کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2579620 | 1130061 | 2007 | 5 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Pour ou contre le phénotypage/génotypage des patients traités par le 5-fluorouracile pour prévenir les effets indésirables ?
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کلمات کلیدی
موضوعات مرتبط
علوم پزشکی و سلامت
داروسازی، سم شناسی و علوم دارویی
فارماکولوژی، سم شناسی و اقلام دارویی (عمومی)
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
5-fluorouracil, (5-FU) is an antimetabolite used in many types of cancers. It has a narrow therapeutic index. More than 80% of administered 5-FU is detoxified in 5-fluoro-5,6-dihydrouracile (5-FUH2) by an enzyme: dihydropyrimidine dihydrogenase (DPD). Half life increased with DPD deficiency. Thus, patients presenting a partial or profound DPD deficiency have an increased risk of severe or lethal toxicity. DPD deficiency was estimated between 3 to 5% in the normal population. Different approaches have been developed: Pharmacogenetic on the DPD gene or pharmacologic measuring DPD activity. More than 30 mutations have been reported on this gene. The more common mutation is the slice-site mutation IVS14Â +Â 1GÂ >Â A. Analysis of the various mutations allowed to identify a population at risk with a DPD deficiency. DPD activity is determined in peripheral blood mononuclear cells. This assay offers the capability of identifying individuals who are completely deficient in DPD activity and those who are partially deficient. Assays to detect DPD deficiency are not used as a screening test to prevent 5-FU toxicity.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Thérapie - Volume 62, Issue 2, MarchâApril 2007, Pages 105-109
Journal: Thérapie - Volume 62, Issue 2, MarchâApril 2007, Pages 105-109
نویسندگان
Romain Coriat, Stanislas Chaussade,