Disulfiram is a drug used to treat alcohol dependence since many years. It interferes with the metabolism of alcohol, may be associated with neurological and dermatological symptoms, and can be hepatotoxic. Due to the frequent coexistent liver test alterations due to alcohol, the true incidence of disulfiram-associated liver injury is unclear and severity of injury may vary from mildly elevated liver enzymes to fulminant hepatitis leading to death. There are several reported cases of disulfiram hepatitis in the literature. Liver histology, when available, demonstrates some degree of portal inflammation with eosinophils and hepatocyte necrosis. We present here a well-documented case of acute hepatitis due to disulfiram with typical histological lesions, favorable outcome following drug withdrawal, and a brief steroid course. The risk of hepatotoxicity should be kept in mind when prescribing disulfiram.

Background and Aim Drug‐induced liver injury (DILI) may present with autoimmune features and require immunosuppressive therapy (IST) to reach biochemical response. Discontinuation of IST without hepatitis relapse may be more frequent in these patients as compared to patients with classical autoimmune hepatitis (AIH). We aimed to determine baseline characteristics and outcome of patients with immune‐mediated drug induced liver injury (IMDILI) with particular emphasis on IST during follow‐up. Methods We performed a single‐center retrospective study of consecutive patients presenting at a tertiary care center between January 2005 and December 2019 either with IMDILI or with classical AIH, for whom full baseline characteristics and a close follow‐up were available over a 12‐month period. Results Overall, 31 patients (IMDILI n = 16, mean age 59 [34–74] years; AIH n = 15, mean age 47 [15–61] years) were included, showing similar biochemical, serological, and histological characteristics. Incriminating drugs in IMDILI patients were mostly represented by nonsteroidal antiinflammatory drugs and sartans. Initial corticosteroids combined with IST led to biochemical response in all patients. Compared to idiopathic AIH, more patients with IMDILI were weaned off corticosteroids at the end of follow‐up (11/16 [68.7%] vs 4/15 [26.6%], P < 0.02). At 1 year of follow‐up, more patients in the IMDILI group compared to the classical AIH group were off any type of IST (13/16 [81%] vs 15/15 [100%], P = 0.08). Conclusions Although presenting with similar baseline biochemical and histological characteristics as idiopathic AIH, patients with IMDILI may not require long‐term IST.

Acute Q fever is a worldwide zoonotic infection due to C. burnetii that may be associated with hepatitis. Nonspecific clinical and biological manifestations may accompany liver involvement, including hepatomegaly and elevated liver biological tests. However, the presence of jaundice is rare. Therefore, making a diagnosis of Q fever hepatitis may be difficult in an afebrile patient with jaundice of recent onset, altered liver function tests, excessive alcohol intake and no reported contact with animals. We report here the diagnostic work-up and complex clinical management of a patient presenting with acute hepatitis resulting from both C. burnetii infection and severe alcoholic steatohepatitis. Positive serology together with a detailed examination of the liver biopsy was able to reveal the coexistence of both Q fever hepatitis with typical fibrin-ring granulomas as well as florid lesions of alcoholic steatohepatitis. A combination of antibiotics, hydroxychloroquine and steroids, guided by the helpful description of changes in histological alterations on repeated liver biopsies during the course of the disease contributed to the slow but favorable outcome.