[Hyperammonemia and hepatic encephalopathy in cirrhotics receiving spironolactone (author's transl)].
The aim of this study was to specify the mechanism of hepatic encephalopathy which may occur in some cirrhotics treated by Spironolactone. In 31 cirrhotics with ascite, this diuretic induced a significant increase in arterial ammonemia; 8 patients developed an impending hepatic coma which was associated with ammonemia levels significantly higher than those observed in the patients without encephalopathy at the end of the treatment. Hyperammonemia induced by Spironolactone does not result from a muscular, renal or hepatic ammonia production but seems related to an increased intestinal ammoniagenesis which which is secondary to the bacterial hydrolysis of urea in the colon; indeed, there is a significant correlation between the ammonemia increase and the simultaneous rise in blood urea during treatment.
D000328:Adult; D000368:Aged; D000641:Ammonia / Q000097:blood* / Q000378:metabolism; D006501:Hepatic Encephalopathy / Q000139:chemically induced*; D006801:Humans; D007413:Intestinal Mucosa / Q000378:metabolism; D008103:Liver Cirrhosis / Q000188:drug therapy* / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D013148:Spironolactone / Q000009:adverse effects* / Q000494:pharmacology; D013268:Stimulation, Chemical; D014508:Urea / Q000378:metabolism; D014511:Uremia / Q000139:chemically induced
D013148:Spironolactone; D000641:Ammonia; D014508:Urea
Hyperammoniémie et encéphalopathie hépatique chez les cirrhotiques traités par la spironolactone.