Pharmacokinetics, metabolism, and renal excretion of sulfadimidine and its N4-acetyl and hydroxy metabolites in humans.
Sulfadimidine is acetylated and hydroxylated in humans. The hydroxylation pathways account for 10-20% of the dose, leaving the acetylation as the major metabolic pathway. The hydroxylation pathways are independent of the acetylator phenotype. The plasma concentration-time curve of sulfadimidine in fast acetylators is biphasic, with half-lives of 1.7 and 5.4 h, whereas that in slow acetylators is monophasic, with a half-life of 7.6 h. Hydroxylation of a methyl group in sulfadimidine lowers the protein binding from 90 to 60%, while acetylation does not affect the protein binding. Methyl hydroxylation markedly increases the renal clearance.
D000107:Acetylation; D000328:Adult; D005260:Female; D006207:Half-Life; D006801:Humans; D007700:Kinetics; D008297:Male; D010641:Phenotype; D011485:Protein Binding; D013418:Sulfamethazine / Q000031:analogs & derivatives* / Q000378:metabolism / Q000652:urine*
C032633:N-acetylsulfamethazine; D013418:Sulfamethazine; C046744:5-hydroxysulfadimidine