Case Presentation: A 35-year-old healthy male veteran presented to the emergency room with painless jaundice. Three days prior to presentation, the patient noticed a yellowing of his eyes, but was otherwise asymptomatic. His history was notable for traumatic brain injury, PTSD, heterozygous gene mutation for hemochromatosis, and alcohol abuse with prior elevations in his aminotransferases to the 400s. Work-up, including a biopsy one year prior to presentation, showed severe steatohepatitis and increased fibrosis in the portal and periportal regions, but no evidence of cirrhosis. LFTs eleven days prior to presentation showed an AST of 53 and ALT of 74 with a bilirubin of 1.0. He was unwavering in his story of having maintained sobriety for two months prior to admission. The patient had recently been discharged from an inpatient alcohol detox facility one month prior and had been initiated on disulfiram. His alcohol screen was negative on admission. His physical exam was notable for icteric sclera, diffuse jaundice, intact mental status and no asterixis. Admission LFTs showed an AST of 1191, ALT of 2658 and a bilirubin of 5.87. His LFTs peaked at an AST of 1207, ALT of 2927 and bilirubin of 8.6. Work-up included an ultrasound showing normal liver echotexture, no splenomegaly, a patent portal vein and no ascites. Lab studies were notable for a negative toxicology screen including acetaminophen. Diagnostic studies for other common causes of acute liver injury were unrevealing including: acute infectious hepatitis, hemochromatosis, autoimmune hepatitis, and Wilson’s disease. After an exhaustive work-up the diagnosis of disulfiram-induced acute liver injury was made. Disulfiram was held from early in his hospitalization and the patient was discharged home to recover. Following discharge his LFTs normalized to an AST of 29, ALT of 32, and bilirubin of 1.0. Repeat biopsy showed moderate portal fibrosis, minimal positive hemosiderin granules in periportal hepatocytes, and no evidence of steatosis or cirrhosis with mild mixed lymphoplasmacytic and eosinophilic infiltrate mainly in the portal region consistent with a toxic insult. Since discharge, the patient has maintained sobriety and is engaged in care for his co-morbid psychiatric and medical co-morbidities.
Discussion: Acute liver injury resulting in elevated liver enzymes (AST and ALT) is a common presentation to many hospital wards. Given the risk of progression to fulminant liver failure, there is an urgency to identifying a diagnosis. Disulfiram use is known to cause mild elevations in serum aminotransferase levels in up to 25% of patients, however more significant elevations leading to acute liver injury were initially reported in the 1970-80s in Scandinavian countries (1, 2). Disulfiram is metabolized in the liver and the mechanism of injury is thought to be idiosyncratic hypersensitivity (3).
Conclusions: This report illustrates a rare case of acute liver injury secondary to disulfiram drug reaction. This case is notable for prompt discontinuation of disulfiram on admission allowing for hepatic recovery. While some patients have recovered hepatic function following discontinuation (4), there are other reports of patients progressing to acute liver failure and death (5, 6). Recognition and early discontinuation of disulfiram in such cases may help optimize chances for hepatic recovery.