, PMR is easy to overdiagnose. Establishing rational PMR diagnosis illustrates a challenge to resist fashion and wishful thinking in medicine. Adherence to the 2012 PMR classification criteria could be beneficial in preventing overdiagnosis because these do not include response to therapy. However, the 'response criterion' will not disappear from the daily practice of the physicians who can appreciate how unique PMR symptoms react to CSs. At least as long as there are no better disease markers.

Conclusion

Lack of specific biomarkers of PMR is problematic and research is needed. Up to now, the diagnosis remains clinical. There are many clinical subtleties to be considered. Usually, PMR responds well to CSs treatment and outcomes are favourable. However, differential diagnosis encompasses diseases with bad prognosis; therefore, PMR overdiagnosis can be detrimental.

Footnotes

Conflicts of Interest: None.

References

33. Żakowska-Wachelko B, editor. Geriatric medicine outline [Zarys medycyny geriatrycznej] Warszawa: Wydawnictwo Lekarskie PZWL; 2000. Musculosceletal diseases and involutional changes; p. 147. [ Google Scholar]

59. Stone JH, Tuckwell K, Dimonaco S, Klearman M, Aringer M, Blockmans D, et al. Efficacy and safety of tocilizumab in patients with giant cell arteritis: Primary and secondary outcomes from a phase 3, randomized, double-blind, placebo-controlled trial [Abstract] Arthritis Rheumatol. 2016;68(Suppl 10):1204-6. [ Google Scholar]

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Diagnosis of polymyalgia rheumatica usually means a favourable outcome for your patient

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Polymyalgia rheumatica (PMR) is a unique disease of elderly people, traditionally diagnosed based on a clinical picture. A typical case is a combination of severe musculoskeletal symptoms and systemic inflammatory response with spectacular response to corticosteroids treatment. The severity of symptoms may be surprising in older patients where immunosenescence is normally expected.

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Definitely not my best performance and a lot of room for improvement. This is the feedback from the new patient experience; I will be getting feedback from the examiners so that I can move forward in a positive way.

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I decided to make the most of my car journeys and subscribe to the podcasts made available by Robert Whitaker, the creator of Instant Anatomy (B2, B3, B4).  I met Robert at the COG prosection/anatomy day in January and he was as inspiring as his book is.

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Initially I wanted to study midwifery, however, when it came to being interviewed, I was rejected and I had to choose something else to study. I wasn't going to let a year of study go wasted or lose interest in obtaining good grades because I had been rejected. I was determined to get the grades I needed for midwifery even I had been rejected. This way I kept up my motivation (B2, B3, B4). Soon after I was interviewed at the ESO and I needed a lot fewer distinctions than those needed for midwifery. Luckily my sense of determination comes into play at these times and I wanted to do well. It mattered to me and wanted to show everyone I knew that I had done well too.

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16 July 2018            bony landmarks of the scapula

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16 July 2018            bony landmarks of the scapula

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I revised the bony landmarks of the scapula to improve my knowledge of where all the 17 muscles of the shoulder attach to the scapula.

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What happened?
I had two new patients with psoriatic arthritis in quick succession; it made me look at the link with coeliac disease as well as the blood markers for psoriasis (B2, B3, B4).
Why did I do this?
Well I knew my knowledge about psoriasis was poor and I wondered about various links with other illnesses. I was also curious about the link with other auto-immune diseases (B2, B3) such as coeliac disease.
What improved? My knowledge about psoriasis (B2, B3, B4). This will help me direct patients in future, if they are at the early stage of diagnosis, or if they haven't got a diagnosis I will be able to give them information about their disease (C3, C5, C7, C8).

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Psoriasis, a disorder that primarily affects the skin, and celiac disease, an allergy to gluten, may be connected according to some experts - and some patients agree. Megan Ancheta of Wasilla, Alaska, has no doubt about this.

Ancheta has had psoriasis since she was 14 and was diagnosed with psoriatic arthritis in 2009. She says adhering to a strict anti-inflammatory diet, which includes no gluten, has given her back her life.

A study published in December 2010 in the journal Clinical and Experimental Dermatology uncovered a link between psoriasis and gluten sensitivity. The researchers found that more than a third of the study participants with psoriasis had elevated antibodies to gliadin in their blood.

Antibodies are proteins that are formed when your body attempts to fight what it suspects are foreign substances, and gliadin is the protein in wheat that cannot be properly digested by people who have celiac disease and gluten sensitivities.

Still, the relationship between psoriasis and celiac disease - both autoimmune disorders - remains controversial.

Valori Treloar, MD, a dermatologist and certified nutrition specialist at Integrative Dermatology in Newton, Massachusetts, notes that some of the controversy may be due to the fact that some people with psoriasis have a sensitivity to gluten, but don't necessarily have celiac disease.

"I think gluten sensitivity occurs along a spectrum, and that celiac disease is at the far end of the spectrum," Dr. Treloar explains. "Not everyone who has gluten sensitivity has celiac disease."

Jerry Bagel, MD, director of the Psoriasis Treatment Center of Central New Jersey in East Windsor, New Jersey, believes that as many as one-quarter of the 7.5 million Americans with psoriasis may benefit from a gluten-free diet. "A 12-week trial can't hurt," Dr. Bagel says.

Pros and Cons of a Gluten-Free Diet

Here are the possible benefits of a gluten-free diet:

It could relieve psoriasis symptoms. "Some people get better and some don't," Treloar says. The only way to find out whether you might benefit is to try it. She says that people with pustular psoriasis, a type of psoriasis that causes blister-like pimples on the palms of the hands and soles of the feet, are most likely to have gluten sensitivity. A gluten-free diet seems to make a big difference to them in particular, she notes.

Ancheta says she's been tested for celiac disease and doesn't have it, but she is gluten-sensitive. Before she went on her anti-inflammatory diet, she had trouble getting out of bed most mornings.

She still has pain from her psoriatic arthritis and secondary Raynaud's phenomenon, which is also an autoimmune disease, but now she's able to function. This makes a big difference, since "life can get pretty hectic raising two small girls and a puppy," she says.

Treloar warns that if you're going to try a gluten-free diet, you should give it time - know that it could take four to six months to see a clear difference.

You'll be eating a healthier diet. Eating a gluten-free diet means eliminating most processed foods and making room for more fresh fruits and vegetables, lean meats, and dairy.

As a huge plus, you'll also help reduce your risk for other diseases that can accompany psoriasis, such as diabetes, heart disease, and obesity. "It might also help with digestion," Bagel says.

You'll likely have more energy. "Lots of patients tell me they feel much better after a few weeks," says Treloar, adding that many didn't realize their problems with digestion were likely caused by their sensitivity to gluten, until they stopped eating it.

Many also report a boost in energy. "That makes it easier for people to stick to the diet, because they're feeling better," she adds.

Here are the possible drawbacks of following a gluten-free diet:

It's not easy to follow. No more bread, bagels, pizza, cookies, or cake - and you'll also have to say no to many processed foods, from lunch meats to salad dressings, because they often contain gluten. You're limited to foods that are 100 percent gluten-free, and you have to shop carefully to be sure of what you're buying. Many people find these limitations to be particularly challenging.

You can't cheat. "For the diet to work, you have to be nuts about it," Treloar says.

Gluten-free foods can be high in sugar and other empty calories. To improve taste, many manufacturers add sugar, saturated fats, and preservatives to packaged gluten-free products. "They tend to be made with refined grains, so they have a high glycemic load," Treloar says. "That can push up your blood sugar."

Some people find they gain weight because they think gluten-free eating is good for them - and they can eat more. "But you can't eat more, especially baked goods, just because they're gluten-free," Treloar cautions.

It can take you longer to shop. You have to read food labels carefully to hunt for gluten. "There's a learning curve," Treloar says. You'll be surprised to find that gluten lurks in many foods you never suspected. Of course, the more you stick to fresh foods, the less hassle you'll have.

Beer is off-limits. A sneaky source of gluten, beer is made from gluten-rich malted barley. In fact, a study published in August 2010 in the journal JAMA Dermatology by researchers at Brigham and Women's Hospital in Boston found that women who drank non-light beer were more likely to develop psoriasis than those who drank light beer, wine, or hard liquor. The authors write that one possible explanation for this is the higher levels of barley in non-light beer.

Shopping for Gluten-Free Foods

"In the 1980s, it was impossible to ask people to eat gluten-free," Treloar says. "Nowadays it's a much easier proposition." You don't have to shop exclusively in health food stores anymore; most supermarkets and even restaurants offer lots of gluten-free options.

When navigating the supermarket aisles, try these tips:

Shop the perimeter. That's where you're most likely to find fresh fruits and vegetables, fish, poultry, and other meats, and dairy - and where you have the widest choices of naturally gluten-free foods.

Talk with the store manager. Although stores are stocking more gluten-free items, including waffles, cereals, pastas, cookies, and pretzels, they may not have a food you want. Make friends with the manager, and he or she might be able to order it for you.

Read labels. Just because something is marked "wheat-free" doesn't mean it's gluten-free. It could contain traces of gluten that may aggravate your psoriasis symptoms. Avoid foods that have even trace amounts of wheat, barley, rye, or malt.

Go online. Before you head to the store, go online to see what brands offer gluten-free foods. If you're just starting out, you may want to prepare a list of gluten-free foods so you know what to look for in each department of the grocery store.

Don't go overboard. Some gluten-free foods can be expensive; others might taste bland. Before you stock up, be sure you like them.

A gluten-free diet can be very restrictive, and following it takes a big commitment. Talk with your doctor and make sure it's a good option for you before you try it.

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Is a Gluten-Free Diet Good for Psoriasis?

# data[].attributes.attachment_link.description
Psoriasis, a disorder that primarily affects the skin, and celiac disease, an allergy to gluten, may be connected according to some experts - and some patients agree. Megan Ancheta of Wasilla, Alaska, has no doubt about this. Ancheta has had psoriasis since she was 14 and was diagnosed with psoriatic arthritis in 2009.

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Is Psoriasis linked to coeliac disease? I have been getting more curious about autoimmune diseases, so I felt a little more research was in order.

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Is Psoriasis linked to coeliac disease? I have been getting more curious about autoimmune diseases, so I felt a little more research was in order.

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What did I learn? Well it would seem there may be a link, but it may be more that people with psoriasis are sensitive to gluten rather than allergic.  I have a patient who has endometriosis and had been suffering with IBS symptoms for a long time.  I suggested to her that it might be worth trying to cut out products with gluten in them, and see if she noticed an improvement. I was impressed because she actually did what I suggested, and cut out gluten products. The change was phenomenal, she has had no more IBS symptoms since and she is very happy with the result. I also suggested to her that she try drinking peppermint tea for relaxing herself and her gut, this was also another success. Wow. It is difficult to know whether patients will take up your suggestion, but this one has noticed a significant improvemnt in her health and wellbeing by taking up my suggestions, so I shall certainly suggest these ideas to patients in the future, when it is appropriate. This was very definitely shared decision making.

# data[].attributes.attachment_link.readable_text
Psoriasis, a disorder that primarily affects the skin, and celiac disease, an allergy to gluten, may be connected according to some experts - and some patients agree. Megan Ancheta of Wasilla, Alaska, has no doubt about this.

Ancheta has had psoriasis since she was 14 and was diagnosed with psoriatic arthritis in 2009. She says adhering to a strict anti-inflammatory diet, which includes no gluten, has given her back her life.

A study published in December 2010 in the journal Clinical and Experimental Dermatology uncovered a link between psoriasis and gluten sensitivity. The researchers found that more than a third of the study participants with psoriasis had elevated antibodies to gliadin in their blood.

Antibodies are proteins that are formed when your body attempts to fight what it suspects are foreign substances, and gliadin is the protein in wheat that cannot be properly digested by people who have celiac disease and gluten sensitivities.

Still, the relationship between psoriasis and celiac disease - both autoimmune disorders - remains controversial.

Valori Treloar, MD, a dermatologist and certified nutrition specialist at Integrative Dermatology in Newton, Massachusetts, notes that some of the controversy may be due to the fact that some people with psoriasis have a sensitivity to gluten, but don't necessarily have celiac disease.

"I think gluten sensitivity occurs along a spectrum, and that celiac disease is at the far end of the spectrum," Dr. Treloar explains. "Not everyone who has gluten sensitivity has celiac disease."

Jerry Bagel, MD, director of the Psoriasis Treatment Center of Central New Jersey in East Windsor, New Jersey, believes that as many as one-quarter of the 7.5 million Americans with psoriasis may benefit from a gluten-free diet. "A 12-week trial can't hurt," Dr. Bagel says.

Pros and Cons of a Gluten-Free Diet

Here are the possible benefits of a gluten-free diet:

It could relieve psoriasis symptoms. "Some people get better and some don't," Treloar says. The only way to find out whether you might benefit is to try it. She says that people with pustular psoriasis, a type of psoriasis that causes blister-like pimples on the palms of the hands and soles of the feet, are most likely to have gluten sensitivity. A gluten-free diet seems to make a big difference to them in particular, she notes.

Ancheta says she's been tested for celiac disease and doesn't have it, but she is gluten-sensitive. Before she went on her anti-inflammatory diet, she had trouble getting out of bed most mornings.

She still has pain from her psoriatic arthritis and secondary Raynaud's phenomenon, which is also an autoimmune disease, but now she's able to function. This makes a big difference, since "life can get pretty hectic raising two small girls and a puppy," she says.

Treloar warns that if you're going to try a gluten-free diet, you should give it time - know that it could take four to six months to see a clear difference.

You'll be eating a healthier diet. Eating a gluten-free diet means eliminating most processed foods and making room for more fresh fruits and vegetables, lean meats, and dairy.

As a huge plus, you'll also help reduce your risk for other diseases that can accompany psoriasis, such as diabetes, heart disease, and obesity. "It might also help with digestion," Bagel says.

You'll likely have more energy. "Lots of patients tell me they feel much better after a few weeks," says Treloar, adding that many didn't realize their problems with digestion were likely caused by their sensitivity to gluten, until they stopped eating it.

Many also report a boost in energy. "That makes it easier for people to stick to the diet, because they're feeling better," she adds.

Here are the possible drawbacks of following a gluten-free diet:

It's not easy to follow. No more bread, bagels, pizza, cookies, or cake - and you'll also have to say no to many processed foods, from lunch meats to salad dressings, because they often contain gluten. You're limited to foods that are 100 percent gluten-free, and you have to shop carefully to be sure of what you're buying. Many people find these limitations to be particularly challenging.

You can't cheat. "For the diet to work, you have to be nuts about it," Treloar says.

Gluten-free foods can be high in sugar and other empty calories. To improve taste, many manufacturers add sugar, saturated fats, and preservatives to packaged gluten-free products. "They tend to be made with refined grains, so they have a high glycemic load," Treloar says. "That can push up your blood sugar."

Some people find they gain weight because they think gluten-free eating is good for them - and they can eat more. "But you can't eat more, especially baked goods, just because they're gluten-free," Treloar cautions.

It can take you longer to shop. You have to read food labels carefully to hunt for gluten. "There's a learning curve," Treloar says. You'll be surprised to find that gluten lurks in many foods you never suspected. Of course, the more you stick to fresh foods, the less hassle you'll have.

Beer is off-limits. A sneaky source of gluten, beer is made from gluten-rich malted barley. In fact, a study published in August 2010 in the journal JAMA Dermatology by researchers at Brigham and Women's Hospital in Boston found that women who drank non-light beer were more likely to develop psoriasis than those who drank light beer, wine, or hard liquor. The authors write that one possible explanation for this is the higher levels of barley in non-light beer.

Shopping for Gluten-Free Foods

"In the 1980s, it was impossible to ask people to eat gluten-free," Treloar says. "Nowadays it's a much easier proposition." You don't have to shop exclusively in health food stores anymore; most supermarkets and even restaurants offer lots of gluten-free options.

When navigating the supermarket aisles, try these tips:

Shop the perimeter. That's where you're most likely to find fresh fruits and vegetables, fish, poultry, and other meats, and dairy - and where you have the widest choices of naturally gluten-free foods.

Talk with the store manager. Although stores are stocking more gluten-free items, including waffles, cereals, pastas, cookies, and pretzels, they may not have a food you want. Make friends with the manager, and he or she might be able to order it for you.

Read labels. Just because something is marked "wheat-free" doesn't mean it's gluten-free. It could contain traces of gluten that may aggravate your psoriasis symptoms. Avoid foods that have even trace amounts of wheat, barley, rye, or malt.

Go online. Before you head to the store, go online to see what brands offer gluten-free foods. If you're just starting out, you may want to prepare a list of gluten-free foods so you know what to look for in each department of the grocery store.

Don't go overboard. Some gluten-free foods can be expensive; others might taste bland. Before you stock up, be sure you like them.

A gluten-free diet can be very restrictive, and following it takes a big commitment. Talk with your doctor and make sure it's a good option for you before you try it.

# data[].attributes.attachment_link.title
Is a Gluten-Free Diet Good for Psoriasis?

# data[].attributes.attachment_link.description
Psoriasis, a disorder that primarily affects the skin, and celiac disease, an allergy to gluten, may be connected according to some experts - and some patients agree. Megan Ancheta of Wasilla, Alaska, has no doubt about this. Ancheta has had psoriasis since she was 14 and was diagnosed with psoriatic arthritis in 2009.

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Gallbladder Surgery and complications - B4, C7, C8, D3

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Gallbladder Surgery and complications - B4, C7, C8, D3

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The patient which will come in for my returning patient part of the exam had her gall bladder removed. In order to be better informed about the process and the possible complications, I decided I should look up this procedure to make sure I can support my patient in caring for herself and any future patients who have gallbladder surgery.

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Cervical spondylosis and cervical myelopathy

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Cervical spondylosis and cervical myelopathy

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see the word document below

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I had a patient present with cervical spondylosis; however my tutor pushed me to question whether it could be a cervical myelopathy. So I realised that I needed to refresh my memory of a cervical myelopathy. What have I learned? How I can distinguish these condiitons and recognise the difference in future patients; it has made me safe because I can recognise the different symptoms of these conditions and I will know when I can help a patient and when the condition is beyond my expertise.

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Cervical myelopathy refers to compression on the cervical spinal cord. Any space occupying lesion within the cervical spine with the potential to compress the spinal cord can cause cervical myelopathy. Cervical myelopathy is predominantly due to pressure on the anterior spinal cord with ischaemia as a result of deformation of the cord by anterior herniated discs, spondylitic spurs, an ossified posterior longitudinal ligament or spinal stenosis

The spontaneous course of myelopathy is characterised either by long periods of stable disability followed by episodes of deterioration or a linear progressive course. The presentation of a cervical myelopathy varies in accordance to the severity of the spinal cord compression as well as its location.

Clinically Relevant Anatomy

There are seven cervical vertebrae and eight cervical nerve roots. The spinal cord is the extension of the central nervous system outside the cranium. It is encased by the vertebral column and begins at the foramen magnum. The spinal cord is an extremely vital part of the central nervous system, and even a small injury can lead to severe disability.

A complex system of ligaments serves to stabilise and protect the cervical spine. For example, ligamentum flavum extends from the anterior surface of the cephalic vertebra to the posterior surface of the caudal vertebra and connects to the ventral aspect of the facet joint capsules. A ligament that is often involved in this condition is the posterior longitudinal ligament. It is situated within the vertebral canal, originating from the body of the axis, where it is continuous with the tectorial membrane, and extends along the posterior surfaces of the bodies of the vertebrae until inserting into the sacrum.

Chronic cervical degeneration is the most common cause of progressive spinal cord and nerve root compression. Spondylotic changes can result in stenosis of the spinal canal, lateral recess, and foramina. Spinal canal stenosis can lead to myelopathy, whereas the latter two can lead to radiculopathy.

Epidemiology

Cervical spondylotic myelopathy is the most common disorder of the spinal cord in persons older than 55 years of age. Radiologic spondylotic changes increase with patient age - 90% of asymptomatic persons older than 70 years have some form of degenerative change in the cervical spine. Cervical spine myelopathy resulting from sagittal narrowing of the spinal canal and compression of the spinal cord is present in 90% of individuals by the seventh decade of life. Both sexes are affected equally. Cervical spondylosis usually starts earlier in men (50 years) than in women (60 years). It causes hospitalisation at a rate of 4.04 per 100,000 person-years.

Pathological Process

The causes of cervical myelopathy can be divided into different categories:

Static factors: A narrowing of the spinal canal size commonly results from degenerative changes in the cervical spine anatomy (cervical spondylosis) such as disc degeneration, spondylosis, stenosis, osteophyte formation at the level of facet joints, segmental ossification of the posterior longitudinal ligament and yellow ligament hypertrophy, calcification or ossification. Patients with a congenitally narrow spinal canal (<13mm) have a higher risk for the development of symptomatic cervical myelopathy.

Cord compression is thought to be a combination of static compression and intermittent dynamic compression from cervical motion (flexion/extension).

Characteristics and Clinical Presentation

Cervical myelopathy can cause a variety of signs and symptoms. Onset is insidious, typically in persons aged 50-60 years.

The symptoms usually develop slowly. Because of the lack of pain, there may be an interval of years between the onset of disease and first treatment. Early symptoms of this condition are 'numb, clumsy, painful hands' and disturbance of fine motor skills. Weakness and numbness occur in a non-specific/non-dermatomal pattern. As spinal cord degeneration progresses, lower motor neuron findings in the upper extremities, such as loss of strength, atrophy of the interosseous muscles and difficulty in fine finger movements, may present.

Additional clinical findings may include: neck pain and stiffness (decreased ROM, especially extension), shoulder and scapular pain, paresthesia in one or both arms or hands, signs of radiculopathy, Babinski and Hoffman's sign, ataxia and dexterity loss. Typical neurological signs of long-tract involvement are exaggerated tendon reflexes (patellar and achilles), presence of pathological reflexes (e.g. clonus, Babinski and Hoffman's sign), spastic quadriplegia, sensory loss and bladder-bowel disturbance.

Once the disorder is diagnosed, complete remission to normality never occurs and spontaneous temporary remission is uncommon. In 75% of the patients, episodic worsening with neurological deterioration occurs, 20% have slow steady progression, and 5% experience rapid onset and progression.

Common Symptoms

Distal weakness

Decreased ROM in the cervical spine, especially extension.

Clumsy or weak hands

Pain in shoulder or arms

Unsteady or clumsy gait

Increased reflexes in the lower extremities and in the upper extremities below the level of the lesion.

Numbness and parasthesia in one or both hands

Radiculopathic signs

Diagnostic Procedures

A detailed and thorough neurological examination plus MRI is the current standard to diagnose the presence of cervical myelopathy.

Plain radiographs alone are of little use as an initial diagnostic procedure. A magnetic resonance image (MRI) is considered the best imaging method for confirming the presence of spinal canal stenosis, cord compression, or myelomalacia, elements germane to cervical spine myelopathy. MRI of the cervical spine can also rule out spinal cord tumours.

An MRI is most useful because it expresses the amount of compression placed on the spinal cord and demonstrates relatively high levels of sensitivity and specificity. Anterior-posterior width reduction, cross-sectional evidence of cord compression, obliteration of the subarachnoid space and signal intensity changes to the cord found on MR imaging are considered the most appropriate parameters for confirmation of a spinal cord compression myelopathy. More than half of patients with cervical spine myelopathy show intramedullary high signal intensity on T2-weighted imaging, mainly in the spinal gray matter. Radiographic cervical spinal cord compression and hyperintense T2 intraparenchymal signal abnormalities (MRI) correlate well with the presence of myelopathic findings on physical examination.

Clinical Examination

1. gait deviation

2. +ve Hoffmann's test

3. inverted supinator sign

4. +ve Babinski test

5. age 45 years or older

Differential Diagnosis

Management

There is no consensus about the treatment of mild and moderate forms of cervical myelopathy. Surgical treatment has no better results than conservative treatment over two years of follow-up. Patients with cervical myelopathy that are treated with a conservative approach (anti-inflammatory medication and physical therapy) may have some short term benefit in relief of painful symptoms. Because the condition is degenerative and progressive, slow and continued progressive neurologic deterioration will occur.

Medical Management

People who have progressive neurologic changes (such as weakness, numbness or falling) with signs of severe spinal cord compression or spinal cord swelling are candidates for surgery. Patients with severe or disabling pain may also be helped with surgery. When myelopathy is caused by factors of a progressive nature, such as spinal cord tumors, surgical treatment is likewise indicated.

People who experience better surgical outcomes often have these characteristics:

The symptom of an electrical sensation that runs down the back and into the limbs

Younger age

Shorter duration of symptoms

Single rather than multiple areas of involvement

Larger areas available for the cord

Physical therapy management

Patients can be treated conservatively. Kadaňka et al. found no difference in long term outcomes (2 years after the intervention) between patient who received conservative or surgical treatment (LoE 2B). Even after 10 years, there were no differences found between the surgery and conservative group (LoE2B). Fouyas et al also confirmed these findings. (LoE1A) The only prognostic factor in which surgery can be generally recommended is with a circumferential spinal cord compression seen on an axial MRI. (LoE2B)

Rhee JM et al. describes myelopathy as a typically progressive disorder and that there is little of evidence that conservative treatment halts or reverses its progression. So they recommend routinely not prescribing non-operative treatment as the primary modality in patients with moderate to severe myelopathy. (LoE 1A)

The goals of physiotherapy treatment are: ( LoE5)

pain relief

to improve function

to prevent neurological deterioration

to reverse or improve neurological deficits

Cervical myelopathy can be treated symptomatically. Possible therapies include:

Cervical traction and manipulation of the thoracic spine: useful for the reduction of pain scores and level of disability in patients with mild cervical myelopathy. Other signs and symptoms, such as weakness, headache, dizziness, and hypoesthesia, can also be positively affected ( LoE4). Cervical traction can be combined with other treatments like electrotherapy and exercises. Joghataei et al. reported a significant increase in grip strength after 10 weeks of this combined treatment(LoE1B)

Manual therapy techniques: used to reduce the neck pain with natural apophyseal glides and sustained natural apophyseal glides for cervical extension and rotation(LoE5) Manipulation and mobilisations can be effective when they are combined with exercise therapy. When you use them without exercises, there is only poor evidence that it could be effective(LoE5)(LoE1A).

Cervical stabilisation exercises: when there is anteroposterior instability of the vertebral bodies of a degenerative nature, vertebral segment stabilisation of the cervical spine can be performed with a pressure biofeedback unit (PBU),.(LoE5)

Improve posture

Mobility and proprioception exercises

In surgical cases, the physiotherapist still has an important role, both before and after the surgery. In the pre-operative phase, the physiotherapist needs to become thoroughly familiar with the patient's history and about their activities of daily living that they are aiming to return to. The physiotherapist will inform the patient about the treatment program and the expectations after the surgery. There are different tests to develop a thorough picture of the patient's baseline pre-operative status such as walking tolerance, Neck Pain and Disability Scale, Neck Disability Index and lung function. Nomura et. al found that the maximum voluntary ventilation should significantly increase after surgery (LoE2B).

Exercises to improve mobility and proprioception are given to the patient. The patient starts with unencumbered stabilisation exercises and then progresses to more active mobilisation exercises. During the day the patient is encouraged to perform their usual ADLs. Intensity of the exercises is increased the following day and are progressed to include standing and walking exercises. Assuming typical progress with rehabilitation, the patient can go home after the ninth day. Physiotherapy continues in the home environment with active exercises and the ability of the patient to perform their normal ADLs is monitored, whilst increasing the intensity of the exercises as appropriate.

Presentations

Case Studies

Clinical Bottom Line

Cervical myelopathy is the result of spinal cord compression in the cervical spine and is a common disorder in persons older than 55 years of age. Cervical compression in myelopathy is predominantly due to pressure on the anterior spinal cord with ischaemia and to deformation of the cord by anterior herniated discs, spondylitic spurs or an ossified posterior longitudinal ligament. Early symptoms of this condition are 'numb, clumsy, painful hands' and disturbance of fine motor skill. The diagnosis of cervical myelopathy is primarily based on the clinical signs found on physical examination and is supported by imaging findings of cervical spondylosis with cord compression. Once the disorder is diagnosed, complete remission to normal fucntion never occurs and spontaneous remission is uncommon. Exercises and techniques that may help relieve symptoms of cervical myelopathy include: cervical traction, manual therapy techniques, proprioceptive neuromuscular facilitation, cervical stabilisation exercises and dynamic upper and lower limb exercises.

References

1. Amenta PS, Ghobrial GM, Krespan K, Nguyen P, Ali M, Harrop JS. Cervical spondylotic myelopathy in the young adult: a review of the literature and clinical diagnostic criteria in an uncommon demographic. Clin Neurol Neurosurg. 2014. 120:68-72.

2. Cook C, Roman M, Stewart KM, Leithe LG, Isaacs R. Reliability and diagnostic accuracy of clinical special tests for myelopathy in patients seen for cervical dysfunction. J Orthop Sports Phys Ther. 2009 Mar;39(3):172-8. doi: 10.2519/jospt.2009.2938.

3. Harrop, James S; Naroji, Swetha; Maltenfort, Mitchell; Anderson, D. Greg; Albert, Todd; Ratliff, John K; Ponnappan, Ravi K; Rihn, Jeffery A; Smith, Harvey E; Hilibrand, Alan; Sharan, Ashwini D; Vaccaro, Alexander. Cervical Myelopathy: A Clinical and Radiographic Evaluation and Correlation to Cervical Spondylotic Myelopathy. Spine 10 February 2010 [epub ahead of print]

4. Physiotutors. Cervical Spondylotic Myelopathy Cluster. Available from: https://www.youtube.com/watch?v=WkRgpMyzQxs

5. Vitzthum H and Dalitz K. Analysis of five specific scores for cervical spondylogenic myelopathy. Eur Spine J. 2007; 16(12): 2096-2103.

6. Fouyas, Ioannis P., Patrick FX Statham, and Peter AG Sandercock. "Cochrane review on the role of surgery in cervical spondylotic radiculomyelopathy." Spine 27.7 (2002): 736-747.

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Cervical myelopathy refers to compression on the cervical spinal cord.

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I have recently been revising the questions for Benign Prostatic Hyperplasia (B2, B3, B4, C1, C2, C3, C5, C7,  C8