The pain and stiffness suffered by a quarter of a million people with the inflammatory spinal condition ankylosing spondylitis can be significantly relieved with a drug already approved for rheumatoid arthritis, according to results of a clinical trial published in The New England Journal of Medicine.
A UCSF study showed that 80 percent of patients taking the immune-blocking drug etanercept experienced relief from their symptoms. The drug worked more quickly than the current therapies such as aspirin-like drugs, other immunosuppressives and physical therapy. And unlike all other current treatments, etanercept relieved intense pain from spinal inflammation in most patients, the study found.
The drug may reduce spinal inflammation and actually slow the progress of the disease, the researchers suggest.
Ankylosing spondylitis, or AS, is a chronic inflammatory arthritis characterized by joint stiffness, pain and extra bone growth that can result in partial or complete fusion of the spine. The bones of the spine may grow together, causing the spine to become rigid and inflexible. Other joints such as the hips, shoulders, knees, or ankles also may become involved.
About 300,000 people in the U.S. suffer from the disease. Symptoms appear most frequently in young men between the ages of 16 and 35. There is currently no cure for ankylosing spondylitis, and there is no drug currently approved by the U.S. Food & Drug Administration (FDA) for this disease.
Like rheumatoid arthritis, the condition is an autoimmune disease in which the immune system loses its capacity to control vigilant proteins known as cytokines, and these soldiers start a relentless attack on the body, prompting a damaging increase in inflammation. A key to this lost immune control is a molecule called tumor necrosis factor-alpha (TNF-alpha) which normally prompts increased cytokine action. Etanercept, on the market for three years to treat rheumatoid arthritis, bloc
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Contact: Wallace Ravven
wravven@pubaff.ucsf.edu
415-476-2557
University of California - San Francisco
1-May-2002