Influence of 5-Fluorouracil on Serum Lipids

Stathopoulos, Georgios; Stergiou, George S.; Perrea-Kostarelis, Despina N.; Dontas, Ismene; Karamanos, B.; Karayiannacos, Panayiotis

doi:10.3109/02841869509093964

Cited by 22 publications

(22 citation statements)

References 11 publications

(8 reference statements)

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“…In the case of CI-HTG, the treatment choices are the discontinuation of capecitabine and the use of lipid-lowering agents such as fenofibrate, gemfibrozil, statins and fish oil [2,3,[7][8][9][10][11][12][13][14]. Our first case was treated with lipid apheresis due to the very high level of TG, with the result that pancreatitis could be prevented probably before overt disease occurred.…”

Section: Discussionmentioning

confidence: 99%

“…Some reports suggested that 5-FU may interfere with lipid metabolism. A study investigating the effect of 5-FU on plasma lipid levels in patients and in animals showed a significant reduction of the total plasma cholestero and a decrease in TG levels in animals [8]. Although cholesterol constitutes a prodrug of 5-FU, recent reports suggest an influence on lipid metabolism through different pathways and that capecitabine may cause HTG [2,3,[7][8][9][10].…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Capecitabine-Induced Hypertriglyceridemia and Hyperglycemia: Two Cases

Duman¹,

Paydaş²,

Tetıker³

et al. 2012

Pharmacology

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Capecitabine has shown significant antitumor activity against anthracycline/taxane refractory breast cancer and advanced colorectal carcinoma. The main drug-related adverse effects are palmar-plantar erythrodysesthesia (hand-foot syndrome), diarrhea and stomatitis. Dyslipidemia is a rare but important side effect of this drug. The mechanism of capecitabine-induced hypertriglyceridemia (CI-HTG) is unclear. It may be due to the decreased activities of lipoprotein lipase and hepatic triglyceride lipase. This report is associated with 2 patients who developed severe HTG when receiving capecitabine. Capecitabine was discountinued and antilipemic treatments were given and both cases are in follow-up with normal lipid levels. This report describes CI-HTG and possible pathogenetic mechanisms and the literature is reviewed.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Capecitabine-Induced Hypertriglyceridemia and Hyperglycemia: Two Cases

Duman¹,

Paydaş²,

Tetıker³

et al. 2012

Pharmacology

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“…Many cases of severe hypertriglyceridaemia were described with capecitabine, but to the best of our knowledge only one study has dealt with the influence of 5-FU on serum and it did not report any changes in triglyceride level in human (Stathopoulos et al , 1995). Recently, a case of recurrent grade-4 hypertriglyceridaemia in a patient treated with capecitabine and tegafur/uracil was reported (Yildiz et al , 2010).…”

mentioning

confidence: 95%

Severe hypertriglyceridaemia during treatment with capecitabine

Javot¹,

Spaëth²,

Scala‐Bertola

et al. 2011

Br J Cancer

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“…It is interesting to note that 5FU, a metabolite of capecitabine, actually reduced cholesterol levels in both patients and animals [3]. However, the literature indicates that another prodrug of 5FU, tegafur, may also cause hypertriglyceridemia [4].…”

Section: Introductionmentioning

confidence: 99%

Increase in triglyceride blood level in patients treated with capecitabine

et al. 2014

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According to registry studies of capecitabine, grade 3-4 hypertriglyceridemia can occur in 0.1-1% of patients, unexplained by the drug's mechanism of action. This retrospective study aimed at estimating the incidence of capecitabine-induced hypertriglyceridemia (CIH) and attempted to identify the risk factors for its occurrence. In a retrospective survey, the files of 289 patients treated with capecitabine as a single agent or combined with other drugs were reviewed. A total of 102 patients without grade 2 or more hypertriglyceridemia at baseline and with at least one test of triglyceride blood level (TGBL) at least 2 months from the start of capecitabine were eligible for the study. The mean TGBL was 149±80 mg/dl at the onset of treatment and the mean maximal level after two or more cycles of capecitabine was 236±137 mg/dl (P<0.001; average increase 93 mg/dl). Nineteen (19%) patients developed grade≥2 CIH, four (4%) of whom had grade 3-4. The median time to developing grade≥2 CIH was 79 days (range, 16-243 days). A high rate of grade≥2 CIH, without statistical significance, was observed on the basis of several risk factors: pre-existing hypertriglyceridemia grade 1 (11/45; 24%), diabetes (7/25; 37%), hypertension (10/60; 17%), and ischemic heart disease (IHD) (5/14; 36%). The only identified risk factor for grade≥3 CIH was IHD (2/14; P=0.02). Increased capecitabine-induced TGBL is common and grade≥2 was detected in 19% of patients in this series. Close monitoring of lipid profile is recommended in patients on capecitabine treatment. IHD may be a risk factor for development of severe hypertriglyceridemia.

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Influence of 5-Fluorouracil on Serum Lipids

Cited by 22 publications

References 11 publications

Capecitabine-Induced Hypertriglyceridemia and Hyperglycemia: Two Cases

Capecitabine-Induced Hypertriglyceridemia and Hyperglycemia: Two Cases

Severe hypertriglyceridaemia during treatment with capecitabine

Increase in triglyceride blood level in patients treated with capecitabine

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