Document Detail


Effect of ethanol on metabolism of purine bases (hypoxanthine, xanthine, and uric acid).
MedLine Citation:
PMID:  15936302     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
There are many factors that contribute to hyperuricemia, including obesity, insulin resistance, alcohol consumption, diuretic use, hypertension, renal insufficiency, genetic makeup, etc. Of these, alcohol (ethanol) is the most important. Ethanol enhances adenine nucleotide degradation and increases lactic acid level in blood, leading to hyperuricemia. In beer, purines also contribute to an increase in plasma uric acid. Although rare, dehydration and ketoacidosis (due to ethanol ingestion) are associated with the ethanol-induced increase in serum uric acid levels. Ethanol also increases the plasma concentrations and urinary excretion of hypoxanthine and xanthine via the acceleration of adenine nucleotide degradation and a possible weak inhibition of xanthine dehydrogenase activity. Since many factors such as the ALDH2*1 gene and ADH2*2 gene, daily drinking habits, exercise, and dehydration enhance the increase in plasma concentration of uric acid induced by ethanol, it is important to pay attention to these factors, as well as ingested ethanol volume, type of alcoholic beverage, and the administration of anti-hyperuricemic agents, to prevent and treat ethanol-induced hyperuricemia.
Authors:
Tetsuya Yamamoto; Yuji Moriwaki; Sumio Takahashi
Publication Detail:
Type:  Journal Article; Review     Date:  2005-03-29
Journal Detail:
Title:  Clinica chimica acta; international journal of clinical chemistry     Volume:  356     ISSN:  0009-8981     ISO Abbreviation:  Clin. Chim. Acta     Publication Date:  2005 Jun 
Date Detail:
Created Date:  2005-06-06     Completed Date:  2005-08-25     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  1302422     Medline TA:  Clin Chim Acta     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  35-57     Citation Subset:  IM    
Affiliation:
Division of Endocrinology and Metabolism, Department of Internal Medicine, Hyogo College of Medicine, Mukogawa-cho 1-1. Nishinomiya, Hyogo 663-8501, Japan. tetsuya@hyo-med.ac.jp
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MeSH Terms
Descriptor/Qualifier:
Acetyl Coenzyme A / biosynthesis
Alcohol Dehydrogenase / genetics
Aldehyde Dehydrogenase / genetics
Ethanol / blood,  pharmacology*
Humans
Hyperuricemia / prevention & control,  therapy
Hypoxanthine / metabolism*
Lactic Acid / blood
NAD / metabolism
Oxidation-Reduction
Uric Acid / metabolism*
Xanthine / metabolism*
Xanthine Dehydrogenase / antagonists & inhibitors
Chemical
Reg. No./Substance:
50-21-5/Lactic Acid; 53-84-9/NAD; 64-17-5/Ethanol; 68-94-0/Hypoxanthine; 69-89-6/Xanthine; 69-93-2/Uric Acid; 72-89-9/Acetyl Coenzyme A; EC 1.1.1.1/ADH1B protein, human; EC 1.1.1.1/Alcohol Dehydrogenase; EC 1.17.1.4/Xanthine Dehydrogenase; EC 1.2.1.3/ALDH2 protein, human; EC 1.2.1.3/Aldehyde Dehydrogenase

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