Gao-Hua Han1, Jun-Xing Huang2. 1. Department of Oncology, The People's Hospital of Taizhou, Taizhou Medical School, Jiangsu and Nantong University, Jiangsu, China. 2. Department of Oncology, The People's Hospital of Taizhou, Taizhou Medical School, Jiangsu and Nantong University, Jiangsu, China hjxtz@sina.cn.
Abstract
BACKGROUND: Capecitabine is a tumor-activated oral fluoropyrimidine used in breast and colorectal cancer. Hypertriglyceridemia associated with this drug has rarely been reported in the literature. METHODS: Two patients with colorectal carcinoma who developed capecitabine-induced hypertriglyceridemia (including a patient who developed hyperglycemia concurrently) were described, treatment modalities were discussed, and the literatures were reviewed. RESULTS: The first patient, a 43-year-old man, developed hyperlipidemia and hyperglycemia after two cycles of XELOX regimen chemotherapy for colorectal cancer. His triglyceride was 2.47 mmol/L (normal range 0.34-1.7 mmol/L) and total cholesterol was 6.93 mmol/L (normal range 3.12-5.9 mmol/L), while blood glucose was abnormal (fasting blood glucose was 10.58-11.9 mmol/L and 2 h postprandial glucose was 14.5-17.2 mmol/L) and glucose was positive in the urine(3+). The second patient, a 47-year-old woman, developed abnormalities in the lipid profile after the sixth cycle of XELOX regimen chemotherapy for colorectal cancer. Her serum triglyceride was 2.41 mmol/L (normal range 0.34-1.7 mmol/L), while the cholesterol level was 7.73 mmol/L (normal range 3.12-5.9 mmol/L). The profile of lipid improved gradually with reduced doses of capecitabine and was well restored after chemotherapy without any lipid-lowering agents. The Naranjo score for capecitabine-induced hypertriglyceridemia was 9 (definite). An analysis of the underlying pathogenic mechanisms was provided. CONCLUSION: It is important of physicians and pharmacists to be aware of the possibility of dyslipidemia, particularly hypertriglyceridemia induced by capecitabine.
BACKGROUND:Capecitabine is a tumor-activated oral fluoropyrimidine used in breast and colorectal cancer. Hypertriglyceridemia associated with this drug has rarely been reported in the literature. METHODS: Two patients with colorectal carcinoma who developed capecitabine-induced hypertriglyceridemia (including a patient who developed hyperglycemia concurrently) were described, treatment modalities were discussed, and the literatures were reviewed. RESULTS: The first patient, a 43-year-old man, developed hyperlipidemia and hyperglycemia after two cycles of XELOX regimen chemotherapy for colorectal cancer. His triglyceride was 2.47 mmol/L (normal range 0.34-1.7 mmol/L) and total cholesterol was 6.93 mmol/L (normal range 3.12-5.9 mmol/L), while blood glucose was abnormal (fasting blood glucose was 10.58-11.9 mmol/L and 2 h postprandial glucose was 14.5-17.2 mmol/L) and glucose was positive in the urine(3+). The second patient, a 47-year-old woman, developed abnormalities in the lipid profile after the sixth cycle of XELOX regimen chemotherapy for colorectal cancer. Her serum triglyceride was 2.41 mmol/L (normal range 0.34-1.7 mmol/L), while the cholesterol level was 7.73 mmol/L (normal range 3.12-5.9 mmol/L). The profile of lipid improved gradually with reduced doses of capecitabine and was well restored after chemotherapy without any lipid-lowering agents. The Naranjo score for capecitabine-induced hypertriglyceridemia was 9 (definite). An analysis of the underlying pathogenic mechanisms was provided. CONCLUSION: It is important of physicians and pharmacists to be aware of the possibility of dyslipidemia, particularly hypertriglyceridemia induced by capecitabine.