S5592 A Harmful Combination of Weight Loss Efforts and Daily Alcohol Use

Introduction: Drug-induced liver injury (DILI) accounts for approximately 19% of hospitalizations due to elevated transaminases greater than 10 times the upper limit of normal. Frequently implicated agents include acetaminophen, antibiotics, and antiepileptics. We present an uncommon cause of DILI secondary to orlistat. Case Description/Methods: A 37-year-old man with history of gastroesophageal reflux disease, obstructive sleep apnea, chronic alcoholic pancreatitis, and alcohol use disorder, presented with nausea and epigastric pain a few hours after his last beer. Upon history taking he declined illicit drug use or new sexual partners. Computed tomography of the abdomen and pelvis revealed a peripancreatic fluid collection, hepatic steatosis, and cholelithiasis. Labs included aspartate aminotransferase (AST) of 3002, alanine aminotransferase (ALT) of 3582, alkaline phosphatase of 111, total bilirubin (T. bili) of 1.9 and international normalized ratio (INR) of 2.0. Lipase was within normal limits and acetaminophen level was negative. Infectious hepatitis (Hep) serologies showed positive hepatitis A IgG, as well as negative hepatitis B surface antigen, hepatitis B surface antibody, hepatitis B core antibody, hepatitis C antibody, and hepatitis E antibody. Antinuclear antibody and smooth muscle antibody were negative. Doppler ultrasonography of the right upper quadrant showed patent hepatic vasculature. Upon further inquiry he admitted to taking orlistat 60 mg daily for weight loss for a few weeks. Given the suspicion of DILI from orlistat, N-acetylcysteine (NAC) infusion was started as per the standard acetaminophen toxicity protocol. The day following NAC administration, liver chemistries improved with AST 368, alanine aminotransferase 1707, T. bili 1.5, and INR 1.2. Liver chemistries and INR continued to downtrend, and the patient was discharged with outpatient follow up. A month later, transaminases had normalized with continued avoidance of orlistat. Discussion: This case illustrates an unusual presentation of DILI with transaminase levels over 3,000 and minimal bilirubin elevation, typically seen in ischemic hepatitis, acute viral hepatitis and acetaminophen toxicity. Although orlistat-induced liver failure has been reported, DILI at a low dose of 60 mg of orlistat is uncommon. This suggests that alcohol may have potentiated the hepatotoxicity of orlistat. This case provides an additional reason to avoid the use of orlistat, beyond its limited efficacy data and side effect profile.

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Publication Details

Journal
The American Journal of Gastroenterology
Published
2025-10-01
DOI
https://doi.org/10.14309/01.ajg.0001149828.79624.c5
Primary Topic
Drug-Induced Hepatotoxicity and Protection
Type
article
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0.00
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article

S5592 A Harmful Combination of Weight Loss Efforts and Daily Alcohol Use

Ambreen Syeda, Kirk Martinez, Alexander J. Kaye, Ivanna Diaz Alcantara et al.
The American Journal of Gastroenterology
Drug-Induced Hepatotoxicity and Protection
article

S5592 A Harmful Combination of Weight Loss Efforts and Daily Alcohol Use

Ambreen Syeda, Kirk Martinez, Alexander J. Kaye, Ivanna Diaz Alcantara, Daniel DiLeo, Bani Chander-Roland
article en

Abstract

Introduction: Drug-induced liver injury (DILI) accounts for approximately 19% of hospitalizations due to elevated transaminases greater than 10 times the upper limit of normal. Frequently implicated agents include acetaminophen, antibiotics, and antiepileptics. We present an uncommon cause of DILI secondary to orlistat. Case Description/Methods: A 37-year-old man with history of gastroesophageal reflux disease, obstructive sleep apnea, chronic alcoholic pancreatitis, and alcohol use disorder, presented with nausea and epigastric pain a few hours after his last beer. Upon history taking he declined illicit drug use or new sexual partners. Computed tomography of the abdomen and pelvis revealed a peripancreatic fluid collection, hepatic steatosis, and cholelithiasis. Labs included aspartate aminotransferase (AST) of 3002, alanine aminotransferase (ALT) of 3582, alkaline phosphatase of 111, total bilirubin (T. bili) of 1.9 and international normalized ratio (INR) of 2.0. Lipase was within normal limits and acetaminophen level was negative. Infectious hepatitis (Hep) serologies showed positive hepatitis A IgG, as well as negative hepatitis B surface antigen, hepatitis B surface antibody, hepatitis B core antibody, hepatitis C antibody, and hepatitis E antibody. Antinuclear antibody and smooth muscle antibody were negative. Doppler ultrasonography of the right upper quadrant showed patent hepatic vasculature. Upon further inquiry he admitted to taking orlistat 60 mg daily for weight loss for a few weeks. Given the suspicion of DILI from orlistat, N-acetylcysteine (NAC) infusion was started as per the standard acetaminophen toxicity protocol. The day following NAC administration, liver chemistries improved with AST 368, alanine aminotransferase 1707, T. bili 1.5, and INR 1.2. Liver chemistries and INR continued to downtrend, and the patient was discharged with outpatient follow up. A month later, transaminases had normalized with continued avoidance of orlistat. Discussion: This case illustrates an unusual presentation of DILI with transaminase levels over 3,000 and minimal bilirubin elevation, typically seen in ischemic hepatitis, acute viral hepatitis and acetaminophen toxicity. Although orlistat-induced liver failure has been reported, DILI at a low dose of 60 mg of orlistat is uncommon. This suggests that alcohol may have potentiated the hepatotoxicity of orlistat. This case provides an additional reason to avoid the use of orlistat, beyond its limited efficacy data and side effect profile.

The American Journal of GastroenterologyVol. 120(10S2)
Openalex Percentile: Top 52%
Drug-Induced Hepatotoxicity and Protection
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