Guillain-Barré syndrome following streptokinase therapy.

Clinical and laboratory data from a patient with Guillain-Barré syndrome indicated a probable etiological correlation of polyradiculitis to the intravenous administration of streptokinase. Oligoclonal IgG bands in the cerebrospinal fluid and serum were shown to be specific for streptokinase. Serum titers of streptokinase were elevated 64-fold for IgG, 16-fold for IgM, and 4-fold for IgA compared to controls. Clinical symptoms of Guillain-Barré syndrome are thought to result from streptokinase antibody complex mediated damage to the local blood-nerve barrier. The pathogenic relevance of autoantibodies to albumin and proteins of the central and peripheral nervous systems, occurring early after onset of symptoms, remains to be determined.