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柳氮磺胺吡啶(简写SAA)原先作为类风湿性关节炎的治疗药开发的,现在主要用于炎症性肠病。SAA是由一分子水杨酸经偶氮键与一分子磺胺吡啶(SP)相联而成。此偶氮键可被结肠细菌断裂,释出5-氨基水杨酸(5-ASA)及SP。后者几乎全由结肠吸收,代谢,经尿排出,SAA的主要副反应均由其产生,且与其血浓度相关,因5-ASA极少从结肠吸收。1977年Azad Khan等发现,5-ASA是治疗溃疡性结肠炎的活性部分。 1.5-AgA和4-氨基水杨酸(4-ASA) 5-ASA口服后迅速由小肠吸收,经乙酰
Sulfasalazine (abbreviated SAA) was originally developed as a therapeutic drug for rheumatoid arthritis and is now mainly used for inflammatory bowel disease. SAA is a molecule of salicylic acid by azo bond with a molecule of sulfapyridine (SP) associated. This azo bond can be broken by colon bacteria releasing 5-aminosalicylic acid (5-ASA) and SP. The latter is almost exclusively absorbed, metabolized and excreted by the colon. The major side effects of SAA are produced by it and are correlated with its blood concentration, since 5-ASA is rarely absorbed from the colon. In 1977 Azad Khan et al. Found that 5-ASA is the active part of the treatment of ulcerative colitis. 1.5-AgA and 4-aminosalicylic acid (4-ASA) 5-ASA quickly absorbed by the small intestine after oral administration of acetyl