Published online Jun 28, 2022. doi: 10.3748/wjg.v28.i24.2654
Peer-review started: August 5, 2021
First decision: September 4, 2021
Revised: September 15, 2021
Accepted: May 14, 2022
Article in press: May 14, 2022
Published online: June 28, 2022
Processing time: 322 Days and 22.3 Hours
Drug-induced autoimmune hepatitis (DIAIH) is a specific phenotype of drug-induced liver injury that may lead to the devastating outcome of acute liver failure requiring liver transplantation. Drugs implicated in DIAIH include antimicrobials such as nitrofurantoin and minocycline, non-steroidal anti-inflammatory drugs, statins as well as anti-tumor necrosis agents. The clinical features of drug-induced liver injury are indistinguishable from idiopathic autoimmune hepatitis (AIH) as both may have positive AIH-related autoantibodies, elevated immunoglobulin G, as well as similar histopathological findings. In patients who show no clinical improvement, or there is progressive liver injury despite cessation of the suspected drug, a liver biopsy should be considered, whereby the presence of advance fibrosis on histology favors the diagnosis of idiopathic AIH. Empirical treatment with corticosteroids may be required in patients with non-resolving liver injury. A typical clinical scenario supportive of DIAIH includes a history of drug exposure with spontaneous resolution of liver injury after drug withdrawal and the absence of relapse after rapid steroid taper. In this article we report two cases of DIAIH secondary to Sorafenib and Atorvastatin along with a review of currently available literature. Early identification and treatment often lead to a favorable outcome in DIAIH.
Core Tip: Drug-induced autoimmune hepatitis is uncommon in clinical practice but may have devastating consequences. It is important to distinguish drug-induced autoimmune hepatitis from idiopathic autoimmune hepatitis as the former may not require prolong course of immunosuppressant. This minireview highlights the key differences between these two closely-linked entities.