scholarly journals Hypertriglyceridemia Induced by Fluorouracil: A Novel Case Report

2021 ◽  
pp. 207-211
Author(s):  
Yoshitaka Saito ◽  
Yoh Takekuma ◽  
Satoshi Yuki ◽  
Yoshito Komatsu ◽  
Mitsuru Sugawara

We had previously reported on S-1-induced hypertriglyceridemia. Here, we report fluorouracil-induced hypertriglyceridemia in a patient with capecitabine-induced hypertriglyceridemia and the corresponding therapeutic process. A woman in her forties who had experienced grade 3 hypertriglyceridemia due to oxaliplatin + capecitabine was administered fluorouracil ± oxaliplatin + levofolinate calcium + panitumumab; however, grade 4 hypertriglyceridemia occurred after the thirteenth administration. Bezafibrate normalized the elevation. Chemotherapy cessation resulted in its decrease to normal, and bezafibrate was stopped. Nine months after cessation, treatment with fluorouracil + irinotecan + levofolinate calcium + ramucirumab was initiated. After four cycles of treatment, her serum triglyceride levels increased again to grade 3, and then, fenofibrate was administered, resulting in a significant decrease to grade 1–2. Serum triglyceride levels significantly reduced after cessation of the prior fluorouracil-containing regimen, although its elevation was observed again following the latter treatment. Therefore, fluorouracil-induced hypertriglyceridemia was strongly speculated in this case. We have speculated that the most probable cause of tegafur and capecitabine-induced hypertriglyceridemia is fluorouracil or its metabolic enzymes since their end product is fluorouracil in the previous report. Results from this patient suggest that our supposition was correct. Fibrates administration, cessation of the treatment, and monitoring of serum triglyceride level was effective in this case as well as previous reports. Fluorouracil-induced hypertriglyceridemia is associated with the one caused by tegafur and capecitabine and presents the possibility of severe complications. Elucidation of its exact mechanism and epidemiological features is needed for better understanding.

2021 ◽  
pp. 1277-1282
Author(s):  
Yoshitaka Saito ◽  
Yoh Takekuma ◽  
Takashi Takeshita ◽  
Mitsuru Sugawara

Docetaxel (DOC) is one of the most effective agents for breast cancer treatment. Here, we report docetaxel-induced severe hypertriglyceridemia in a patient previously diagnosed with hyperlipidemia and corresponding therapeutic intervention. A postmenopausal woman, with previously controlled hyperlipidemia using rosuvastatin 5 mg daily, was diagnosed with stage IIB breast cancer with human epidermal growth factor receptor-2 overexpression; she received DOC (75 mg/m<sup>2</sup>), pertuzumab, and trastuzumab treatment as neoadjuvant chemotherapy. The serum triglyceride level was mildly higher than normal, and cholesterol level was normal at baseline. The serum triglyceride level was almost stable after chemotherapy initiation but suddenly increased to grade 3 (770 mg/dL) after the third cycle of the treatment without any symptoms. Sustained-release bezafibrate 400 mg was administered, resulting in a significant decrease to the baseline level; bezafibrate was discontinued on day 28 of the fourth chemotherapy as neoadjuvant chemotherapy was completed. The level was stable around the baseline level during adjuvant chemotherapy with pertuzumab and trastuzumab. Therefore, DOC-induced severe hypertriglyceridemia was strongly indicated in this case. The mechanism underlying the symptoms remains unclear; we speculate that it could be a resultant of a decrease in lipid metabolism as the patient had grade 2 diarrhea. Moreover, her backgrounds, such as mild hypertriglyceridemia, postmenopausal, diabetes, and obesity, in addition to DOC administration might have affected the outcome. Fibrate administration and cessation of treatment were as effective as in previous reports. DOC-induced hypertriglyceridemia presents with the possibility of severe complications. Elucidation of the exact mechanisms and epidemiological features is required for better management.


2021 ◽  
Vol 9 (5) ◽  
pp. 505
Author(s):  
Jingyi Yuan ◽  
Song Qin ◽  
Wenjun Li ◽  
Yubing Zhang ◽  
Yuting Wang ◽  
...  

Fucoidan is a kind of polysaccharide with antitumor and antioxidant properties, which is mainly isolated from brown algae. Although there are many reports about the prebiotic effects of polysaccharides on hosts, there are few reports about the effects of fucoidan on blood biochemical indexes, intestinal microbiome, and metabolic function on healthy hosts. We applied 16S rRNA gene amplicon sequencing and LC-MS/MS metabolomics to evaluate the changes in the gut microbiome and metabolite profiles of fucoidan treatment in mice over 10 weeks. Fucoidan treatment modulated lipid metabolism, including significantly decreasing serum triglyceride level in healthy mice. Fucoidan also significantly inhibited serum lipopolysaccharide-binding protein (LBP) concentration, a biomarker of endotoxemia. Correlation analysis further showed that Lactobacillus animalis populations that were enriched by fucoidan demonstrated significantly negative correlations with serum triglyceride level. The abundance of Lactobacillus gasseri and Lactobacillus reuteri, increased by fucoidan supplementation, demonstrated significantly negative correlation with lipopolysaccharide-binding protein levels. Lactobacillus gasseri also demonstrated significantly positive correlations with three tryptophan-related metabolites, including indoleacrylic acid, 3-indoleacrylic acid, and 5-hydroxytryptamine, which were all increased by fucoidan administration. Combined with the previous evidence, the results indicate that fucoidan exerts prebiotic effects, such as lipid metabolism suppression and metabolic endotoxemia suppression, by modulating the abundance of gut microbiota, such as Lactobacillus animalis, Lactobacillus gasseri, and Lactobacillus reuteri, as well as microbiota-dependent metabolites, such as tryptophan-related metabolites.


2021 ◽  
Vol 141 (5) ◽  
pp. 95-103
Author(s):  
Pham Thuy Phuong ◽  
Pham Thi Van Anh ◽  
Dang Thi Thu Hien ◽  
Nguyen Trong Thong ◽  
Pham Quoc Binh

This study evaluated the effects of Hamo NK hard capsule on athresclerosis using experimental atherosclerosis model. NewZealand White rabbits were fed a high-fat diet (HFD) containing cholesterol and peanut oil. The animals received oral administration of HFD and Hamo NK hard capsule at two doses of 0.126 and 0.378 g/kg bw/day for 8 consecutive weeks. Blood samples were collected for analyis of biochemical parameters at before treatment, week 4 and week 8. Histopathology assessments of the aortic artery and liver were carried out at the end of the experiment. Hamo NK was effective in reducing serum triglyceride level after 8 weeks of the experiment. In addition, Hamo NK at two doses of 0.126 g/kg b.w and 0.378 g/kg b.w for 8 consecutive weeks did not affect the cholesterol, LDL-C and HDL-C concentrations induced by a HFD. Hamo NK at the dose of 0.126 g/kg bw/day was not only able to decrease significant aortic surface lesions but also capable of managing atherosclerosis plaques formation in aorta; whereas theses activities were not notiaceable at the dose of 0.378 g/kg b.w.


2020 ◽  
Vol 13 (1) ◽  
pp. 304-308 ◽  
Author(s):  
Alyssa Schlotman ◽  
Adam Stater ◽  
Kyle Schuler ◽  
Judd Heideman ◽  
Vandana Abramson

A 49-year-old woman with ER-positive/PR-negative/HER2-negative metastatic breast cancer experienced Grade 3 hepatotoxicity following initiation of a clinical trial of fulvestrant, palbociclib, and erdafitinib. Fulvestrant was determined to be the drug most likely responsible for this hepatotoxic effect. This case report details the timing and nature of this drug-induced liver injury, adding support to an area that has yet to be described adequately in the existing literature.


2000 ◽  
Vol 151 (1) ◽  
pp. 47
Author(s):  
A Branchi ◽  
A.M Fiorenza ◽  
A Torri ◽  
F Muzio ◽  
A Rovellini ◽  
...  

2016 ◽  
Vol 64 (2) ◽  
pp. 383-387 ◽  
Author(s):  
Amani Beshara ◽  
Eytan Cohen ◽  
Elad Goldberg ◽  
Pearl Lilos ◽  
Moshe Garty ◽  
...  

The relationship between triglyceridemia and diabetes mellitus remains unclear. This study evaluated the risk of diabetes and impaired fasting glucose associated with a wide range of triglyceride levels. A longitudinal retrospective study was carried out employing data from a screening center between the years 2000 and 2012. Inclusion criteria were absence of diabetes at baseline and attendance at the center at least twice over a 5-year period. Participants were divided by fasting blood glucose level (normal/impaired) at the first visit. A total of 5085 participants were eligible for the study. Of the 4164 normoglycemic participants at baseline, 40 (0.96%) had diabetes and 998 (24%) had impaired fasting glucose by the end of the study. On stepwise logistic regression analysis, every 10 mg/dL increase in triglyceride level significantly increased the risk of diabetes by 4% and of impaired fasting glucose by 2% (p<0.001). This association held true even when rising triglyceride levels remained within the accepted normal range (<150 mg/dL, p<0.001). Sustained increments in serum triglyceride level, even within the accepted normal range, are an independent risk factor for diabetes mellitus and impaired fasting glucose in normoglycemic participants.


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