Summary

Guillain-Barré syndrome (GBS) constitutes a heterogeneous group of immune-mediated peripheral neuropathic disorders that can be triggered by a variety of antecedent events. Clinical symptoms are thought to result from streptokinase antibody-mediated damage to the local blood–nerve barrier. We report the case of a 50-year-old man with acute anterior wall myocardial infarction who developed GBS as a manifestation of autoimmune hypersensitivity reaction to the drug 17 days after thrombolytic therapy with streptokinase. The patient was treated with a 5-day course of intravenous γ globulin and his symptoms improved and there was no residual deficit. The case forms a reminder of the autoimmune complications of non-fibrin specific agents that can sometimes be catastrophic and require persistent and vigilant in-hospital and immediate postdischarge follow-up and immediate management.