Premium
Effects of Alcohol Intake and Low K m Aldehyde Dehydrogenase on Hepatic Function in a High Hepatitis C Virus‐Prevalent Japanese Island Population
Author(s) -
Yang Xing,
Takeshita Tatsuya,
Hirata Mari,
Sato Shigeaki,
Morimoto Kanehisa
Publication year - 1999
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.1999.tb04179.x
Subject(s) - aldh2 , hepatitis c virus , aldehyde dehydrogenase , liver injury , medicine , liver function , alanine transaminase , hepatitis c , alcohol , population , aspartate transaminase , genotype , liver function tests , alcohol dehydrogenase , gastroenterology , physiology , immunology , virus , biology , environmental health , enzyme , biochemistry , gene , alkaline phosphatase
In Asians from the Pacific rim countries, alcohol sensitivity has been attributed mainly to a highly prevalent polymorphism in low K m aldehyde dehydrogenase ( ALDH2 ). Chronic alcohol abuse may accelerate or aggravate the liver injury in chronic hepatitis C virus (HCV)‐infected subjects. In this study, we examined the relationships among alcohol intake, ALDH2 genotypes, and liver injury in a high HCV‐prevalent Japanese native island population. The ALDH2 genotypes are significantly associated with drinking habits. In HCV RNA positive subjects, serum alanine aminotransferase (ALT), as well as aspartate transaminase (AST) and γ‐glutamyl transpeptidase (GGT), were significantly higher in habitual drinkers than in nonhabitual drinkers. In male habitual drinkers, the ALDH2*1/*1 subjects had higher liver necroinflammatory scores than the ALDH2*1/*2 subjects in all groups classified as: I, anti‐HCV‐seronegative; II, anti‐HCV‐seropositive with negative HCV RNA; and III, HCV RNA positive, although scores for the latter two groups were not statistically significant because of limited sample size. It was suggested that the liver function might be affected by the interaction between the ALDH2 genotypes and alcohol intake. These findings indicate that HCV‐infected ALDH2*1/*1 habitual drinkers are the major target for the prevention of alcoholic liver diseases.