Testing for 5-FU Toxicity: DPD Mechanism of Action
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5-Fluorouracil and capecitabine are two of the most frequently prescribed chemotherapeutic drugs for patients with cancers of the gastrointestinal tract, breast, and head and neck. In most patients, nearly 85% of 5-FU administered is metabolized by dihydropyrimidine dehydrogenase (DPD), with about 15% of the dose remaining active.
However, individuals with complete or partial DPD deficiency have a strongly reduced capacity to metabolize 5-FU and therefore experience severe, and sometimes life-threatening, toxic effects from the increased levels of active drug.
Testing for DPD deficiency, and thus identifying patients with an increased risk for toxicity to 5-FU and capecitabine, lends itself to the unique opportunity to prescreen patients and to minimize, or even eliminate, these toxicities. Furthermore, DPD deficiency is now recognized formally as a contraindication for the use of capecitabine and other fluoropyrimidines, lending additional support to the necessity of developing a prescreening program for a DPD deficiency.1,2,3
- Van Kuilenburg. Screening for Dihydropyrimidine Dehydrogenase Deficiency: To Do or Not To Do, That’s The Question. Cancer Investigation. 2006;24:215-17.
- http://www.fda.gov/medwatch/SAFETY/2003/mar03.htm#xeloda
- http://www.merck.com/mmpe/lexicomp/fluorouracil.html
Additional Articles
- Testing for 5-FU Toxicity: DPYD (DPD) and TYMS (TS)
- Testing for 5-FU Toxicity: DPYD
- Testing for 5-FU Toxicity: TYMS (TS)
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