Case-control studies that have investigated the association between alcoholism and alcohol-induced liver damage and the ADH2, ADH3, CYP2E1, and ADLH2 polymorphisms have reported controversial or inconclusive results. Thus, we conducted a meta-analysis of 50 association studies of the above polymorph
Alcoholism and alcoholic organ damage and genetic polymorphisms of alcohol metabolizing enzymes in Chinese patients
β Scribed by Y. Chao; T. Young; H. Tang; C. Hsu
- Publisher
- John Wiley and Sons
- Year
- 1997
- Tongue
- English
- Weight
- 190 KB
- Volume
- 25
- Category
- Article
- ISSN
- 0270-9139
No coin nor oath required. For personal study only.
β¦ Synopsis
The physical complications of alcoholism are numerous. 1
It is still not clear why some alcoholic patients acquire
Different mechanisms are probably involved in different alcocertain organ-specific complications of alcoholism hol-induced end organ diseases, such as those in the liver, whereas other alcoholic patients acquire different ones.
pancreas, heart and neuromuscular system. It is still not As we know the liver alcohol dehydrogenase (ADH), clear why some alcoholic patients acquire certain organ-spealdehyde dehydrogenase (ALDH), and cytochrome cific complications of alcoholism, whereas other alcoholics ac-P4502E1 (P4502E1) are polymorphic at the ADH2, ADH3, quire different ones.
and ALDH2 loci and the 5-flanking region of the
Alcohol is metabolized in the hepatocyte via three path-P4502E1. The aim of this study was to investigate the ways: the alcohol dehydrogenase (ADH) pathway in the cytodifferences between Chinese alcoholic patients with cirsol, the microsomal ethanol oxidizing system in the endoplasrhosis and acute pancreatitis by studying the genetic mic reticulum, and catalase in the peroxisomes. ADH and polymorphisms of ADH2, ADH3, ALDH2, and P4502E1.
the microsomal ethanol oxidizing system produce specific Genotyping of ADH2, ADH3, ALDH2, and P4502E1 was metabolic and toxic disturbances, and all three pathways reperformed using polymerase chain reaction-restriction sult in the production of acetaldehyde, which then is metabofragment length polymorphism (PCR-RFLP) methods on lized by aldehyde dehydrogenase (ALDH) into acetate. [2] Acperipheral white blood cell DNA from 75 alcoholic ciretaldehyde, a metabolite more toxic than alcohol itself, is one rhotic patients, 48 acute alcoholic pancreatitis patients, of several factors implicated in the onset or development of 19 heavy drinkers without liver disease or pancreatitis, cirrhosis. 5 Genetic polymorphisms in ADH2, ADH3, and and 235 controls. The results showed that the frequen-ALDH2 and in the 5-flanking region of the human cytocies of the alleles ADH2*1 and ALDH2*1 in the alcoholic chrome P4502E1 gene (P4502E1) and its ethnic variations cirrhotic patients were significantly higher than those have been reported. [2][7][9][10][11][12][13][14] A number of studies have looked for in the nonalcoholic controls. In acute alcoholic pancredifferences in alcohol metabolizing enzymes to explain susatitis patients, only the frequency of allele ALDH2*1, not ceptibility to alcoholism and to alcohol-induced liver dis-ADH2*1 was significantly higher than in the nonalcoease. [9][10][11][12][15][16][17][18] We previously reported that the ADH2*1, holic controls. The allele frequency of ADH2*1 in acute ADH3*2, and ALDH2*1 genes can affect predisposition to pancreatitis patients was significantly lower (P Γ΅ .01) alcoholism in Chinese patients. 15 In that study, we investithan in alcoholic cirrhotic patients. The daily amount of gated only alcohol-induced cirrhotic patients but no other alcohol consumption was significantly lower in patients subpopulation of alcoholic patients with different organ comwith acute pancreatitis than in patients with cirrhosis plications such as alcohol-induced acute pancreatitis. (P Γ΅ .0005). The genotype distributions of P4502E1, de-Whether the allele frequencies of alcohol metabolizing entected by RsaI and PstI, were not different among alcozyme genes in patients with alcohol-induced cirrhosis and holic cirrhotic patients, alcoholic pancreatitis patients, alcohol-induced acute pancreatitis are different or not is unheavy drinker, and nonalcoholic controls. In conclusion, clear. In another study which included a small number of ALDH2*1 is the most important alcohol metabolizing patients with acute alcoholic pancreatitis (n Γ 23), we regene affecting predisposition to alcoholism whereas the ported that the amount of daily alcohol consumption was ADH2*2 gene may influence susceptibility to acute alcosignificantly lower in patients with alcohol-induced acute holic pancreatitis. The patients with alcohol-induced pancreatitis than with alcoholic cirrhosis. 12 In this study, we cirrhosis and with alcohol-induced acute pancreatitis wanted to evaluate whether the drinking behavior in a speare of two different subpopulations. (HEPATOLOGY cific subpopulation of alcoholic patients is influenced by ge-1997;25:112-117.) netic polymorphisms of alcohol metabolizing enzyme and whether the allele frequencies of alcohol metabolizing enzymes genes are different in subpopulations of alcoholic patients with certain specific organ complications. The genotypes of ADH2, ADH3, and ALDH2 and the RsaI and PstI
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