Potential Benefit of Alcohol Intake in Patients With Acetaminophen Toxicity: A Propensity Matched Analysis

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Conference Proceeding

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American Journal of Gastroenterology


Introduction: Acetaminophen toxicity (AT) is the most common cause of acute liver failure and it works by reversibly inhibiting cyclooxygenase and forming a hepatotoxic metabolite, N-acetyl-Pbenzoquinoneimine (NAPQI). There are overlaps in the pathways between ethanol and acetaminophen metabolism, so this study was done to determine if concomitant alcohol use affects patient outcomes in those with AT. Methods: To identify primary AT hospitalizations, we used the National Inpatient Sample (NIS) database from 2016 to 2020. We included adult AT patients (age $ 18) with alcohol blood levels . 80mg/dl or an alcohol intake related acute complication other than alcoholic hepatitis, and excluded patients with cirrhosis, or active liver disease of another etiology. Using a 1:1 matching method based on biodemographics, hospital characteristics, and Elixhauser comorbidities, we developed a matched comparison cohort of AT with concomitant alcohol intake. Results: We matched 6,210 AT patients without alcohol use to the same number of AT patients with active alcohol use and found no significant difference in inpatient mortality between matched cohorts (adjusted Odds ratio (AOR)50.73, 95% confidence interval (CI)50.49-1.10, P-value50.137). However, alcohol use with AT was associated with a shorter length of stay (LOS), a lower mean inpatient cost (MIC), lower odds of transaminitis, coagulopathy, acute liver failure, hepatic encephalopathy, disseminated intravascular coagulation (DIC), sepsis without shock, acute kidney injury (AKI), and a need for blood product transfusion (see Table 1). Conclusion: Concomitant alcohol intake is not associated with improved inpatient mortality in patients with AT, but it is associated with lower odds of transaminitis, acute liver failure, and hepatic encephalopathy. This is likely due to alcohol’s effect as a competitive inhibitor of the enzyme CYP2E1, which metabolizes acetaminophen to hepatotoxic NAPQI in the absence of glutathione and is also involved in the reaction converting ethanol to acetaldehyde. This likely results in shunting of the pathway away from the production of toxic NAPQI, thereby lowering the rate of hepatic injury. Our study associates alcohol blood level above . 80 mg/dl with improved inpatient outcomes in AT patients and supports a need for further research in this area.





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American College of Gastroenterology Annual Scientific Meeting, October 20-25, 2023, Vancouver, Canada

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