Abstract
Thank you for the recently published paper “Cost Implication of Reactive Versus Prospective Testing for DPD Deficiency in Patients with Colorectal Cancer: A Single Institution Experience.” We appreciate this straightforward, informative communication and important contribution in the care and safety of patients with cancer treated with 5-fluorouracil (5-FU) and capecitabine. This paper stimulated a number of questions, and we wonder if the source data collected by the authors may include some of the answers. When did the grade 3 or 4 toxicity appear in each patient? Was it “early onset” (ie, within days of the first administration of 5-FU or during the first course of capecitabine treatment)? Or was it cumulative toxicity (after multiple courses of 5FU or capecitabine)? In patients who developed grade 3 or 4 toxicities and did not have a discernable DPYD mutation, were other nongenetic causative or contributory factors identifiable? For example, renal function, body mass index, age? (eg, see Meulendijks D, et al. Eur J Cancer. 2016; 54:120-130) Were assessments made of any other potential mutations, such as TYMS, MTHFR, or CDA, that can result in increased toxicity? Were the types of toxicity in the patients who did not have DPYD mutations comparable to those who did—primarily gastrointestinal and hematologic? Did any patients experience cardiotoxicity? (eg, see Polk A, et al. BMJ Open. 2016; 6(10); Sara JD, et al. Ther Adv Med Oncol. 2018. 10: doi:1758835918780140)
We have been working in this field for many years to better understand such toxicities and to provide treatment for patients receiving 5-FU or capecitabine who develop severe toxicity or who have been overdosed with these chemotherapy agents. Uridine triacetate (Vistogard) was approved by the US Food and Drug Administration in late 2015 for this purpose. We applaud the efforts of the authors to ensure the safety of patients with cancer receiving fluoropyrimidine treatment and thank you for this important publication.