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Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Periodontal disease is a chronic infection of the gums characterized by a loss of attachment between the tooth and bone, and by bone loss. We evaluated cross-sectionally the association between periodontal disease and C-reactive protein (CRP), fibrinogen, factor VII, tissue plasminogen activator (t-PA), LDL-C, von Willebrand factor, and soluble tumor necrosis factor receptors 1 and 2. The final sample consisted of 468 men (ages 47-80 yrs), participating in the Health Professional Follow-up Study, who provided blood and were free of CVD, diabetes, and cancer. In multivariate regression models controlling for age, cigarette smoking, alcohol intake, physical activity, and aspirin intake, self-reported periodontal disease was associated with significantly higher levels of CRP (30% higher among periodontal cases compared with non-cases), t-PA (11% higher), and LDL-C (11% higher). Based on our data, periodontal disease showed significant associations with biomarkers of endothelial dysfunction and dyslipidemia, which may potentially mediate the association between periodontal and cardiovascular disease.
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PMID:Periodontal disease and biomarkers related to cardiovascular disease. 1474 54

The ability of insulin to stimulate glucose disposal varies more than six-fold in apparently healthy individuals. The one third of the population that is most insulin resistant is at greatly increased risk to develop cardiovascular disease (CVD), type 2 diabetes, hypertension, stroke, nonalcoholic fatty liver disease, polycystic ovary disease, and certain forms of cancer. Between 25-35% of the variability in insulin action is related to being overweight. The importance of the adverse effects of excess adiposity is apparent in light of the evidence that more than half of the adult population in the United States is classified as being overweight/obese, as defined by a body mass index greater than 25.0 kg/m(2). The current epidemic of overweight/obesity is most-likely related to a combination of increased caloric intake and decreased energy expenditure. In either instance, the fact that CVD risk is increased as individuals gain weight emphasizes the gravity of the health care dilemma posed by the explosive increase in the prevalence of overweight/obesity in the population at large. Given the enormity of the problem, it is necessary to differentiate between the CVD risk related to obesity per se, as distinct from the fact that the prevalence of insulin resistance and compensatory hyperinsulinemia are increased in overweight/obese individuals. Although the majority of individuals in the general population that can be considered insulin resistant are also overweight/obese, not all overweight/obese persons are insulin resistant. Furthermore, the cluster of abnormalities associated with insulin resistance - namely, glucose intolerance, hyperinsulinemia, dyslipidemia, and elevated plasma C-reactive protein concentrations -- is limited to the subset of overweight/obese individuals that are also insulin resistant. Of greater clinical relevance is the fact that significant improvement in these metabolic abnormalities following weight loss is seen only in the subset of overweight/obese individuals that are also insulin resistant. In view of the large number of overweight/obese subjects at potential risk to be insulin resistant/hyperinsulinemic (and at increased CVD risk), and the difficulty in achieving weight loss, it seems essential to identify those overweight/obese individuals who are also insulin resistant and will benefit the most from weight loss, then target this population for the most-intensive efforts to bring about weight loss.
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PMID:Obesity, insulin resistance, and cardiovascular disease. 1474 3

The dyslipidemia of the metabolic syndrome is associated with alterations in triglyceride and high-density lipoprotein (HDL) metabolism. We examined the serum levels of glycosylphosphatidylinositol-specific phospholipase D (GPI-PLD), a minor HDL-associated protein, in a cohort with a wide range of insulin sensitivity. The mean serum GPI-PLD mass from 109 subjects was 58.9 +/- 18.4 microg/mL (mean +/- SD). GPI-PLD levels directly correlated with cholesterol, apolipoprotein AI, triglycerides, insulin, and homeostasis model assessment (HOMA) but not C-reactive protein. These results suggest that increased serum GPI-PLD is associated with the insulin resistance.
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PMID:Insulin resistance is associated with increased serum levels of glycosylphosphatidylinositol-specific phospholipase D. 1476 61

Cardiovascular disease (CVD) is the leading cause of mortality in women and a major cause of morbidity. Coronary heart disease (CHD) accounts for nearly half of all CVD deaths. Gender differences in CHD include a later age of onset for women, a greater prevalence of comorbid diseases, and differences in the initial manifestations of the disease. Traditional risk factors for CHD include tobacco use, hypertension, diabetes mellitus, dyslipidemia, obesity, sedentary lifestyle, and atherogenic diet. More recently identified risk factors in women include high sensitivity C-reactive protein (hsCRP), homocysteine, and lipoprotein (a). Appropriate management of risk factors is associated with a reduced incidence of CHD, yet poor implementation in women is widely documented. Barriers to optimal risk factor management in women should be identified and overcome in an effort to maximize the cardiovascular health of women.
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PMID:Epidemiology of coronary heart disease in women. 1496 52

There is increasing evidence that an ongoing cytokine-induced acute-phase response (sometimes called low-grade inflammation, but part of a widespread activation of the innate immune system) is closely involved in the pathogenesis of type 2 diabetes and associated complications such as dyslipidemia and atherosclerosis. Elevated circulating inflammatory markers such as C-reactive protein and interleukin-6 predict the development of type 2 diabetes, and several drugs with anti-inflammatory properties lower both acute-phase reactants and glycemia (aspirin and thiazolidinediones) and possibly decrease the risk of developing type 2 diabetes (statins). Among the risk factors for type 2 diabetes, which are also known to be associated with activated innate immunity, are age, inactivity, certain dietary components, smoking, psychological stress, and low birth weight. Activated immunity may be the common antecedent of both type 2 diabetes and atherosclerosis, which probably develop in parallel. Other features of type 2 diabetes, such as fatigue, sleep disturbance, and depression, are likely to be at least partly due to hypercytokinemia and activated innate immunity. Further research is needed to confirm and clarify the role of innate immunity in type 2 diabetes, particularly the extent to which inflammation in type 2 diabetes is a primary abnormality or partly secondary to hyperglycemia, obesity, atherosclerosis, or other common features of the disease.
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PMID:Inflammation and activated innate immunity in the pathogenesis of type 2 diabetes. 1498 10

A rapidly growing body of evidence demonstrates important associations between the metabolic syndrome, characterized by a cluster of risk factors or phenotypes that include dyslipidemia, central obesity, hypertension, and hyperinsulinemia, and both cardiovascular disease and type 2 diabetes. The purpose of the present study was to characterize the metabolic syndrome in a sample of 432 individuals from 68 Japanese-American families, using factor analysis of quantitative phenotypes, and to estimate the heritability of these independent factors. Using nine characteristic phenotypes that included LDL particle size and C-reactive protein (CRP), factor analysis identified three multivariate factors interpreted as lipids, body fat/insulin/glucose/CRP, and blood pressure, explaining 65% of the variance. Heritability analysis revealed significant genetic effects on all of the factors: lipids (h(2) = 0.52, P < 0.001), body fat/insulin/glucose/CRP (h(2) = 0.27, P = 0.016), and blood pressure (h(2) = 0.25, P = 0.026). This analysis shows that independent, multivariate factors of the metabolic syndrome are heritable, demonstrating genetic influences on the underlying pathophysiological mechanisms of the syndrome.
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PMID:Heritability of multivariate factors of the metabolic syndrome in nondiabetic Japanese americans. 1504 37

Evolution of the National Cholesterol Education Program (NCEP) Adult Treatment Panel (ATP) guidelines for lipid lowering reflects a movement toward global risk assessment, including improved identification of risk in individuals without established coronary heart disease (CHD), and toward more aggressive lipid-lowering targets to reduce CHD risk. The current guidelines, for example, identify a segment of the population without established CHD as being at high risk on the basis of criteria that indicate CHD risk equivalency, recommend a low-density lipoprotein cholesterol (LDL-C) plasma level <100 mg/dL as optimal in all individuals, and establish the metabolic syndrome as a secondary target for therapeutic intervention. Many questions remain for future guidelines to address: To what extent should plasma levels of LDL-C be lowered by therapy to afford optimal risk reduction? Can risk assessment be improved, e.g., by using novel risk measures (such as high-sensitivity C-reactive protein) to indicate patients at higher risk who may benefit from more aggressive interventions? Should the metabolic syndrome be considered a high-risk state warranting aggressive intervention irrespective of risk categorization using current scoring methods? Guidelines for lipid management represent a synthesis of constantly emerging and evolving data: ongoing efforts to improve understanding of the relation between dyslipidemia and cardiovascular disease, to increase knowledge of and ability to measure other CHD risk factors, and to improve therapeutic practices and options will be reflected in future guidelines.
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PMID:Past, present, and future standards for management of dyslipidemia. 1505 Jan 86

Cardiovascular disease is the leading cause of death in the industrialized world, and a number of well-characterized factors, including advanced age, hypertension, dyslipidemia, diabetes, and smoking, contribute to cardiovascular risk. Integration of these factors using the Framingham calculation estimates the absolute 10-year risk for coronary heart disease (CHD), which can be used to guide therapy. Recent studies have demonstrated that additional markers, including elevated lipoprotein(a), homocysteine, sitosterol, and particularly C-reactive protein (CRP), are also associated with increased risk for CHD. In particular, high-sensitivity CRP has been shown to identify patients with high CHD risk who may not have elevated low-density lipoprotein cholesterol (LDL-C) and may add to the predictive value of the Framingham functions for CHD risk assessment. Assessment of global risk is particularly important in lipid management, as the LDL-C target goals are determined by risk category.
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PMID:Assessing coronary heart disease risk with traditional and novel risk factors. 1523 85

Dyslipidemia is an important risk factor for cardiovascular disease in patients with chronic renal failure (CRF). We evaluated the safety and efficacy of atorvastatin in patients with dyslipidemia associated with CRF who were undergoing hemodialysis (HD). Thirty-five patients who were receiving HD were given atorvastatin (10 mg/d) for 3 months. Chylomicron (CM), light and dense very-low-density lipoprotein (VLDL), intermediate-density lipoprotein (IDL), and light and dense low-density lipoprotein (LDL) were separated by ultracentrifugation. Apolipoprotein (apo) B was measured by electroimmunoassay. Mean LDL particle diameter was measured by gradient gel electrophoresis. Atorvastatin therapy reduced LDL-cholesterol (C) by 36% and remnant-like particle (RLP)-C by 58%. Atorvastatin significantly reduced apo B, apo CIII, and apo E in VLDL by 40% to 46% and IDL-apo B by 66%. Atorvastatin also significantly reduced cholesterol in CM, light VLDL, and dense VLDL without consistently affecting triglyceride (TG) in these lipoproteins. Atorvastatin similarly reduced both light and dense LDL-apo B by 38%. LDL particle size in the HD patients significantly increased during atorvastatin treatment from 25.7 +/- 0.4 to 26.2 +/- 0.6 nm. High sensitive C-reactive protein (HS-CRP) was halved by atorvastatin decreasing from 0.08 +/- 0.05 to 0.04 +/- 0.03 mg/dL. Atorvastatin treatment did not affect the creatinine kinase level, and no classical adverse effects were observed during the study. These results suggest that atorvastatin is safe and effective for the management of dyslipidemia in patients with CFR who are receiving HD, which may help to suppress the development of atherosclerosis.
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PMID:Effects of atorvastatin on triglyceride-rich lipoproteins, low-density lipoprotein subclass, and C-reactive protein in hemodialysis patients. 1533 69

Impairment of peroxisome proliferator-activated receptor-gamma (PPAR-gamma), a nuclear receptor that regulates genes involved in lipid and glucose metabolism, may contribute to the onset of metabolic disorders such as diabetes and the accompanying dyslipidemia. Fat-derived tumor necrosis factor alpha (TNF-alpha) and the acute-phase response protein, C-reactive protein (CRP), may also have a role in the development of obesity-related insulin resistance and type 2 diabetes mellitus. In this study, a group of 14 naturally occurring, insulin-requiring, type 2 diabetic cynomolgus monkeys were used to evaluate the effects of the PPAR-gamma agonist, rosiglitazone, on glycemic and lipid parameters and serum levels of TNF-alpha and CRP. The animals were randomized into 2 groups of 7. One group was treated with 0.5 mg/kg rosiglitazone orally once a day for 7 weeks. Blood was collected for evaluation at baseline, at 2 and 7 weeks during the treatment period, and at 7 and 13 weeks after treatment. Daily insulin requirements were recorded during the entire study. Results showed daily exogenous insulin requirements were significantly reduced (P <.01) in those treated with rosiglitazone, while glycemic control was maintained. Plasma triglyceride concentrations were significantly lower (P <.01) whereas plasma cholesterol levels tended to be lower and high-density lipoprotein (HDL) concentrations tended to be higher after treatment. No significant differences were noted in TNF-alpha and CRP serum levels during the treatment period. Body weights remained steady in both groups during the study. These results suggest overall improvement in insulin regulation and lipid profiles during treatment with rosiglitazone.
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PMID:Rosiglitazone treatment improves insulin regulation and dyslipidemia in type 2 diabetic cynomolgus monkeys. 1533 71


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