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二氢嘧啶脱氢酶家族性缺乏。家族性嘧啶血症和严重5-氟尿嘧啶诱导毒性的生化基础。

Familial deficiency of dihydropyrimidine dehydrogenase. Biochemical basis for familial pyrimidinemia and severe 5-fluorouracil-induced toxicity.

作者信息

Diasio R B, Beavers T L, Carpenter J T

机构信息

Division of Clinical Pharmacology, University of Alabama, Birmingham 35294.

出版信息

J Clin Invest. 1988 Jan;81(1):47-51. doi: 10.1172/JCI113308.

Abstract

Severe neurotoxicity due to 5-fluorouracil (FUra) has previously been described in a patient with familial pyrimidinemia. We now report the biochemical basis for both the pyrimidinemia and neurotoxicity in a patient we have recently studied. After administration of a "test" dose of FUra (25 mg/m2, 600 microCi[6-3H]FUra by intravenous bolus) to a patient who had previously developed neurotoxicity after FUra, a markedly prolonged elimination half-life (159 min) was observed with no evidence of FUra catabolites in plasma or cerebrospinal fluid and with 89.7% of the administered dose being excreted into the urine as unchanged FUra. Using a sensitive assay for dihydropyrimidine dehydrogenase in peripheral blood mononuclear cells, we demonstrated complete deficiency of enzyme activity in the patient and partial deficiency of enzyme activity in her father and children consistent with an autosomal recessive pattern of inheritance. Patients who are deficient in this enzyme are likely to develop severe toxicity after FUra administration.

摘要

先前曾有一名患有家族性嘧啶血症的患者出现了由5-氟尿嘧啶(FUra)引起的严重神经毒性。我们现在报告我们最近研究的一名患者嘧啶血症和神经毒性的生化基础。在给一名先前使用FUra后出现神经毒性的患者静脉推注一剂“试验”剂量的FUra(25mg/m²,600微居里[6-³H]FUra)后,观察到消除半衰期明显延长(159分钟),血浆或脑脊液中没有FUra分解代谢物的证据,且给药剂量的89.7%以未改变的FUra形式排泄到尿液中。使用对外周血单核细胞中二氢嘧啶脱氢酶的灵敏检测方法,我们证明该患者酶活性完全缺乏,其父亲和子女酶活性部分缺乏,符合常染色体隐性遗传模式。缺乏这种酶的患者在使用FUra后可能会出现严重毒性。

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