HENOCH-SCHONLEIN PURPURA DUE TO STREPTOKINASE

The syndrome of Henoch-Schoenlein purpura developed in a 74-year-old w oman after receiving streptokinase as thrombolytic therapy for an acut e myocardial infarction. Renal biopsy revealed mesangial hypercellular ity with deposits of IgA. Skin biopsy also revealed IgA deposition. Im munological studies showed evidence of sensitization to streptokinase. Elevated IgG, IgA, IgM, and IgE antistreptokinase antibodies were det ected in the acute serum. Positive immediate skin reactivity to strept okinase was also present. Serum precipitins to streptokinase disappear ed when IgA was removed from the serum. Positive staining with biotiny lated streptokinase was seen in the skin in the same pattern of distri bution as IgA. These findings strongly support the role of streptokina se and IgA in the pathogenesis of Henoch-Schoenlein purpura in this pa tient. A control group of streptococcal-infected patients showed no im mune response to streptokinase. Another control group of streptokinase -treated patients, who had no untoward reaction, had elevated immunogl obulin classes and precipitins to streptokinase. However, the precipit ating antibody was IgG and streptokinase skin tests were negative.