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Citation
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Schmeltzer PA, Kosinski AS, Kleiner DE, Hoofnagle JH, Stolz A, Fontana RJ, Russo MW. Liver Int. 2015; 36(4): 603-609. |
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Abstract
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BACKGROUND: Nonsteroidal anti-inflammatory drugs (NSAIDs) are commonly used and have been associated with hepatotoxicity. Studies of liver injury from NSAIDs have been retrospective and prospective data are lacking.
AIM: To report the features and outcomes of subjects with severe drug induced liver injury from NSAIDS.
METHODS: The U.S. Drug Induced Liver Injury Network is a prospective registry of idiosyncratic drug hepatotoxicity. All patients are evaluated in a standard fashion and followed for at least 6 months.
RESULTS: Of 1,221 DILIN cases that were adjudicated, 30 cases were attributed to 8 different NSAIDs. The mean age was 52 years old, 24 (80%) were women, and 21 (70%) were Caucasian. The mean latency was 67 days. Common signs and symptoms at presentation were nausea (73%), jaundice (67%), and dark urine (67%). Mean peak serum AST, ALT, total bilirubin, and alkaline phosphatase were 898 U/L, 1060 U/L, 12.2 mg/dL, and 326 U/L. The most common pattern of injury was hepatocellular (70%) and autoantibodies were detected in 33% of cases. Diclofenac, was the most frequently implicated NSAID (16/30 cases), and characterized by hepatocellular injury. Seventeen cases resulted in hospitalization or prolongation of hospitalization and one patient died from complications of Stevens-Johnson syndrome due to diclofenac.
CONCLUSIONS: Hepatocellular injury is the most common pattern seen with NSAID hepatotoxicity and diclofenac is the most frequently implicated agent. Given the number of NSAID alternatives, diclofenac should be reserved for patients who fail other NSAIDs and a high level of suspicion for hepatotoxicity should be maintained. This article is protected by copyright. All rights reserved.
Language: en |