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本文引用的文献

1
Protein measurement with the Folin phenol reagent.使用福林酚试剂进行蛋白质测定。
J Biol Chem. 1951 Nov;193(1):265-75.
2
CEREBELLAR ATAXIA ASSOCIATED WITH FLUORINATED PYRIMIDINE THERAPY.与氟嘧啶治疗相关的小脑共济失调
Cancer Chemother Rep. 1964 Sep;41:15-8.
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THE REDUCTION OF THYMINE BY HUMAN LEUKOCYTES.
Arch Biochem Biophys. 1964 Jan;104:146-9. doi: 10.1016/s0003-9861(64)80046-1.
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"Organic brain syndrome" secondary to 5-fluorouracil toxicity.继发于5-氟尿嘧啶毒性的“器质性脑综合征”
Dis Colon Rectum. 1981 Mar-Apr;24(2):130-1. doi: 10.1007/BF02604302.
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Rapid catabolism of 5-fluorouracil in freshly isolated rat hepatocytes as analyzed by high performance liquid chromatography.通过高效液相色谱法分析新鲜分离的大鼠肝细胞中5-氟尿嘧啶的快速分解代谢。
J Biol Chem. 1982 Jul 25;257(14):8171-6.
6
New defects of pyrimidine metabolism.嘧啶代谢的新缺陷
Adv Exp Med Biol. 1984;165 Pt A:109-14. doi: 10.1007/978-1-4684-4553-4_19.
7
Dihydropyrimidine dehydrogenase deficiency leading to thymine-uraciluria. An inborn error of pyrimidine metabolism.
Clin Chim Acta. 1984 Aug 31;141(2-3):227-34. doi: 10.1016/0009-8981(84)90014-7.
8
Elevated urine, blood and cerebrospinal fluid levels of uracil and thymine in a child with dihydrothymine dehydrogenase deficiency.一名患有二氢胸腺嘧啶脱氢酶缺乏症的儿童尿液、血液和脑脊液中尿嘧啶和胸腺嘧啶水平升高。
Clin Chim Acta. 1984 Jul 31;140(3):247-56. doi: 10.1016/0009-8981(84)90206-7.
9
Biochemical basis for fluorouracil neurotoxicity. The role of Krebs cycle inhibition by fluoroacetate.氟尿嘧啶神经毒性的生化基础。氟乙酸对三羧酸循环抑制的作用。
Arch Neurol. 1970 Aug;23(2):155-60. doi: 10.1001/archneur.1970.00480260061008.
10
Biochemical basis of the acute cerebellar syndrome in 5-fluorouracil chemotherapy.5-氟尿嘧啶化疗所致急性小脑综合征的生化基础
Trans Am Neurol Assoc. 1969;94:290-2.

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.

DOI:10.1172/JCI113308
PMID:3335642
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC442471/
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。