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European Heart Journal 1992 13(11):1514-1520;
Copyright © 1992 by the European Society of Cardiology.
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© 1992 The European Society of Cardiology

Prevalence and mechanism of streptokinase-induced platelet stimulation. Effect of acetylsalicylic acid

W. TERRES, K. KRÜGER and W. BLEIFELD

Department of Cardiology, Medical Clinic, Eppendorf University Hospital Hamburg, Germany

Received 13 May 1991; revised 26 May 1992; .

Correspondence: Dr Wolfram Terres, Department of Cardiology, Medical Clinic, Eppendorf University Hospital, Martinistr. 52, 2000 Hamburg 20, Germany

Abstract

It was recently shown that streptokinase may induce clot formation in vivo by immunoglobulin G mediated platelet stimulation. We evaluated the in vitro effect of streptokinase on platelet function in 103 subjects, of whom 52 were ≤30 years and 51 were ≥50 years old. Although streptokinase inhibited platelet aggregation in the majority of cases, in nine the threshold concentration of ADP required to induce irreversible aggregation decreased with streptokinase (1 million Units . l–1) by 30% or more. This observation was confirmed in five of the nine by repeated measurements indicating reproducible streptokinase-induced platelet stimulation. Among the five, two were ≤30, and three were ≥50 years old. In none of the five subjects did the radio allergo sorbent test detect type E immunoglobulins directed against streptokinase in the serum. In contrast, in four of the five subjects, streptokinase-induced platelet hyperaggregability was suppressed by addition of goat antibodies against human immunoglobulin G, or F(ab')2-fragments of such antibodies. Acetylsalicylic acid did not prevent streptokinase-induced platelet stimulation, but in three of five cases, led to an increase in the control threshold concentration for ADP, so that after the decrease induced by streptokinase the threshold concentration for ADP was in the same range as before acetylsalicylic acid and streptokinase administration.

Thus, streptokinase led to an inhibition of platelet aggregation in the majority of subjects evaluated. In a minority of five out of 103, however, streptokinase reproducibly caused platelet stimulation, presumably mediated by immunoglobulin G. The platelet stimulatory effect of streptokinase was partly counteracted in three cases by application of acetylsalicylic acid.

Key Words: Acetylsalicylic acid • immunoglobulin E • immunoglobulin G • platelet aggregation • streptokinase • thromboxane A2


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