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Retinoids in Lymphoma
Published in Ayse Serap Karadag, Berna Aksoy, Lawrence Charles Parish, Retinoids in Dermatology, 2019
Bexarotene can also cause hyperlipidemia and hypercholesterolemia (28). Prior to initiating oral bexarotene, baseline lipid levels should be established. If there are abnormalities, they should be corrected prior to initiation. Once oral bexarotene has begun, close monitoring should occur. The most common lipid abnormality is hypertriglyceridemia at 79% (28). To combat this, patients are started on fenofibrate. If LDL cholesterol levels also rise, atorvastatin can be initiated; however, we preemptively initiate atorvastatin 40 mg at baseline. Finally, with the possibility of hepatotoxicity, liver enzymes should be monitored. Additional side effects may be peripheral edema and nausea, with pancreatitis rarely occurring but also being avoidable by monitoring triglyceride levels.
Mechanisms of action
Published in Fazal-I-Akbar Danish, Ahmed Ehsan Rabbani, Pharmacology in 7 Days for Medical Students, 2018
Fazal-I-Akbar Danish, Ahmed Ehsan Rabbani
Fenofibrate is a prodrug. It is converted to an active metabolite ‘fenofibric acid’ which is responsible for the triglyceride-lowering effect of the drug. Fenofibric acid, once formed, attaches to its receptor: peroxisome proliferator-activated receptor-alpha (PPAR-α). The activated receptor then binds to peroxisome proliferator response elements located in various gene promoters. These elements increase the expression of genes encoding for lipoprotein lipase. This enzyme is primarily found on the surface of endothelial cells. Its main function is to clip off free fatty acids from within the lipoprotein complexes so that the same can be taken up into the cells. This leads to depletion of triglycerides (3 × fatty acids + glycerol) from the lipoprotein complexes. Increased expression of lipoprotein lipase means increased clearance of triglyceride-rich lipoproteins from the circulation leading to a fall in triglyceride levels. This also in turn leads to decreased cholesterol biosynthesis in the liver.
Inhibiting Insulin Resistance and Accumulation of Triglycerides and Cholesterol in the Liver
Published in Christophe Wiart, Medicinal Plants in Asia for Metabolic Syndrome, 2017
Aqueous fraction of Ocimum basilicum L. given orally at a daily dose of 200 mg/kg for 5 weeks to mice on hypercholesterolemic diet lowered plasma cholesterol by 42%, triglycerides by 42%, and lowered low-density lipoprotein–cholesterol by 88% and increased high-density lipoprotein by 80%.486 This treatment reduced atherogenic index by 88%.486 Fenofibrate given orally at a dose of 200 mg/kg lowered plasma cholesterol by 25%, triglycerides by 52%, low-density lipoprotein–cholesterol by 84%.486 The aqueous fraction lowered hepatic cholesterol by 52% and hepatic triglycerides by 58%.486 Fenofibrate lowered hepatic cholesterol and triglyceride by 59% and 71%, respectively.486 Clinical trials are warranted.
Fenofibrate therapy to lower serum triglyceride concentrations in persons with spinal cord injury: A preliminary analysis of its safety profile
Published in The Journal of Spinal Cord Medicine, 2020
Michael F. La Fountaine, Christopher M. Cirnigliaro, Joshua C. Hobson, Alexander T. Lombard, Adam F. Specht, Trevor A. Dyson-Hudson, William A. Bauman
A screening visit was performed on 70 persons with SCI to identify subjects with elevated serum TG concentrations (i.e. paraplegia: ≥135 mg/dl; tetraplegia ≥115 mg/dl)29 after a ≥12-hour overnight fast. Fifteen participants were identified as having elevated serum TG values and received once-daily fenofibrate therapy (145 mg tablet; Tricor®, AbbVie Inc., North Chicago, IL, USA) (Table 1). The clinically acceptable time point in deciding whether to withdraw or continue fenofibrate treatment is 2-months and is based on whether there was a ≥25% reduction in the serum TG concentration; in the absence of an improvement, drug therapy was discontinued. For those who responded to fenofibrate therapy (e.g. a reduction of serum TG ≥25%), treatment was continued for an additional 2 months in the trial. At baseline and then at each month thereafter, a review of systems was obtained to identify any deviation from baseline status and venous blood collection was performed between 8 am and noon after an overnight fast. The blood specimen were sent to a commercial laboratory (LabCorp, Raritan, NJ, USA) for evaluation of liver function tests (LFTs), kidney function (i.e. estimated glomerular filtration rate), and a complete blood count with differential.
Efficacy and safety of coenzyme A versus fenofibrate in patients with hyperlipidemia: a multicenter, double-blind, double-mimic, randomized clinical trial
Published in Current Medical Research and Opinion, 2020
Ya-Qin Chen, Shui-ping Zhao, Hui-Jun Ye
The dyslipidemias may necessitate an almost lifelong administration. Many people prefer natural products instead of chemical drugs because they believe these products are natural, safer, cheaper and easier to ingest24. With the wider use of fibrates, more side effects have been detected. The most frequent side effects are liver dysfunction, gastrointestinal tract symptoms and musculoskeletal symptoms. In the present trial, the incidence of side effects caused by fenofibrate is significantly higher than that caused by CoA. There was no occurrence of myopathy or obvious damage of liver and kidney function in the CoA group. Furthermore, the incidence of gastrointestinal tract symptoms and complications by CoA therapy was rare. All of this evidence demonstrated that CoA is a well tolerated lipid-lowering agent.
Effect of Fenofibrate on the Expression of Inflammatory Mediators in a Diabetic Rat Model
Published in Current Eye Research, 2019
Po-Ting Yeh, Lu-Chun Wang, Shu-Wen Chang, Wei-Shiung Yang, Chung-May Yang, Chang-Hao Yang
The most concerned issue of fenofibrate treatment is its hepatotoxicity. Impaired liver functions caused by fenofibrate have been found in animal and human studies.38,40 In our study, fenofibrate 30 mg/kg/day and 100 mg/kg/day were given to diabetic rats according to the previous reports.20,21 Compared with the treatment dose in the FIELD study (200 mg daily in human), we used a relatively large dose in our study. No hepatotoxicity was observed in the experimental animals except mild fatty liver. In the FIELD and ACCORD eye study, type 2 diabetic patients who received long-term fenofibrate treatment were evaluated. In contrast, the in vivo animal experiments can only demonstrated the short-term effect. STZ injection causes type 1 diabetes, which results in acute elevation of blood sugar and acute inflammatory reaction within retina of diabetic rats. Relative large dose of fenofibrate with short-term treatment (3 months) should be applied to suppress the acute inflammatory reaction within diabetic retina in this animal model. Although our short-term, large-dose fenofibrate treatment only indicated mild fatty liver, long-term usage may result in adverse effects such as hepatotoxicity and gallstones.38,40 To confirm this treatment in preventing DR progression and possible side effects clinically, more animal studies with type 2 diabetes model and human clinical trials are necessary to further delineate the safety dosage and exact treatment guidelines of fenofibrate.