Acute liver injury (ALI) following acetaminophen overdose (AO) occurs in less than 10% of cases, but that risk is increased among alcoholics and those with chronic alcoholic liver disease. We sought to assess whether coexistent hepatitis C virus (HCV) infection potentiated the hepatotoxic effects of acetaminophen. We queried the Nationwide Inpatient Sample (1998-2005), a 20% sample of U.S. hospitals, to identify admissions for AO using International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM) codes. Outcomes were development of ALI (ICD-9-CM: 570.0, 572.2, 573.3), in-hospital mortality, severe liver failure, and resource utilization. There were 42,781 admissions for AO in the sample, yielding a national estimate of 210,436 AO hospitalizations. HCV prevalence increased from 0.5% to 1.5% between 1998 and 2005 (P<0.0001). The rate of ALI was 7.2%. After adjusting for confounders and excluding patients with cirrhosis, the risk of ALI increased with HCV (adjusted odds ratio [aOR] 1.80; 95% con.dence interval [CI]: 1.30-2.48), nonalcoholic fatty liver disease (aOR 7.43; 95% CI: 3.30-16.7), alcoholic liver disease (aOR 6.46; 95% CI: 4.53-9.21), and malnutrition (aOR 3.84; 95% CI: 2.61-5.65). HCV was associated with greater risk of progression to severe liver failure (aOR 3.55; 95% CI: 1.88-6.70). Crude mortality was higher in patients with HCV compared to those without HCV (2.1% versus 0.9%, P = 0.01); patients with ALI had an overall mortality of 8.6%. Length of stay was longer in patients with HCV (4.0 versus 2.6 days, P < 0.0001). Admissions with coexistent HCV also incurred two-fold higher hospital charges than those that did not ($21,400 versus $11,400, P < 0.0001). Conclusion: Our retrospective analysis suggests that patients with HCV may be at increased risk of ALI following AO. These findings warrant further confirmation in prospective studies.
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