Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The Study of Health Assessment and Risk in Ethnic groups (SHARE) is a study to determine the risk factors for atherosclerosis among three ethnic populations in Canada. Three hundred and thirty South Asian Canadian, 320 Chinese Canadian and 320 European Canadian men and women between 35 and 75 years of age are being randomly sampled from communities in Hamilton and Toronto, Ontario and Edmonton, Alberta for assessment of conventional (i.e., smoking, dyslipidemia, diabetes and hypertension) and emerging (i.e., candidate genes for atherosclerosis, homocysteine, fibrinolytic parameters, neurohormones, glucose intolerance, markers of infection, socioeconomic status, psychosocial status and diet) cardiovascular disease risk factors. Subclinical atherosclerosis is measured by quantitative B-mode ultrasonography of the carotid arteries, and other objective measures of vascular disease are a 12-lead electrocardiogram, a two-dimensional echocardiogram, ankle to arm blood pressure ratio and urine microalbumin concentration. The relationship between the conventional and emerging risk factors, and atherosclerosis, vascular disease and markers of end-organ damage will be evaluated between and within ethnic groups.
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PMID:The Study of Health Assessment and Risk in Ethnic groups (SHARE): rationale and design. The SHARE Investigators. 985 15

Immediate-release niacin manifests beneficial effects in cardiovascular disease with respect to dyslipidemic states. It lowers low-density lipoprotein (LDL) cholesterol, triglycerides, lipoprotein(a), and apoprotein B; at the same time, it increases high-density lipoprotein (HDL) cholesterol, HDL2, and apoprotein A-I. However, use of crystalline niacin has drawbacks: therapy requires multidose regimens, and side effects include flushing and pruritus. Slowing absorption with sustained-release formulations succeeds in decreasing flushing and increasing tolerance, but increases in hepatic enzyme levels have raised safety concerns. A new extended-release, once-daily formulation of niacin (Niaspan) shows promise in minimizing flushing while avoiding hepatotoxicity. A multicenter, randomized, double-blind clinical trial of Niaspan enrolled 122 patients with confirmed diagnosis of primary dyslipidemia (LDL cholesterol >4.14 mmol/L [160 mg/dL] and triglycerides <9 mmol/L [800 mg/dL]) into 3 treatment groups: (1) Niaspan 1,000 mg/day; (2) Niaspan 2,000 mg/day; and (3) placebo. The primary treatment endpoint was LDL-cholesterol level. This endpoint was not significantly affected by placebo (0.2% increase), but Niaspan decreased LDL cholesterol by 5.8% (1,000 mg/day) and 14.6% (2,000 mg/day) (p <0.001). Likewise, with placebo there were significant changes in total cholesterol, triglycerides, lipoprotein(a), and apoprotein B, whereas both Niaspan 1,000 and 2,000 mg/day significantly (p <0.001) decreased these parameters. In addition, both Niaspan groups showed significant (p <0.001) increases in HDL cholesterol (17% and 23%, respectively), including HDL subfractions. With respect to flushing, 20% of the placebo group reported at least 1 episode, whereas 88% and 83% of the Niaspon 1,000- and 2,000-mg/day groups, respectively, reported episodes. There was no hepatotoxicity as liver enzyme levels remained within clinically accepted limits in all treatment groups. However, Niaspan 2,000 mg/day showed a significant increase in aspartate aminotransferase compared with baseline and placebo. This trial demonstrated a cholesterol-modifying effect of Niaspan consistent with those reported for niacin, but demonstrated a better tolerance for flushing. Moreover, in contrast to sustained-release formulations, Niaspan showed relatively mild hepatic effects.
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PMID:A new extended-release niacin (Niaspan): efficacy, tolerability, and safety in hypercholesterolemic patients. 991 60

There is a high prevalence of type 2 diabetes mellitus and coronary artery disease among urban and migrant Asian Indians despite the absence of traditional risk factors. Evidence exists that Asian Indians are more hyperinsulinemic than Caucasians and that hyperinsulinemia may be important in the development of these diseases. To test whether insulin action was related to total or regional adiposity and to explore the potential role of plasma leptin and lipids, we measured insulin-mediated glucose disposal by the euglycemic insulin clamp, adipose distribution and muscle volume using computed axial tomography, and fasting serum leptin and lipid levels in 20 healthy Asian Indian male volunteers (age, 36 +/- 10 yr). A mean body mass index of 24.5 +/- 2.5 kg/m2 was associated with an unusually high percentage of body fat (33 +/- 7%). The majority of the fat was sc, and 16% was visceral (intraabdominal) adipose tissue. The majority (66%) of these nonobese men were insulin resistant. The mean fasting serum leptin level was 7.6 +/- 3.3 ng/mL. Insulin action was inversely correlated with visceral adipose tissue, not total or abdominal sc adipose tissue. In contrast, leptin levels correlated with sc and total (not visceral) adipose tissue. Serum triglyceride and high density lipoprotein cholesterol levels were inversely correlated with each other and were directly related to insulin resistance and visceral (not subcutaneous) fat. Increased visceral fat in Asian Indians is associated with increased generalized obesity, which is not apparent from their nonobese body mass index. Increased visceral fat is related to dyslipidemia and increased frequency of insulin resistance and may account for the increased prevalence of diabetes mellitus and cardiovascular disease in Asian Indians.
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PMID:Body composition, visceral fat, leptin, and insulin resistance in Asian Indian men. 992 74

Approximately 80% of all patients with diabetes die of cardiovascular disease. The traditional management of type 2 diabetes has been ineffective in altering this dismal prognosis. Insulin resistance is the fundamental defect of type 2 diabetes. Insulin resistance often leads to hyperinsulinemia, which is associated with hypertension, atherogenic dyslipidemia, left ventricular hypertrophy, impaired fibrinolysis, visceral obesity, and sedentary lifestyle. Although all these conditions are associated with atherosclerosis and adverse cardiovascular events, the therapeutic efforts in patients with diabetes have focused predominantly on normalizing glucose levels. Improved insulin sensitivity through lifestyle modifications or pharmacologic therapy (troglitazone and metformin) will lower both insulin and glucose levels as well as diminish dyslipidemia and hypertension. In contrast, sulfonylurea agents lower glucose by increasing insulin levels and may increase the risk of cardiovascular events. Therapy including aspirin, lipid agents (for example, statins), angiotensin-converting enzyme inhibitors, beta-adrenergic blockers, postmenopausal estrogen replacement, and vitamin E should be considered for patients with type 2 diabetes. In most patients with diabetes who have multivessel coronary artery disease, coronary artery bypass grafting is superior to coronary angioplasty for improving long-term cardiovascular prognosis. This superiority is mediated in part by the use of a left internal mammary graft to the left anterior descending coronary artery. Urgent coronary angioplasty or thrombolytic therapy should be considered for all patients with diabetes who have acute myocardial infarction.
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PMID:Improving the adverse cardiovascular prognosis of type 2 diabetes. 1006 57

Many patients with type 2 diabetes require insulin therapy for improved glycemic control after beta-cell failure. However, many physicians are reluctant to institute insulin therapy in type 2 diabetes for fear of accelerating atherosclerosis. The epidemiological evidence is reasonably sound that hyperinsulinism correlates with increased cardiovascular disease in nondiabetic people and those with early type 2 diabetes. It is much less clear, however, that insulin concentration plays a negative role when less well controlled diabetes is considered. The data are more consistent, in fact, with the glucose hypothesis, i.e., that hyperglycemia is a risk factor, although the magnitude of the glucose effect is not well defined. Certainly, the dysmetabolism associated with poor glycemic control could increase the risk of macrovascular events through well-known mechanisms. There is direct evidence that insulin therapy can reduce the risk of macrovascular events by improving glycemic control and diabetes-associated dyslipidemias, although the beneficial effects may be significantly compromised by excessive weight gain. Insulin therapy does not appear to induce hypertension independent of changes in body weight. It is concluded that optimal glycemic control confers a known benefit and can only be achieved with insulin therapy in some people with type 2 diabetes. In these circumstances, the use of insulin has a net benefit on cardiovascular risk, mediated primarily through improvement in dyslipidemia and glycemia itself.
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PMID:Effect of insulin therapy on macrovascular risk factors in type 2 diabetes. 1018 62

There is considerable evidence that insulin and insulin-like growth factors regulate a number of important physiological functions in a variety of tissues, some not considered to be classically insulin sensitive. Impaired biological responses to insulin and related insulin-like growth factors are referred to as insulin resistance. Persons with insulin resistance often display clinical abnormalities other than impaired glucose tolerance, including central obesity, hypertension, dyslipidemia, microalbuminuria, and abnormal coagulation and fibrinolytic systems. The mechanisms leading to development of insulin resistance are not fully understood. However, in addition to abnormalities of phosphorylation processes, it appears that alterations in cellular cation metabolism contribute to diminished cellular actions of insulin (i.e., glucose transport and hemodynamic actions). This review focuses on known cellular cation abnormalities and associated insulin resistance and cardiovascular disease.
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PMID:Insulin, cation metabolism and insulin resistance. 1021 36

Mild hyperhomocysteinemia, a putative risk factor for atherothrombotic cardiovascular disease morbidity and mortality, may contribute to the excess incidence of atherothrombotic outcomes in the dialysis-dependent end-stage renal disease population. Hemodialysis access (fistula or graft) thrombosis is an unfortunately common and costly morbidity in this patient population. In this study, using a prospective design, the potential relationship between baseline nonfasting, predialysis plasma total homocysteine (tHcy) levels and vascular access-related morbidity was examined in a cohort of 84 hemodialysis patients with a fistula or prosthetic graft as their primary hemodialysis access. Vascular access thrombotic episodes were recorded over a subsequent 18-mo follow-up period. Forty-seven patients (56% of the total) had at least one access thrombosis during the 18-mo follow-up period (median follow-up, 13 mo; rate, 0.6 events per patient-year of follow-up). Proportional hazards modeling revealed that each 1 microM/L increase in the tHcy level was associated with a 4.0% increase in the risk of access thrombosis (95% confidence interval, 1.0 to 6.0%, P = 0.008). This association persisted after adjustment for type of access (fistula versus graft), age, gender, time on dialysis, diabetes, smoking, hypertension, nutritional status, urea reduction ratio, dyslipidemia, and the presence of previous vascular disease. Elevated tHcy levels appear to confer a graded, independent increased risk for hemodialysis access thrombosis. A randomized, controlled trial examining the effect of tHcy-lowering intervention on hemodialysis access thrombosis appears to be justified.
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PMID:Plasma total homocysteine and hemodialysis access thrombosis: a prospective study. 1023 97

In Western countries, cardiovascular disease accounts for substantial morbidity and mortality. In the US, where medical costs and intervention rates are the highest in the world, the direct and indirect costs of cardiovascular disease and stroke have been estimated at $US274 billion (1998 dollars), with the costs of hospitalisation ($US119.9 billion) and lost productivity because of early mortality ($US77.9 billion) representing the largest proportions of this amount. Dyslipidaemia is an important risk factor for coronary heart disease (CHD), a condition which accounts for $US39.3 billion and $US37.9 billion (1998 dollars) in hospitalisation/nursing home costs and lost productivity, respectively, annually in the US. Similarly, the UK National Health Service spends more than 500 million pounds sterling annually on the treatment of CHD. Numerous studies have shown the benefit of lowering cholesterol levels in terms of decreasing CHD-associated morbidity and mortality; however, drug therapy costs for dyslipidaemia can be high. US and European treatment guidelines for dyslipidaemia recommend aggressive treatment for those at highest CHD event risk. Because of the high prevalence of dyslipidaemia in Western countries, these recommendations impact on a substantial proportion of the population and have increased the use of cholesterol-lowering medications. In a limited number of economic studies using clinical data from large prevention trials, the cost of drug therapy was nearly offset by the reduction in costs associated with hospitalisation and revascularisation procedures. Therefore, it appears that the strategy of identifying and treating individuals at highest risk for CHD, although expensive in terms of drug costs, would be expected to reduce the substantial direct and indirect costs associated with this condition.
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PMID:Resource utilisation in the management of dyslipidaemia. 1034 24

Polycystic ovary syndrome is a common problem affecting approximately 5% of women of reproductive age when defined by clinical features of anovulation and hyperandrogenism. Metabolic derangements associated with this condition may predispose to a range of diseases with attendant morbidity and mortality risks. In general, available data support significantly increased rates of type II diabetes mellitus, dyslipidemia, and endometrial cancer in PCOS that are not completely explained by obesity; data also suggest that rates of hypertension, gestational diabetes, and pregnancy-induced hypertension may likewise be increased, although the extent to which obesity mediates these risks is not clear. The increased prevalence of several cardiovascular risk factors in PCOS and limited cross-sectional data suggest that cardiovascular disease should be more likely in PCOS, but prospective data are lacking to confirm this supposition. Limited data have suggested an association between PCOS and ovarian cancer risk and require further study. The present data do not support an increased risk for breast cancer in this condition. Long-term prospective data are clearly needed to better delineate the nature and magnitude of disease risks associated with PCOS, with appropriate adjustment for associated obesity. Such information is a necessary background for understanding the role of established and emerging PCOS therapies, including oral contraceptives, intermittent progesterone, ovulation induction agents, and insulin sensitizers, in modifying such risks. In the meantime, close follow-up of women with PCOS and encouragement of lifestyle practices likely to reduce disease risks, such as regular exercise and weight control, should be standard practice.
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PMID:The epidemiology of polycystic ovary syndrome. Prevalence and associated disease risks. 1035 18

The metabolic syndrome consists of a cluster of metabolic disorders, many of which promote the development of atherosclerosis and increase the risk of cardiovascular disease events. Insulin resistance may lie at the heart of the metabolic syndrome. Elevated serum triglycerides commonly associate with insulin resistance and represent a valuable clinical marker of the metabolic syndrome. Abdominal obesity is a clinical marker for insulin resistance. The metabolic syndrome manifests 4 categories of abnormality: atherogenic dyslipidemia (elevated triglycerides, increased small low-density lipoproteins, and decreased high-density lipoproteins), increased blood pressure, elevated plasma glucose, and a prothrombotic state. Various therapeutic approaches for the patient with the metabolic syndrome should be implemented to decrease the risk of cardiovascular disease events. These interventions include decreasing obesity, increasing physical activity, and managing dyslipidemia; the latter may require the use of pharmacotherapy with cholesterol-lowering and triglyceride-lowering drugs.
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PMID:Hypertriglyceridemia, insulin resistance, and the metabolic syndrome. 1035 72


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