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Sir, We read with great interest the study of Michie et al (2010) evaluating capecitabine-induced hypertriglyceridaemia (CIHT). The authors suggest that it should be classified as a common adverse effect and we fully agree with their recommendation for targeted screening in patients with diabetes or pre-existing hyperlipidaemia. Here we report an additional case of severe CIHT in a patient with pre-existing hyperlipidaemia to focus attention on possible mechanisms. A 50-year-old woman with a history of breast cancer, treated by surgery and hyperlipidaemia stabilised with pravastatin, was diagnosed in January 2009 with a progression of her breast cancer. Before receiving carboplatin, TAXOL (Bristol Myers Squibb, France) and bevacizumab, cholesterolaemia level was 6.68 mmol l−1 (2.59 g l−1) and triglyceridemia level was 2.51 mmol l−1 (2.20 g l−1) (Figure 1). During the 6-month treatment, a transient increase in triglycerides was observed and pravastatin was replaced by rosuvastatin. In July 2009, bevacizumab alone was administered once a week as maintenance treatment. In August 2009, because of secondary gastric and ganglion infiltration, carboplatin and taxol were stopped and the patient received a combination of capecitabine and bevacizumab. Nine cycles of this treatment were scheduled. After six cycles, in December 2009, highly raised triglycerides (26.77 mmol l−1 (23.48 g l−1)) and slightly raised cholesterol levels (8.75 mmol l−1 (3.39 g l−1)) were observed, without any clinical sign of pancreatitis. At no time had the patient reported alcohol consumption or dietary changes and no weight gain was observed. The replacement of rosuvastatin by fenofibrate was followed 1 week later by a significant decrease in her triglyceride level to 6.26 mmol l−1 (5.49 g l−1). However, 1 month later, the triglycerides level again increased to 11.33 g l−1 (9.94 mmol l−1). Owing to both side effects and progression of her cancer, capecitabine and bevacizumab were stopped and replaced by fulvestrant (FASLODEX; Astrazeneca, Cheshire, UK). A return to baseline triglyceridaemia values (3.27 mmol l−1 (2.87 g l−1)) was observed within 2 months. Our case fulfils the criteria for a probable case of CIHT. Concomitant bevacizumab was not suspected because the increase in triglycerides during first-line chemotherapy resolved spontaneously, whereas treatment with rosuvastatin was unchanged. We would like to propose two ways to improve our understanding of CIHT:  A lipid survey should be mandatory before initiation of capecitabine or other 5-FU prodrugs. Patients with dyslipidaemia should be closely monitored and further studied.

Severe hypertriglyceridaemia during treatment with capecitabine