Metabolism of procainamide and p-aminobenzoic acid in patients with chronic liver disease.
Procainamide acetylation and hydrolysis, procainamide-derived p-amino-benzoic acid acetylation, and plasma hydrolysis of procaine were studied in normal volunteers and in 20 patients with chronic liver disease, Impairment of procainamide acetylation was evident in the patients, but no correlations were demonstrable between the degree of impairment and the severity of the disease. On the other hand, procainamide hydroylsis was diminished in liver disease, and as indicated by depression of serum albumin levels and plasma prothrombin activity this alteration did correlate with the degree of impairment of liver function. Procaine hydrolysis in plasma was also affected, the mean in vitro plasma half-life being prolonged in the patients with liver disease and correlating with the degree of hepatic impairment. A correlation of procainamide hydrolysis with procaine hydrolysis was also observed. Finally, acetylation of procainamide-derived p-aminobenzoic acid appeared to increase in patients with liver disease, the degree of acetylation increasing with decreasing procainamide hydrolysis capacity.
D010129:4-Aminobenzoic Acid / Q000378:metabolism*; D000107:Acetylation; D000328:Adult; D000368:Aged; D062365:Aminobenzoates / Q000378:metabolism*; D002908:Chronic Disease; D005260:Female; D006207:Half-Life; D006801:Humans; D006868:Hydrolysis; D008107:Liver Diseases / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D011342:Procainamide / Q000378:metabolism*; D011516:Prothrombin / Q000378:metabolism; D012709:Serum Albumin / Q000378:metabolism
D062365:Aminobenzoates; D012709:Serum Albumin; D011516:Prothrombin; D011342:Procainamide; D010129:4-Aminobenzoic Acid