Successful use of clopidogrel for cerebrovascular accident in a patient with suspected ticlopidine-induced hepatotoxicity.
Ключови думи
Резюме
OBJECTIVE
To report a case of successful clopidogrel use in a patient who developed suspected ticlopidine-induced hepatotoxicity during therapy for a cerebrovascular accident.
METHODS
A 79-year-old white woman with a history of hypertension, type 2 diabetes, Alzheimer disease, and coronary artery disease started receiving ticlopidine 250 mg twice daily three days after hospital admission for a cerebrovascular accident. Medications prior to admission included quinapril, furosemide, insulin, atorvastatin, conjugated estrogen, medroxyprogesterone, donepezil, and vitamin E. The estrogen, medroxyprogesterone, and donepezil were discontinued on admission. Laboratory tests on admission revealed that total bilirubin, alkaline phosphatase, and aspartate aminotransferase (AST) were within normal limits. On day 39 of hospitalization, laboratory tests showed marked increases in alkaline phosphatase, AST, alanine aminotransferase, gamma-glutamyl-transferase, and 5' nucleotidase. Physical examination revealed no signs of jaundice or hepatomegaly, and laboratory tests for viral hepatitis were negative. A presumptive diagnosis of ticlopidine-induced hepatotoxicity was made and ticlopidine was discontinued. The following day, clopidogrel 75 mg/d was initiated. Liver function tests returned to baseline over the following four months with ongoing clopidogrel therapy.
CONCLUSIONS
Ticlopidine-induced hepatotoxicity is well documented in the literature. In the present case, clopidogrel, a structurally similar thienopyridine, was substituted for ticlopidine following the development of presumptive ticlopidine-induced hepatotoxicity. Serum liver enzyme concentrations returned to baseline with continued clopidogrel therapy, suggesting that clopidogrel is a suitable alternative in patients who develop ticlopidine-induced hepatotoxicity.
CONCLUSIONS
Clopidogrel may be a suitable alternative for patients who develop ticlopidine-induced hepatotoxicity.
