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• W2163729260 abstract "Background & AimsTumor necrosis factor (TNF)-α antagonists have been associated with drug-induced liver injury (DILI). We reviewed cases of DILI in the United States to identify those associated with use of TNF-α antagonists.MethodsWe searched the U.S. DILI Network (DILIN) database, from 2003 to 2011, for cases associated with TNF-α antagonists. Mean Roussel-Uclaf Causality Assessment Method scores were calculated. A DILIN severity score was assigned according to a previously published scale, and we identified 6 subjects likely to have DILI associated with use of TNF-α antagonists. We also searched PubMed for articles that reported hepatotoxicity from TNF-α antagonists, identifying 28 additional cases suitable for analysis.ResultsThe drugs presumed to have caused DILI were infliximab (n = 26), etanercept (n = 4), and adalimumab (n = 4). The anti–TNF-α agent was the probable cause of 12 cases of DILI (35%), a very likely cause for 21 (62%), and a definite cause for 1 (3%). Median latency was 13 weeks (range, 2–104); however, 7 cases (20%) had latency periods longer than 24 weeks. Twenty-two of 33 subjects who underwent serologic analysis (67%) tested positive for anti-nuclear and/or smooth muscle antibodies. Of these 22, 17 underwent liver biopsy; 15 subjects had clear features of autoimmunity. The 22 subjects with autoimmune features had longer median latency (16 vs 10 weeks) and higher peak levels of alanine aminotransferase (784 vs 528 U/L) than the 12 without such features. There was 1 case of severe cholestasis. All but one subject improved after discontinuation of the implicated drug; 12 subjects received corticosteroid therapy. No deaths were attributed to liver injury, although one patient with preexistent cirrhosis required liver transplantation.ConclusionsAcute liver injury caused by TNF-α antagonists may be a class effect because multiple agents in this category have been implicated. The most common presentation is an autoimmune phenotype with marked hepatocellular injury, but a mixed non-autoimmune pattern or predominant cholestasis also occurs. The prognosis is usually good after drug discontinuation, although some patients may benefit from a course of corticosteroids. ClinicalTrials.gov: Number, NCT00345930 Tumor necrosis factor (TNF)-α antagonists have been associated with drug-induced liver injury (DILI). We reviewed cases of DILI in the United States to identify those associated with use of TNF-α antagonists. We searched the U.S. DILI Network (DILIN) database, from 2003 to 2011, for cases associated with TNF-α antagonists. Mean Roussel-Uclaf Causality Assessment Method scores were calculated. A DILIN severity score was assigned according to a previously published scale, and we identified 6 subjects likely to have DILI associated with use of TNF-α antagonists. We also searched PubMed for articles that reported hepatotoxicity from TNF-α antagonists, identifying 28 additional cases suitable for analysis. The drugs presumed to have caused DILI were infliximab (n = 26), etanercept (n = 4), and adalimumab (n = 4). The anti–TNF-α agent was the probable cause of 12 cases of DILI (35%), a very likely cause for 21 (62%), and a definite cause for 1 (3%). Median latency was 13 weeks (range, 2–104); however, 7 cases (20%) had latency periods longer than 24 weeks. Twenty-two of 33 subjects who underwent serologic analysis (67%) tested positive for anti-nuclear and/or smooth muscle antibodies. Of these 22, 17 underwent liver biopsy; 15 subjects had clear features of autoimmunity. The 22 subjects with autoimmune features had longer median latency (16 vs 10 weeks) and higher peak levels of alanine aminotransferase (784 vs 528 U/L) than the 12 without such features. There was 1 case of severe cholestasis. All but one subject improved after discontinuation of the implicated drug; 12 subjects received corticosteroid therapy. No deaths were attributed to liver injury, although one patient with preexistent cirrhosis required liver transplantation. Acute liver injury caused by TNF-α antagonists may be a class effect because multiple agents in this category have been implicated. The most common presentation is an autoimmune phenotype with marked hepatocellular injury, but a mixed non-autoimmune pattern or predominant cholestasis also occurs. The prognosis is usually good after drug discontinuation, although some patients may benefit from a course of corticosteroids. ClinicalTrials.gov: Number, NCT00345930" @default.
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• W2163729260 date "2013-05-01" @default.
• W2163729260 modified "2023-09-26" @default.
• W2163729260 title "Liver Injury From Tumor Necrosis Factor-α Antagonists: Analysis of Thirty-four Cases" @default.
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• W2163729260 cites W1986617379 @default.
• W2163729260 cites W2001143625 @default.
• W2163729260 cites W2001288327 @default.
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• W2163729260 cites W2013511746 @default.
• W2163729260 cites W2014370035 @default.
• W2163729260 cites W2018626170 @default.
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• W2163729260 cites W2036791601 @default.
• W2163729260 cites W2037442557 @default.
• W2163729260 cites W2041808735 @default.
• W2163729260 cites W2045716633 @default.
• W2163729260 cites W2046166122 @default.
• W2163729260 cites W2047233853 @default.
• W2163729260 cites W2055202209 @default.
• W2163729260 cites W2056529714 @default.
• W2163729260 cites W2062185109 @default.
• W2163729260 cites W2064049859 @default.
• W2163729260 cites W2067292160 @default.
• W2163729260 cites W2069757747 @default.
• W2163729260 cites W2077358378 @default.
• W2163729260 cites W2081424106 @default.
• W2163729260 cites W2084780145 @default.
• W2163729260 cites W2101690589 @default.
• W2163729260 cites W2113183888 @default.
• W2163729260 cites W2116981696 @default.
• W2163729260 cites W2124074159 @default.
• W2163729260 cites W2125081368 @default.
• W2163729260 cites W2127767188 @default.
• W2163729260 cites W2142434338 @default.
• W2163729260 cites W2144511941 @default.
• W2163729260 cites W2148497851 @default.
• W2163729260 cites W2152084270 @default.
• W2163729260 cites W2153910121 @default.
• W2163729260 cites W2154976029 @default.
• W2163729260 cites W2157225692 @default.
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• W2163729260 doi "https://doi.org/10.1016/j.cgh.2012.12.025" @default.
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