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DPYD genotype-guided fluoropyrimidines dose: is it ready for prime time?
Annals of Oncology ( IF 50.5 ) Pub Date : 2017-12-01 , DOI: 10.1093/annonc/mdx632
D Páez 1 , R Salazar 2 , J Tabernero 3
Affiliation  

For over 50 years, fluoropyrimidines have been the cornerstone of anticancer drugs for various types of solid cancers. Treatment with these drugs—5-fluorouracil (FU) and its oral prodrugs, capecitabine and tegafur—is generally well-tolerated, except in a small proportion of patients who develop severe and life-threatening early toxicity. This toxicity is mainly associated with a deficiency of the primary fluoropyrimidine detoxifying enzyme, dihydropryrimidine dehydrogenase (DPD) [1]. The drug labels of FU and capecitabine state DPD deficiency as a contraindication, but they give no warning for the 3%–8% of the population who are partially DPD deficient.

中文翻译:

DPYD基因型指导的氟嘧啶剂量:是否准备好接受黄金时段?

超过50年来,氟嘧啶一直是用于各种类型实体癌的抗癌药物的基石。这些药物(5-氟尿嘧啶(FU)及其口服前药,卡培他滨和替加福)的治疗耐受性一般良好,只有一小部分患者出现严重且危及生命的早期毒性。这种毒性主要与氟代嘧啶脱氧酶二氢嘧啶脱氢酶(DPD)的缺乏有关[1]。FU和卡培他滨的药物标签规定了DPD缺乏症为禁忌,但对于部分DPD缺乏的3%–8%的人群,它们没有给出警告。
更新日期:2017-10-05
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