RHABDOMYOLYSIS INDUCED BY EPSILON-AMINOCAPROIC ACID

OBJECTIVE: To report a case of rhabdomyolysis associated with epsilon- aminocaproic acid (epsilon-ACA). CASE SUMMARY: A 33-year-old female pa tient with chronic granulocytic leukemia was treated with epsilon-ACA for approximately 3.5 months for thrombocytopenic bleeding, The initia l dosage was 4 g po q6h. One month after an increase in dosage to 5 g po q4h the patient developed severe lower extremity myalgia and marked weakness. Laboratory investigations revealed an elevated creatine kin ase (CK), lactate dehydrogenase (LDH), aspartate aminotransferase (AST ), and myoglobinemia. Epsilon-ACA was thought to be the causative agen t and was discontinued. Tile patient received intravenous fluids to mi nimize renal damage due to myoglobin. Serum enzyme concentrations did not return to normal. The patient died of a central nervous system hem orrhage 1 week after the epsilon-AGA was discontinued. DISCUSSION: The re were 31 cases of epsilon-ACA-induced myopathies published in the li terature (MEDLINE) from 1972 to June 1995. Of these, 10 cases were rev iewed. In all cases, patients received epsilon-ACA in doses ranging fr om 16 to 36 g/d for more than 28 days. Clinical findings varied from e xtreme muscle weakness to myopathic changes in electromyelograms. All patients recovered following discontinuation of epsilon-ACA. CONCLUSIO NS: Long-term therapy with high-dose epsilon-ACA may produce muscle we akness or rhabdomyolysis. Patients who require long-term, high-dose ep silon-ACA therapy should be monitored for myoglobinuria and changes in serum CK, LDH, and AST, for myoglobinemia, for decreases in muscle st rength, and/or for myalgia Significant changes in these parameters com pared with baseline values should suggest a need to discontinue epsilo n-ACA therapy.