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Racial and ethnic differences in alcohol-associated aspartate aminotransferase and γ-glutamyltransferase elevation

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74 Scopus citations

Abstract

Background: Recent analyses have confirmed that Hispanic and black non-Hispanic Americans are at an increased risk for death from liver cirrhosis. The reasons for this are unknown. As a common cause of cirrhosis, differing sensitivities to alcohol-related hepatocellular injury may play a role. This study compared racial and ethnic aspartate aminotransferase and γ-glutamyltransferase level elevations within alcohol-drinking categories. Methods: A cross-sectional analysis of adult subjects from the Third National Health and Nutrition Examination Survey. Logistic regression models were used to estimate the risk for elevation of aspartate aminotransferase and γ-glutamyltransferase levels among Mexican American and black non-Hispanic subjects compared with white non-Hispanic subjects within categories of alcohol use. Adjustment was made for age, sex, exposure to hepatitis C and B, and body mass index. Results: Among current drinkers, black non-Hispanic and Mexican Americans were more likely to have a 2-fold elevation in aspartate aminotransferase levels when compared with white non-Hispanic Americans. This was most pronounced in the highest-frequency drinkers (Mexican Americans: odds ratio, 9.1 [95% confidence interval, 3.9-21.0]; and black non-Hispanic Americans: odds ratio, 3.1 [95% confidence interval, 1.4-6.8]). No racial and ethnic differences were apparent among current abstainers. A similar pattern was found for 2-fold γ-glutamyltransferase level elevations. Conclusions: Among current drinkers, Mexican and black non-Hispanic Americans may have an increased risk for hepatocellular injury. These results require confirmation in other study populations for whom validated measures of quantity and pattern of drinking exist.

Original languageEnglish
Pages (from-to)2236-2239
Number of pages4
JournalArchives of internal medicine
Volume162
Issue number19
DOIs
StatePublished - Oct 28 2002

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