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A prospective study of acute drug‐induced liver injury in patients suffering from non‐alcoholic fatty liver disease
Author(s) -
Tarantino Giovanni,
Conca Paolo,
Basile Vincenzo,
Gentile Antonio,
Capone Domenico,
Polichetti Giuliano,
Leo Emilio
Publication year - 2007
Publication title -
hepatology research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.123
H-Index - 75
eISSN - 1872-034X
pISSN - 1386-6346
DOI - 10.1111/j.1872-034x.2007.00072.x
Subject(s) - medicine , fatty liver , gastroenterology , liver injury , steatohepatitis , odds ratio , cirrhosis , drug , liver disease , population , disease , pharmacology , environmental health
Aim: Liver damage due to facultative hepatotoxins is scarcely foreseeable. We evaluated the prevalence of acute drug‐induced liver injury (DILI) in a specific setting, assessing eventual interactions with pre‐existing hepatic illnesses. Methods: The research was carried out in an Italian tertiary care hospital, by analyzing 248 patients with non‐advanced liver disease, divided into two well‐matched groups: 174 patients (median age 53, 94 females) with hepatitis C virus‐related chronic hepatitis; and 74 (median age 55, 39 females) with non‐alcoholic fatty liver disease (NAFLD). Results: Six patients (2.4% of the whole population) belonging to the NAFLD group (χ 2 ‐test, P = 0.004) suffered from acute hepatoxicity related to the following drugs, that is antihypertensive, acting on platelet aggregation, antimicrobial, non‐steroidal anti‐inflammatory and proton pump inhibitor. The NAFLD presence was an independent risk factor in determining drug‐related acute hepatitis, with an odds ratio of 3.95 (95% confidence intervals: 11.48–1.35). Central obesity was relevant in every patient with acute toxicity. Alcohol consumption and drug association did not influence the acute drug‐induced liver damage. Conclusion: NAFLD conveys a nearly fourfold increase of DILI risk in obese middle‐aged patients. NAFLD, characterized by mitochondrial dysfunction, could predispose to drug‐induced hepatotoxicity that probably shares the same pathophysiological mechanism.