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An immunologic mechanism, possibly immune complex mediated, has been suggested as the basis for the pathogenesis of thrombotic thrombocytopenic purpura (TTP). The evidence supporting this concept has been the association of TTP with systemic lupus erythematosus and the successful therapy of TTP by plasmapheresis. However, most investigators have failed to demonstrate elevated circulating immune complexes during the course of TTP. This report describes a young woman with systemic lupus who developed TTP as a terminal event. Elevated levels of immune complexes were associated with periods of active lupus but were not detectable at the time she developed TTP.Thrombotic thrombocytopenic purpura (TTP) is a disorder of unknown etiology manifested clinically by the pentad of microangiopathic hemolytic anemia, central nervous system and renal dysfunction, thrombocytopenic purpura, and fever (1). Pathologically the hallmark of the disease is widely disseminated hyaline microthrombi in the terminal arterioles and capillaries (2) often associated with microaneurismal formation at

Immunoglobulins, including rheumatoid factors, are produced by the rheumatoid synovial membrane. A significant contribution of the synovial membrane to the total IgG and IgM detected in the synovial fluid has been documented. The present study was designed to examine the contribution of the synovial membrane to the rheumatoid factors detected in the synovial fluid. Analysis of the data demonstrated that the synovial membrane was the source of a significant component of the total synovial fluid IgA rheumatoid factor and IgM rheumatoid factor. While some fluids possessed extremely elevated concentrations of the IgG rheumatoid factor, the data suggested that IgG rheumatoid factor was preferentially reduced, relative to total IgG, by the rheumatoid inflammatory process. These observations suggest a potentially important role for IgG rheumatoid factor in rheumatoid synovitis.The synovial membrane and the synovial fluid are the focal points of the inflammatory process in patients with rheumatoid arthritis. The rheumatoid synovium is capable of locally synthesizing many or all of the immune reactants involved in this condition.

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