View clinical trials related to Hyperlipidemias.
Filter by:This study was conducted to investigate the effects of daily supplementation of Citron(Citrus Junos Siebold ex Tanaka) Peel Extract on improvement of Blood Cholesterol.
The purpose of this study is to conduct a preliminary test of the effectiveness of various educational interventions to promote adoption of a whole-food, plant-strong diet and reduce specific cardiovascular risk factors in Veterans, and subsequently perform a preliminary pilot study on whether this dietary approach will change plaque inflammation and endothelial function.
Dyslipidemias are a major risk factor for the onset of cardiovascular disease, while early diagnosis and appropriate treatment approaches significantly reduce cardiovascular morbidity and mortality. The aim is to provide revised Greek guidelines for the diagnosis and treatment of dyslipidaemias. The lipids of the human body are cholesterol (it is used to synthesize cell membranes, adrenal hormones and gonads and is a component of bile) and triglycerides (used as a fuel and as a storage of energy in adipose tissue). Dyslipidemias are disorders (quantitative or qualitative) of the metabolism of lipoprotein particles [low density lipoproteins (LDL), chylomic, high density lipoproteins (HDL), very low density lipoproteins (VLDL)] that carry lipids into the body. Primary prevention in subjects aged 40-65 years with no known clinical atherosclerotic disease and without diabetes or chronic renal disease should evaluate the likelihood of a fatal cardiovascular event over the next 10 years. For this purpose, it is recommended to use the Greek version of the SCORE of the Hellenic Heart SCORE.
Lipoprotein lipase deficiency (LPLD) is a rare autosomal recessive disorder, characterized by loss-of function mutations in the LPL gene, leading to the inability to produce functionally active lipoprotein lipase (LPL). LPL is the key enzyme in the metabolism of triglyceride (TG)-rich lipoproteins (chylomicrons (CM) and very low-density lipoproteins (VLDL)). LPLD results in extremely high concentrations of circulating TG-rich lipoproteins. No drug therapy for LPLD is currently available. Clinical management of LPLD patients consists of severe dietary fat restriction and the use of medium-chain triglycerides to substitute for normal dietary fats. Alipogene tiparvovec (Glybera®) received marketing authorisation from the European commission on 25 October 2012. Glybera® aims to correct lipoprotein lipase deficiency sufficiently to decrease the morbidity and lower the risk of inherent complications of LPLD, in adult patients genetically diagnosed with LPLD. The Glybera Registry is designed to collect the long-term safety and efficacy data of GLYBERA®
The purpose of the study is to investigate the cholesterol lowering efficacy of a cereal based snack bar with added plant stanol ester when used between meals as part of a habitual diet by subjects with mild to moderate hypercholesterolemia.
The chronic disease burden is increasing worldwide leading to a rise in the demand for primary healthcare and a shortage of primary care physicians. Addressing this shortage entails a multi-prong approach with innovations in care delivery, greater use of healthcare technology, and more efficient use of all healthcare providers on the care team. We previously developed an interactive self-service healthcare kiosk (Self-empowering and enabling kiosk - SEEK® MyHealthKiosk) for the management of patients with stable chronic disease in the primary care setting. A feasibility study using SEEK showed high levels of acceptance and satisfaction from patients and healthcare providers. The aim of this follow-up study is to evaluate the health outcomes of patients with stable chronic disease who are on kiosk management compared to patients who are on routine management by nurse clinicians. We hypothesize that patients who are managed by the kiosk continue to maintain good disease control that are comparable to patients who are managed by a nurse clinician.
Background: Cisplatin is a chemotherapy drug. It is used to treat head and neck squamous cell carcinoma (HNSCC) and other cancers. It can cause hearing loss for some people. It is not known how many people will get hearing loss from cisplatin. It is also not known what other factors might influence who gets hearing loss. Factors could include age, sex, noise exposure, and other drugs the person is taking. Statins are drugs used to lower cholesterol. Statins may also reduce cisplatin-induced hearing loss. Objectives: To see if statins reduce hearing loss in people getting cisplatin therapy to treat HNSCC. To find out how many people taking cisplatin get hearing loss from it. To find out if other factors might influence whether cisplatin causes hearing loss. Eligibility: People ages 18 and older who are getting treatment with cisplatin for HNSCC Design: Participants will be screened with a review of their medical records. Participants will have 3 visits. These will be before the onset of cisplatin therapy, at about 4 weeks after they finish therapy, and about 6 months after they finish therapy. Each visit will include: Medication history Audiogram/hearing tests. Participants will wear headphones and indicate when they hear different sounds. Questions about their noise exposure history and whether they have ringing in the ears
Theranostic translation applications against viral, metabolic liver diseases and hepatic oncogenesis: lipoprotein and apolipoproteins at a crossroad
The primary aim of this study is to directly compare the two major types of anthocyanins found in the diet (cyanidin-type and delphinidin-type) on lipid status in adults.
Cardiovascular Diseases (CVDs) are the leading causes of death in the world and in Brazil. In 2001, 12.45 million deaths on the globe (21% of the total) were caused by some CVD. The composition of modern man's diet has changed drastically with the industrialization of food, resulting in the transition from a diet rich in fibers and complex carbohydrates to one with a high content of sugars and fats. Since the current dietary pattern is characterized by the consumption of three or more meals a day, containing a quantity of fat in the range of 20 to 70 g, individuals spend a large part of the day in the postprandial state, with continuous fluctuation of lipemia Over 18 hours. Food intake (postprandial state) is the dynamic, unstable response of the body that refers to rapid hormonal and lipoprotein remodeling. It is well established in the literature that high-fat meals (lipid overload) cause an increase in plasma triglycerides. Hypertriglyceridemia and / or elevated triglyceride-rich lipoproteins (LRT) (chylomicrons, VLDL and their remnants) in the postprandial state induces endothelial dysfunction via increased oxidative stress and is an independent risk factor for CVDs. Therefore, Postprandial Lipemia (PPL) is counted as an early marker of atherosclerotic process, metabolic abnormalities and endothelial dysfunction. High-carbohydrate (CHO) diets may promote increased LDL-c, TG, VLDL and HDL-c reduction, as well as PPL, generating a lipid profile associated with an increased risk of CVDs. This effect appears to be more pronounced with the inclusion of simple carbohydrates (mono and disaccharides), although it also occurs with diets rich in complex carbohydrates (polysaccharides). High fructose diets (HFDs) are a known model of induction of insulin resistance, dyslipidemia and DM2 in primates and humans. The chronic effect of fructose consumption has been well studied in the last decades due to its connection with obesity, resistance to Insulin, accumulation of visceral fat and dyslipidemia. As the consumption of fructose is progressively increasing in society and its chronic exposure can generate a phenotypic effect of dyslipidemia and, consequently, the increased risk of CVDs, prevention and treatment strategies should be seen as an important public health issue . Thus, the objective of this study is to understand the effects of exercise on fat metabolism, since there is a lack of robust evidence about the possible cardioprotective and hypolipemic role of the same on HFD.