Purpose
Metastatic breast cancer (mBC) patients with
DPYD
genetic variants linked to loss of dihydropyrimidine dehydrogenase (DPD) activity are at risk of severe capecitabine-associated toxicities. However, prospective
DPYD
genotyping has not yet been implemented in routine clinical practice. Following a previous internal review in which two patients underwent lengthy hospitalisations whilst receiving capecitabine, and were subsequently found to be DPD deficient, we initiated routine
DPYD
genotyping prior to starting capecitabine. This study evaluates the clinical application of routine
DPYD
screening at a large cancer centre in London.
Methods
We reviewed medical records for consecutive patients with mBC who underwent DPYD genotyping before commencing capecitabine between December 2014 and December 2017. Patients were tested for four
DPYD
variants associated with reduced DPD activity.
Results
Sixty-six patients underwent
DPYD
testing. Five (8.4%) patients were found to carry
DPYD
genetic polymorphisms associated with reduced DPD activity; of these, two received dose-reduced capecitabine. Of the 61 patients with
DPYD
wild-type, 14 (23%) experienced grade 3 toxicities which involved palmar–plantar erythrodysesthesia (65%), and gastrointestinal toxicities (35%); no patient was hospitalised due to toxicity.
Conclusions
Prospective
DPYD
genotyping can be successfully implemented in routine clinical practice and can reduce the risk of severe fluoropyrimidine toxicities.
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