Roy M T, First M R, Myre S A, Cacini W
Ther Drug Monit. 1982;4(1):77-9. doi: 10.1097/00007691-198204000-00011.
Significant elevation of serum creatinine concentration and reduction in creatinine clearance have been reported following cotrimoxazole therapy in patients with normal and impaired renal function. Both components of co-trimoxazole, trimethoprim and sulfamethoxazole, have been proposed as the causative agent. Ten healthy male volunteers were treated for seven days with either sulfamethoxazole (5 subjects) or co-trimoxazole (5 subjects) in the usual recommended doses. After a one-week recovery period, the subjects were allocated to the alternate treatment regimen for another seven days. Cotrimoxazole caused a mean elevation in the serum creatinine concentration of 0.12 mg/dl over the base-line value (p less than 0.05). Sulfamethoxazole produced an insignificant fall in the serum creatinine level. The increase in the serum creatinine concentration induced by co-trimoxazole was reversed seven days after discontinuation of the drug. From this study, it can be concluded that either trimethoprim alone or an interaction between trimethoprim and sulfamethoxazole is responsible for the increase in serum creatinine observed following co-trimoxazole therapy and that sulfamethoxazole alone is not the causative agent.
据报道，在肾功能正常和受损的患者中，服用复方新诺明治疗后血清肌酐浓度显著升高，肌酐清除率降低。复方新诺明的两种成分，甲氧苄啶和磺胺甲恶唑，都被认为是致病因素。10名健康男性志愿者以常用推荐剂量接受了7天的磺胺甲恶唑（5名受试者）或复方新诺明（5名受试者）治疗。经过一周的恢复期后，受试者被分配接受另一种治疗方案，为期7天。复方新诺明使血清肌酐浓度比基线值平均升高0.12mg/dl（p小于0.05）。磺胺甲恶唑使血清肌酐水平出现不显著下降。复方新诺明引起的血清肌酐浓度升高在停药7天后恢复正常。从这项研究可以得出结论，单独的甲氧苄啶或甲氧苄啶与磺胺甲恶唑之间的相互作用是复方新诺明治疗后血清肌酐升高的原因，而单独的磺胺甲恶唑不是致病因素。
