# data[].attributes.body
https://www.mayoclinic.org/diseases-conditions/acromegaly/symptoms-causes/syc-20351222?page=0&citems=10

# data[].attributes.body
https://www.mayoclinic.org/diseases-conditions/addisons-disease/symptoms-causes/syc-20350293?page=0&citems=10

# data[].attributes.body
https://www.mayoclinic.org/diseases-conditions/cushing-syndrome/diagnosis-treatment/drc-20351314

# data[].attributes.body
https://www.mayoclinic.org/diseases-conditions/diabetes-insipidus/symptoms-causes/syc-20351269?page=0&citems=10

# data[].attributes.body
https://www.mayoclinic.org/diseases-conditions/graves-disease/symptoms-causes/syc-20356240

# data[].attributes.body
https://www.mayoclinic.org/diseases-conditions/type-1-diabetes/symptoms-causes/syc-20353011

# data[].attributes.body
https://www.mayoclinic.org/diseases-conditions/dwarfism/symptoms-causes/syc-20371969?page=0&citems=10

# data[].attributes.body
https://www.mayoclinic.org/diseases-conditions/type-2-diabetes/symptoms-causes/syc-20351193?page=0&citems=10

# data[].attributes.body
https://www.mayoclinic.org/diseases-conditions/hypercalcemia/symptoms-causes/syc-20355523?page=0&citems=10

# data[].attributes.body
https://www.mayoclinic.org/diseases-conditions/hyperthyroidism/symptoms-causes/syc-20373659?page=0&citems=10

# data[].attributes.body
https://www.healthline.com/health/calcium-deficiency-disease

# data[].attributes.body
https://www.nicklauschildrens.org/genetic/neonatal-hypothyroidism

# data[].attributes.body
Myxedema

# data[].attributes.body
https://www.mayoclinic.org/diseases-conditions/pheochromocytoma/symptoms-causes/syc-20355367?page=0&citems=10

# data[].attributes.body
https://www.mayoclinic.org/diseases-conditions/hypothyroidism/symptoms-causes/syc-20350284?page=0&citems=10

# data[].attributes.body
https://www.mayoclinic.org/diseases-conditions/addisons-disease/symptoms-causes/syc-20350293?page=0&citems=10

# data[].attributes.attachment_link.readable_text
Infectious Diseases Care at Mayo Clinic

Our caring teams of professionals offer expert care to people with infectious diseases, injuries and illnesses.

Infectious diseases are disorders caused by organisms - such as bacteria, viruses, fungi or parasites. Many organisms live in and on our bodies. They're normally harmless or even helpful. But under certain conditions, some organisms may cause disease.

Some infectious diseases can be passed from person to person. Some are transmitted by insects or other animals. And you may get others by consuming contaminated food or water or being exposed to organisms in the environment.

Signs and symptoms vary depending on the organism causing the infection, but often include fever and fatigue. Mild infections may respond to rest and home remedies, while some life-threatening infections may need hospitalization.

Many infectious diseases, such as measles and chickenpox, can be prevented by vaccines. Frequent and thorough hand-washing also helps protect you from most infectious diseases.

From Mayo Clinic to your inbox

Sign up for free and stay up to date on research advancements, health tips, current health topics, and expertise on managing health. Click here for an email preview.

To provide you with the most relevant and helpful information, and understand which information is beneficial, we may combine your email and website usage information with other information we have about you. If you are a Mayo Clinic patient, this could include protected health information. If we combine this information with your protected health information, we will treat all of that information as protected health information and will only use or disclose that information as set forth in our notice of privacy practices. You may opt-out of email communications at any time by clicking on the unsubscribe link in the e-mail.

Infectious diseases can be caused by:

Bacteria. These one-cell organisms are responsible for illnesses such as strep throat, urinary tract infections and tuberculosis.

Viruses. Even smaller than bacteria, viruses cause a multitude of diseases ranging from the common cold to AIDS.

Fungi. Many skin diseases, such as ringworm and athlete's foot, are caused by fungi. Other types of fungi can infect your lungs or nervous system.

Parasites. Malaria is caused by a tiny parasite that is transmitted by a mosquito bite. Other parasites may be transmitted to humans from animal feces.

Direct contact

An easy way to catch most infectious diseases is by coming in contact with a person or an animal with the infection. Infectious diseases can be spread through direct contact such as:

Person to person. Infectious diseases commonly spread through the direct transfer of bacteria, viruses or other germs from one person to another. This can happen when an individual with the bacterium or virus touches, kisses, or coughs or sneezes on someone who isn't infected.

These germs can also spread through the exchange of body fluids from sexual contact. The person who passes the germ may have no symptoms of the disease, but may simply be a carrier.

Animal to person. Being bitten or scratched by an infected animal - even a pet - can make you sick and, in extreme circumstances, can be fatal. Handling animal waste can be hazardous, too. For example, you can get a toxoplasmosis infection by scooping your cat's litter box.

Mother to unborn child. A pregnant woman may pass germs that cause infectious diseases to her unborn baby. Some germs can pass through the placenta or through breast milk. Germs in the vagina can also be transmitted to the baby during birth.

Indirect contact

Disease-causing organisms also can be passed by indirect contact. Many germs can linger on an inanimate object, such as a tabletop, doorknob or faucet handle.

When you touch a doorknob handled by someone ill with the flu or a cold, for example, you can pick up the germs he or she left behind. If you then touch your eyes, mouth or nose before washing your hands, you may become infected.

Insect bites

Some germs rely on insect carriers - such as mosquitoes, fleas, lice or ticks - to move from host to host. These carriers are known as vectors. Mosquitoes can carry the malaria parasite or West Nile virus. Deer ticks may carry the bacterium that causes Lyme disease.

Food contamination

Disease-causing germs can also infect you through contaminated food and water. This mechanism of transmission allows germs to be spread to many people through a single source. Escherichia coli (E. coli), for example, is a bacterium present in or on certain foods - such as undercooked hamburger or unpasteurized fruit juice.

1. Facts about infectious disease. Infectious Disease Society of America. https://www.idsociety.org/public-health/facts-about-id/. Accessed May 29, 2019.

2. Jameson JL, et al., eds. Approach to the patient with an infectious disease. In: Harrison's Principles of Internal Medicine. 20th ed. New York, N.Y.: The McGraw-Hill Companies; 2018. https://accessmedicine.mhmedical.com. Accessed May 29, 2019.

3. Clean hands count for safe health care. Centers for Disease Control and Prevention. https://www.cdc.gov/features/handhygiene/index.html. Accessed May 29, 2019.

4. Kumar P, et al., eds. Infectious diseases and tropical medicine. In: Kumar and Clark's Clinical Medicine. 11th ed. Philadelphia, Pa.: Elsevier; 2017. https://www.clinicalkey.com. Accessed May 29, 2019.

5. LaRocque R, et al. Causes of infectious diarrhea and other foodborne illnesses in resource-rich settings. https://www.uptodate.com/contents/search. Accessed May 29, 2019.

6. Ryan KJ, ed. Infectious diseases: Syndromes and etiologies. In: Sherris Medical Microbiology. 7th ed. New York, N.Y.: McGraw-Hill Education; 2018. https://accessmedicine.mhmedical.com. Accessed May 29, 2019.

7. File TM, et al. Epidemiology, pathogenesis, and microbiology of community-acquired pneumonia in adults. https://www.uptodate.com/contents/search. Accessed May 29. 2019.

8. DeClerq E, et al. Approved antiviral drugs over the past 50 years. Clinical Microbiology Reviews. 2016;29:695.

9. Mousa HAL. Prevention and treatment of influenza, influenza-like illness and common cold by herbal, complementary, and natural therapies. Journal of Evidence-Based Complementary & Alternative Medicine. 2017;22:166.

10. Caring for someone sick. Centers for Disease Control and Prevention. https://www.cdc.gov/flu/treatment/caring-for-someone.htm. Accessed May 29, 2019.

# data[].attributes.attachment_link.title
Infectious diseases-Infectious diseases - Symptoms & causes - Mayo Clinic

# data[].attributes.attachment_link.description
Viruses, bacteria, fungi and parasites can all cause infection. Find out more about how to prevent and treat these conditions.

# data[].attributes.attachment_link.readable_text
Overview

Acromegaly is a hormonal disorder that develops when your pituitary gland produces too much growth hormone during adulthood. When this happens, your bones increase in size, including those of your hands, feet and face. Acromegaly usually affects middle-aged adults.

Acromegaly usually affects middle-aged adults, though it can develop at any age. In children who are still growing, too much growth hormone can cause a condition called gigantism. These children have exaggerated bone growth and an abnormal increase in height.

Because acromegaly is uncommon and physical changes occur gradually, the condition sometimes takes a long time to recognize. If it's not treated promptly, acromegaly can lead to serious illness and may even become life-threatening. But available treatments can reduce your risk of complications and significantly improve characteristics of the condition, including the enlargement of your features.

Symptoms

A common sign of acromegaly is enlarged hands and feet. People with this disorder often notice that they aren't able to put on rings that used to fit and that their shoe size has progressively increased.

Acromegaly may also cause gradual changes in the shape of your face, such as a protruding lower jaw and brow, an enlarged nose, thickened lips, and wider spacing between your teeth.

Because acromegaly tends to progress slowly, early signs may not be obvious for years. Sometimes, people notice the condition only by comparing old photographs with newer ones.

Acromegaly may produce the following signs and symptoms, which can vary from one person to another:

Enlarged hands and feet

Coarsened, enlarged facial features

Coarse, oily, thickened skin

Excessive sweating and body odor

Small outgrowths of skin tissue (skin tags)

Fatigue and muscle weakness

A deepened, husky voice due to enlarged vocal cords and sinuses

Severe snoring due to obstruction of the upper airway

Impaired vision

Headaches

Enlarged tongue

Pain and limited joint mobility

Menstrual cycle irregularities in women

Erectile dysfunction in men

Enlarged organs, such as the heart

Loss of interest in sex

When to see a doctor

If you have signs and symptoms associated with acromegaly, contact your doctor for an evaluation.

Acromegaly usually develops slowly. Even your family members may not initially notice the gradual physical changes that occur with this disorder, but early diagnosis is important so that you can start getting proper care. Acromegaly can lead to serious complications if it's not treated.

Causes

Acromegaly is caused by the pituitary gland overproducing growth hormone (GH) over time. The pituitary gland, a small gland situated at the base of your brain behind the bridge of your nose, produces a number of hormones. GH plays an important role in managing your physical growth.

When GH is secreted into your bloodstream, it triggers your liver to produce a hormone called insulin-like growth factor-I (IGF-I). In turn, IGF-I stimulates the growth of bones and other tissues.

If your pituitary gland makes too much GH, excessive amounts of IGF-I can result. Too much IGF-I can cause abnormal growth of your soft tissues and skeleton and other signs and symptoms characteristic of acromegaly and gigantism.

In adults, a tumor is the most common cause of too much GH production:

Pituitary tumors. Most cases of acromegaly are caused by a noncancerous (benign) tumor (adenoma) of the pituitary gland. The tumor secretes excessive amounts of growth hormone, causing many of the signs and symptoms of acromegaly. Some of the symptoms of acromegaly, such as headaches and impaired vision, are due to the tumor mass pressing on nearby brain tissues.

Nonpituitary tumors. In a few people with acromegaly, tumors in other parts of the body, such as the lungs or pancreas, cause the disorder. Sometimes, these tumors secrete GH. In other cases, the tumors produce a hormone called growth hormone-releasing hormone (GH-RH), which stimulates the pituitary gland to make more GH.

Complications

Progression of acromegaly can result in major health problems. Complications may include:

High blood pressure (hypertension)

Cardiovascular disease, particularly enlargement of the heart (cardiomyopathy)

Osteoarthritis

Diabetes mellitus

Goiter

Precancerous growths (polyps) on the lining of your colon

Sleep apnea, a condition in which breathing repeatedly stops and starts during sleep

Carpal tunnel syndrome

Spinal cord compression

Vision loss

Early treatment of acromegaly can prevent these complications from developing or becoming worse. Untreated, acromegaly and its complications can lead to premature death.

The Mayo Clinic experience and patient stories

Our patients tell us that the quality of their interactions, our attention to detail and the efficiency of their visits mean health care like they've never experienced. See the stories of satisfied Mayo Clinic patients.

# data[].attributes.attachment_link.description
Acromegaly is a hormonal disorder that develops when your pituitary gland produces too much growth hormone during adulthood. When this happens, your bones increase in size, including those of your hands, feet and face. Acromegaly usually affects middle-aged adults. Acromegaly usually affects middle-aged adults, though it can develop at any age.

# data[].attributes.attachment_link.provider_name
NORD (National Organization for Rare Disorders)

# data[].attributes.attachment_link.readable_text
The treatment of acromegaly is directed toward the specific symptoms that are apparent in each individual. Treatment may require the coordinated efforts of a team of specialists. The goals of treatment of acromegaly are to return growth hormone levels to normal, decrease the size of a pituitary adenoma (if present) thereby relieving pressure on the surrounding tissue, maintain normal pituitary function, and reverse or improve associated symptoms.

Acromegaly is usually treated by surgery, medications and/or radiation therapy. No single therapeutic option is effective for everyone. An individual's specific treatment plan will based on several factors including the size and location of the pituitary tumor; the presence or absence of certain symptoms; an individual's age and general health; and/or other elements. Decisions concerning the use of particular therapies should be made by physicians and other members of the health care team in careful consultation with the patient based upon the specifics of his or her case; a thorough discussion of the potential benefits and risks, including possible side effects and long-term effects; patient preference; and other appropriate factors.

Acromegaly is usually treated by transsphenoidal surgery; a procedure in which all or part of a pituitary tumor is removed. Surgery often results in a rapid therapeutic response, immediately relieving pressure on surrounding brain structures and lowering growth hormone levels. When surgery is successful, soft tissue swelling may decrease in just a few days. Surgery is more effective in individuals with small tumors (microadenomas) than in those with large tumors (macroadenomas). Surgery may not successfully improve all symptoms (e.g., headaches may persist) and, in some cases, removal of the entire tumor may not be possible, resulting in growth hormone levels that remain too high.

Individuals treated by surgery should be periodically monitored by a physician because of the possible recurrence of the disorder. In some cases, surgery will improve the hormone levels, but not return them to normal, which necessitates further treatment often with medications.

Certain medications may be used to treat individuals with acromegaly. Medical therapy may be recommended in individuals in whom surgery in contraindicated, in whom surgery did not work or failed to return hormone levels to normal or to shrink large tumors before surgery.

Three different classes of medications are often used to treat individuals with acromegaly. These are somatostatin analogues including octreotide, lanreotide and pasireotide; growth hormone receptor antagonists such as pegvisomant; and dopamine antagonists.

The Food and Drug Administration (FDA) has approved the drug octreotide acetate (Sandostatin® LAR) for its use in the treatment of acromegaly. Octreotide is an artificially produced (synthetic) compound similar to somatostatin (somatostatin analog), a natural hormone produced by the hypothalamus that serves to inhibit the secretion of growth hormone. (The hypothalamus is an area of the brain that plays a role in coordinating hormone function.) Treatment with octreotide has demonstrated decreases in serum levels of GH and IGF-I, and tumor shrinkage in some patients receiving the drug. Safety and efficacy studies have been extensively published with decades of experience in treating patients with acromegaly.

The FDA has approved the drug pasireotide (Signifor LAR®) for injectable suspension in the treatment of acromegaly. Pasireotide is indicated for patients who have had an inadequate response to surgery, or for whom surgery is not an option. Similar to octreotide, pasireotide acts on the somatostatin receptors, with interactions with somatostatin receptor subtypes 1, 2, 3, and 5. Recent publications have demonstrated the safety and efficacy of pasireotide in comparison to octreotide LAR in a randomized, double-blind clinical trial, open label extension studies, and crossover studies comparing pasireotide to octreotide or lanreotide. Signifor LAR is manufactured by Novartis Pharmaceuticals Corporation.

The FDA has also approved Somatuline® Depot (lanreotide) Injection for the treatment of acromegaly. The FDA approved Somatuline® Depot (lanreotide) Injection for the long-term treatment of individuals with acromegaly who have had inadequate response to or cannot be treated with surgery and/or radiation therapy. This treatment lowers the levels of GH and insulin-like growth factor-1. Somatuline Depot is manufactured by Ipsen.

The FDA has approved the orphan drug Somavert® (pegvisomant for injection) for the treatment of acromegaly in individuals who have had an inadequate response to surgery and/or radiation therapy and/or other medical therapies, or for whom these therapies are not appropriate. Somavert, which blocks the effects of excess growth hormone in acromegaly, is administered by subcutaneous injection. Somavert is manufactured by Pfizer, Inc.

The third class of medications sometimes used to treat individuals with acromegaly is dopamine agonists. However, these drugs, which include bromocriptine and cabergoline, are generally effective for fewer individuals than other medications. Physicians may prescribe these medications in conjunction with other medications used to treat acromegaly.

Surgery and medications may be supplemented by radiation treatment (proton beam, heavy particle, and supravoltage irradiation) or drug therapy. Radiation therapy is most often used in individuals in whom surgery has failed to sufficiently reduce tumor size or growth hormone levels. Conventional fractionated radiation therapy usually requires daily treatments over a four to six week period and may reduce growth hormones levels by 50 percent, but successful results may not occur until two to five years later. Because results are delayed, radiation therapy is rarely used to treat acromegaly without combining it with surgery or drug therapy.

After initial therapies, individuals with acromegaly will need to be routinely monitored by a physician to ensure that the pituitary is functioning normally and that the existing symptoms continue to improve.

In addition to conventional radiation therapy described above, some individuals may be treated by other forms radiotherapy. This forms of radiotherapy offers more precise targeting of high-beam radiation delivered at varying angles. This option limits the damage to surrounding tissue and can be delivered in a single session. A person is not eligible for this form of radiotherapy if the pituitary tumor is not at least 5mm away from the spot where the optic nerves from eyes cross at the base of the brain (optic chiasm). More research is necessary to determine the long-term safety and effective of this form of therapy for individuals with acromegaly.

# data[].attributes.attachment_link.title
Acromegaly - NORD (National Organization for Rare Disorders)

# data[].attributes.attachment_link.description
The treatment of acromegaly is directed toward the specific symptoms that are apparent in each individual. Treatment may require the coordinated efforts of a team of specialists.

# data[].attributes.attachment_link.readable_text
Named after Thomas Addison, a graduate of the University of Edinburgh Medical School, who first discovered and described the illness in 1855, Addison's disease is a rare illness that affects one out of every 100,000 individuals. The disease can affect both men and women of any age, but it is predominantly diagnosed in middle-aged women, and former president John F. Kennedy was known to suffer from the condition as well. Learn more now about this autoimmune condition, its causes, signs and symptoms, and treatment options available for patients afflicted by it.

# data[].attributes.attachment_link.description
Named after Thomas Addison, a graduate of the University of Edinburgh Medical School, who first discovered and described the illness in 1855, Addison's disease is a rare illness that affects one out of every 100,000 individuals. The disease can affect both men and women of any age, but it is predominantly diagnosed in middle-aged women, [...]

# data[].attributes.attachment_link.description
Addison's disease, also called adrenal insufficiency, is an uncommon disorder that occurs when your body doesn't produce enough of certain hormones. In Addison's disease, your adrenal glands, located just above your kidneys, produce too little cortisol and, often, too little aldosterone. Addison's disease occurs in all age groups and both sexes, and can be life-threatening.

# data[].attributes.attachment_link.readable_text
Causes of excess IGF-I action can be divided into the following three categories:

By far, most people with gigantism or acromegaly have GH-secreting pituitary adenomas or hyperplasia. Other causes of increased and unregulated GH production, all very rare, include increased GHRH from hypothalamic tumors; ectopic GHRH from nonendocrine tumors; and ectopic GH secretion by nonendocrine tumors.

Although gigantism is typically an isolated disorder, rare cases occur as a feature of other conditions, such as the following:

Approximately 20% of patients with gigantism have McCune-Albright syndrome (the triad of precocious puberty, café au lait spots, fibrous dysplasia) and may have either pituitary hyperplasia or adenomas. (See the image below.)

A 12-year-old boy with McCune-Albright syndrome. His growth-hormone excess manifested as tall stature, coarse facial features, and macrocephaly.

More than 95% of acromegaly cases are caused by a pituitary adenoma that secretes excess amounts of GH. Histopathologically, tumors include acidophil adenomas, densely granulated GH adenomas, sparsely granulated GH adenomas, somatomammotropic adenomas, and plurihormonal adenomas.

Ectopic production of GH and GHRH by malignant tumors accounts for other causes of IGF-I excess. (Ectopic GHRH-producing tumors, usually seen in the lung or pancreas, may occasionally be evident elsewhere, such as in the duodenum as a neuroendocrine carcinoma.)

Of these tumors, up to 40% have a mutation involving the alpha subunit of the stimulatory guanosine triphosphate (GTP)-binding protein. In the presence of a mutation, persistent elevation of cyclic adenosine monophosphate (cAMP) in the somatotrophs results in excessive GH secretion.

The pathologic effects of GH excess include acral overgrowth, insulin antagonism, nitrogen retention, increased risk of colon polyps/tumors, and acral overgrowth (ie, macrognathia; enlargement of the facial bone structure, as well as of the hands and feet; and visceral overgrowth, including macroglossia and enlargement of the heart muscle, thyroid, liver, and kidney).

Pathologic studies on acromegalic hearts have shown extensive interstitial fibrosis, suggesting the existence of a specific acromegalic cardiomyopathy.

GH/IGF-I excess

Despite diverse pathophysiologic mechanisms, the final common abnormality in gigantism and acromegaly is IGF-I excess. Elevated tissue levels of free IGF-I, which is produced primarily in hepatocytes in response to excess GH, mediate most, if not all, growth-related outcomes in gigantism. Transgenic mice that overexpressed GH, GHRH, or IGF-I were found to have dramatically accelerated somatic growth compared with control litter mates.

One acromegalic patient had low serum GH levels and elevated serum total IGF-I levels; this finding implicates IGF-I as the key pathologic factor in this disease. Serum levels of IGF-I are consistently elevated in patients with acromegaly and, therefore, are used to monitor treatment success. The conditions described below can cause IGF-I oversecretion.
Primary pituitary GH excess
In most individuals with GH excess, the underlying anomaly is a benign pituitary tumor composed of somatotrophs (GH-secreting cells) or mammosomatotrophs (GH-secreting and prolactin-secreting cells) in the form of a pituitary microadenoma (< 1 cm) or macroadenoma (>1 cm). The adenomas are most characteristically well-demarcated and confined to the anterior lobe of the pituitary gland. In some people with GH excess, the tumor spreads outside the sella, invading the sphenoid bone, optic nerves, and brain. GH-secreting tumors are more likely to be locally invasive or aggressive in pediatric patients than in adults.
Gs-alpha (Gsa) mutation
G proteins play an integral role in postligand signal transduction in many endocrine cells by stimulating adenyl cyclase, resulting in an accumulation of cyclic adenosine monophosphate (cAMP) and subsequent gene transcription. About 20% of patients with gigantism have McCune-Albright syndrome and pituitary hyperplasia or adenomas.

Activating mutations of the stimulatory Gsa protein have been found in the pituitary lesions in McCune-Albright syndrome and are believed to cause the other glandular adenomas observed. Point mutations found in several tissues affected in McCune-Albright syndrome involve a single amino-acid substitution in codon 201 (exon 8) or 227 (exon 9) of the gene for Gsa. Somatic point mutations have been identified in the somatotrophs of less than 40% of sporadic GH-secreting pituitary adenomas. The resulting oncogene ( gsp) is thought to induce tumorigenesis by persistently activating adenyl cyclase, with subsequent GH hypersecretion.
Loss of band 11q13 heterozygosity
Loss of heterozygosity at the site of a putative tumor-suppressor gene on band 11q13 was first identified in tumors from patients with MEN type I and GH excess. Loss of heterozygosity at band 11q13 has also been observed in all types of sporadically occurring pituitary adenomas. It is associated with an increased propensity for tumoral invasiveness and biologic activity.

Isolated familial somatotropinoma, a rare disease, refers to the occurrence of two or more cases of acromegaly or gigantism in a family in whom the features of Carney complex or MEN type 1 are absent.It appears to be inherited as an autosomal dominant disease with incomplete penetrance. Although an association exists between isolated familial somatotropinoma and loss of heterozygosity on 11q13, the responsible gene remains unknown.
Abnormality at Carney loci on chromosomes 2 and 17
The Carney complex, which is characterized by myxomas, endocrine tumors, and spotty pigmentation, is transmitted as an autosomal dominant trait. About 8% of affected individuals have GH-producing pituitary adenomas. The causative gene for this disease was mapped to bands 2p16 and 17q22-24. Germline mutations in PRKAR1A (which encodes for the protein kinase A type I-alpha regulatory subunit, an apparent tumor-suppressor gene on chromosome arm 17q) were detected in several families with Carney complex.
Secondary GH excess
Causes of secondary GH excess include increased secretion of GHRH due to an intracranial or ectopic source and dysregulation of the hypothalamic-pituitary-GH axis.
GHRH excess
Hypothalamic GHRH excess is postulated as a cause for gigantism, possibly secondary to an activating mutation in hypothalamic GHRH neurons. Excess GHRH secretion may be due to an intracranial or ectopic tumor. Several well-documented incidents of hypothalamic GHRH excess demonstrated intracranial gangliocytomas associated with gigantism or acromegaly.

Ectopic GHRH-secreting tumors have included carcinoid, pancreatic islet-cell, and bronchial neoplasms. Prolonged tumoral secretion of GHRH leads to pituitary hyperplasia, with or without adenomatous transformation, that increases levels of GH and other adenohypophyseal peptides.
Disruption of somatostatin tone
Tumoral infiltration into somatostatinergic pathways are hypothesized to be the basis for GH excess in rare incidents of gigantism associated with neurofibromatosis and optic glioma or astrocytomas.

# data[].attributes.attachment_link.description
Gigantism refers to abnormally high linear growth due to excessive action of insulinlike growth factor I (IGF-I) while the epiphyseal growth plates are open during childhood. Acromegaly is the same disorder of IGF-I excess but occurs after the growth plate cartilage fuses in adulthood.

# data[].attributes.attachment_link.readable_text
Your adrenal glands are located on top of your kidneys. These glands produce many of the hormones that your body needs for normal functions.

Addison's disease occurs when the adrenal cortex is damaged, and the adrenal glands don't produce enough of the steroid hormones cortisol and aldosterone.

Cortisol regulates the body's reaction to stressful situations. Aldosterone helps with sodium and potassium regulation. The adrenal cortex also produces sex hormones (androgens).

People who have Addison's disease may experience the following symptoms:

muscle weakness

fatigue and tiredness

darkening in skin color

weight loss or decreased appetite

a decrease in heart rate or blood pressure

low blood sugar levels

fainting spells

sores in the mouth

cravings for salt

nausea

vomiting

People living with Addison's disease may also experience neuropsychiatric symptoms, such as:

irritability or depression

lack of energy

sleep disturbances

If Addison's disease goes untreated for too long, it can become an Addisonian crisis. Symptoms associated with an Addisonian crisis can :

agitation

delirium

visual and auditory hallucinations

An Addisonian crisis is a life-threatening medical emergency. Call 911 immediately if you or someone you know begins to experience:

mental status changes, such as confusion, fear, or restlessness

loss of consciousness

sudden pain in the lower back, belly, or legs

An untreated Addisonian crisis can lead to shock and death.

There are two major classifications for Addison's disease: primary adrenal insufficiency and secondary adrenal insufficiency. In order to treat the disease, your doctor will need to find out which type is responsible for your condition.

Primary adrenal insufficiency

Primary adrenal insufficiency occurs when your adrenal glands are damaged so severely that they can no longer produce hormones. This type of Addison's disease is most often caused when your immune system attacks your adrenal glands. This is called an autoimmune disease.

In an autoimmune disease, your body's immune system mistakes any organ or area of the body for a virus, bacteria, or another outside invader.

Other causes of primary adrenal insufficiency include:

prolonged administration of glucocorticoids (e.g. prednisone)

infections in your body

cancer and abnormal growths (tumors)

certain blood thinners used to control clotting in the blood

Secondary adrenal insufficiency

Secondary adrenal insufficiency occurs when the pituitary gland (located in your brain) can't produce adrenocorticotropic hormone ( ACTH). ACTH tells the adrenal glands when to release hormones.

It's also possible to develop adrenal insufficiency if you do not take the corticosteroid medications your doctor prescribes. Corticosteroids help control chronic health conditions like asthma.

There are also many other causes of secondary adrenal insufficiency, including:

You may be at a higher risk for Addison's disease if you:

Your doctor will ask you about your medical history and the symptoms you've been experiencing. They will do a physical examination, and they may order some lab tests to check your potassium and sodium levels.

Your doctor may also order imaging tests and measure your hormone levels.

Your treatment will depend on what's causing your condition. Your doctor may prescribe medications that regulate your adrenal glands.

Following the treatment plan that your doctor creates for you is very important. Untreated Addison's disease can lead to an Addisonian crisis.

If your condition has gone untreated for too long, and has progressed to a life-threatening condition called Addisonian crisis, your physician may prescribe medication to treat that first.

Addisonian crisis causes low blood pressure, high potassium in the blood, and low blood sugar levels.

Medications

You may need to take a combination of glucocorticoids medications (drugs that stop inflammation) to improve your health. These medications will be taken for the rest of your life and you cannot miss a dose.

Hormone replacements may be prescribed to replace hormones that your adrenal glands are not making.

Home care

Keep an emergency kit that contains your medications on hand at all times. Ask your doctor to write a prescription for an injectable corticosteroid for emergencies.

You may also want to keep a medical alert card in your wallet and a bracelet on your wrist to let others know about your condition.

Alternative therapies

It's important to keep your stress level down if you Addison's disease. Major life events, such as a death of a loved one or an injury, can raise your stress level and affect the way you respond to your medications. Talk to your doctor about alternative ways to relieve stress, such as yoga and meditation.

Addison's disease requires lifelong treatment. Treatments, such as hormone replacement medications, can help you manage your symptoms.

Following the treatment plan your doctor creates is an important step in helping you live a productive life.

Remember, always take your medications exactly as directed. Taking too little or too much medication can negatively affect your health.

Your treatment plan may need to be reevaluated and changed depending on your condition. For this reason, it's important that you see your doctor regularly.

# data[].attributes.attachment_link.description
Addison's disease occurs when the adrenal cortex is damaged, and the adrenal glands do not produce enough cortisol and aldosterone. Cortisol regulates the body's reaction to stressful situations. Aldosterone helps with sodium and potassium regulation. Learn causes, risks, and treatment of Addison's disease.

# data[].attributes.attachment_link.readable_text
Diabetes insipidus is a condition where the body loses too much fluid through urination, causing a significant risk of dangerous dehydration as well as a range of other illnesses and conditions.

It is a rare disorder affecting the regulation of body fluid levels.

People with diabetes insipidus produce excessive amounts of urine, resulting in frequent urination and thirst. However, the underlying cause of these two symptoms differs from types 1 and 2 diabetes.

The disease takes two main forms: Mephrogenic diabetes insipidus and central or neurogenic diabetes insipidus.

Central diabetes insipidus occurs when the pituitary gland fails to secrete the hormone vasopressin, which regulates bodily fluids. In nephrogenic diabetes insipidus, vasopressin secretion is normal, but the kidneys do not correctly respond to the hormone.

Diabetes insipidus affects roughly 1 in every 25,000 people in the United States.

Share on Pinterest
The need to urinate in large volumes can wake people with diabetes insipidus.

The main symptom of all cases of diabetes insipidus is frequently needing to pass high volumes of diluted urine.

The second most common symptom is polydipsia, or excessive thirst.

In this case, results from the loss of water through urine. The thirst prompts the person with diabetes insipidus to drink large volumes of water.

The need to urinate can disturb sleep. The volume of urine passed each day can be anywhere between 3 liters and 20 liters, and up to 30 liters in cases of central diabetes insipidus.

Another secondary symptom is dehydration due to the loss of water, especially in children who may not be able to communicate their thirst. Children may become listless and feverish, experience vomiting and diarrhea, and may show delayed growth.

Other people unable to help themselves to water, such as people with dementia, are also at risk of dehydration.

Extreme dehydration can lead to hypernatremia, a condition in which the sodium concentration of the serum in the blood becomes very high due to low water retention. The cells of the body also lose water.

Hypernatremia can lead to neurological symptoms, such as overactivity in the brain and nerve muscles, confusion, seizures, or even coma.

Without treatment, central diabetes inspidus can lead to permanent kidney damage. In nephrogenic DI, serious complications are rare, so long as water intake is sufficient.

Diabetes insipidus becomes a serious problem only for people who cannot replace the fluid that is lost in the urine. Access to water and other fluids makes the condition manageable.

If there is a treatable underlying cause of the high urine output, such as diabetes mellitus or drug use, addressing this should help resolve the diabetes insipidus.

For central and pregnancy-related diabetes insipidus, drug treatment can correct the fluid imbalance by replacing vasopressin. For nephrogenic diabetes insipidus, the kidneys will require treatment.

Vasopressin hormone replacement uses a synthetic analog of vasopressin called desmopressin.

The drug is available as a nasal spray, injection, or tablet, and is taken when needed.

Care should be taken not to overdose, as this can lead to excessive water retention and, in rare, severe cases, hyponatremia and fatal water intoxication.

The drug is otherwise generally safe when used at appropriate dosages, with few side effects. It is, however, not effective if diabetes insipidus occurs as a result of kidney dysfunction.

Mild cases of central diabetes insipidus may not need hormone replacement and can be managed through increased water intake.

Nephrogenic diabetes insipidus treatments may include:

anti-inflammatory medicines, such as non-steroidal anti-inflammatory drugs (NSAIDS)

diuretics, such as amiloride and hydrochlorothiazide

reducing sodium intake and increasing water intake

A doctor may also advise a low-salt diet, and a person with diabetes insipidus may be referred to a nutritionist to organize a diet plan.

Reducing caffeine and protein intake and removing processed foods from the diet can be effective steps to controlling water retention, as well as consuming foods with high water content, such as melons.

Both types of diabetes insipidus are linked to a hormone called vasopressin but occur in different ways.

Vasopressin promotes water retention in the kidneys. This also keeps blood pressure at a healthy level.

The main symptom, excessive urine output, can have other causes. These would usually be ruled out before making a diagnosis of diabetes insipidus.

For example, undiagnosed or poorly managed diabetes mellitus can cause frequent urination.
Central diabetes insipidus
Central diabetes insipidus is caused by reduced or absent levels of vasopressin.

The condition can be present from birth, or primary. Secondary central diabetes insipidus is acquired later in life.

The cause of primary central diabetes insipidus is often unknown. Some causes result from an abnormality in the gene responsible for vasopressin secretion.

The secondary type is acquired through diseases and injuries that affect how vasopressin is produced.

These can include brain lesions resulting from head injuries, cancers, or brain surgery. Other body-wide conditions and infections can also trigger central diabetes insipidus.
Nephrogenic diabetes insipidus
Nephrogenic diabetes insipidus can also be inherited or acquired. This type affects the response of the kidneys to vasopressin.

Depending on a person's genes, the condition results in the kidneys either completely or partially not responding to vasopressin. This affects water balance to varying degrees.

The acquired form of nephrogenic diabetes insipidus also reduces the kidneys' ability to concentrate urine when water needs to be conserved.

Secondary nephrogenic diabetes insipidus can have numerous causes, including:

kidney cysts that have developed due to a number of conditions, such as autosomal dominant polycystic kidney disease (ADPKD), nephronophthisis, medullary cystic disease complex, and medullary sponge kidney

the release of an outlet tube obstruction from a kidney

kidney infection

high blood calcium levels

some cancers

certain medications, especially lithium, but also demeclocycline, amphotericin B, dexamethasone, dopamine, ifosfamide, ofloxacin, and orlistat

rarer conditions, including amyloidosis, Sjögren's syndrome, and Bardet-Biedl syndrome

chronic hypokalemic nephropathy, a kidney disease caused by low blood potassium levels

a cardiopulmonary bypass, which can affect vasopressin levels and may require treatment with desmopressin

Gestational diabetes insipidus
In rare cases, pregnancy can cause a disturbance of vasopressin, especially during the third trimester. This occurs due to the placenta releasing an enzyme that degrades vasopressin.

Pregnancy also causes a lower thirst threshold in women, stimulating them to drink more fluids, while other normal physiological changes during pregnancy can also affect the kidneys' response to vasopressin.

Gestational diabetes insipidus is treatable during gestation and resolves 2 or 3 weeks following childbirth. The condition affects only a few women out of every 100,000 women who are pregnant.
Drugs that affect water balance
Diuretic drugs, commonly referred to as water pills, can also cause increased urine output.

Fluid imbalance can also occur after fluids are administered intravenously (IV). In these cases, the rate of the drip is stopped or slowed, and the need to urinate resolves. High-protein tube feeds may also increase urine output.

The water deprivation test is a reliable test to help diagnose diabetes insipidus. However, the test has to be performed by a specialist, as it can be dangerous without proper supervision.

The water deprivation test challenges the body's hormonal and kidney responses to dehydration.

The water deprivation test involves allowing a patient to become increasingly dehydrated while taking blood and urine samples.

Vasopressin is also given to test the kidneys' ability to conserve water during dehydration.

In addition to managing the dangers of dehydration, close supervision also allows psychogenic polydipsia to be definitively ruled out. This condition causes a person to compulsively or habitually drink large volumes of water.

Someone with psychogenic polydipsia may try to drink some water during this test, despite strict instructions against drinking.

Samples taken during the water deprivation test are assessed to determine the concentration of urine and blood, and to measure levels of electrolytes, particularly sodium, in the blood.

Under normal circumstances, dehydration triggers the secretion of vasopressin from the pituitary gland in the brain, telling the kidneys to conserve water and concentrate the urine.

In diabetes insipidus, either insufficient vasopressin is released, or the kidneys are resistant to the hormone. Testing these dysfunctions will help define and treat the type of diabetes insipidus.

The two types of the condition are further defined if the urine concentration then responds to injection or nasal spray of vasopressin.

Improvements in urine concentration demonstrate that the kidneys are responding to the hormone's message to improve water conservation, suggesting that the diabetes insipidus is central.

If the kidneys do not respond to the synthetic vasopressin, the cause is likely to be nephrogenic.

Before the water deprivation test is carried out by specialists, investigations are done to rule out other explanations for the high volumes of diluted urine, including:

Diabetes mellitus: Blood sugar levels in types 1 and 2 diabetes affect urine output and thirst.

Current courses of medication: The doctor will rule out the role of any current medications, such as diuretics, in affecting water balance.

Psychogenic polydipsia: Excessive water intake as a result of this condition can create the high urine output. It can be associated with psychiatric illnesses, such as schizophrenia.

Diabetes insipidus and diabetes mellitus are not related to one another. Their symptoms, however, can be similar.

The words 'mellitus' and 'insipidus' come from the early days of diagnosing the condition. Doctors would taste the urine to gauge sugar content. If the urine tasted sweet, it meant that too much sugar was leaving the body in the urine, and the doctor would reach a diabetes mellitus diagnosis.

However, if the urine tasted bland or neutral, it meant that water concentration was too high, and diabetes inspidus would be diagnosed. "Insipidus" comes from the word "insipid," meaning weak or tasteless.

In diabetes mellitus, elevated blood sugar prompts the production of large volumes of urine to help remove the excess sugar from the body. In diabetes insipidus, it is the water balance system that is not functioning correctly.

Diabetes mellitus is far more common than diabetes insipidus. Diabetes insipidus, however, progresses far more rapidly.

Of the two conditions, diabetes mellitus is more harmful and harder to manage.

Diabetes inspidus is often difficult or impossible to prevent, as it results either from genetic problems or other conditions. However, symptoms can be managed effectively.

It is often a lifelong condition. With ongoing treatment, the outlook can be good.

# data[].attributes.attachment_link.title
Diabetes insipidus: Causes, symptoms, and treatment

# data[].attributes.attachment_link.description
Diabetes insipidus is a rare condition that affects a person's ability to regulate their fluid level. People with this disease produce excessive amounts of urine, which can result in severe dehydration. The condition is different to the well-known diabetes mellitus. Here we look at the causes, diagnosis, and treatment.

# data[].attributes.attachment_link.readable_text
Where is the pancreas?

The pancreas is a large gland that lies alongside the stomach and the small bowel. It is about six inches (approximately 15 cm) long and is divided into the head, body and tail.

What does the pancreas do?

The pancreas carries out two important roles:

1. It makes digestive juices, which consist of powerful enzymes. These are released into the small bowel after meals to break down and digest food.

2. It makes hormones that control blood glucose levels.

The pancreas produces hormones in its 'endocrine' cells. These cells are gathered in clusters known as islets of Langerhans and monitor what is happening in the blood. They then can release hormones directly into the blood when necessary. In particular, they sense when sugar (glucose) levels in the blood rise, and as soon as this happens the cells produce hormones, particularly insulin. Insulin then helps the body to lower blood glucose levels and 'store' the sugar away in fat, muscle, liver and other body tissues where it can be used for energy when required.

The pancreas is very close to the stomach. As soon as food is eaten, the pancreas releases digestive enzymes into the bowel to break food down. As the food is digested, and nutrient levels in the blood rise, the pancreas produces insulin to help the body store the glucose (energy) away. Between meals, the pancreas does not produce insulin and this allows the body to gradually release stores of energy back into the blood as they are needed.

Glucose levels remain very stable in the blood at all times to ensure that the body has a steady supply of energy. This energy is needed for metabolism, exercise and, in particular, to fuel the parts of the brain that 'run' on glucose. This makes sure that the body doesn't starve between meals.

What hormones does the pancreas produce?

The most important hormone that the pancreas produces is insulin. Insulin is released by the 'beta cells' in the islets of Langerhans in response to food. Its role is to lower glucose levels in the bloodstream and promote the storage of glucose in fat, muscle, liver and other body tissues.

' Alpha cells' in the islets of Langerhans produce another important hormone, glucagon. This has the opposite effect to insulin, by helping release energy into the bloodstream from where it is stored, thus raising blood sugar levels. Therefore, glucagon and insulin work in tandem to control the balance of glucose in the bloodstream.

Other hormones produced by the pancreas include pancreatic polypeptide and somatostatin. They are believed to play a part in regulating and fine-tuning the insulin and glucagon-producing cells.

What could go wrong with the pancreas?

When the cells that make insulin either stop working altogether, or become inefficient and do not make enough insulin, this causes diabetes mellitus. Type 1 diabetes mellitus is caused when the body's immune system attacks its own cells in the islets of Langerhans, meaning that these cells cannot produce insulin. Type 2 diabetes mellitus is a metabolic disorder where the body is no longer able to produce or respond to insulin.

Some women also get diabetes temporarily when they are pregnant. This is called gestational diabetes. There are other rarer forms of diabetes, some of which are inherited. In addition, people will get diabetes if their pancreas is taken away surgically or damaged (for instance by severe pancreatitis).

Very rarely, patients develop growths (tumours) of the cells that make up the islets of Langerhans. These may be benign tumours, where a particular kind of cell multiplies and makes large quantities of its hormone whether it is needed or not. For example, if the tumour is made of insulin-producing cells, it is called an insulinoma. This is where too much insulin is produced when it is not required. This also happens with glucagon-producing cells, or a glucagonoma, which produces too much glucagon. These and other hormone-producing tumours in the pancreas are very rare, but endocrinology specialists have important parts to play in diagnosing patients with these tumours and contributing to their management and treatment.

The digestive cells of the pancreas can be involved in the condition known as pancreatitis. This is a very painful and serious condition caused by digestive enzymes 'leaking' into the pancreas itself and damaging the delicate tissues in and around it.

It is also possible for a tumour to develop in the part of the pancreas that produces the digestive juices that are released into the bowel. This condition is called pancreatic cancer.

Last reviewed: Mar 2018

# data[].attributes.attachment_link.description
The pancreas is a large gland that lies alongside the stomach and the small bowel. It is about six inches (approximately 15 cm) long and is divided into the head, body and tail. The pancreas carries out two important roles: It makes digestive juices, which consist of powerful enzymes.

# data[].attributes.attachment_link.readable_text
Overview

Cushing syndrome occurs when your body is exposed to high levels of the hormone cortisol for a long time. Cushing syndrome, sometimes called hypercortisolism, may be caused by the use of oral corticosteroid medication. The condition can also occur when your body makes too much cortisol on its own.

Too much cortisol can produce some of the hallmark signs of Cushing syndrome - a fatty hump between your shoulders, a rounded face, and pink or purple stretch marks on your skin. Cushing syndrome can also result in high blood pressure, bone loss and, on occasion, type 2 diabetes.

Treatments for Cushing syndrome can return your body's cortisol production to normal and noticeably improve your symptoms. The earlier treatment begins, the better your chances for recovery.

Symptoms

The signs and symptoms of Cushing syndrome can vary depending on the levels of excess cortisol.

Common signs and symptoms of Cushing syndrome

Weight gain and fatty tissue deposits, particularly around the midsection and upper back, in the face (moon face), and between the shoulders (buffalo hump)

Pink or purple stretch marks (striae) on the skin of the abdomen, thighs, breasts and arms

Thinning, fragile skin that bruises easily

Slow healing of cuts, insect bites and infections

Acne

Signs and symptoms women with Cushing syndrome may experience

Thicker or more visible body and facial hair (hirsutism)

Irregular or absent menstrual periods

Signs and symptoms men with Cushing syndrome may experience

Decreased libido

Decreased fertility

Erectile dysfunction

Other signs and symptoms that may occur with Cushing syndrome

Severe fatigue

Muscle weakness

Depression, anxiety and irritability

Loss of emotional control

Cognitive difficulties

New or worsened high blood pressure

Headache

Increased pigmentation of the skin

Bone loss, leading to fractures over time

In children, impaired growth

When to see a doctor

Contact your doctor if you have symptoms that suggest Cushing syndrome, especially if you're taking corticosteroid medication to treat a condition, such as asthma, arthritis or inflammatory bowel disease.

Causes

Excess levels of the hormone cortisol are responsible for Cushing syndrome. Cortisol, which is produced in the adrenal glands, plays a variety of roles in your body.

For example, cortisol helps regulate your blood pressure, reduces inflammation, and keeps your heart and blood vessels functioning normally. Cortisol helps your body respond to stress. It also regulates the way you convert (metabolize) proteins, carbohydrates and fats in your diet into usable energy.

However, when the level of cortisol is too high in your body, you may develop Cushing syndrome.

The role of corticosteroid medications

Cushing syndrome can develop from a cause outside of your body (exogenous Cushing syndrome). One example is taking oral corticosteroid medications in high doses over an extended period of time. These medications, such as prednisone, have the same effect in the body as does cortisol produced by your body.

Oral corticosteroids may be necessary to treat inflammatory diseases, such as rheumatoid arthritis, lupus and asthma. It may also be used to prevent your body from rejecting a transplanted organ. Because the doses required to treat these conditions are often higher than the amount of cortisol your body normally needs each day, side effects from excess cortisol can occur.

It's also possible to develop Cushing syndrome from injectable corticosteroids - for example, repeated injections for joint pain, bursitis and back pain. Inhaled steroid medicines (taken for asthma) and steroid skin creams (used for skin disorders such as eczema) are generally less likely to cause Cushing syndrome than are oral corticosteroids. But, in some individuals, these medications may cause Cushing syndrome, especially if taken in high doses.

Your body's own overproduction

The condition may also be due to your body's own overproduction of cortisol (endogenous Cushing syndrome). This may occur from excess production by one or both adrenal glands, or overproduction of the adrenocorticotropic hormone (ACTH), which normally regulates cortisol production.

A pituitary gland tumor (pituitary adenoma). A noncancerous (benign) tumor of the pituitary gland, located at the base of the brain, produces an excess amount of ACTH, which in turn stimulates the adrenal glands to make more cortisol. When this form of the syndrome develops, it's called Cushing disease. It occurs much more often in women and is the most common form of endogenous Cushing syndrome.

An ACTH-secreting tumor. Rarely, a tumor that develops in an organ that normally does not produce ACTH will begin to secrete this hormone in excess, resulting in Cushing syndrome. These tumors, which can be noncancerous (benign) or cancerous (malignant), are usually found in the lungs, pancreas, thyroid or thymus gland.

A primary adrenal gland disease. In some people, the cause of Cushing syndrome is excess cortisol secretion that doesn't depend on stimulation from ACTH and is associated with disorders of the adrenal glands. The most common of these disorders is a noncancerous tumor of the adrenal cortex, called an adrenal adenoma.

Cancerous tumors of the adrenal cortex (adrenocortical carcinomas) are rare, but they can cause Cushing syndrome as well. Occasionally, benign, nodular enlargement of both adrenal glands can result in Cushing syndrome.

Familial Cushing syndrome. Rarely, people inherit a tendency to develop tumors on one or more of their endocrine glands, affecting cortisol levels and causing Cushing syndrome.

Complications

Without treatment, complications of Cushing syndrome may include:

Bone loss (osteoporosis), which can result in unusual bone fractures, such as rib fractures and fractures of the bones in the feet

High blood pressure (hypertension)

Type 2 diabetes

Frequent or unusual infections

Loss of muscle mass and strength

# data[].attributes.attachment_link.description
Cushing syndrome occurs when your body is exposed to high levels of the hormone cortisol for a long time. Cushing syndrome, sometimes called hypercortisolism, may be caused by the use of oral corticosteroid medication. The condition can also occur when your body makes too much cortisol on its own.

# data[].attributes.attachment_link.readable_text
The pancreas is an organ located behind the lower part of the stomach, in front of the spine and plays an important part in diabetes.

The pancreas is the organ which produces insulin, one the main hormones that helps to regulate blood glucose levels

The role of the pancreas in the body

The pancreas plays a part in two different organ systems, the endocrine system and the exocrine system.

The endocrine system includes all the organs which produce hormones, chemicals which are delivered via the blood to help regulate our mood, growth, metabolism and reproduction.

Two of the hormones produced by the pancreas are insulin and glucagon

The exocrine system is made up of a number of glands which release substances such as sweat (to the skin), saliva (in the mouth) or, in the case of the pancreas, digestive enzymes

The pancreas and insulin

The pancreas is responsible for producing insulin. The cells which produce insulin are beta cells. These cells are distributed in a cluster of cells in the pancreas called the Islets of Langerhans, named after the anatomist who discovered them

Insulin is a hormone that helps to regulate blood sugar levels by assisting the transport of glucose from the blood into neighbouring cells.

The pancreas and type 1 diabetes

In type 1 diabetes , the beta cells that produce insulin are attacked by the body's immune system.

As more beta cells get killed off, the pancreas struggles to produce enough insulin to keep blood sugar levels down and the symptoms of diabetes begin to appear.

Research has shown that whilst many beta cells are killed off, the body can continue to produce very small amounts of insulin even after decades have passed.

The pancreas and type 2 diabetes

In type 2 diabetes, the body builds up resistance to insulin and more insulin is needed to bring down blood glucose levels. As a result the pancreas needs to produce more insulin than it would normally need to.

If the pancreas can no longer produce enough insulin to bring down sugar levels, the symptoms of diabetes will begin to appear. Type 2 diabetes comes on gradually and it can take up to years for symptoms to appear.

Further development of type 2 diabetes can lead to loss of insulin producing beta cells from the pancreas which can lead to the need for insulin to be administered.

# data[].attributes.attachment_link.title
The pancreas is an organ located behind the lower part of the stomach, in front of the spine and plays an important part in diabetes.

# data[].attributes.attachment_link.description
The pancreas is an organ located behind the lower part of the stomach, in front of the spine and plays an important part in diabetes. The pancreas is the organ which produces insulin, one the main hormones that helps to regulate blood glucose levels The pancreas plays a part in two different organ systems, the endocrine system and the exocrine system.

# data[].attributes.attachment_link.readable_text
Diabetes insipidus is a rare condition where you pee a lot and often feel thirsty.
Diabetes insipidus is not related to diabetes, but it does share some of the same signs and symptoms.

The 2 main symptoms of diabetes insipidus are:

extreme thirst (polydipsia)

peeing a lot, even at night (polyuria)

In very severe cases of diabetes insipidus, a person can pee up to 20 litres of urine in a day.
Find out more about the symptoms of diabetes insipidus

When to seek medical advice

You should always see your GP if you're feeling thirsty all the time.

Although it may not be diabetes insipidus, it should be investigated.

Also see your GP if you're:

peeing more than normal - most healthy adults pass urine 4 to 7 times in a 24-hour period

needing to pee small amounts at frequent intervals - sometimes this can occur along with the feeling that you need to pee immediately

Children tend to pee more frequently because they have smaller bladders.

But seek medical advice if your child pees more than 10 times a day.

Your GP will be able to carry out a number of tests to help determine what's causing the problem.
Find out more about diagnosing diabetes insipidus

What causes diabetes insipidus

Diabetes insipidus is caused by problems with a hormone called vasopressin (AVP), also called antidiuretic hormone (ADH).

AVP plays a key role in regulating the amount of fluid in the body.

It's produced by specialist nerve cells in a part of the brain known as the hypothalamus.

AVP passes from the hypothalamus to the pituitary gland, where it's stored until needed.

The pituitary gland releases AVP when the amount of water in the body becomes too low.

It helps retain water in the body by reducing the amount of water lost through the kidneys, making the kidney produce more concentrated urine.

In diabetes insipidus, the lack of production of AVP means the kidney cannot make enough concentrated urine and too much water is passed from the body.

In rare cases, the kidney does not respond to AVP. This causes a specific form of diabetes insipidus called nephrogenic diabetes insipidus.

People feel thirsty as the body tries to compensate for the increased loss of water by increasing the amount of water taken in.
Find out more about the causes of diabetes insipidus

Who's affected by diabetes insipidus

Diabetes insipidus affects about 1 in 25,000 people in the general population.

Adults are more likely to develop the condition, but it can occur at any age.

In rarer cases, diabetes insipidus can develop during pregnancy, known as gestational diabetes insipidus.

Types of diabetes insipidus

There are 2 main types of diabetes insipidus:

cranial diabetes insipidus

nephrogenic diabetes insipidus

Cranial diabetes insipidus

Cranial diabetes insipidus occurs when there's not enough AVP in the body to regulate urine production.

Cranial diabetes insipidus is the most common type of diabetes insipidus.

It can be caused by damage to the hypothalamus or pituitary gland - for example, after an infection, operation, brain tumour or head injury.

In about 1 in 3 cases of cranial diabetes insipidus there's no obvious reason why the hypothalamus stops making enough AVP.

Nephrogenic diabetes insipidus

Nephrogenic diabetes insipidus occurs when there's enough AVP in the body but the kidneys fail to respond to it.

It can be caused by kidney damage or, in some cases, inherited as a problem on its own.

Some medications, particularly lithium (used to help stabilise mood in some people with specific mental health conditions, such as bipolar disorder), can cause nephrogenic diabetes insipidus.

Treating diabetes insipidus

Treatment is not always needed for mild cases of cranial diabetes insipidus.

You just need to increase the amount of water you drink to compensate for the fluid lost through urination.

If necessary, a medication called desmopressin can be used to replicate the functions of AVP.

Nephrogenic diabetes insipidus is often treated with medications called thiazide diuretics, which reduce the amount of urine the kidneys produce.
Find out more about treating diabetes insipidus

Complications

As diabetes insipidus increases water loss in the urine, the amount of water in the body can become low. This is known as dehydration.

Rehydration with water can be used to treat mild dehydration. Severe dehydration will need to be treated in hospital.
Find out more about the complications of diabetes insipidus

# data[].attributes.attachment_link.description
Diabetes insipidus is a rare condition where you pee a lot and often feel thirsty. Diabetes insipidus is not related to diabetes, but it does share some of the same signs and symptoms. The 2 main symptoms of diabetes insipidus are: extreme thirst (polydipsia) peeing a lot, even at night (polyuria) In very severe cases of diabetes insipidus, a person can pee up to 20 litres of urine in a day.

# data[].attributes.attachment_link.title
Addison's Disease - Overview (clinical features, pathophysiology, investigations, treatment)

# data[].attributes.body
https://www.mayoclinic.org/diseases-conditions/acromegaly/symptoms-causes/syc-20351222?page=0&citems=10

# data[].attributes.attachment_link.title
Addisons Disease Made Simple - Primary Adrenal Faliure

# data[].attributes.attachment_link.readable_text
Your adrenal glands are located on top of your kidneys. These glands produce many of the hormones that your body needs for normal functions.

Addison's disease occurs when the adrenal cortex is damaged, and the adrenal glands don't produce enough of the steroid hormones cortisol and aldosterone.

Cortisol regulates the body's reaction to stressful situations. Aldosterone helps with sodium and potassium regulation. The adrenal cortex also produces sex hormones (androgens).

People who have Addison's disease may experience the following symptoms:

muscle weakness

fatigue and tiredness

darkening in skin color

weight loss or decreased appetite

a decrease in heart rate or blood pressure

low blood sugar levels

fainting spells

sores in the mouth

cravings for salt

nausea

vomiting

People living with Addison's disease may also experience neuropsychiatric symptoms, such as:

irritability or depression

lack of energy

sleep disturbances

If Addison's disease goes untreated for too long, it can become an Addisonian crisis. Symptoms associated with an Addisonian crisis can :

agitation

delirium

visual and auditory hallucinations

An Addisonian crisis is a life-threatening medical emergency. Call 911 immediately if you or someone you know begins to experience:

mental status changes, such as confusion, fear, or restlessness

loss of consciousness

sudden pain in the lower back, belly, or legs

An untreated Addisonian crisis can lead to shock and death.

There are two major classifications for Addison's disease: primary adrenal insufficiency and secondary adrenal insufficiency. In order to treat the disease, your doctor will need to find out which type is responsible for your condition.

Primary adrenal insufficiency

Primary adrenal insufficiency occurs when your adrenal glands are damaged so severely that they can no longer produce hormones. This type of Addison's disease is most often caused when your immune system attacks your adrenal glands. This is called an autoimmune disease.

In an autoimmune disease, your body's immune system mistakes any organ or area of the body for a virus, bacteria, or another outside invader.

Other causes of primary adrenal insufficiency include:

prolonged administration of glucocorticoids (e.g. prednisone)

infections in your body

cancer and abnormal growths (tumors)

certain blood thinners used to control clotting in the blood

Secondary adrenal insufficiency

Secondary adrenal insufficiency occurs when the pituitary gland (located in your brain) can't produce adrenocorticotropic hormone ( ACTH). ACTH tells the adrenal glands when to release hormones.

It's also possible to develop adrenal insufficiency if you do not take the corticosteroid medications your doctor prescribes. Corticosteroids help control chronic health conditions like asthma.

There are also many other causes of secondary adrenal insufficiency, including:

You may be at a higher risk for Addison's disease if you:

Your doctor will ask you about your medical history and the symptoms you've been experiencing. They will do a physical examination, and they may order some lab tests to check your potassium and sodium levels.

Your doctor may also order imaging tests and measure your hormone levels.

Your treatment will depend on what's causing your condition. Your doctor may prescribe medications that regulate your adrenal glands.

Following the treatment plan that your doctor creates for you is very important. Untreated Addison's disease can lead to an Addisonian crisis.

If your condition has gone untreated for too long, and has progressed to a life-threatening condition called Addisonian crisis, your physician may prescribe medication to treat that first.

Addisonian crisis causes low blood pressure, high potassium in the blood, and low blood sugar levels.

Medications

You may need to take a combination of glucocorticoids medications (drugs that stop inflammation) to improve your health. These medications will be taken for the rest of your life and you cannot miss a dose.

Hormone replacements may be prescribed to replace hormones that your adrenal glands are not making.

Home care

Keep an emergency kit that contains your medications on hand at all times. Ask your doctor to write a prescription for an injectable corticosteroid for emergencies.

You may also want to keep a medical alert card in your wallet and a bracelet on your wrist to let others know about your condition.

Alternative therapies

It's important to keep your stress level down if you Addison's disease. Major life events, such as a death of a loved one or an injury, can raise your stress level and affect the way you respond to your medications. Talk to your doctor about alternative ways to relieve stress, such as yoga and meditation.

Addison's disease requires lifelong treatment. Treatments, such as hormone replacement medications, can help you manage your symptoms.

Following the treatment plan your doctor creates is an important step in helping you live a productive life.

Remember, always take your medications exactly as directed. Taking too little or too much medication can negatively affect your health.

Your treatment plan may need to be reevaluated and changed depending on your condition. For this reason, it's important that you see your doctor regularly.

# data[].attributes.attachment_link.description
Addison's disease occurs when the adrenal cortex is damaged, and the adrenal glands do not produce enough cortisol and aldosterone. Cortisol regulates the body's reaction to stressful situations. Aldosterone helps with sodium and potassium regulation. Learn causes, risks, and treatment of Addison's disease.

# data[].attributes.attachment_link.readable_text
Am Fam Physician. 2000 Dec 1;62(11):2485-2490.

Myxedema coma, the extreme manifestation of hypothyroidism, is an uncommon but potentially lethal condition. Patients with hypothyroidism may exhibit a number of physiologic alterations to compensate for the lack of thyroid hormone. If these homeostatic mechanisms are overwhelmed by factors such as infection, the patient may decompensate into myxedema coma. Patients with hypothyroidism typically have a history of fatigue, weight gain, constipation and cold intolerance. Physicians should include hypothyroidism in the differential diagnosis of every patient with hyponatremia. Patients with suspected myxedema coma should be admitted to an intensive care unit for vigorous pulmonary and cardiovascular support. Most authorities recommend treatment with intravenous levothyroxine (T ₄) as opposed to intravenous liothyronine (T ₃). Hydrocortisone should be administered until coexisting adrenal insufficiency is ruled out. Family physicians are in an important position to prevent myxedema coma by maintaining a high level of suspicion for hypothyroidism.

Myxedema coma is an extreme complication of hypothyroidism in which patients exhibit multiple organ abnormalities and progressive mental deterioration. The term myxedema is often used interchangeably with hypothyroidism and myxedema coma. Myxedema also refers to the swelling of the skin and soft tissue that occurs in patients who are hypothyroid. Myxedema coma occurs when the body's compensatory responses to hypothyroidism are overwhelmed by a precipitating factor such as infection.

A common misconception is that a patient must be comatose to be diagnosed with myxedema coma. However, myxedema coma is a misnomer because most patients exhibit neither the nonpitting edema known as myxedema nor coma. 1, 2 Instead, the cardinal manifestation of myxedema coma is a deterioration of the patient's mental status.

When only comatose patients are considered, myxedema coma is exceedingly rare: one study reports 200 cases between 1953 and 1996. 3 Applying a broader definition results in a significantly higher number of cases. While the actual prevalence of myxedema coma is unknown, its lethal nature demands recognition. Even with early detection and appropriate treatment, mortality ranges from 30 to 60 percent. 3, 4 Family physicians must be alert to the possibility of undiagnosed hypothyroidism in their patients.

Epidemiology

Hypothyroidism is four times more common in women than in men; 80 percent of cases of myxedema coma occur in females. 5, 6 Myxedema coma occurs almost exclusively in persons 60 years and older. 5 More than 90 percent of cases occur during the winter months. 6 This seasonal presentation is probably due to age-related loss of the ability to sense temperature and lower heat production secondary to hypothyroidism. 7

Historical Features

Patients with myxedema coma usually have longstanding hypothyroidism, although it may not have been previously diagnosed. They often demonstrate classic symptoms of hypothyroidism: fatigue; constipation; weight gain; cold intolerance; a deep voice; coarse hair; and dry, pale, cool skin. However, elderly patients with hypothyroidism often have atypical presentations, such as decreased mobility, 8 and some patients with compensated hypothyroidism are asymptomatic. 9

PRECIPITATING EVENT

Decompensation into myxedema coma occurs when the hypothyroid patient's homeostatic mechanisms are disrupted. Multiple factors can precipitate myxedema coma ( Table 1). 1- 3, 10- 14 Some of the more common precipitating factors include infections, particularly pneumonia and urosepsis, and certain medications. Another potential risk factor is failure to reinstate thyroid replacement therapy during hospitalization.

Physical Findings

Physical findings in myxedema coma ( Table 2) may include the classic myxedematous face, which is characterized by generalized puffiness, macroglossia, ptosis, periorbital edema, and coarse, sparse hair. Nonpitting edema of the lower extremities is sometimes present. The findings from a thyroid examination are usually normal, but a goiter may be present in some patients. The presence of a scar on the neck might suggest postsurgical hypothyroidism and may be an important clue in the diagnosis of a patient who is comatose. A neurologic examination may reveal decreased reflex tendon relaxation and will invariably reveal altered mentation.

ALTERED MENTATION

All patients with myxedema coma display deterioration of their mental status. This decline may be subtle, manifesting as apathy, neglect or a decrease in intellectual function; more obvious changes include confusion, psychosis and, rarely, coma. While all patients with myxedema coma present with some degree of mental status change, few progress to coma. When there is doubt about a change in mental status, formal mental status testing should be performed.

Physicians should also be alert to the possibility of depression in the seemingly demented patient and perform depression screening in any patient with mental status changes. Lumbar puncture may also be clinically appropriate.

HYPOTHERMIA

Another common clinical feature of myxedema coma is hypothermia. The patient's temperature is usually less than 35.5°C (95.9°F). 13 Conditions that may precipitate myxedema coma such as hypoglycemia and cold exposure may exacerbate the hypothermia. However, the patient's temperature is not always an accurate diagnostic aid because some patients present with a normal temperature.

BLOOD PRESSURE CHANGES

Patients with compensated hypothyroidism often exhibit diastolic hypertension. Decreased oxygen consumption and lowered body temperature result in peripheral vasoconstriction and central shunting. 2 Only when the patient has begun to decompensate do these neurovascular mechanisms fail. The patient may then display the hypotension characteristically associated with myxedema coma. Bradycardia, low cardiac output and overall blood volume deficit frequently exacerbate the hypotension.

HYPOVENTILATION

Hypoventilation in myxedema coma results from the body's decreased ventilatory response to hypoxia and hypercapnia. 15 Respiratory dysfunction may lead to sleep apnea, 16 and respiratory difficulties may be exacerbated by myxedematous infiltration of the tongue and pharynx. 15, 17 The diaphragmatic weakness induced by hypothyroidism is reversed by thyroid hormone replacement. 16, 18

Diagnostic Testing

Multiple diagnostic findings are reported in patients with myxedema coma. This disorder impacts thyroid hormone levels, electrolyte levels, creatine kinase (CPK) levels and other laboratory values ( Table 3).

THYROID HORMONE

Primary hypothyroidism results from the inability of the thyroid gland to produce adequate amounts of thyroid hormone. Typically, patients with myxedema coma have primary hypothyroidism manifested by low serum levels of thyroxine (T ₄) and triiodothyronine (T ₃) and a high thyroid stimulating hormone (TSH) level. However, primary hypothyroidism should be differentiated from secondary hypothyroidism, tertiary hypothyroidism and the low T ₄ level/low T ₃ level syndrome (euthyroid sick syndrome).

Secondary hypothyroidism is a result of pituitary dysfunction; tertiary hypothyroidism is caused by a hypothalamic abnormality. If the patient has hypopituitarism, the level of TSH is not increased. The findings of a low T ₄ level and low-normal or decreased TSH level mandate a search for pituitary abnormalities. However, a low level of serum T ₄ (and T ₃) with a normal TSH level may simply indicate that the patient's thyroid function tests have been altered as a result of illness unrelated to the thyroid (euthyroid sick syndrome).

ELECTROLYTE ABNORMALITIES

The hyponatremia seen in myxedema coma is a result of decreased free water clearance. Elevated levels of antidiuretic hormone and/or diminished blood flow to the kidneys are believed to be responsible for the inability to excrete free water. 19, 20 Hyponatremia is classically associated with a low serum osmolality. The level of serum creatinine is usually high, and while the level of calcium is generally low, it may be elevated. 21 Hypoglycemia may be a result of the down-regulation of metabolism seen in hypothyroidism 2; it may also indicate the possibility of adrenal insufficiency.

ELEVATED CREATINE KINASE

Patients with myxedema coma may be mis-diagnosed with myocardial infarction based on elevated CPK levels in association with nonspecific electrocardiographic (ECG) findings. Increased CPK and other transaminases are thought to result from altered membrane permeability. 22 Fractionation of the CPK reveals a skeletal muscle source. ECG changes include bradycardia, decreased voltages, non-specific ST and T changes, varying types of block and a prolonged QT interval. Conversely, physicians should be alert to the possibility of myocardial infarction as a triggering event for myxedema coma.

OTHER ABNORMALITIES

Arterial blood gases often reveal respiratory acidosis, hypoxia and hypercapnia. Mild leukopenia and a normocytic anemia are also frequently present. However, macrocytic anemia and pernicious anemia caused by associated immune dysfunction are sometimes present. 13, 23 A chest radiograph may show cardiomegaly and pleural effusions. If cardiomegaly is present, an echocardiogram should be obtained to rule out a pericardial effusion. When performed, lumbar puncture typically reveals elevated protein levels 13, 15, 24 and a high opening pressure. Results of electroencephalography are nonspecific. 13

Treatment

The patient with myxedema coma should be admitted to the intensive care unit, and hypovolemia and electrolyte abnormalities corrected. Mechanical ventilation may be necessary. Cardiovascular status should be monitored carefully, especially after intravenous thyroid hormone replacement. Myocardial infarction must be ruled out and blood pressure stabilized. If possible, pressors and ionotropes should be avoided because of their tendency to provoke arrhythmias in the setting of intravenous thyroid replacement. Patients with hypothermia should be covered with regular blankets; the use of warming blankets should be avoided because the resulting peripheral dilatation may lead to hypotension and cardiovascular collapse.

THYROID HORMONE REPLACEMENT

Any patient with suspected myxedema coma should be treated presumptively with thyroid hormone. While there is concern regarding the precipitation of arrhythmias or myocardial infarction by administering large doses of intravenous levothyroxine, this concern must be balanced against T ₄'s potentially life-saving and usually nondetrimental effect. 25

While the necessity of intravenous thyroid hormone replacement is apparent, some controversy exists regarding the use and dosages of levothyroxine (T ₄) and liothyronine (T ₃). Because of the relatively small number of patients with myxedema coma, controlled studies comparing various dosages of T ₄ and T ₃ are lacking. Because T ₃ is more biologically active than T ₄, and because the conversion of 26, 27 T ₄ to T ₃ is suppressed in myxedema coma, some have advocated T ₃ replacement. However, parental T ₃ is not only expensive and difficult to obtain, it may also contribute to increased mortality. 27

Most authorities therefore recommend use of T ₄ alone. 2, 7, 13, 14, 27 An initial levothyroxine dose of 100 to 500 μg administered intravenously should be followed by 75 to 100 μg administered intravenously daily until the patient is able to take oral replacement. The lower initial dose should be administered to patients who are frail or have other comorbidities, particularly cardiovascular disease. Elderly patients typically require 100 to 170 μg of oral levothyroxine daily. 13

ANTIBIOTICS

Infection is often the cause of the patient's decompensation; therefore, an infectious etiology should be sought with blood and urine cultures as well as a chest radiograph. Some authorities advocate empiric therapy with broad-spectrum intravenous antibiotics. 2

STEROIDS

Because of the possibility of secondary hypothyroidism and associated hypopituitarism, hydrocortisone should be administered until adrenal insufficiency has been ruled out. Hydrocortisone should be administered intravenously at a dosage of 100 mg every eight hours. Failure to treat with hydrocortisone in the face of adrenal insufficiency may result in the precipitation of adrenal crisis. A random cortisol level should be drawn prior to therapy, and if not depressed, the hydrocortisone can be discontinued without tapering. An adrenocorticotropic hormone stimulation test can be administered if clinically warranted.

Prognosis

The prognosis for patients with myxedema coma is difficult to define because of the small number of cases reported in the literature. The severity of the condition, however, is clear. One study reported a mortality rate of about 30 percent, while another suggests the mortality rate may be as high as 60 percent. 3, 4 Factors associated with a poor prognosis include advanced age, bradycardia and persistent hypothermia. 27

Final Comment

Family physicians should be alert for myxedema coma, particularly in elderly women with mental status changes who present during the winter months. An accurate diagnosis generally follows a careful history, physical examination and laboratory evaluation. The most important elements in treatment of myxedema coma are early recognition, presumptive thyroid hormone replacement, hydrocortisone and appropriate supportive care. While myxedema coma carries a significant mortality rate even with appropriate testing and treatment, an early diagnosis of hypothyroidism may well save a patient's life.

The Author

CRISTEN RHODES WALL, M.D., is an assistant professor in the Department of Family Practice and Community Medicine at the University of Texas Southwestern Medical Center at Dallas, where she received her medical degree. Dr. Wall is a recent graduate of the Baylor-Garland Family Practice Residency Program, Garland, Tex....

Address correspondence to Cristen R. Wall, M.D., University of Texas Southwestern Medical Center at Dallas, 5323 Harry Hines Blvd., Dallas, TX 75390-9067. Reprints are not available from the author.

The author thanks the Baylor-Garland Family Practice Residency, Garland, Tex., the Faculty Development Center in Waco, Tex., and the University of Texas Southwestern Medical Center at Dallas for assistance with the manuscript, and Teresa Hanson for her research support.

REFERENCES

1. Jordan RM. Myxedema coma: Pathophysiology, therapy, and factors affecting prognosis. Med Clin North Am. 1995;79:185-94. ...

3. Werner SC, Ingbar SH, Braverman LE, Utiger RD. Werner &Ingbar's The thyroid: a fundamental and clinical text. 8th ed. Philadelphia: Lipincott Williams &Wilkins;2000.

15. Bardin CW, ed. Current therapy in endocrinology and metabolism. 6th ed. St. Louis, Mo: Mosby; 1997.

MOST RECENT ISSUE

Feb 15, 2020
Access the latest issue of American Family Physician
Read the Issue

Email Alerts

Don't miss a single issue. Sign up for the free AFP email table of contents.
Sign Up Now

# data[].attributes.attachment_link.description
Myxedema coma, the extreme manifestation of hypothyroidism, is an uncommon but potentially lethal condition. Patients with hypothyroidism may exhibit a number of physiologic alterations to compensate for the lack of thyroid hormone. If these homeostatic mechanisms are overwhelmed by factors such as infection, the patient may decompensate into myxedema coma.

# data[].attributes.attachment_link.keywords[]
myxedemma myexdema mmyxedema myxedma kyxedema myxedeam mxedema myxeedema mxyedema myxedema

# data[].attributes.attachment_link.description
Myxedema Information Including Symptoms, Diagnosis, Treatment, Causes, Videos, Forums, and local community support. Find answers to health issues you can trust from Healthgrades.com

# data[].attributes.attachment_link.title
Diabetes Insipidus - Overview (causes, pathophysiology, investigations)

# data[].attributes.attachment_link.readable_text
What is the medical definition of myxedema (crisis) coma?

A coma is a state of decreased consciousness whereby a patient cannot react to the surrounding environment.

Myxedema (crisis) coma is a loss of brain function as a result of the severe, longstanding low level of thyroid hormone in the blood ( hypothyroidism). Myxedema coma is considered a rare life-threatening complication of hypothyroidism and represents one of the more serious sides of thyroid disease.

What causes myxedema coma?

Most patients with myxedema coma have a history of hypothyroidism.

Most patients with myxedema coma have a history of hypothyroidism, thyroid surgery, or radioactive iodine treatment for thyroid disease. Very rarely, the problem is not caused by the inability of the thyroid gland to make thyroid hormone; but rather is caused by the failure of the pituitary gland or the hypothalamus to correctly signal the thyroid gland to perform its normal functions. In this situation, the thyroid gland is normal, but it is not receiving the signals from the pituitary gland or hypothalamus to make the thyroid hormone it is capable of producing.

What triggers of myxedema coma?

Certain factors may suddenly trigger myxedema coma in a person with poorly controlled hypothyroidism. These include drugs (particularly sedatives, narcotics, anesthesia, lithium (Eskalith, Lithobid), and amiodarone ( Cordarone), infections, stroke, trauma, heart failure, digestive (gastrointestinal, GI) bleeding, hypothermia (abnormally low body temperature), and failing to take thyroid medications as prescribed by their doctor.

What are the symptoms of hypothyroidism?

Before a person develops myxedema coma, signs and symptoms of hypothyroidism usually are present and may have gone undiagnosed for a long time.

Symptoms of hypothyroidism include:

What are the symptoms of myxedema coma?

People with myxedema coma may have symptoms and signs, for example:

The body temperature is usually abnormally low (hypothermia), and the core temperature may be as low as 80 F (26.6 C);

Severe mental changes including hallucinations, disorientation, seizures, and ultimately, deep coma;

Significant swelling (edema) all over the body with swollen eyes and thickening of the tongue,

Sparse, dry hair, and loss of the outer thirds of the eyebrows;

Difficulty breathing;

Collections of fluid around the lungs and heart (pleural effusion and pericardial effusions);

The heart may slow down and its ability to pump blood forward can be impaired;

The gastrointestinal tract does not function well and sometimes it becomes paralyzed, thereby necessitating surgery; and

Blood test abnormalities are a result of the increased fluid in the body. For example, sodium levels drop because of dilution, which is caused by the body retaining extra water.

SLIDESHOW
See Slideshow

What procedures and tests diagnose myxedemia coma?

Initial laboratory evaluation usually includes a test for thyroid function (TSH, T3, and T4 levels). Other blood tests and heart and lung function tests may be needed.

What is the treatment for myxedema coma? Is it life threatening?

Treatment may include assisting the patient to breathe and warming them to raise the body temperature to normal. Often, antibiotics are started until it is certain that an infection is not present.

The method of replacing the thyroid hormone in patients with myxedema coma is controversial. Many different approaches are used. In general, initial replacement is done by intravenous infusion, since the intestinal system may not be absorbing properly.

While common hypothyroidism without myxedema is usually treated with T4 replacement (the hormone produced in greatest quantity by the thyroid gland), in the case of myxedema coma, management is different. The thyroid gland also produces a small amount of another hormone, T3. This is the more metabolically active of the two hormones. In patients who are well, T4 is converted into T3 in the bloodstream. However, patients with myxedema coma are often so sick that this conversion is impaired. As a result, many doctors choose to treat these patients with T3 initially and start T4 therapy as well. Since T4 therapy can take a month or so to work, there is usually an overlap of these two hormones. Care is taken to avoid heart rhythm abnormalities (arrhythmias) and stress on the heart, which can be caused by replacing thyroid hormone too quickly, particularly in elderly patients.

Mild thyroid disorders can be managed by primary or internal medicine doctors, however; it usually is managed by a thyroid specialist (endocrinologist) because treatment can be complicated and critical.

How can myxedema coma be prevented?

The ideal way to manage this condition is to prevent it from occurring in the first place. An individual with hypothyroidism should visit their doctor regularly for follow-up and blood testing to be certain that their replacement dose is appropriate.

If an individual has symptoms that concern them but have not been diagnosed with hypothyroidism, they should visit their healthcare practitioner to discuss their concerns and explore the option of testing for thyroid imbalance.

Eledrisi, MS, MD, et al. Myxedema Coma or Crisis. Medscape. Updated: Oct 18, 2018."
<https://emedicine.medscape.com/article/123577-overview>

Top Myxedema Coma Related Articles

Coma Causes and Glasgow Coma Scale

Coma is the inability to waken or react to the surrounding environment. The Glasgow Coma Scale is frequently used to measure the depth of coma. Causes of coma include trauma, bleeding, edema, lack...

# data[].attributes.attachment_link.title
Myxedema Coma Causes, Symptoms, Treatment, Hypothyroidism

# data[].attributes.attachment_link.description
Myxedema coma or myxedema crisis is a life-threatening complication of hypothyroidism. Learn the causes, triggers, symptoms, diagnosis, treatment, and medication for myxedema coma.

# data[].attributes.attachment_link.readable_text
Myxedema refers to a severe form of hypothyroidism than can occur when the condition is left untreated or is not treated sufficiently. The term also applies to the effects that hypothyroidism can have on the skin, making it appear swollen and puffy.

When thyroid hormone levels become extremely low, a person may experience symptoms such as drowsiness, confusion, and hypothermia, as well as changes to the skin.

One life-threatening complication of hypothyroidism is myxedema coma. This complication is also known as myxedema crisis, which is a more accurate term, as a person experiencing myxedema coma may not fall into a comatose state.

# data[].attributes.attachment_link.description
Myxedema refers to both a form of severe hypothyroidism and a number of effects that hypothyroidism can have on the skin and other body tissues. Find out here why myxedema occurs, and the symptoms it can cause. We also examine a rare, life-threatening complication called myxedema coma that can occur in untreated cases.

# data[].attributes.attachment_link.readable_text
Am Fam Physician. 2000 Dec 1;62(11):2485-2490.

Myxedema coma, the extreme manifestation of hypothyroidism, is an uncommon but potentially lethal condition. Patients with hypothyroidism may exhibit a number of physiologic alterations to compensate for the lack of thyroid hormone. If these homeostatic mechanisms are overwhelmed by factors such as infection, the patient may decompensate into myxedema coma. Patients with hypothyroidism typically have a history of fatigue, weight gain, constipation and cold intolerance. Physicians should include hypothyroidism in the differential diagnosis of every patient with hyponatremia. Patients with suspected myxedema coma should be admitted to an intensive care unit for vigorous pulmonary and cardiovascular support. Most authorities recommend treatment with intravenous levothyroxine (T ₄) as opposed to intravenous liothyronine (T ₃). Hydrocortisone should be administered until coexisting adrenal insufficiency is ruled out. Family physicians are in an important position to prevent myxedema coma by maintaining a high level of suspicion for hypothyroidism.

Myxedema coma is an extreme complication of hypothyroidism in which patients exhibit multiple organ abnormalities and progressive mental deterioration. The term myxedema is often used interchangeably with hypothyroidism and myxedema coma. Myxedema also refers to the swelling of the skin and soft tissue that occurs in patients who are hypothyroid. Myxedema coma occurs when the body's compensatory responses to hypothyroidism are overwhelmed by a precipitating factor such as infection.

A common misconception is that a patient must be comatose to be diagnosed with myxedema coma. However, myxedema coma is a misnomer because most patients exhibit neither the nonpitting edema known as myxedema nor coma. 1, 2 Instead, the cardinal manifestation of myxedema coma is a deterioration of the patient's mental status.

When only comatose patients are considered, myxedema coma is exceedingly rare: one study reports 200 cases between 1953 and 1996. 3 Applying a broader definition results in a significantly higher number of cases. While the actual prevalence of myxedema coma is unknown, its lethal nature demands recognition. Even with early detection and appropriate treatment, mortality ranges from 30 to 60 percent. 3, 4 Family physicians must be alert to the possibility of undiagnosed hypothyroidism in their patients.

Epidemiology

Hypothyroidism is four times more common in women than in men; 80 percent of cases of myxedema coma occur in females. 5, 6 Myxedema coma occurs almost exclusively in persons 60 years and older. 5 More than 90 percent of cases occur during the winter months. 6 This seasonal presentation is probably due to age-related loss of the ability to sense temperature and lower heat production secondary to hypothyroidism. 7

Historical Features

Patients with myxedema coma usually have longstanding hypothyroidism, although it may not have been previously diagnosed. They often demonstrate classic symptoms of hypothyroidism: fatigue; constipation; weight gain; cold intolerance; a deep voice; coarse hair; and dry, pale, cool skin. However, elderly patients with hypothyroidism often have atypical presentations, such as decreased mobility, 8 and some patients with compensated hypothyroidism are asymptomatic. 9

PRECIPITATING EVENT

Decompensation into myxedema coma occurs when the hypothyroid patient's homeostatic mechanisms are disrupted. Multiple factors can precipitate myxedema coma ( Table 1). 1- 3, 10- 14 Some of the more common precipitating factors include infections, particularly pneumonia and urosepsis, and certain medications. Another potential risk factor is failure to reinstate thyroid replacement therapy during hospitalization.

Physical Findings

Physical findings in myxedema coma ( Table 2) may include the classic myxedematous face, which is characterized by generalized puffiness, macroglossia, ptosis, periorbital edema, and coarse, sparse hair. Nonpitting edema of the lower extremities is sometimes present. The findings from a thyroid examination are usually normal, but a goiter may be present in some patients. The presence of a scar on the neck might suggest postsurgical hypothyroidism and may be an important clue in the diagnosis of a patient who is comatose. A neurologic examination may reveal decreased reflex tendon relaxation and will invariably reveal altered mentation.

ALTERED MENTATION

All patients with myxedema coma display deterioration of their mental status. This decline may be subtle, manifesting as apathy, neglect or a decrease in intellectual function; more obvious changes include confusion, psychosis and, rarely, coma. While all patients with myxedema coma present with some degree of mental status change, few progress to coma. When there is doubt about a change in mental status, formal mental status testing should be performed.

Physicians should also be alert to the possibility of depression in the seemingly demented patient and perform depression screening in any patient with mental status changes. Lumbar puncture may also be clinically appropriate.

HYPOTHERMIA

Another common clinical feature of myxedema coma is hypothermia. The patient's temperature is usually less than 35.5°C (95.9°F). 13 Conditions that may precipitate myxedema coma such as hypoglycemia and cold exposure may exacerbate the hypothermia. However, the patient's temperature is not always an accurate diagnostic aid because some patients present with a normal temperature.

BLOOD PRESSURE CHANGES

Patients with compensated hypothyroidism often exhibit diastolic hypertension. Decreased oxygen consumption and lowered body temperature result in peripheral vasoconstriction and central shunting. 2 Only when the patient has begun to decompensate do these neurovascular mechanisms fail. The patient may then display the hypotension characteristically associated with myxedema coma. Bradycardia, low cardiac output and overall blood volume deficit frequently exacerbate the hypotension.

HYPOVENTILATION

Hypoventilation in myxedema coma results from the body's decreased ventilatory response to hypoxia and hypercapnia. 15 Respiratory dysfunction may lead to sleep apnea, 16 and respiratory difficulties may be exacerbated by myxedematous infiltration of the tongue and pharynx. 15, 17 The diaphragmatic weakness induced by hypothyroidism is reversed by thyroid hormone replacement. 16, 18

Diagnostic Testing

Multiple diagnostic findings are reported in patients with myxedema coma. This disorder impacts thyroid hormone levels, electrolyte levels, creatine kinase (CPK) levels and other laboratory values ( Table 3).

THYROID HORMONE

Primary hypothyroidism results from the inability of the thyroid gland to produce adequate amounts of thyroid hormone. Typically, patients with myxedema coma have primary hypothyroidism manifested by low serum levels of thyroxine (T ₄) and triiodothyronine (T ₃) and a high thyroid stimulating hormone (TSH) level. However, primary hypothyroidism should be differentiated from secondary hypothyroidism, tertiary hypothyroidism and the low T ₄ level/low T ₃ level syndrome (euthyroid sick syndrome).

Secondary hypothyroidism is a result of pituitary dysfunction; tertiary hypothyroidism is caused by a hypothalamic abnormality. If the patient has hypopituitarism, the level of TSH is not increased. The findings of a low T ₄ level and low-normal or decreased TSH level mandate a search for pituitary abnormalities. However, a low level of serum T ₄ (and T ₃) with a normal TSH level may simply indicate that the patient's thyroid function tests have been altered as a result of illness unrelated to the thyroid (euthyroid sick syndrome).

ELECTROLYTE ABNORMALITIES

The hyponatremia seen in myxedema coma is a result of decreased free water clearance. Elevated levels of antidiuretic hormone and/or diminished blood flow to the kidneys are believed to be responsible for the inability to excrete free water. 19, 20 Hyponatremia is classically associated with a low serum osmolality. The level of serum creatinine is usually high, and while the level of calcium is generally low, it may be elevated. 21 Hypoglycemia may be a result of the down-regulation of metabolism seen in hypothyroidism 2; it may also indicate the possibility of adrenal insufficiency.

ELEVATED CREATINE KINASE

Patients with myxedema coma may be mis-diagnosed with myocardial infarction based on elevated CPK levels in association with nonspecific electrocardiographic (ECG) findings. Increased CPK and other transaminases are thought to result from altered membrane permeability. 22 Fractionation of the CPK reveals a skeletal muscle source. ECG changes include bradycardia, decreased voltages, non-specific ST and T changes, varying types of block and a prolonged QT interval. Conversely, physicians should be alert to the possibility of myocardial infarction as a triggering event for myxedema coma.

OTHER ABNORMALITIES

Arterial blood gases often reveal respiratory acidosis, hypoxia and hypercapnia. Mild leukopenia and a normocytic anemia are also frequently present. However, macrocytic anemia and pernicious anemia caused by associated immune dysfunction are sometimes present. 13, 23 A chest radiograph may show cardiomegaly and pleural effusions. If cardiomegaly is present, an echocardiogram should be obtained to rule out a pericardial effusion. When performed, lumbar puncture typically reveals elevated protein levels 13, 15, 24 and a high opening pressure. Results of electroencephalography are nonspecific. 13

Treatment

The patient with myxedema coma should be admitted to the intensive care unit, and hypovolemia and electrolyte abnormalities corrected. Mechanical ventilation may be necessary. Cardiovascular status should be monitored carefully, especially after intravenous thyroid hormone replacement. Myocardial infarction must be ruled out and blood pressure stabilized. If possible, pressors and ionotropes should be avoided because of their tendency to provoke arrhythmias in the setting of intravenous thyroid replacement. Patients with hypothermia should be covered with regular blankets; the use of warming blankets should be avoided because the resulting peripheral dilatation may lead to hypotension and cardiovascular collapse.

THYROID HORMONE REPLACEMENT

Any patient with suspected myxedema coma should be treated presumptively with thyroid hormone. While there is concern regarding the precipitation of arrhythmias or myocardial infarction by administering large doses of intravenous levothyroxine, this concern must be balanced against T ₄'s potentially life-saving and usually nondetrimental effect. 25

While the necessity of intravenous thyroid hormone replacement is apparent, some controversy exists regarding the use and dosages of levothyroxine (T ₄) and liothyronine (T ₃). Because of the relatively small number of patients with myxedema coma, controlled studies comparing various dosages of T ₄ and T ₃ are lacking. Because T ₃ is more biologically active than T ₄, and because the conversion of 26, 27 T ₄ to T ₃ is suppressed in myxedema coma, some have advocated T ₃ replacement. However, parental T ₃ is not only expensive and difficult to obtain, it may also contribute to increased mortality. 27

Most authorities therefore recommend use of T ₄ alone. 2, 7, 13, 14, 27 An initial levothyroxine dose of 100 to 500 μg administered intravenously should be followed by 75 to 100 μg administered intravenously daily until the patient is able to take oral replacement. The lower initial dose should be administered to patients who are frail or have other comorbidities, particularly cardiovascular disease. Elderly patients typically require 100 to 170 μg of oral levothyroxine daily. 13

ANTIBIOTICS

Infection is often the cause of the patient's decompensation; therefore, an infectious etiology should be sought with blood and urine cultures as well as a chest radiograph. Some authorities advocate empiric therapy with broad-spectrum intravenous antibiotics. 2

STEROIDS

Because of the possibility of secondary hypothyroidism and associated hypopituitarism, hydrocortisone should be administered until adrenal insufficiency has been ruled out. Hydrocortisone should be administered intravenously at a dosage of 100 mg every eight hours. Failure to treat with hydrocortisone in the face of adrenal insufficiency may result in the precipitation of adrenal crisis. A random cortisol level should be drawn prior to therapy, and if not depressed, the hydrocortisone can be discontinued without tapering. An adrenocorticotropic hormone stimulation test can be administered if clinically warranted.

Prognosis

The prognosis for patients with myxedema coma is difficult to define because of the small number of cases reported in the literature. The severity of the condition, however, is clear. One study reported a mortality rate of about 30 percent, while another suggests the mortality rate may be as high as 60 percent. 3, 4 Factors associated with a poor prognosis include advanced age, bradycardia and persistent hypothermia. 27

Final Comment

Family physicians should be alert for myxedema coma, particularly in elderly women with mental status changes who present during the winter months. An accurate diagnosis generally follows a careful history, physical examination and laboratory evaluation. The most important elements in treatment of myxedema coma are early recognition, presumptive thyroid hormone replacement, hydrocortisone and appropriate supportive care. While myxedema coma carries a significant mortality rate even with appropriate testing and treatment, an early diagnosis of hypothyroidism may well save a patient's life.

The Author

CRISTEN RHODES WALL, M.D., is an assistant professor in the Department of Family Practice and Community Medicine at the University of Texas Southwestern Medical Center at Dallas, where she received her medical degree. Dr. Wall is a recent graduate of the Baylor-Garland Family Practice Residency Program, Garland, Tex....

Address correspondence to Cristen R. Wall, M.D., University of Texas Southwestern Medical Center at Dallas, 5323 Harry Hines Blvd., Dallas, TX 75390-9067. Reprints are not available from the author.

The author thanks the Baylor-Garland Family Practice Residency, Garland, Tex., the Faculty Development Center in Waco, Tex., and the University of Texas Southwestern Medical Center at Dallas for assistance with the manuscript, and Teresa Hanson for her research support.

REFERENCES

1. Jordan RM. Myxedema coma: Pathophysiology, therapy, and factors affecting prognosis. Med Clin North Am. 1995;79:185-94. ...

3. Werner SC, Ingbar SH, Braverman LE, Utiger RD. Werner &Ingbar's The thyroid: a fundamental and clinical text. 8th ed. Philadelphia: Lipincott Williams &Wilkins;2000.

15. Bardin CW, ed. Current therapy in endocrinology and metabolism. 6th ed. St. Louis, Mo: Mosby; 1997.

MOST RECENT ISSUE

Feb 15, 2020
Access the latest issue of American Family Physician
Read the Issue

Email Alerts

Don't miss a single issue. Sign up for the free AFP email table of contents.
Sign Up Now

# data[].attributes.attachment_link.description
Myxedema coma, the extreme manifestation of hypothyroidism, is an uncommon but potentially lethal condition. Patients with hypothyroidism may exhibit a number of physiologic alterations to compensate for the lack of thyroid hormone. If these homeostatic mechanisms are overwhelmed by factors such as infection, the patient may decompensate into myxedema coma.

# data[].attributes.attachment_link.title
The endocrine system be secreting hormones like | Make a Meme

# data[].attributes.attachment_link.description
The endocrine system be secreting hormones like

# data[].attributes.body
https://www.youtube.com/watch?v=Ky4SfAcRANc&feature=youtu.be

# data[].attributes.attachment_link.readable_text
Definition

Neonatal hypothyroidism is decreased thyroid hormone production in a newborn. In very rare cases, no thyroid hormone is produced.

If the baby was born with the condition, it is called congenital hypothyroidism. If it develops soon after birth, it is called hypothyroidism acquired in the newborn period.

Alternative Names

Cretinism; Congenital hypothyroidism; Hypothyroidism - infants

Causes, incidence, and risk factors

Hypothyroidism in the newborn may be caused by:

A missing or poorly developed thyroid gland

A pituitary gland that does not stimulate the thyroid gland

Thyroid hormones that are poorly formed or do not work

A thyroid gland that is not fully developed is the most common defect. Girls are affected twice as often as boys.

Symptoms

Most affected infants have few or no symptoms. This is because their thyroid hormone level is only slightly low. Infants with severe hypothyroidism often have a unique appearance, including:

Puffy face

Thick tongue that sticks out

This appearance usually develops as the disease gets worse.

The child may also have:

Choking episodes

Constipation

Dry, brittle hair

Lack of muscle tone (floppy infant)

Low hairline

Poor feeding

Short height

Sleepiness

Sluggishness

Signs and tests

A physical exam may show:

Decreased muscle tone

Failure to grow

Hoarse-sounding cry or voice

Short arms and legs

Very large soft spots on the skull (fontanelles)

Wide hands with short fingers

Widely separated skull bones

Blood tests are done to check thyroid function. Other tests may include:

Treatment

Early diagnosis is very important. Most of the effects of hypothyroidism are easy to reverse.

Thyroxine is usually given to treat hypothyroidism. Once the child starts taking this medicine, blood tests are regularly done to make sure thyroid hormone levels are in a normal range.

Expectations (prognosis)

Getting diagnosed early usually leads to a good outcome. Newborns who are diagnosed and treated in the first month or so usually have normal intelligence.

Untreated mild hypothyroidism can lead to severe intellectual disability and growth problems. The nervous system goes through important development during the first few months after birth. Lack of thyroid hormones can cause damage that cannot be reversed.

Complications

Intellectual disability

Growth problems

Heart problems

Calling your health care provider

Call your health care provider if:

You feel your infant shows signs or symptoms of hypothyroidism

You are pregnant and have been exposed to antithyroid drugs or procedures

Prevention

If a pregnant women takes radioactive iodine for thyroid cancer, the thyroid gland may be destroyed in the developing fetus. Infants whose mothers have taken such medicines should be observed carefully after birth for signs of hypothyroidism.

Most states require a routine screening test to check all newborns for hypothyroidism.

References

LeFranchi S. Hypothyroidism. In: Kliegman RM, Stanton BF, St. Geme III JW, et al., eds. Nelson Textbook of Pediatrics. 19th ed. Philadelphia, Pa.: Elsevier Saunders; 2011;chap 559.

# data[].attributes.attachment_link.description
Neonatal hypothyroidism is decreased thyroid hormone production in a newborn. In very rare cases, no thyroid hormone is produced. If the baby was born with the condition, it is called congenital hypothyroidism. If it develops soon after birth, it is called hypothyroidism acquired in the newborn period.

# data[].attributes.body
https://www.sciencedirect.com/topics/medicine-and-dentistry/dwarfism

# data[].attributes.body
https://emedicine.medscape.com/article/919758-overview

# data[].attributes.body
https://www.mayoclinic.org/diseases-conditions/pheochromocytoma/symptoms-causes/syc-20355367?page=0&citems=10

# data[].attributes.body
https://medlineplus.gov/pheochromocytoma.html

# data[].attributes.body
https://www.youtube.com/watch?v=ea1sXgd5ui8&feature=youtu.be

# data[].attributes.body
https://rarediseases.org/rare-diseases/pheochromocytoma/

# data[].attributes.body
https://www.healthline.com/health/pheochromocytoma

# data[].attributes.body
https://www.youtube.com/watch?v=FR2r30NXzng&feature=youtu.be

# data[].attributes.body
https://my.clevelandclinic.org/health/diseases/17365-pheochromocytoma

# data[].attributes.body
https://www.youtube.com/watch?v=-B-RVybvffU&feature=youtu.be

# data[].attributes.body
https://www.mayoclinic.org/diseases-conditions/diabetes-insipidus/symptoms-causes/syc-20351269?page=0&citems=10

# data[].attributes.body
https://www.youtube.com/watch?v=CpBHQSJUrWY&feature=youtu.be

# data[].attributes.body
https://www.healthline.com/health/hypothyroidism/symptoms-treatments-more

# data[].attributes.body
https://www.youtube.com/watch?v=U5VVSCVJt_w&feature=youtu.be

# data[].attributes.body
https://www.mayoclinic.org/diseases-conditions/acromegaly/symptoms-causes/syc-20351222?page=0&citems=10

Fun fact: Andre the Giant had this

# data[].attributes.body
https://www.healthline.com/health/hypocalcemia#symptoms

# data[].attributes.body
https://www.mayoclinic.org/diseases-conditions/addisons-disease/diagnosis-treatment/drc-20350296

# data[].attributes.body
https://www.google.com/search?kgmid=/m/0hg25&hl=en-US&kgs=52a483e876d5032e&q=Acromegaly&shndl=0&source=sh/x/kp/osrp&entrypoint=sh/x/kp/osrp&safe=active&surl=1

# data[].attributes.body
https://www.mayoclinic.org/diseases-conditions/hypercalcemia/symptoms-causes/syc-20355523?page=0&citems=10

# data[].attributes.body
https://www.medicalnewstoday.com/articles/172744

# data[].attributes.body
https://www.mayoclinic.org/diseases-conditions/cushing-syndrome/symptoms-causes/syc-20351310

# data[].attributes.body
https://www.mayoclinic.org/diseases-conditions/cushing-syndrome/symptoms-causes/syc-20351310

# data[].attributes.body
https://www.mayoclinic.org/diseases-conditions/graves-disease/symptoms-causes/syc-20356240

# data[].attributes.body
https://www.niddk.nih.gov/health-information/endocrine-diseases#topics

# data[].attributes.body
https://www.niddk.nih.gov/health-information/endocrine-diseases#topics

# data[].attributes.body
https://www.mayoclinic.org/diseases-conditions/acromegaly/symptoms-causes/syc-20351222?page=0&citems=10

# data[].attributes.body
https://www.niddk.nih.gov/health-information/endocrine-diseases/cushings-syndrome

# data[].attributes.body
https://www.endocrineweb.com/conditions

# data[].attributes.body
https://www.yourhormones.info/glands/pituitary-gland/

# data[].attributes.body
https://www.merckmanuals.com/professional/endocrine-and-metabolic-disorders/electrolyte-disorders/hypocalcemia

# data[].attributes.body
https://academic.oup.com/qjmed/article/110/7/411/2631713

# data[].attributes.body
https://medlineplus.gov/pheochromocytoma.html

# data[].attributes.body
https://www.aans.org/en/Patients/Neurosurgical-Conditions-and-Treatments/Cushings-Disease

# data[].attributes.body
https://www.webmd.com/diabetes/endocrine-system-disorders#1

# data[].attributes.body
https://www.healthline.com/health/hypothyroidism/symptoms-treatments-more

# data[].attributes.body
https://en.wikipedia.org/wiki/Graves%27_disease

# data[].attributes.attachment_link.readable_text
Symptoms of hypocalcemia arise from lower than normal levels of calcium in the blood. Some affected people, especially if the condition is mild, will not have symptoms. Others may have severe and life-threatening symptoms. Symptoms include

Psychoemotional symptoms can also be seen, including

Causes of hypocalcemia

There are a number of medical conditions that can cause hypocalcemia. Some of the most common include renal (kidney) failure, hyperphosphatemia (elevated blood phosphate levels), hypoalbuminemia (low albumin), vitamin D deficiency, magnesium deficiency, pancreatitis, and hypoparathyroidism.

Other hypocalcemia symptoms and signs

See Answer

# data[].attributes.attachment_link.title
Hypocalcemia: Symptoms, Signs, Causes & Treatment

# data[].attributes.attachment_link.description
Symptoms of hypocalcemia arise from lower than normal levels of calcium in the blood. Some affected people, especially if the condition is mild, will not have symptoms. Others may have severe and life-threatening symptoms. Symptoms include Psychoemotional symptoms can also be seen, including Causes of hypocalcemia There are a number of medical conditions that can cause hypocalcemia.

# data[].attributes.body
https://www.medicinenet.com/hypocalcemia_symptoms_and_signs/symptoms.htm

# data[].attributes.body
https://medlineplus.gov/pheochromocytoma.html

# data[].attributes.body
https://www.healthline.com/health/myxedema

# data[].attributes.body
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6021313/

# data[].attributes.body
phenochromocytoma
https://www.mayoclinic.org/diseasesconditions/
pheochromocytoma/diagnosis-treatment/drc-
20355372

# data[].attributes.body
https://www.nicklauschildrens.org/genetic/neonatalhypothyroidism

# data[].attributes.body
| https://www.mayoclinic.org/diseases-conditions/addisons-disease/symptoms-causes/syc-20350293?page=0&amp;citems=10

# data[].attributes.body
| https://www.medicalnewstoday.com/articles/321886

# data[].attributes.body
| Lauren W
https://www.mayoclinic.org/diseases-conditions/cushing-syndrome/symptoms-causes/syc-20351310

# data[].attributes.body
| https://www.mayoclinic.org/diseases-conditions/acromegaly/symptoms-causes/syc-20351222?page=0&amp;citems=10

# data[].attributes.body
| https://www.mayoclinic.org/diseases-conditions/acromegaly/symptoms-causes/syc-20351222?page=0&amp;citems=10

# data[].attributes.body
| https://m.ufhealth.org/neonatal-hypothyroidism

# data[].attributes.body
| https://www.healthline.com/health/cushings-syndrome

# data[].attributes.body
| https://www.webmd.com/diabetes/endocrine-system-disorders

# data[].attributes.body
| Jasmine Mhamdi
https://www.health.harvard.edu/a_to_z/type-2-diabetes-mellitus-a-to-z

# data[].attributes.body
| https://www.niddk.nih.gov/health-information/endocrine-diseases/acromegaly

# data[].attributes.body
| https://medlineplus.gov/dwarfism.html

# data[].attributes.body
| https://www.webmd.com/children/dwarfism-causes-treatments

# data[].attributes.body
https://www.healthline.com/health/addisons-disease#symptoms

# data[].attributes.body
| Jasmine Mhamdi
Https://www.mayoclinic.org/diseases-conditions/hypercalcemia/symptoms-causes/syc-20355523?page=0&amp;citems=10