Alcohol Does Not Appear to Increase Acetaminophen-Related Acute Liver Failure: Presented at AASLD
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Alcohol Does Not Appear to Increase Acetaminophen-Related Acute Liver Failure: Presented at AASLD

By Cheryl Lathrop

BOSTON -- November 2, 2009 -- While alcohol use is common in acetaminophen-related acute liver failure (ALF), it does not appear to increase acetaminophen-related mortality or the need for liver transplantation, according to research presented here at the Liver Meeting 2009, the 60th Annual Meeting of the American Association for the Study of Liver Diseases (AASLD).

Alcohol users, however, have lower acetaminophen levels, higher aspartate aminotransferase (AST), renal insufficiency, and higher Model for End-Stage Liver Disease (MELD) scores than nonusers, noted Lulu Iles-Shih, MD, Oregon Health and Sciences University, Portland, Oregon, speaking here at a poster session on October 31.

Acetaminophen is the most common cause of ALF in the United States. Although alcohol can potentiate hepatotoxicity, its impact on the outcome of acetaminophen-related ALF was unknown. The aim of this study was to assess the association between alcohol use and adverse outcomes. The hypothesis was that individuals who consume alcohol do indeed have worse outcomes than those that do not. The authors, however, decided that alcohol does not appear to increase acetaminophen-related mortality or the need for liver transplantation.

Dr. Iles-Shih and colleagues examined 622 subjects (74% female) with acetaminophen-related ALF who had enrolled in the prospective US Acute Liver Failure Study (January 1998 to November 2008). Binary logistic regression was used to characterise the effect of alcohol on rates of death or liver transplantation (after controlling for confounders).

Data regarding alcohol use were available for 99% of patients: 51.2% (n = 315) consumed alcohol. The amount of alcohol was quantified in 56% of this group of consumers -- the median alcohol consumed was 40 g/day; the mean alcohol consumed was 69.4 g/day (range 10 to 1,000 g). It was noted that females were less likely to drink alcohol; there were 67.7% females in the alcohol group and 82.7% females in the non-alcohol group.

Death occurred in 25.2% (n = 157) of subjects, and 8.4% (n = 52) had a liver transplant.

Alcohol users had a higher admission creatinine (2.68 mg/dL [standard error {SE} +- 0.1] vs 2.34 mg/dL [SE +- 0.13]), higher AST (6,701 IU/L +- 428 vs 4,696 IU/L +- 258), higher MELD scores (32.3 vs 29.7), and lower acetaminophen levels (52.4 mg/L +- 4.01 vs 76.7 +- 6.75) than non-alcohol users.

No differences were observed in age, race, international normalised ratio upon admission, body mass index, mean arterial pressure, or mode of toxicity (intentional or unintentional).

[Presentation title: Role of Alcohol in Acetaminophen-Related Acute Liver Failure. Abstract 272]


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