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Aldehyde dehydrogenase 2 polymorphism for development to hepatocellular carcinoma in E ast A sian alcoholic liver cirrhosis
Author(s) -
Abe Hiroshi,
Aida Yuta,
Seki Nobuyoshi,
Sugita Tomonori,
Tomita Yoichi,
Nagano Tomohisa,
Itagaki Munenori,
Sutoh Satoshi,
Nagatsuma Keisuke,
Itoh Kyoko,
Matsuura Tomokazu,
Aizawa Yoshio
Publication year - 2015
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1111/jgh.12948
Subject(s) - aldh2 , hepatocellular carcinoma , medicine , cirrhosis , aldehyde dehydrogenase , gastroenterology , alcoholic liver disease , genotype , adh1b , biology , dehydrogenase , gene , genetics , branched chain alpha keto acid dehydrogenase complex , biochemistry , enzyme
Background and Aim We aimed to clarify the influences of aldehyde dehydrogenase 2 ( ALDH2 ), alcohol dehydrogenase 1B ( ADH1B ) polymorphisms, and ethanol consumption profile to hepatocellular carcinoma ( HCC ) development in alcoholic liver cirrhosis without chronic hepatitis B and C virus infection (non‐ B non‐ C ). Methods Of 236 freshly diagnosed non‐ B non‐ C alcoholic liver cirrhosis patients, 67 were diagnosed as HCC and the remaining 169 as not having HCC . The relationship between the genetic polymorphisms and development to HCC were evaluated in well‐matched patients with HCC ( HCC group, n = 67) and without HCC (non‐ HCC group, n = 67) using propensity scores in age, sex, and prevalence of diabetes mellitus. Results Daily amount of ethanol consumption was significantly lower ( P = 0.005), and consumptive period was significantly longer ( P = 0.003) in HCC group than non‐ HCC group. Of 134 well‐matched patients, 113 (84.3%) had ALDH2 *1/*1 genotype and 21 (15.7%) had ALDH2 *1/*2 genotype. In HCC development, consumptive long period ( P = 0.007) and carrying ALDH2 *1/*2 genotype ( P = 0.026) were identified as significant factors independently participated, while there was no relation to ADH1B polymorphism. In addition, consumptive period was significantly longer in HCC group than non‐ HCC group in ALDH2 *1/*1 genotype patients ( P = 0.0005), while there was no difference in profile of ethanol consumption in ALDH2 *1/*2 genotype patients. Among HCC group, daily ( P = 3.78 × 10 −6 ) and cumulative amount ( P = 4.89 × 10 −6 ) of ethanol consumption were significantly higher in ALDH2 *1/*1 genotype patients than ALDH2 *1/*2 genotype patients. Conclusion In alcoholic liver cirrhosis, investigations of ALDH2 polymorphism and ethanol consumption profile are useful for prediction of HCC development.