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

The metabolic syndrome represents the association in a single individual of a cluster of metabolic and hemodynamic factors, leading to an increased risk of type 2 diabetes and/or cardiovascular diseases. Several definitions exist (WHO, EGIR, NCEP-ATP III, AACE), but all of them include a cluster of criteria (hyper glycemia or type 2 diabetes, arterial hypertension, dyslipidemia, abdominal obesity) which increased these risks in parallel to their aggregation. The prevalence of the metabolic syndrome in industrialized countries represents 10 to 30% of the adult population, depending on the definition used and of the range of age, with a regular progression, particularly in women. Thus, it is needed to identify subjects with metabolic syndrome in the general population, and not only in overweight/obese subjects. This review, briefly presents the main definitions, as well as current data on pathophysiology, prevalence and consequences of the metabolic syndrome. Steps to diagnose it and guidance for the therapeutic management of metabolic syndrome in primary care practice are described.
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PMID:[How to manage the metabolic syndrome?]. 1595 95

Patients with diabetes mellitus have a 2- to 4-fold increased risk of atherosclerotic cardiovascular, peripheral vascular, and cerebrovascular disease, which are the leading causes of morbidity and mortality in this population. Several epidemiological studies have shown an association between diabetic dyslipidemia, which is characterized by hypertriglyceridemia, low levels of high density lipoprotein-cholesterol, postprandial lipemia and small, dense low density lipoprotein-cholesterol (LDL-C) particles, and the occurrence of cardiovascular disease. Other studies have established the beneficial effects of lipid lowering on the reduction of major coronary events in diabetic patients. The recent National Cholesterol Education Program (NCEP) Adult Treatment Panel III (ATP III) guidelines emphasize diabetes as a coronary heart disease risk equivalent. The NCEP ATP III states that elevated LDL-C is a major risk factor for coronary heart disease, and the primary goal of risk-reduction therapy is the reduction of LDL-C levels to 100 mg/dL. This article defines and describes diabetic dyslipidemia and its etiology and pathogenesis, as well as reviewing guidelines and recommendations for treatment of this disorder. Treatment of diabetic dyslipidemia includes 1) lifestyle modifications: physical activity and a diet low in saturated fats and cholesterol and high in complex carbohydrates and fiber; and 2) pharmacological treatment with (i) oral antihyperglycemic agents: metformin and thiazolidinediones; (ii) weight reduction drugs: orlistat and sibutramine and; (iii) lipid-lowering drugs: HMG-CoA reductase inhibitors, fibric acid derivatives, nicotinic acid, and bile acid sequestrants.
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PMID:Pathogenesis and management of diabetic dyslipidemia. 1596 59

At present, dyslipidemia is most commonly treated with drug therapy. However, because safety concerns regarding the use of pharmaceutical agents have arisen, a need for alternative nonpharmacological therapies has become increasingly apparent. The National Cholesterol Education Program (NCEP) Adult Treatment Panel III (ATP III) recommends lifestyle therapies, which include a combination of diet and exercise modifications, in place of drug treatment for patients who fall into an intermediate range of coronary heart disease (CHD) risk. This review examined the cholesterol lowering efficacy of the following 2 NCEP-recommended combination therapies: 1) low saturated fat diets combined with exercise, and 2) nutritional supplementation, i.e., fish oil, oat bran, or plant sterol supplementation, combined with exercise, in the treatment of dyslipidemia. Combination therapies are particularly advantageous because diet and exercise elicit complementary effects on lipid profiles. More specifically, diet therapies, with some exceptions, lower total (TC) and LDL cholesterol (LDL-C) concentrations, whereas exercise interventions increase HDL cholesterol (HDL-C) while decreasing triglyceride (TG) levels. With respect to specific interventions, low saturated fat diets combined with exercise lowered TC, LDL-C, and TG concentrations by 7-18, 7-15, and 4-18%, respectively, while increasing HDL-C levels by 5-14%. Alternatively, nutritional supplements combined with exercise, decreased TC, LDL-C, and TG concentrations by 8-26, 8-30, and 12-39%, respectively, while increasing HDL-C levels by 2-8%. These findings suggest that combination lifestyle therapies are an efficacious, preliminary means of improving cholesterol levels in those diagnosed with dyslipidemia, and should be implemented in place of drug therapy when cholesterol levels fall just above the normal range.
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PMID:Combination diet and exercise interventions for the treatment of dyslipidemia: an effective preliminary strategy to lower cholesterol levels? 1604 4

The recent ATP III classification defines metabolic syndrome as including > or = 3 of the following characteristics: abdominal adiposity, atherogenic dyslipidemia, high blood pressure, and insulin resistance. In these patients the visceral fat may produce inflammatory cytokines that may account for an enhanced cardiovascular risk. The treatment of obese patients is complex and often ineffective: patients may initially reduce weight but subsequently regain or even increase it, according to the so-called "yo-yo syndrome". Given the difficulties of treatment of patients with increased BMI, visceral adiposity, or metabolic syndrome, a multidisciplinary approach to these patients may yield more frequent positive results. The different strategies that may be applied, in varying mix targeted to the individual patient, include diet, drugs, educational and psychological support and, in few selected cases, surgery.
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PMID:[Obesity and metabolic syndrome: clinical and therapeutic review]. 1612 65

A decrease in the number of functional insulin-producing beta-cells contributes to the pathophysiology of type 2 diabetes. Opinions diverge regarding the relative contribution of a decrease in beta-cell mass versus an intrinsic defect in the secretory machinery. Here we review the evidence that glucose, dyslipidemia, cytokines, leptin, autoimmunity, and some sulfonylureas may contribute to the maladaptation of beta-cells. With respect to these causal factors, we focus on Fas, the ATP-sensitive K+ channel, insulin receptor substrate 2, oxidative stress, nuclear factor-kappaB, endoplasmic reticulum stress, and mitochondrial dysfunction as their respective mechanisms of action. Interestingly, most of these factors are involved in inflammatory processes in addition to playing a role in both the regulation of beta-cell secretory function and cell turnover. Thus, the mechanisms regulating beta-cell proliferation, apoptosis, and function are inseparable processes.
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PMID:Mechanisms of beta-cell death in type 2 diabetes. 1630 27

The objective of this study was to determine the proportion of Greek patients referred to outpatient clinics for dyslipidemia who achieved the low-density lipoprotein cholesterol (LDL-C) goal defined by the National Cholesterol Education Program Adult Treatment Panel III (NCEP-ATP III) guidelines, using lifestyle changes, lipid-lowering drug treatment (LLDT), or both. Adult patients with dyslipidemia, who had been receiving a hypolipidemic diet and/or LLDT for at least 3 months were assessed in a multicenter study performed at 66 sites across Greece. Patients were followed up for an additional 3-month treatment period. Lipid levels were recorded at baseline and at the end of the study. The primary endpoint was the proportion of patients achieving their individual LDL-C target at the end of the study, according to their coronary heart disease (CHD) risk status or its equivalents, as defined by the NCEP-ATP III guidelines. Multivariate logistic models were used to identify determinants of undertreatment. The study included 2,660 adults (20-75 years) from 7 regions of Greece. Of the evaluable sample (n = 2,211; men 51%; mean age 62 +/-9 years) 81% were receiving LLDT (96% with statins and 3% with fibrates), 44% had a history of CHD, 61% arterial hypertension, 36% diabetes, and 26% a family history of premature CHD. Overall, 6% were at low CHD risk, 30% at medium CHD risk, and 63% at high CHD risk. At the end of the study, 26% of all patients and 30% of those receiving LLDT achieved the NCEP-specified LDL-C target levels. The percentage of patients at LDL-C goal according to CHD risk status was: low risk 67% (95% CI = 59-75), medium risk 29% (95% CI = 26-33), and high risk 20% (95% CI = 18-22). Statins proved to be more effective than fibrates (p <0.0001). Atorvastatin-treated subjects (n = 1,222, mean dose 19 mg/day) attained the LDL-C target (31% of the cases) at a higher rate than those receiving other LLDT (n = 574, 26% at target, p <0.01) or not receiving drug treatment (n = 415, 8%, p <0.001). This outcome was more evident in the high-CHD risk group (n = 1,402, 26% with atorvastatin vs 16% with other LLDT and 3% not receiving LLDT attained the LDL-C goal, ANOVA, p <0.001). The majority of dyslipidemic patients receiving LLDT, mainly those with high-CHD risk, are not achieving the NCEP LDL-C target. This is mainly explained by inadequate dose titration to ensure target goals are met. Promoting healthy lifestyle and appropriate LLDT (potent statins with sufficient dose titration) must be implemented to ensure that patients attain LDL-C treatment goals and thus benefit from the reduction in individual CHD risk.
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PMID:The control of dyslipidemia in outpatient clinics in Greece (OLYMPIC) Study. 1632 50

It has been suggested that hyperuricemia and possibly gout are associated with the metabolic syndrome, but there have been no direct studies. This study was undertaken to obtain the prevalence of the metabolic syndrome in patients with gout and to compare it with those from the general population studies. This was a 4-institutional case-historical control study composed of 168 patients with gout. We assessed the prevalence of metabolic syndrome according to the ATP III criteria and compared the prevalence with that of the historical controls. To elucidate the factors in gout that were associated with metabolic syndrome, a multivariate analysis was done. The age-adjusted prevalence of metabolic syndrome in gout patients was 43.6%, which was significantly higher than that of the Korean control population (5.2%) from the previous studies. Patients with gout had more components of metabolic syndrome than did the controls. Body mass index (BMI, OR = 1.357 (95%CI 1.111-1.657)) and high density lipoprotein (HDL, OR = 0.774 (95%CI 0.705-0.850)) were the variables most significantly associated with the occurrence of metabolic syndrome in gout, but alcohol consumption did not show such associations. Gout is associated with the metabolic syndrome, and furthermore, obesity and dyslipidemia were the factors most associated with the syndrome in these patients.
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PMID:The prevalence of metabolic syndrome in patients with gout: a multicenter study. 1636 17

Dyslipidemia is an important, modifiable CHD risk factor. Previous studies have reported the prevalence of dyslipidemia particularly in urban populations. However, its prevalence in rural Northeast Thailand has not been well documented since extensive dietary and lifestyle transitions induced by the rapid socio-economic development of the late 1990s and early 2000s. The authors, therefore, conducted a cross-sectional assessment for the prevalence of dyslipidemia among rural Thais (in Khon Kaen province) using the National Cholesterol Education Program (NCEP) Adult Treatment Panel (ATP III) Guidelines. The 325 subjects recruited (136 men; 189 women) averaged 53.8 +/- 17.6 years of age (range, 20-88). After having the subjects fast 12 hours, serum samples were collected. Total cholesterol, triglycerides, low-density lipoprotein (LDL-C) and high-density lipoprotein (HDL-C) cholesterols were measured. The prevalence of hypercholesterolemia (> 200 mg/dL), hypertriglyceridemia (> 150 mg/dL), high LDL-C (> 130 mg/dL) and low HDL-C (< 40 mg/dL) was 31, 40, 20 and 14 per cent, respectively. Women had a 2- to 3.5-fold higher prevalence of hypercholesterolemia and high LDL-C than men, while the prevalence of hypertriglyceridemia was comparable. The prevalence of dyslipidemia increased with advancing age and increasing BMI; notwithstanding, a high prevalence of dyslipidemia was observed in the youngest tertile as well. In conclusion, the present study demonstrated a high prevalence of dyslipidemia in rural Thai adults; consequently, primary lipid screening should be considered for all ages.
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PMID:Prevalence of dyslipidemia in rural Thai adults: an epidemiologic study in Khon Kaen province. 1640 37

MDR1/ABCB1, MRP2/ABCC2, and breast cancer resistance protein (BCRP)/ABCG2 are expressed in the liver and intestine and contribute to the disposition of many drugs. Rosuvastatin, a 3-hydroxy-3-methylglutaryl-CoA reductase inhibitor for the treatment of patients with dyslipidemia, is primarily excreted via bile as unchanged drug. The present study was designed to determine whether rosuvastatin is transported by MDR1, MRP2, and BCRP. The apparent permeability value for rosuvastatin across MDR1-Madin-Darby canine kidney cells was low ( approximately 8 nm/s), and no directional transport was observed. Rosuvastatin uptake into control Sf9 membranes and membranes expressing MRP2 was similar in the presence or absence of GSH. In contrast, ATP dramatically stimulated rosuvastatin uptake into membranes expressing BCRP, but not control membranes. Rosuvastatin transport occurred into an osmotically sensitive space and was saturable. An Eadie-Hofstee analysis suggested that there were two transport sites in BCRP, with an apparent K(m) of 10.8 muM for the high affinity site and 307 microM for the low affinity site. These data demonstrate that rosuvastatin is transported efficiently by BCRP and suggest that BCRP plays a significant role in the disposition of rosuvastatin.
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PMID:ATP-dependent transport of rosuvastatin in membrane vesicles expressing breast cancer resistance protein. 1641 24

The Metabolic syndrome is a widely prevalent and multi-factorial disorder. The syndrome has been given several names, including- the metabolic syndrome, the insulin resistance syndrome, the plurimetabolic syndrome, and the deadly quartet. With the formulation of NCEP/ATP III guidelines, some uniformity and standardization has occurred in the definition of metabolic syndrome and has been very useful for epidemiological purposes. The mechanisms underlying the metabolic syndrome are not fully known; however resistance to insulin stimulated glucose uptake seems to modify biochemical responses in a way that predisposes to metabolic risk factors. The clinical relevance of the metabolic syndrome is related to its role in the development of cardiovascular disease. Management of the metabolic syndrome involves patient-education and intervention at various levels. Weight reduction is one of the main stays of treatment. In this article we comprehensively discuss this syndrome- the epidemiology, pathogenesis, clinical relevance and management. The need to do a comprehensive review of this particular syndrome has arisen in view of the ever increasing incidence of this entity. Soon, metabolic syndrome will overtake cigarette smoking as the number one risk factor for heart disease among the US population. Hardly any issue of any primary care medical journal can be opened without encountering an article on type 2 diabetes, dyslipidemia or hypertension. It is rare to see type 2 diabetes, dyslipidemia, obesity or hypertension in isolation. Insulin resistance and resulting hyperinsulinemia have been implicated in the development of glucose intolerance (and progression to type 2 diabetes), hypertriglyceridemia, hypertension, polycystic ovary syndrome, hypercoagulability and vascular inflammation, as well as the eventual development of atherosclerotic cardiovascular disease manifested as myocardial infarction, stroke and myriad end organ diseases. Conversely, treatment and consequent improvement of insulin resistance have been shown to result in better outcomes in virtually all of these conditions.
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PMID:Metabolic syndrome. 1650 79


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