Woody R C, Brewster M A
Department of Pediatrics, University of Maryland, Baltimore 21201.
Dev Med Child Neurol. 1990 Jul;32(7):639-42. doi: 10.1111/j.1469-8749.1990.tb08549.x.
A child with dihydropteridine reductase (DHPR) deficiency developed signs of dopamine insufficiency after being given trimethoprim-sulfamethoxazole (TMP-SMX). She recovered function after the antibiotic was stopped, which suggests that it adversely influenced dopamine metabolism in the CNS. The authors speculate that TMP, a dihydrofolate reductase inhibitor, was the major cause of the patient's deterioration, and suggest that it and other dihydrofolate inhibitors, notably methotrexate, are contra-indicated for patients with DHPR deficiency.
一名患有二氢蝶啶还原酶(DHPR)缺乏症的儿童在服用甲氧苄啶-磺胺甲恶唑(TMP-SMX)后出现多巴胺不足的症状。停用抗生素后她的功能恢复,这表明该药物对中枢神经系统的多巴胺代谢产生了不利影响。作者推测,作为二氢叶酸还原酶抑制剂的甲氧苄啶是导致患者病情恶化的主要原因,并建议患有DHPR缺乏症的患者禁用该药物及其他二氢叶酸抑制剂,尤其是甲氨蝶呤。