title: Capecitabine-induced severe hypertriglyceridemia: report of two cases.
abstract: OBJECTIVE
  To report 2 cases of severe hypertriglyceridemia associated with the use of oral capecitabine.
  
  
  METHODS
  The first patient was a 73-year-old woman with metastatic breast carcinoma who received capecitabine 2500 mg/m2/day in 2 divided doses for 2 weeks followed by a one week rest period. The baseline triglyceride level was 324 mg/dL; after 2 cycles of capecitabine, levels increased to 916 mg/dL. Although lipid-lowering treatment was initiated, triglyceride levels peaked at 1782 mg/dL by the end of the seventh cycle. Eight weeks after capecitabine treatment was stopped, triglyceride levels decreased to 118 mg/dL. The second patient was a 59-year-old man with metastatic colorectal carcinoma who was placed on capecitabine treatment at a dosage of 2500 mg/m2/day in 2 divided doses for 2 weeks followed by a one week rest period. The baseline triglyceride level was 244 mg/dL; levels peaked at 1455 mg/dL at the end of the fifth cycle. Capecitabine treatment was discontinued due to disease progression, and triglyceride levels decreased to 154 mg/dL after 11 weeks.
  
  
  CONCLUSIONS
  The most frequently reported adverse effects of capecitabine are gastrointestinal and hematologic effects and palmar-plantar erythrodysesthesia. Drug-induced hyperlipidemia may appear more readily in individuals with hereditary lipoprotein lipase deficiency because decreased lipoprotein lipase activity might make these individuals more susceptible to a rise in triglyceride levels. The Naranjo probability scale indicated a probable relationship between capecitabine and severe hypertriglyceridemia.
  
  
  CONCLUSIONS
  Capecitabine should be prescribed with care, especially in patients with preexisting hypertriglyceridemia. The question of whether capecitabine actually causes hypertriglyceridemia needs careful consideration, and the possible mechanism by which it may cause this adverse effect requires further investigation.
authors.affiliation: Department of Internal Medicine, Faculty of Medicine, Hacettepe University, Ankara, Turkey. mkurt@hacettepe.edu.tr
authors.forename: Mevlut
authors.initials: M
authors.lastname: Kurt
authors.forename: Melih O
authors.initials: MO
authors.lastname: Babaoglu
authors.forename: Umit
authors.initials: U
authors.lastname: Yasar
authors.forename: Ali
authors.initials: A
authors.lastname: Shorbagi
authors.forename: Nilufer
authors.initials: N
authors.lastname: Guler
mesh_terms: D000368:Aged; D000964:Antimetabolites, Antineoplastic / Q000008:administration & dosage / Q000009:adverse effects* / Q000627:therapeutic use; D001943:Breast Neoplasms / Q000188:drug therapy; D000069287:Capecitabine; D015179:Colorectal Neoplasms / Q000188:drug therapy; D003841:Deoxycytidine / Q000008:administration & dosage / Q000009:adverse effects / Q000031:analogs & derivatives* / Q000627:therapeutic use; D005260:Female; D005472:Fluorouracil / Q000031:analogs & derivatives; D006801:Humans; D015228:Hypertriglyceridemia / Q000097:blood / Q000139:chemically induced*; D008297:Male; D008875:Middle Aged; D014280:Triglycerides / Q000097:blood
chemical_list: D000964:Antimetabolites, Antineoplastic; D014280:Triglycerides; D003841:Deoxycytidine; D000069287:Capecitabine; D005472:Fluorouracil