Liver and Bile
J Hepatol. 2022;76(1):86–92
Infliximab-induced liver injury: Clinical phenotypes, autoimmunity and the role of corticosteroid treatment
Background and aims: Infliximab has been associated with drug-induced liver injury (DILI), particularly drug-induced autoimmune hepatitis (DIAIH). DIAIH is commonly treated with corticosteroids, but there is limited data on the efficacy of corticosteroids in infliximab-induced DILI.
Methods: Patients were included for assessment if they had been treated with infliximab between 2009 and 2020 in Iceland and had developed elevated liver tests. Other specific etiologies of liver enzyme elevations were excluded. Patients treated with corticosteroids were compared to patients not receiving corticosteroids.
Results: A total of 36 patients with infliximab-induced DILI were identified: median age was 46 (interquartile range [IQR], 32–54) years and 28 (78%) were female. Type of liver injury was predominantly hepatocellular (64%). Median peak liver enzymes were: alanine aminotransferase (ALT) 393 (IQR, 328–695) U/l, aspartate aminotransferase (AST) 283 (IQR, 158–564) U/l, alkaline phosphatase 116 (IQR, 83–205) U/l, and bilirubin 13 (IQR, 10–20) μmol/l. A total of 25 patients (69%) were positive for anti-nuclear antibody and/or had elevated immunoglobulin G. Corticosteroids were initiated in 17 (47%). Median time from onset of liver injury to peak ALT value was longer in patients treated with corticosteroids, 22 (IQR, 12–59) days vs. 0 (IQR, 0–3) days (p = 0.001). Time from peak ALT to normalization of liver enzymes was 45 days in the corticosteroid group versus 77 days in others (p = 0.062). Corticosteroids were tapered in all patients, with no cases of relapse during the follow-up period of 1245 (IQR, 820–2698) days. Overall 75% received another biologic, mostly adalimumab, without evidence of liver injury.
Conclusion: Approximately half of patients with infliximab-induced liver injury had slow improvement in alanine aminotransferase despite cessation of therapy and were treated with corticosteroids. Treatment response was good with prompt resolution of liver test abnormalities. Relapse of liver injury was not observed after tapering of corticosteroids despite prolonged follow-up and no patients developed drug-induced liver injury due to a second biologic.