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Dyslipidemia
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
Primary and secondary causes of dyslipidemia may influence the disease in different amounts. Familial combined hyperlipidemia may only develop, for example, when there are strong secondary causes present. Primary causes of dyslipidemia involve single or multiple gene mutations that cause overproduction or poor clearance of LDL and triglycerides. There can also be underproduction or extreme clearance of HDL. Previously, lipoproteins were described by how the separated into alpha (HDL) or beta (LDL) bands on electrophoretic gels.
Identification and Management of Children with Dyslipidemia
Published in James M. Rippe, Lifestyle Medicine, 2019
Julie A. Brothers, Stephen R. Daniels
Another common cause of hypercholesterolemia is familial combined hyperlipidemia (FCHL) or type IIb hyperlipoproteinemia (Table 79.5). This is an autosomal dominant genetic disorder that is the most common genetic lipid disorder in the United States, affecting approximately 1 in 200 people. There is phenotypic variation among family members with FCHL, with the most common lipid phenotype showing elevated LDL-C with elevated TGs and very-low-density lipoprotein cholesterol (VLDL-C), and low HDL-C. FCHL may also be seen in those with overweight, insulin resistance, and hypertension.
Lipid Subfraction Testing
Published in Stephen T. Sinatra, Mark C. Houston, Nutritional and Integrative Strategies in Cardiovascular Medicine, 2015
Patients with familial combined hyperlipidemia have predominantly small dense LDL lipoproteins and these particles appear to be directly related to cardiovascular events, independent of metabolic syndrome, total cholesterol, and apoB.91
Safety and efficacy of therapies for chylomicronemia
Published in Expert Review of Clinical Pharmacology, 2022
Isabel Shamsudeen, Robert A. Hegele
Vupanorsen (IONIs-ANGPTL3-LRx, Akcea, and Pfizer) is an GalNac conjugated ASO therapy targeting ANGPTL3 mRNA in hepatocytes by efficient delivery through the cell surface asialoglycoprotein receptor [72,73]. There was some initial excitement about the potential value of vupanorsen in patients with moderate HTG and insulin resistance, as suggested by a phase 2, randomized, double-blind, placebo-controlled study, which showed a reduction of TG and LDL cholesterol by up to 63.1% and 32.9%, respectively [73]. However, in a phase 3 dose-finding study among patients with combined hyperlipidemia, vupanorsen was observed to have only modest lipid lowering effects that were associated with elevations in liver enzymes (alanine aminotransferase and aspartate aminotransferase) and increased hepatic fat, leading to the termination of the drug development program in early 2022 [74]. These adverse effects were not observed with evinacumab, which only interacts with extracellular ANGPTL3, suggesting that interfering with intracellular ANGPTL3 through RNA silencing may target an additional mechanism that promotes a net negative metabolic outcome.
Characteristics of patients with dyslipidemia treated in routine care setting in China
Published in Journal of Drug Assessment, 2019
Gordon Liu, Jason Shepherd, Pratik Rane, Zhongyun Zhao, Hollie Bailey, Nathan Williams, Yi Qian
This study included 195 physicians (40 endocrinologists, 75 internists, 80 cardiologists) who provided data on 1870 patients of whom 852 had been diagnosed with diabetes by the time of the survey. All patients completed the patient survey. Characteristics of study patients at diagnosis are provided in Table 1. Compared with non-diabetic patients (n = −1,018), individuals with diabetes (n = 852) were older on average (p < 0.0001) and a greater percentage of diabetic patients were retired or had a caregiver (p < .0001, p < .005, respectively). Among diabetic patients, 47% had been diagnosed with combined hyperlipidemia (hypercholesterolemia/hypertriglyceridemia) compared with 39% of patients without diabetes (p < .001). This finding was reversed for the diagnosis of hypercholesterolemia alone (p < .0050). Similar percentages of patients with and without diabetes carried a diagnosis of hypertriglyceridemia and familial combined hyperlipidemia (p > .6).
Benefits and risks of the treatment with fibrates––a comprehensive summary
Published in Expert Review of Clinical Pharmacology, 2018
Bogusław Okopień, Łukasz Bułdak, Aleksandra Bołdys
Fibrates are the most effective drugs in the therapy of hypertriglyceridemia and are the treatment of choice in severe hypertriglyceridemia [1]. The unique benefit of fibrate therapy is its strong impact on postprandial/non-fasting hypertriglyceridemia, which is considered as one of the novel cardiovascular risk factors. Due to above-mentioned increased LPL activity, the postprandial rise in the level of highly atherogenic remnant lipoprotein level may be prevented [42]. According to a large-scale meta-analysis (examining data from 16,802 patients and 53 trials) the TG decrease during treatment reached 36%, varying between 18% for clofibrate and 48% for gemfibrozil [43]. Impact of fibrates on LDL-C reduction is less prominent than on TG and averages around 11%, but these drugs have unique ability to significantly increase HDL-C by 10% [43]. These features are ideal to treat patients with atherogenic dyslipidemia [4]. What is more, they are very effective in patients with combined hyperlipidemia [44]. In this setting 200 mg per day of fenofibrate was superior to 10 mg of atorvastatin in TG reducing potential (28% vs. 12%; p < 0.001) and was similarly effective in LDL-C reduction (−18.9% vs. 24.9%; p > 0.05). Recently, several studies on the combination therapy with fibrates and ezetimibe have also been performed. EFECTL Study showed benefits of combined treatment with fenofibrate and ezetimibe compared to both monotherapies in patients with combined hyperlipidemia [45]. A specific additive effect of combined treatment was clearly noted in the magnitude of LDL-C reduction that reached