Extracorporeal Immunoparmacotherapy in Rheumatoid Arthritis

This disease causes inflammatory changes in the synovial membranes and periarticular structures associated with severe pain, joint stiffness up to ankylosis, and bone atrophy. The blood serum of the patients with rheumatoid arthritis contains high titres of antistreptokinase and anti-plasminogen autoantibodies of class IgG and IgA, as a rule after streptococcal infection. There are also antineutrophil autoantibodies – both anti-nuclear and cytoplasmic. Plasminogen synthesized by the liver is distributed in the vessels both internally and externally. At activation plasminogen turns in plasmin, regulating extracellular proteolytic activity, activating proteases. In these patient’s fibrinogen level is increased, and insoluble fibrin is found on the synovial membranes. Plasmin, in turn, inhibits the cartilages proteoglycan. All of it leads to destruction of the joints and the synovial membranes proliferation.