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However, 31–34% of patients encountered grade 3–4 adverse events (AEs) with 0.5% mortality often-necessitating dose reduction or discontinuation [5]. A significant proportion of these AEs are likely to be the result of inter-individual genetic variation, in particularly such as dihydropyrimidine dehydrogenase (DPYD). DPYD gene encodes DPD, the ratelimiting enzyme responsible for catabolism of 5-FU and is responsible for >85% of 5-FU elimination. Deficiency of DPD due to DPYD polymorphism gives rise to severe 5-FU AEs from reduced catabolism [6]. This pharmacogenetic ‘DPD syndrome’ manifests typically as severe or fatal diarrhea, mucositis/stomatitis, myelosuppression and even rare toxicities, such as hepatitis, encephalopathy and acute cardiac ischemia following first or second dose of 5-FU [6–8]. DPYD mutations are found in 50% of severe 5-FU toxicity cases [6–10]. Different methods have been developed to test DPYD abnormalities [11,12].

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Pharmacogenetic Variants in the DPYD and TYMS Genes are Clinically Significant Predictors of Fluoropyrimidine Toxicity: Are We Ready for Use in our Clinical Practice