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Rumatoid arthritis (RA) has a prevalence of 0.5-1.0%, and it affects women more often than men. RA tends to develop during early or middle adulthood (between the ages of 20 and 50 years), but it can also begin in childhood or old age. It has only a slight tendency to run in families. RA is a chronic illness.
Pathogenesis. RA is an autoimmune disease, although a virus may trigger the chronic rheumatoid process in vulnerable individuals. This process causes the immune system to attack the synovium of various joints, leading to synovitis. Synovial inflammation accounts for the typical pain warmth, and swelling of the involved joints.
Clinical manifestations
Rumatoid arthritis (rumatism) is a chronic, symmetric polyarthritis. The polyarthritis is often deforming. About 80% of patients describe a slowly progressive onset over weeks or months. RA may wax and wane.
Inflammatory features
The joints in rumatoid are swollen, tender, slightly warm, and stiff. Synovial fluid shows active inflammation:
Patients with RA usually have profound and prolonged morning stiffness. Fatigue, anemia of chronic disease, and severe constitutional illness (eg, fever, vasculitis, pericarditis, myocarditis, Felty's syndrome) are common.
Joint involvement. RA may begin in one or two joints, but it almost invariably progresses to affect 20 or more. In some cases, joint involvement is nearly symmetric, affecting the same finger joints.
Proliferative/erosive features. The inflamed synovial tissue evolves into a thickened, boggy mass.
Joint deformity. Deformities of RA are more likely to be the result of damage to the soft tissues.
Diagnosis
Rumatoid arthritis is a clinical diagnosis. The presence of arthritis excludes the many forms of soft tissue rheumatism (eg, tendinitis, bursitis).
The pannus is often palpable as a rubbery mass of tissue around a joint.
Laboratory tests
The rheumatoid factor assay helps to confirm the diagnosis of RA. Rheumatoid factor serves as a marker for RA, but it is not reliable because 1-2% of the normal population have low levels.
Treatment of rheumatoid arthritis
Disease-modifying antirheumatic drugs
Virtually all patients should start taking a disease-modifying antirheumatic drug (DMARDs) as soon as the diagnosis of RA is made. Treatment should continue for the duration of the disease.
The early and aggressive use of these agents reduces acute symptoms and decreases disability over the long term. These drugs are no more toxic than high-dose NSAIDs.
Methotrexate is the treatment of choice because of demonstrated efficacy and long-term tolerability.
Hydroxychloroquine ( Plaquenil), 200-400 mg PO qd, is recommended for patients with mild disease.
Etanercept ( Enbrel). After twice-weekly subcutaneous injections of etanercept (recombinant human tumor necrosis factor receptor), 25 mg, at 3 months, 62% improve.
Infliximab ( Remicade) is given intravenously for use in refractory disease. Infliximab is an anti-tumor necrosis factor monoclonal antibody.
Leflunomide ( Arava), which inhibits pyrimidine synthesis, is an oral drug considered as a possible alternative to methotrexate. The dosage is 100 mg PO daily for three days.
Nonsteroidal antiinflammatory drugs. Most patients will gain short-term symptomatic relief.
Corticosteroids . These drugs may relieve the symptoms of RA, but they are potentially dangerous, with many long-term side effects.