Unfavorable prognosis of patients with acute liver injury due to drug-induced liver injury and acute exacerbation of hepatitis B virus infection

Hepatol Res. 2019 Nov;49(11):1286-1293. doi: 10.1111/hepr.13397. Epub 2019 Jul 26.

Abstract

Aim: Acute liver injury (ALI) has a favorable prognosis, whereas acute liver failure (ALF) leads to organ failure and thus has an unfavorable prognosis. The effect of each etiology on the clinical course of ALI remains unclear. This study aimed to determine how each etiology and glucocorticoid on the unfavorable etiology affects the clinical course of ALI.

Methods: This prospective observational study enrolled 522 patients with ALI/ALF from 2004 and 2017. To evaluate the influence of etiology on prognosis, decision tree analysis was carried out using age, disease type, etiology, and the presence of hepatic encephalopathy.

Results: Of 522 patients, 398 patients satisfied the ALI criteria at registration in this study. The ALI etiologies were as follows: viral hepatitis through oral infection (n = 54), acute hepatitis B virus (HBV) infection (n = 24), acute exacerbation of HBV infection (n = 30), de novo hepatitis due to HBV (n = 5), autoimmune hepatitis (n = 59), drug-induced liver injury (DILI; n = 85), other viruses (n = 12), and undetermined (n = 129). ALI in 46 patients progressed to ALF after registration. Of 11 patients (age >52 years) with ALF due to acute exacerbation of HBV infection or DILI, seven patients (63.6%) died. Whether glucocorticoid affected the clinical course of ALI due to acute exacerbation of HBV infection or DILI was evaluated using propensity score matching (age, sex, alanine aminotransferase, total bilirubin, and prothrombin time-international normalized ratio). Glucocorticoid did not improve the prognosis of ALI patients due to the two etiologies.

Conclusions: Progression of ALI due to DILI or acute exacerbation of HBV infection to ALF showed a poor prognosis.

Keywords: acute liver failure; acute liver injury; drug-induced liver injury; glucocorticoid.