Rheumatoid Arthritis and Genetics – Nitric Oxide overproduction and Joint Damage

Rheumatoid Arthritis and Genetics – Nitric Oxide overproduction and Joint Damage

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Researchers from the University of Michigan Medical School have discovered data that questions the belief that rheumatoid arthritis (RA) is strictly an autoimmune disorder. This study was first published in the November 2006 issue of Arthritis and Rheumatism.

Rheumatoid arthritis is a chronic inflammatory disease that causes damage to the joints. This joint damage increases pain, loss of movement and bone deformities. There is an estimated 2.1 million people in the United States that have rheumatoid arthritis.

Most researchers believe that RA is an autoimmune disorder. The location in the DNA human genome for causing the RA disease is found in the location that is responsible for the body’s ability to identify antigens. In nearly 95% of RA patients they share a common sequence of DNA. If almost all of the RA patients have the same arrangement of DNA that causes this disease why would there be such a wide range of severely affected to symptom free individuals?

"Although the hypothesis that RA is an autoimmune disorder is widely accepted, there is no convincing evidence that it is correct," says Joseph Holoshitz, M.D., associate professor of internal medicine at U-M Medical School who directed the study. "We see this same type of association with HLA genes in other diseases, which we know are not autoimmune diseases."

In this study, the researchers found a shared genetic sequence that was responsible for the body to increase the levels of nitric oxide in other cells. This nitric oxide is unrelated to the immune system antigen response. When there is an increase in nitric oxide, cell death (apoptosis) is slowed down and can cause the joints of an RA patient to become inflamed.

In this study the researchers studied genetic sequences from individuals that had a shared sequence that was resistant to the cell death compared to individuals who did not have the same identifying genetic sequence trait.

"Our findings suggest this activity is unrelated to antigen presentation," says Holoshitz. "This is the first direct evidence that the shared epitope may be responsible for the overproduction of nitric oxide seen in patients with RA."

"It was previously postulated that nitric oxide plays a role in RA, since patients have higher levels of it in their joint tissue. When we looked at the rate of NO generation in these patients, we found that it was significantly higher for people with the shared epitope," says Holoshitz.

Even though there is a strong relationship between genetic sequences that can contribute to RA, there are still approximately 10 percent of affected individuals that do not have a relationship with these DNA indicators. The researchers will need to continue their studies to understand more about how nitric oxide is overproduced in rheumatoid arthritis patients.



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