Hepatotoxicity With Elevated Bilirubin Secondary to Prophylactic Doses of Unfractionated Heparin: A Case Report and Review of Heparin-Induced Hepatotoxicity

Author:

Bosco Michael1ORCID,Kish Troy2

Affiliation:

1. James J. Peters VA Medical Center, Bronx, NY, USA

2. Arnold and Marie Schwartz College of Pharmacy and Health Sciences, Long Island University, Brooklyn, NY, USA

Abstract

Objective: To report a case of heparin-induced hepatotoxicity in a patient without prior liver dysfunction who received prophylactic doses of unfractionated heparin (UFH). Case Summary: A 70-year-old man with no prior liver dysfunction was admitted to the hospital for presyncope, secondary to dehydration, and new-onset congestive heart failure. Prophylactic UFH was initiated for deep vein thrombosis prophylaxis. Within 2 days, he developed increases in aspartate aminotransferase and alanine aminotransferase. By day 4, aspartate aminotransferase and alanine aminotransferase were greater than 5 and 9 times the upper limit of normal, respectively. Alkaline phosphatase and bilirubin were markedly elevated as well. UFH was discontinued on day 4, and liver enzymes subsequently normalized. Discussion: Hepatotoxicity, defined as increases in transaminases greater than 3 times the upper limit of normal, is relatively rare—estimated to occur in only 5% of those receiving therapy with UFH. Concurrent elevations in bilirubin have rarely been reported. Enzymes typically begin to rise after 4 to 5 days of UFH use and return to normal within 2 weeks of discontinuation. Previously published case reports of heparin-induced hepatotoxicity have occurred with therapeutic doses of either UFH or low-molecular-weight heparins. Conclusions: Heparin-induced hepatotoxicity may occur more rapidly than previously described, and even with the use of prophylactic doses of UFH. Given their widespread use, it is important for clinicians to consider heparins in their differential as a potential cause of hepatotoxicity especially in patients without underlying hepatic disease.

Publisher

SAGE Publications

Subject

Pharmaceutical Science

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