[Alcohol ingestion and hyperuricemia].
Purine nucleotide degradation during ethanol catabolism, inhibition of renal excretion of urate by lactic acid, and high purine content of certain kinds of beverage are responsible for the elevation of serum uric acid level following alcohol drinking. It is well documented that rapid consumption of ATP produces uric acid via purine nucleotide degradation. Since individuals with ALDH2*1 can catalyze ethanol readily, they consume large amount of ATP, and thus produce more hypoxanthine than those with ALDH2*2. Thus, daily drinker and heavy drinker tend to readily induce hyperuricemia after alcohol ingestion. A high purine content in beer may contribute to the increasing frequency of hyperuricemia. Restriction of any kind of alcohol beverages, especially beer, is necessary in the medical control of patients with gout or hyperuricemia.
Yamanaka
H
H
Institute of Rheumatology, Tokyo Women's Medical College.
D000255:Adenosine Triphosphate / Q000378:metabolism; D000428:Alcohol Drinking / Q000009:adverse effects*; D000444:Aldehyde Dehydrogenase / Q000235:genetics / Q000378:metabolism; D001515:Beer / Q000009:adverse effects; D000431:Ethanol / Q000378:metabolism; D005260:Female; D005838:Genotype; D006073:Gout / Q000209:etiology*; D006801:Humans; D019271:Hypoxanthine / Q000378:metabolism; D011247:Pregnancy; D011685:Purine Nucleotides / Q000378:metabolism; D014527:Uric Acid / Q000097:blood*
D011685:Purine Nucleotides; D014527:Uric Acid; D019271:Hypoxanthine; D000431:Ethanol; D000255:Adenosine Triphosphate; D000444:Aldehyde Dehydrogenase