Rheumatoid arthritis (RA) is the most common inflammatory form of arthritis and affects approximately 2 million Americans. It is a chronic, autoimmune, systemic disease for which there is no known cure; however, it is capable of being put into remission.
RA develops as a result of chronic inflammation involving the synovium- the lining of the joint- which results in damage to the joint. Damage can occur early in the disease and is irreversible.
New diagnostic criteria formulated in 2010 by a combined effort of the American College of Rheumatology as well as the European League Against Rheumatism have helped establish parameters that allow for the detection of early disease.
It is quite clear that early diagnosis and aggressive treatment results in improved functional outcome for patients with RA. Currently, the target or goal is remission. In fact, the "treat to target" approach is the new buzz word in rheumatology.
Treatment approaches designed to effect remission vary depending upon the treating rheumatologist.
Some arthritis specialists feel that a combination of disease modifying anti-rheumatic drugs (DMARDS) including drugs such as methotrexate, hydroxychloroquine (Plaquenil), sulfasalazine (Azulfidine), and leflunomide (Arava) should be employed for at least six months before switching to biologic therapies.
In most instances, methotrexate is the DMARD of choice and is started at a dose of 10-15 mgs per week and increased to about 20 mgs over an 8 week period. Folic acid is given in a dose of 1 mg per day to help counteract some of the untoward effects of methotrexate.
While there is some data to support this approach, many other rheumatologists feel that six months is far too long to wait before initiation of biologic therapy.
Most rheumatologists do agree that for patients with active disease, low doses of corticosteroids can act as a "bridge" until the disease is controlled.
Biologic therapies are much more selective in their effects on RA. They are specifically designed to hit certain inflammatory proteins or cells that produce these inflammatory proteins.
The difference between DMARDS and biologic therapies can be likened to the difference between a shotgun versus a rifle.
As can be surmised, there is potential for side effects from both DMARDS as well as biologics. The use of either category of drug needs to be instituted and followed by a physician with much experience in their use.
While much has been written about the potential hazards of biologic therapy, there has been relatively little attention paid to the potential hazards of combination DMARD therapy.
It can be emphatically said that neither approach is side-effect free.
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