View clinical trials related to Hyperlipidemias.
Filter by:People with psoriasis have significantly higher rates of obesity, diabetes, heart failure and high blood pressure than the general public. The purpose of this study is to determine how substances produced in the fat (inflammatory markers) relate to the risk of heart disease in people with the metabolic syndrome and psoriasis. People with metabolic syndrome have insulin resistance, increased waist size, high blood pressure, or high cholesterol.
The primary purpose of this trial is to determine if the treatment with rosuvastatin 10 and 20mg/day during 8 weeks in hypertriglyceridemic patients will reduce their triglyceride levels.
Compare the effectiveness of 3 strategies by pharmacists to decrease the time to refill of prescriptions for common chronic diseases (diabetes, hypertension, hyperlipidemia, heart failure, depression, psychoses).
The purpose of this study is to determine whether chenodeoxycholic acid decreases de novo hepatic lipogenesis, hepatic fat content, hepatic triglyceride production and plasma triglyceride concentrations and improves hepatic glucose metabolism in patients with the metabolic syndrome, Familial Hypertriglyceridemia and Familial Combined Hyperlipidemia.
To demonstrate that niacin ER and simvastatin (NS) tablets, when compared to atorvastatin (Lipitor®; Pfizer, Inc.), has superior high-density lipoprotein cholesterol (HDL-C) elevating effects at Week 12 in subjects with type II hyperlipidemia or mixed dyslipidemia who are currently off lipid-modifying therapy. This was a prospective, randomized, open-label, blinded endpoint (PROBE) study.
This is a multi-center, double blind, prospective, longitudinal, randomized, 12-week study with a 52-week open-label follow-up to evaluate the safety and efficacy of daily administration of Pravastatin 40 mg or Fenofibrate 160 mg or Pravafen (the combination of both Pravastatin and Fenofibrate 40/160 mg) in the treatment of combined hyperlipidemia. There will be an open-label, 8-week, Selection Phase prior to randomization in which all patients will be stabilized on Pravastatin 40 mg/day. Following the Selection Phase, and if the patients meet all inclusion/exclusion criteria, they will be randomized to a three arm, double blind, 12-week Efficacy Phase during which they would receive either Pravastatin 40 mg or Fenofibrate 160 mg or Pravafen (the combination of Pravastatin and Fenofibrate 40/160 mg). The 12-week Efficacy Phase will be followed by an open-label, 52-week, Safety Phase in which all patients will receive Pravafen. After the 8-week Selection Phase, patients that still meet the inclusion/exclusion criteria will be randomized on a 1:1:2 ratio to Pravastatin 40 mg or Fenofibrate 160 mg or Pravafen (the combination of both Pravastatin and Fenofibrate 40/160 mg) for 12 weeks. After the completion of the 12-week double-blind phase of the study, all patients that haven't had changes in their well being, will be allowed to roll-over into the 52-week, open-label, follow-up portion of the study. During the 52 week, open label, Safety Phase of the study, all patients will receive Pravafen (the combination of Pravastatin and Fenofibrate 40/160 mg). Patients will be evaluated at baseline and every three weeks thereafter throughout the initial 12-week Efficacy Phase of the study. Patients that roll-over into the 52-week, open-label, follow-up Safety Phase will be evaluated at 12, 24, 36 and 52 weeks. Participation in the study can be up to 72 weeks.
paraoxonase 1 is involved to prevent LDL and HDL oxidation,so increase of it's activity leads to lower risk of coronary heart disease.In postmenopausal women ,we have decrease of paraoxonase1 activity and soy proteins may increase paraoxonase1 activity
The overall objective of the CAP study was to determine genetic influences on efficacy of simvastatin treatment with regard to LDL cholesterol reduction and changes in other markers of cardiovascular disease risk.
Cardiovascular-related diseases have been the majorities of the leading ten causes of death in Taiwan. Atherosclerotic cardiovascular diseases are multifactorial. Some non-modifiable risk factors (e.g. genetic trait) may attenuate the benefit of risk modification of the modifiable factors (e.g. the effect of drug treatment). Genetic epidemiology has being widely used to analyze the underline risk of cardiovascular diseases and to point the direction of treatment or prevention. Lipoprotein is composed of lipid and protein. The genetic variation or mutation of apolipoprotein, the protein of lipoprotein, has been linked to some lipid abnormality resulting severe atherosclerotic cardiovascular diseases. ApoA-I, apo A-II, apo A-IV, apo B100, apo B48, apo C-I, apo C-II, apo C-III, apo D, and apo E are currently thought to affect lipid abnormalities. In addition, it has been documented that genetic variations are presented among different races. Apolipoprotein genetic variations or genetic polymorphism study has been emerged as an important role in the field of genetic therapy. The purpose of this 3-year study is to continue the lipid study in our laboratory, identifying the apolipoprotein genotyping in our pooled hyperlipidemic patients and normal control subjects living in Taiwan. We will observe the incidence and link apo A-I, apo A-II, apo A-IV and apo C-III genetic variations to the related lipid abnormality and cardiovascular diseases. The changes of genotyping after lipid lowering drug treatment using statin or fibrate in hypercholesterolemic or hypertriglyceridemic patients is another goal of this project.
The purpose of this study is to evaluate the long term effectiveness of the dietary portfolio, consisting of viscous fibers, soy products, nuts and plant sterols, as well as the effects of removing single food components from the dietary portfolio on cholesterol reduction and other cardiovascular risk factors.