The Annals Take our Readership Survey!
home help contact us subscription past issues search current issue
 QUICK SEARCH:   [advanced]


     


The Annals of Pharmacotherapy: Vol. 33, No. 9, pp. 939-941. DOI 10.1345/aph.18435
© 1999 Harvey Whitney Books Company.
This Article
Right arrow PDF
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Articles Ahead of Print
Right arrow [Order Reprint]
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Zeolla, M.
Right arrow Articles by Carson, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Zeolla, M.
Right arrow Articles by Carson, J.


Research Articles

Successful use of clopidogrel for cerebrovascular accident in a patient with suspected ticlopidine-induced hepatotoxicity

MM Zeolla and JJ Carson

OBJECTIVE: To report a case of successful clopidogrel use in a patient who developed suspected ticlopidine-induced hepatotoxicity during therapy for a cerebrovascular accident. CASE REPORT: 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. DISCUSSION: 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.


This article has been cited by other articles:


Home page
Drug Metab. Dispos.Home page
D. K. Dalvie and T. N. O'Connell
CHARACTERIZATION OF NOVEL DIHYDROTHIENOPYRIDINIUM AND THIENOPYRIDINIUM METABOLITES OF TICLOPIDINE IN VITRO: ROLE OF PEROXIDASES, CYTOCHROMES P450, AND MONOAMINE OXIDASES
Drug Metab. Dispos., January 1, 2004; 32(1): 49 - 57.
[Abstract] [Full Text] [PDF]


Home page
The Annals of PharmacotherapyHome page
Y. D Skurnik, A. Tcherniak, K. Edlan, and Z. Sthoeger
Ticlopidine-Induced Cholestatic Hepatitis
Ann. Pharmacother., March 1, 2003; 37(3): 371 - 375.
[Abstract] [Full Text] [PDF]




homecopy help contact us subscription past issues search current issue
Copyright © 1999 by Harvey Whitney Books Company.