Abstract

e24107 Background: Capecitabine is a prodrug activated to its cytotoxic form 5-fluorouracil by thymidine phosphorylase whose active metabolites inhibit DNA synthesis by reducing thymidine production and also inhibits RNA and protein synthesis by competing with uridine triphosphate. Capecitabine is used in many types of tumors and its main reported side effects are diarrhea, hand-foot syndrome and hematologic toxicity. Methods: Retrospective analysis of a cohort of patients visited in a private hospital in Mexico City, that has a basal triglyceride profile and at least two determinations during treatment with capecitabine with or without oxaliplatin. Results: We analyzed 14 patients with a mean age of 55 years (IQR 40-73), 12 patients with colorectal cancer, 78.5% in the adjuvant setting, a half of patients with capecitabine monotherapy and the other half in combination with oxaliplatin. Comorbidities as overweight/obesity were seen in a half of the patients, diabetes in 21.4% and hypertriglyceridemia at baseline in 57.1% of patients all of them G1. The mean baseline glucose was 99.5 mg/dl (IQR 74-174), the mean baseline cholesterol was 180.8 mg/dl (IQR 85-243), the mean baseline triglycerides was 153.3 mg/dl (IQR 85-243). During capecitabine treatment a total of 85.7% of patients developed hypertriglyceridemia: G3/4 of 21.4%, G2 of 28.5%, G1 of 35.7%. No patient developed a serious complication associated with hypertriglyceridemia such as pancreatitis. There was no association between monotherapy or combination treatment with oxaliplatin, of patients with grade ≥2 hypertriglyceridemia, five received capecitabine monotherapy and two in combination with oxaliplatin. Also, no association was found among the highest levels of cholesterol, glucose, disease stage, age or body mass index. All of the 6 patients with normal baseline triglycerides developed hypertriglyceridemia 66.6% G1 and 33.3% G2. All the patients who present with hypertriglyceridemia G3/4 had baseline hypertriglyceridemia and 66.6% also diabetes. Conclusions: This analysis shows the high prevalence of hypertriglyceridemia associated with the use of capecitabine as monotherapy or combined with oxaliplatin in a Mexican cohort, with an incidence of 21.4% of hypertriglyceridemia G3/4 having the pre-existing hypertriglyceridemia and diabetes as risk factors. The cause of the worsening of the lipid profile requires more research but justify lipid profile at baseline and during the treatment with capecitabine. Due to the small size of the sample, the findings need to be confirmed with a prospective study with a larger number of patients.

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