Rheumatoid arthritis active phase

Find information on medical topics, symptoms, drugs, procedures, news and more, written for the health rheumatoid arthritis active phase professional. This is the Professional Version. RA causes damage mediated by cytokines, chemokines, and metalloproteases.

Diagnosis is based on specific clinical, laboratory, and imaging features. Treatment involves drugs, physical measures, and sometimes surgery. Disease-modifying antirheumatic drugs help control symptoms and slow disease progression. Women are affected 2 to 3 times more often than men. Prominent immunologic abnormalities include immune complexes produced by synovial lining cells and in inflamed blood vessels. Released inflammatory mediators and various enzymes contribute to the systemic and joint manifestations of RA, including cartilage and bone destruction.

In chronically affected joints, the normally thin synovium proliferates, thickens, and develops many villous folds. Fibrin deposition, fibrosis, and necrosis are also present. WBCs in the synovial fluid. They are granulomas consisting of a central necrotic area surrounded by palisaded histiocytic macrophages, all enveloped by lymphocytes, plasma cells, and fibroblasts.

Nodules and vasculitis can also develop in visceral organs. Antibodies against cyclic citrullinated peptide and IgA rheumatoid factor predict the development of rheumatoid arthritis. Anti-carbamylated protein antibodies in the pre-symptomatic phase of rheumatoid arthritis, their relationship with multiple anti-citrulline peptide antibodies and association with radiological damage. Autoantibody epitope spreading in the pre-clinical phase predicts progression to rheumatoid arthritis. Onset of rheumatoid arthritis is usually insidious, often beginning with systemic and joint symptoms.

Systemic symptoms include early morning stiffness of affected joints, generalized afternoon fatigue and malaise, anorexia, generalized weakness, and occasionally low-grade fever. Joint symptoms include pain, swelling, and stiffness. Occasionally, the disease begins abruptly, mimicking an acute viral syndrome. The course is unpredictable in individual patients. Joint symptoms are characteristically symmetric. Involved joints become tender, with erythema, warmth, swelling, and limitation of motion.

The axial skeleton is rarely involved except for the upper cervical spine. Joints are often held in flexion to minimize pain, which results from joint capsular distention. Joint instability due to stretching of the joint capsule can also occur. Carpal tunnel syndrome can result from wrist synovitis compressing the median nerve. Pulmonary nodules of RA cannot be distinguished from pulmonary nodules of other etiology without biopsy. Other extra-articular signs include vasculitis causing leg ulcers or mononeuritis multiplex, pleural or pericardial effusions, pulmonary infiltrates or fibrosis, pericarditis, myocarditis, lymphadenopathy, Felty syndrome, Sjögren syndrome, scleromalacia, and episcleritis.

Importantly, cervical spine instability is most often asymptomatic. RA should be suspected in patients with polyarticular, symmetric arthritis, particularly if the wrists and 2nd and 3rd metacarpophalangeal joints are involved. Classification criteria serve as a guide for establishing the diagnosis of RA and are helpful in defining standardized treatment populations for study purposes. Other causes of symmetric polyarthritis, particularly hepatitis C, must be excluded. Patients should have a serum RF test, hand and wrist x-rays, and baseline x-rays of affected joints to document future erosive changes.