The prolonged administration of epsilon-aminocaproic acid (EACA) resulted in the development of severe proximal myopathy associated with high plasma creatine kinase values, rhabdomyolysis, myoglobinuria, and mild hyperbilirubinaemia. Withdrawal of the drug led to spontaneous resolution of the clinical and biochemical syndrome. Structural and enzyme studies of a biopsy specimen of the involved skeletal muscle supported the presence of subclinical myopathy. The mechanism whereby EACA produces its toxicity in muscle may in part be due to inhibition of cathepsin D, but the possibility that other proteases are involved has not been excluded. The fact that this clinical syndrome is rare despite the widespread use of EACA may be because it only occurs in subjects with a subclinical skeletal muscle disorder which is unmasked by the drug.
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