Active clinical trials for "Hypertriglyceridemia"

A prospective observational program using digital technology tools to enhance patient adherence to Omacor therapy

Elevated plasma triglycerides (TG) are due to an excess of TG-rich lipoproteins of several different types, most commonly of very-low-density lipoproteins (VLDL), but also intermediate-density lipoproteins (IDL, or VLDL remnants), chylomicrons, and/or chylomicron remnants. Epidemiologic evidence that a moderate elevation in TG is often associated with increased atherosclerotic cardiovascular disease (ASCVD) risk, and more recent evidence from Mendelian randomization studies has shown that elevated TG associated with genetic variants may be a causal factor for ASCVD and possibly for premature all-cause mortality.[1-6] Fasting plasma TG concentrations may be categorized as: normal (< 150 mg/dL ), borderline (150-199 mg/dL), high TG (HTG, 200-499 mg/dL), and very high TG (VHTG, ≥ 500 mg/dL).[7, 8] Risk of acute pancreatitis is increased in VHTG patients, especially those with TG ≥ 1000 mg/dL.[9] For VHTG, the primary goal of therapy is to reduce TG to < 500 mg/dL,[10] whereas there is no specific treatment goal for HTG nor prescription indication. However, the omega-3 fatty acids, EPA and DHA have well-established efficacy in reducing TG in the range of 150-500 when administered at doses of > or = 3 g/d EPA+DHA (reviewed in Skulas-Ray et al. in press). Importantly, administration of omega-3 fatty acids to people with TG in this range lead to a 25% reduction in major adverse cardiovascular endpoints in the recently completed "Reduction of Cardiovascular Events with EPA Intervention Trial" (REDUCE-IT).[11] The results of REDUCE-IT provide compelling evidence for the use 3 g/d omega-3 fatty acid supplementation to reduce cardiovascular risk among patients with TG 150-500 mg/dL. The concentrated EPA supplement used in REDUCE-IT is just one of three long chain n-3 omega-3 fatty acids that influence lipids and lipoproteins and other aspects of cardiovascular risk. Most research has focused on the evaluation of EPA and DHA, which are the two predominant n-3 FA in fish and in n-3 agents, but docosapentaenoic acid (DPA) is present in fish oil, as well, and accumulates in the blood at similar concentrations. The carbon length of the n-3 FA appears important for physiological effects. EPA has a carbon length of 20, DHA has a carbon length of 22, and DPA, the metabolic intermediate of EPA and DHA, is a 22-carbon n-3 FA. DPA may have significant potential for treating HTG and VHTG,[12, 13] but research on this fatty acid remains limited. In a 2-week open-label crossover comparison of 4 g/d of a DPA concentrate (containing unspecified amounts of free DPA and EPA) vs. 4 g/d EPA concentrate in people with HTG, plasma TG were reduced 33% by the DPA concentrate, which was significantly more than the 11% reduction with EPA.[13] Thus, a recent scientific advisory from the American Heart Association (Skulas-Ray et al, in press) concluded that more research is needed to elaborate the lipid and lipoprotein effects of DPA. Additional biomarker research suggests DPA similarly can influence health outcomes that respond to EPA and DHA. For instance, decreased serum concentrations of DPA and DPA + DHA have been associated with increased risk of risk of acute coronary events[14] and myocardial infarction[15], respectively. Plasma DPA was also inversely associated with incident cardiovascular disease (CVD) in some ethnic groups.[16] In conclusion evidence supports a potential role of DPA in improving health, but results from clinical supplementation studies are needed to clarify the effect of DPA supplementation on lipids and lipoproteins as well as other cardiovascular disease risk factors-relative to supplementation with EPA and DHA-to ascertain whether enrichment of omega-3 concentrates with DPA could offer health benefits above and beyond concentrates that only contain EPA and DHA.

) Finding a unique pattern in the triglyceride composition of patients with hypertriglyceridemia that increases the chances of getting pancreatitis and which can serve as a laboratory predictive tool for patients and define them as a at-risk population. 2) Finding the typical fatty acid composition in triglycerides for patients at high risk of pancreatic acute inflammation that can be used to develop unique drugs for pancreatic acute inflammation caused by high levels of triglycerides.

Introduction: Hypertriglyceridemia is one of the etiologies of acute pancreatitis. It may cause severe multi-system disease resulting in high morbidity and mortality. There is controversy regarding the best method to treat it, which includes, among other therapies, high-dose insulin and performing plasma exchange (apheresis). Aims: Primary outcome - Comparison of 28- day mortality between hypertriglyceridemia-induced acute pancreatitis patients who received conservative therapy versus those who received apheresis therapy. Secondary outcomes: Comparison of morbidity parameters and rate of blood triglycerides level decrease between the groups. Materials and Methods: A retrospective study based on observational data collection, which will include all patients aged 18--99 who were admitted to the intensive care unit in 2010-2020 in the diagnosis of acute pancreatitis secondary to high blood lipids. Data will be collected from hospital files and computerized systems. Data will include demographics, admission times, ventilation days, pressor support, 28- day mortality,daily triglyceride level, medical history, APACHE-2 score, lactate level, need for dialysis, need for antibiotics and surgical intervention. The study will include 29 patients. All demographic and patient parameters will be statistically examined by a qualified statistician depending on the type of data.

Subjects with elevated serum triglycerides in the 4th Tromso study in 1994/1995 were re-examined with an oral glucose tolerance test to see predictive value of triglycerides regarding development of type 2 diabetes

To study the effect of genes on lipid-lowering drug treatment in hypertriglyceridemia.

This study is a prospective observational program within the frames of which Tricor (fenofibrate) is prescribed to patients with hypertriglyceridemia within a routine procedure as a part of the combination therapy with statins.

Acute pancreatitis (AP) is a one of the potentially life-threatening complication of severe hypertriglyceridemia (HTG), with mortality around to 30%. HTG-associated PA and their complications management has to be the same as the other pancreatitis, but they are associated with the worse clinical outcomes. Triglycerides levels are correlated with the risk of pancreatitis and severity. Therapeutic plasma exchange (TPE) could provide positive effects in reducing triglyceridemia plasma levels during the acute phase of HTG-AP, and in prevention of recurrence. There is currently no difference about mortality in studies. Some authors have recommended its use only in severe HTG-AP and have precised the need of early initiation to have positive results. Despite such promising findings from studies, the effects of therapeutic plasma exchange on HTG-associated PA have never been specifically assessed and its benefits in critically ill patients with AP remains uncertain.

Adipose tissue secreting a number of adipokines which regulate insulin sensitivity, energy metabolism and vascular homeostasis, so the dysfunction of adipose tissue is linked with the incidence of obesity accompanied with insulin resistance, hypertension and cardiovascular disease (1). Obesity is known to alters the expression of adipokines due to the adipose tissue hypertrophy (2), including adiponectin, in which able to exert a potent anti-inflammatory and vascular protective effect (2). It has been proposed that adiponectin acts to prevent the vascular dysfunction due to obesity and diabetes by improves insulin sensitivity and metabolic profiles to reduce the risk factors for cardiovascular disease and protects the vasculature through its pleiotropic actions on endothelial cells, endothelial progenitor cells, smooth muscle cells and macrophages (1). The concentrations of adiponectin of 5 to 25 mg/mL had a significant inhibitory effect on the expression of monocyte adhesion and adhesion molecule induced by TNF-α in vitro. Atherosclerosis is an inflammatory disease in which adhesion molecules on arterial endothelial cells are responsible for the accumulation of monocytes/macrophages and T lymphocytes. While obesity is low-grade inflammation in which make a contribution on endothelial dysfunction by increasing the oxygen-derived free radicals (ROS) due to adipocyte hypertrophy, leads to an endoplasmic reticulum (ER) stress and mitochondrial dysfunction (3). Adiponectin is accumulated in the vasculature, and it reduced on obesity due to suppression by TNF-α and lead to adiponectin-deficiency which stimulate the significant increases of Vascular cell adhesion protein 1 (VCAM-1) and Intercellular Adhesion Molecule 1 (ICAM-1) or known as CD54 in aortic intima (4). Here we investigate the level of adiponectin, ICAM-1, VCAM-1 with the incidence of MetS in obese adolescents.

To conduct a comprehensive epidemiologic investigation into the relationship between serum triglyceride (TG) levels and coronary heart disease (CHD).