Francois Poumeaud*, Arthur Glenet, Marion Montastruc, Blandine Delaunay, Beatrice Laudet and Florence Dalenc
Severe adverse events with both 5-Fluorouracile (5-FU) and capecitabine, one of its prodrugs, have been extensively studied and primarily related to a partial or complete Dihydropyrimidine Dehydrogenase (DPD) deficiency. However, rare and atypical side effects such as hypertriglyceridemia might still occur in the absence of DPD deficiency. We report the case of a 61- year-old woman with early-stage triple negative breast cancer treated with adjuvant capecitabine. While having no phenotypic DPD deficiency, she developed severe Capecitabine-Induced Hypertriglyceridemia (CIHT, 49 g/L) after four treatment cycles at a reduced dose (1000 mg/m2 ). Notably, the patient experienced only grade I hand-foot syndrome at initiation with no other capecitabine-associated toxicities. CIHT spontaneously resolved after interrupting treatment with no relapse and no further treatment. We suggest that Carboxylesterase (CES1), an enzyme involved in both capecitabine and lipid metabolism, might contribute to such toxicity. Further studies are required to validate this hypothesis.