Active clinical trials for "Hyperlipoproteinemias"

The purpose of this study is to create a model enabling us to predict pancreatitis, hyperlipidemia and hepatotoxicity during treatment with PEG-Asparaginase in children with Acute Lymphoblastic Leukemia.

The study is planned to show whether monotherapies or combined hypolipemic therapy influence the fasting plasma glucose, serum adipokines (leptin, adiponectin, resistin) and proinflammatory cytokines (interleukin-6, TNF alpha) during 30 and 90 day course.

The role of hyperlipidemia and lipid lowering therapy (LLT) in Amyotrophic Lateral Sclerosis (ALS) pathophysiology and its impact on disease progression and survival is unclear. The investigators analyzed the correlation between lipid levels with disease progression and survival in ALS patients and the association of LLT with these outcomes.

To determine prospectively the role of elevated plasma triglyceride (TG) as a risk factor for 20-year coronary heart disease (CHD) mortality in familial combined hyperlipidemia (FCHL) and familial hypertriglyceridemia (FHTG), the familial forms of hypertriglyceridemia. Also, to perform genetic epidemiologic studies of recently identified lipoprotein risk factors for CHD, including Atherogenic Lipoprotein Phenotypes (ALP) based on subclasses of low-density lipoproteins (LDL), Lipoprotein(a) (Lp(a)) and apolipoprotein (apo) B plasma levels, and apo E isoforms.

The primary objective is to survey the efficacy of various commercially available statins (a class of lipid-lowering agents, for example, rosuvastatin, atorvastatin, simvastatin, lovastatin, pravastatin and fluvastatin) under local clinical practice in treating patients with hyperlipidemia. Surveillance data (Lipid Profile) will be collected during course of usual clinical practice or captured upon its availability.

A screening project of diabetics with a very high cardiovascular risk (e.g. diabetes plus coronary heart disease) who already receive cholesterol-lowering therapy. Lipid profile and rate of patients who are treated to target (which is <70mg/dl for such patients with very high risk) are screened. The doctors therapy decisions after the screening will be documented and 8-10 weeks later the lipid profile of each patient will be evaluated again. Our aim is to evaluate dosing habits, to evaluate how many patients are treated to their LDL-C target and to underline the importance of treating patients to their cholesterol targets.

To conduct epidemiologic surveys of the distribution, causes, and consequences of the dyslipoproteinemias. The Population Studies include the Prevalence Study, the Family Study, and the Mortality Follow-up Study and shared the same general population base.

To conduct focused studies of lipoprotein physiology and pathophysiology in genetically characterized patients with the objectives of understanding disease mechanisms, developing better treatments, and identifying and preventing early vascular disease.

Some HIV-infected adults develop lipodystrophy that includes significant changes in body shape, with fat losses in the face, arms and legs, and fat gain in the trunk. This lipodystrophy is often accompanied by other disorders of metabolism, such as increased levels of fat and insulin in the blood. The majority of these cases have been seen when patients are taking medications called protease inhibitors. These are anti-retroviral medications designed to treat patients with HIV. It is unclear if lipodystrophy is a result of having HIV or the medication used to treat HIV. It has been suggested, but not proven, that lipodystrophy is a direct side effect of protease inhibitors. In addition, it is unknown if HIV-infected children develop significant lipodystrophy after taking protease inhibitors. This study will investigate the prevalence of metabolic disorders and changes in body fat distribution in children taking protease inhibitor anti-retroviral medications. The results will be compared to three other groups; (1) children suffering from other non-HIV chronic infections, (2) HIV-infected children not taking protease inhibitors, and (3) healthy children. The study will look at HIV-infected children who have already started taking protease inhibitors. It will evaluate these children for disorders in metabolism as well as body fat changes. In addition, the study will follow HIV-infected children who will begin taking protease inhibitors. The study will follow these children for 18 months to detect the development of disorders in metabolism and / or body fat changes.

Animal studies have found that vitamin K-dependent proteins matrix Gla protein and osteocalcin beneficially influence lipid and glucose metabolism, respectively. However, this concept has not been tested in humans at risk for dyslipidemia and diabetes risk. Vitamin K supplementation presents an opportunity to test the hypothesized link between the vitamin K-dependent proteins and markers of lipid and glucose metabolism. The investigators will conduct an 8-week vitamin K intervention (to manipulate carboxylation of matrix Gla protein and osteocalcin) and determine its effects on markers of dyslipidemia and diabetes risk. Sixty obese children will be randomly allocated to either the control group receiving placebo or the low-dose (45 mcg/d) or high-dose group (90 mcg/d) receiving vitamin K (menaquinone-7).