# data[].attributes.attachment_link.description
Gout is a form of inflammatory arthritis that develops in some people who have high levels of uric acid in the blood. It occurs in about 4 percent of American adults, but is more likely to affect men than women.

# data[].attributes.attachment_link.readable_text
WASHINGTON - Refuting a belief long held by many physicians, a Mayo Clinic study found that rheumatoid arthritis patients also can get gout. The research is among several studies Mayo Clinic is presenting at the American College of Rheumatology annual meeting in Washington. Researchers also found that gut bacteria has potential to treat autoimmune disorders, rheumatoid arthritis patients are at higher risk for cancer, broken bones put rheumatoid arthritis patients in greater danger of heart disease and death, and corticosteroids are a mainstay of rheumatoid arthritis treatment even as new drugs emerge.

VIDEO ALERT: For an interview with Dr. Matteson and Mayo Clinic News Network membership, visit the Mayo Clinic News Network.

The gout study shows that, contrary to conventional wisdom, rheumatoid arthritis patients aren't immune to the nation's obesity-fueled gout epidemic, says lead author Eric Matteson, M.D., chair of the Division of Rheumatology at Mayo Clinic in Rochester, Minn. The two are distinct conditions, treated differently. Rheumatoid arthritis is an autoimmune disease in which the immune system mistakenly attacks tissues, inflaming joints. In gout, the body produces too much uric acid or has problems flushing it out, and urate crystals build up in joints, causing inflammation and intense pain.

The reason it was thought that rheumatoid arthritis patients didn't get gout likely had to do with the way rheumatoid arthritis used to be treated, Dr. Matteson says. Such patients used to be given aspirin in high doses, and that coincidentally helped their kidneys expel uric acid. Aspirin is no longer used much for rheumatoid arthritis, and that, combined with a rise in obesity, is likely fueling gout in rheumatoid arthritis patients, he says.

"It is probably true that flares of rheumatoid arthritis in some cases might have actually been flares of gout, and that the gout wasn't diagnosed; it wasn't realized that it was a coexistent problem," Dr. Matteson says. "Awareness that gout does exist in patients with rheumatoid arthritis hopefully will lead to better management of gout in those patients."

Researchers studied 813 patients diagnosed with rheumatoid arthritis between 1980 and 2007 and followed them as long as they were alive and in the county, until last April. The study used the Rochester Epidemiology Project, a National Institutes of Health-supported pool of Olmsted County, Minn., patient medical records from Mayo and other health care providers.

Twenty-two patients developed gout over the study period, most often in the big toe. Gout was more common in patients diagnosed with rheumatoid arthritis from 1995 on. The risk factors for gout were the same as in the general population: being overweight, being older and being male.

Other Mayo studies being presented at the rheumatology conference found that:
*Gut bacteria, specifically Prevotella histicola, have anti-inflammatory benefits that could help treat autoimmune disorders such as lupus, rheumatoid arthritis and ankylosing spondylitis. Researchers examined the possibility using mice, and more studies are planned. "This is a hot area of research now," says Dr. Matteson, who wasn't part of the study team.

* Corticosteroids, whose discovery at Mayo Clinic earned the Nobel Prize in 1950, are still a common treatment for rheumatoid arthritis even as newer drugs with fewer side effects emerge. The proportion of patients on the drugs at any given point in their rheumatoid arthritis is actually higher than it used to be, the study found. "Not only do we think that they're helpful in controlling symptoms of disease, especially in the first year, but we also are realizing that they have some effect in modifying the disease course," says Dr. Matteson, the lead author. "We try to use the minimum amount possible for the shortest time necessary."

*Rheumatoid arthritis patients have a higher risk of developing blood cancers, particularly lymphoma. One of the immune system's top jobs is to seek and destroy cancer cells, and in rheumatoid arthritis patients that can fail due to the autoimmune disorder itself and to drugs that treat it by suppressing the immune system, Dr. Matteson, the lead author, says. More research is needed to understand the risk factors in individual patients. A small number of patients get lymphoma, and they tend to have more severe rheumatoid arthritis, Dr. Matteson says.

*Rheumatoid arthritis patients who have cardiovascular disease are more likely to test positive for rheumatoid factor in their blood, and those who are positive for rheumatoid factor seem to have immune systems that age faster and also have accelerated risk of cardiovascular disease.

*Rheumatoid arthritis patients who have broken bones are at higher risk of cardiovascular disease and death. The chronic inflammation in rheumatoid arthritis may be a factor.

The following abstracts included conflict-of-interest disclosures: rheumatoid arthritis and gout; mortality after fragility fractures; accelerated aging; and fractures associated with increased risk of cardiovascular events. For more information, see the ACR abstract supplement.
Media Contact: Sharon Theimer, 507-284-5005 (days), newsbureau@mayo.edu

# data[].attributes.attachment_link.title
Rheumatoid Arthritis Patients Can Get Gout Too, Mayo Clinic Study Finds

# data[].attributes.attachment_link.description
WASHINGTON - Refuting a belief long held by many physicians, a Mayo Clinic study found that rheumatoid arthritis patients also can get gout. The research is among several studies Mayo Clinic is presenting at the American College of Rheumatology annual meeting in Washington.

# data[].attributes.attachment_link.readable_text
What are autoimmune diseases?

Your immune system protects you from disease and infection by attacking germs that get into your body, such as viruses and bacteria. Your immune system can tell that the germs aren't part of you, so it destroys them. If you have an autoimmune disease, your immune system attacks the healthy cells of your organs and tissues by mistake.

There are more than 80 types of autoimmune diseases. They can affect almost any part of your body. For example, alopecia areata is an autoimmune disease of the skin that causes hair loss. Autoimmune hepatitis affects the liver. In type 1 diabetes, the immune system attacks the pancreas. And in rheumatoid arthritis, the immune system can attack many parts of the body, including the joints, lungs, and eyes.

What causes autoimmune diseases?

No one is sure why autoimmune diseases happen. But you can't catch them from other people.

Autoimmune diseases do tend to run in families, which means that certain genes may make some people more likely to develop a problem. Viruses, certain chemicals, and other things in the environment may trigger an autoimmune disease if you already have the genes for it.

Who is at risk for autoimmune diseases?

Millions of Americans of all ages have autoimmune diseases. Women develop many types of autoimmune diseases much more often than men. And if you have one autoimmune disease, you are more likely to get another.

What are the symptoms of autoimmune diseases?

The symptoms of an autoimmune disease depend on the part of your body that's affected. Many types of autoimmune diseases cause redness, swelling, heat, and pain, which are the signs and symptoms of inflammation. But other illnesses can cause the same symptoms.

The symptoms of autoimmune diseases can come and go. During a flare-up, your symptoms may get severe for a while. Later on, you may have a remission, which means that your symptoms get better or disappear for a period of time.

How are autoimmune diseases diagnosed?

Doctors often have a hard time diagnosing autoimmune diseases. There's usually not a specific test to show whether you have a certain autoimmune disease. And the symptoms can be confusing. That's because many autoimmune diseases have similar symptoms. And some symptoms, such as muscle aches, are common in many other illnesses. So it can take a long time and some visits to different types of doctors to get a diagnosis.

To help your doctor find out if an autoimmune disease is causing your symptoms,:

Learn about the health conditions in your family history. What health problems did your grandparents, aunts, uncles, and cousins have? Write down what you learn and share it with your doctor.

Keep track of your symptoms, including how long they last and what makes them better or worse. Share your notes with your doctor.

See a specialist who deals with the symptoms that bother you most. For example, if you have rash, see a dermatologist (skin doctor).

What are the treatments for autoimmune diseases?

The treatment depends on the disease. In most cases, the goal of treatment is to suppress (slow down) your immune system, and ease swelling, redness, and pain from inflammation. Your doctor may give you corticosteroids or other medicines to help you feel better. For some diseases, you may need treatment for the rest of your life.

# data[].attributes.attachment_link.title
Autoimmune Diseases | Autoimmune Disease Symptoms | MedlinePlus

# data[].attributes.attachment_link.description
Your immune system protects you from disease and infection by attacking germs that get into your body, such as viruses and bacteria. Your immune system can tell that the germs aren't part of you, so it destroys them. If you have an autoimmune disease, your immune system attacks the healthy cells of your organs and tissues by mistake.

# data[].attributes.attachment_link.readable_text
Scientists have identified a chain reaction that explains why our own bodies can turn against healthy cells, potentially transforming the way we look at autoimmune diseases and the way we treat them.

The reaction, discovered after four years of research in mice, has been described as a "runaway train" where one error leads the body to develop a very efficient way of attacking itself.

The study focussed on B cells gone rogue. Ordinarily these cells produce antibodies and program the immune cells to attack unwanted antigens (or foreign substances), but scientists found an 'override switch' in mouse B cells that distorted this behaviour and caused autoimmune attacks.

"Once your body's tolerance for its own tissues is lost, the chain reaction is like a runaway train," says one of the team, Michael Carroll from Boston Children's Hospital and Harvard Medical School (HMS).

"The immune response against your own body's proteins, or antigens, looks exactly like it's responding to a foreign pathogen."

These B-cells-gone-awry could in turn explain the biological phenomenon known as epitope spreading, where our bodies start to hunt down different antigens that shouldn't be on the immune system's 'kill list'.

Epitope spreading has long been observed in the lab but scientists have been in the dark about how it happens, and why autoimmune diseases evolve over time to target an ever-expanding catalogue of healthy organs and tissues.

In this case the research looked at a mouse model of the lupus autoimmune disease, considered an archetypal or 'classic' type of autoimmune disease that many others are based on.

"Lupus is known as 'the great imitator' because the disease can have so many different clinical presentations resembling other common conditions," says one of the researchers, Søren Degn from Boston Children's Hospital and Aarhus University in Denmark.

"It's a multi-organ disease with a plethora of potential antigenic targets, tissues affected and 'immune players' involved."

The team used what's known as a 'confetti' technique in their imaging, where fluorescent marker proteins were used to track different B cells in the body.

When B cells sense a foreign body - or something healthy that appears to be a foreign body - they swing into action in clusters called germinal centres. Those centres are why your lymph nodes become swollen when you've got a cold coming on, for example.

B cell clones actually battle each other out inside these centres so the body can determine which antibody is best suited to fight the threat, and in the case of this study that meant one colour of protein winning out against the others.

The problem comes when the body incorrectly identifies a normal protein as a threat. When that happens, the B cell selection process produces what are known as autoantibodies that prove very effective at harming our own bodies.

"Over time, the B cells that initially produce the 'winning' autoantibodies begin to recruit other B cells to produce additional damaging autoantibodies - just as ripples spread out when a single pebble is dropped into water," says Degn.

This has only been examined in mice so far, but the researchers now want to use the confetti model to look at how B cell production of autoantibodies is regulated and gets sped up.

Eventually, blocking the germinal centres in some way could put a break in the vicious cycle that autoimmune diseases create. It would effectively block the immune system's short term memory, but that kind of treatment is still a long way off.

For now, it's a promising step towards a better understanding of this runaway biological train that's so hard to stop.

"This finding was such a surprise," says Carroll. "It not only tells us that autoreactive B cells are competing inside germinal centres to design an autoantibody, but then we also see that the immune response broadens to attack other tissues in the body, leading to epitope spreading at the speed of wildfire."

The research has been published in .

# data[].attributes.attachment_link.title
We May Have Finally Discovered The Trigger That Starts Autoimmune Diseases

# data[].attributes.attachment_link.description
Scientists have identified a chain reaction that explains why our own bodies can turn against healthy cells, potentially transforming the way we look at autoimmune diseases and the way we treat them. The reaction, discovered after four years of research in mice, has been described as a "runaway train" where one error leads the body to develop a very efficient way of attacking itself.