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Review
. 2010 Dec 7;16(45):5651-61.
doi: 10.3748/wjg.v16.i45.5651.

Non-steroidal anti-inflammatory drugs: What is the actual risk of liver damage?

Fernando Bessone
Review

Non-steroidal anti-inflammatory drugs: What is the actual risk of liver damage?

Fernando Bessone. World J Gastroenterol. .

Abstract

Non-steroidal anti-inflammatory drugs (NSAIDs) constitute a family of drugs, which taken as a group, represents one of the most frequently prescribed around the world. Thus, not surprisingly NSAIDs, along with anti-infectious agents, list on the top for causes of Drug-Induced Liver Injury (DILI). The incidence of liver disease induced by NSAIDs reported in clinical studies is fairly uniform ranging from 0.29/100 000 [95% confidence interval (CI): 0.17-051] to 9/100 000 (95% CI: 6-15). However, compared with these results, a higher risk of liver-related hospitalizations was reported (3-23 per 100 000 patients). NSAIDs exhibit a broad spectrum of liver damage ranging from asymptomatic, transient, hyper-transaminasemia to fulminant hepatic failure. However, under-reporting of asymptomatic, mild cases, as well as of those with transient liver-tests alteration, in conjunction with reports non-compliant with pharmacovigilance criteria to ascertain DILI and flawed epidemiological studies, jeopardize the chance to ascertain the actual risk of NSAIDs hepatotoxicity. Several NSAIDs, namely bromfenac, ibufenac and benoxaprofen, have been withdrawn from the market due to hepatotoxicity; others like nimesulide were never marketed in some countries and withdrawn in others. Indeed, the controversy concerning the actual risk of severe liver disease persists within NSAIDs research. The present work intends (1) to provide a critical analysis of the dissimilar results currently available in the literature concerning the epidemiology of NSAIDS hepatotoxicity; and (2) to review the risk of hepatotoxicity for each one of the most commonly employed compounds of the NSAIDs family, based on past and recently published data.

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Figures

Figure 1
Figure 1
Piroxicam induced hepato-canalicular cholestasis associated with ductopenia (notice absence of bile duct in the portal tract).
Figure 2
Figure 2
Latency (time from nimesulide intake to clinical onset) in 43 patients.
Figure 3
Figure 3
Acute hepatitis induced by nimesulide (hepatocellular collapsed areas are shown with arrows).
See this image and copyright information in PMC

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