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Query: UMLS:C0948265 (metabolic syndrome)
 24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clustering of risk factors for cardiovascular disease (CVD) and non-insulin-dependent diabetes mellitus (NIDDM) in obese patients may be attributable to a disturbed metabolism caused by hypophosphataemia. A low serum phosphate (S-P) level may be a limiting factor for glucose metabolism and may account for hyperglycaemia, with an increased risk of NIDDM and hypertension and consequent increased risk of stroke. Low S-HDL levels, known to exist in the metabolic syndrome, as well as high serum triglycerides may also have been the results of phosphate depletion. The hypothesis presents a new serious disturbance which accounts for the dyslipidaemia, hyperglycaemia and the hypertension in metabolic syndrome. The proposed causal relationship between low S-P and the clustering of risk factors is based on results from a cross-sectional study of obese patients, where low S-P was associated with high body mass index (BMI), high blood glucose (B-glu), high systolic blood pressure (SBP), high diastolic blood pressure (DBP), but low serum high density lipoprotein (S-HDL) and serum magnesium (S-Mg) levels. Knowledge from experimental and clinical studies on hypophosphataemia and/or phosphate depletion are referred to when discussing the hypothesis.
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PMID:Hypophosphataemia: cause of the disturbed metabolism in the metabolic syndrome. 1139 16

Obesity is one of the most important predictors and causes of such lifestyle diseases as metabolic syndrome, type 2 diabetes, and cardiovascular disease. It is thus imperative to follow the trend longitudinally in the population. Measurement of obesity in children and adolescents is difficult; many studies use the body mass index as a measure, regardless of the fact that it is inappropriate. Skinfolds or the ponderal index should be used, instead. Recent Danish studies suggest that the incidence of childhood and adolescent obesity is increasing and that those who are overweight are even more so today than earlier. Obesity is caused by a number of factors, genetic, social, environmental, and lifestyle, all of which play an important role. One of the main causes of the increase in childhood obesity in Denmark today is the lower level of physical activity than formerly. The prospects for the future are an increase in obesity and incidence of lifestyle diseases with a poorer quality of life and a shorter life time expectancy.
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PMID:[Obesity among children--with particular reference to Danish circumstances]. 1140 67

Considerable progress has been made in our understanding of the role of high heart rate in determining cardiovascular morbidity and mortality. However, whether the association between fast heart rate and cardiovascular disease is equally strong in males and females is still a matter for debate. In most studies, the predictive value of tachycardia for all-cause mortality has been found to be weaker in women than in men, and in some studies no association between heart rate and cardiovascular mortality was observed. In particular, high heart rate appeared to be a weak predictor of death from coronary heart disease in the female gender. Multiple mechanisms by which sympathetic overactivity could cause hypertension and the metabolic syndrome of insulin resistance have been documented. Recent results obtained at the Ann Arbor laboratory from the analysis of four populations indicate that these mechanisms are operative mostly in males in whom tachycardia reflects a heightened sympathetic tone. In women, fast heart rate would merely represent the extreme of a normal distribution. However, tachycardia can also have a direct impact on the arterial wall, as demonstrated in laboratory studies, and can favour the occurrence of cardiac arrhythmias. The impact of these mechanisms may be similar in men and women and could explain why a high heart rate has been found to have a detrimental effect also in the female gender. Pharmacological reduction of high heart rate is an additional desirable goal of therapy in several clinical conditions such as hypertension, myocardial infarction and congestive heart failure. Although a greater effect is expected in men, cardiac slowing could counteract the detrimental haemodynamic effect of tachycardia also in women.
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PMID:Heart rate as a cardiovascular risk factor: do women differ from men? 1140 41

Dyslipidemia emerges as an important modifiable risk factor for cardiovascular disease in diabetes mellitus, especially as part of the metabolic syndrome in type 2 diabetes. In type 1 diabetes mellitus, tight glucose regulation usually will correct dyslipidemia. Both total cholesterol and triglyceride levels predict cardiovascular disease in diabetes, and HDL-cholesterol may prove to be an even better predictor. In type 2 diabetes, increased triglyceride and reduced HDL-cholesterol levels are the key characteristics of dyslipidemia. Increased hepatic VLDL production and impaired catabolism of triglyceride-rich particles contribute to hypertriglyceridemia. Subsequent formation of small dense LDL particles leads to increased atherogenicity. Small dense LDL particles have a longer circulation time, are susceptible to glycoxidation, and are taken up by macrophages and the vessel wall. Post-hoc analysis of diabetic subgroups in primary and secondary prevention trials suggest that individuals with diabetes may enjoy substantial cardiovascular risk reduction from lipid-lowering therapy. Trials prospectively addressing the benefit of lipid lowering therapy in diabetes are under way. Target levels for lipid lowering therapy in diabetes at present stem from pathophysiological plausibility rather than from clinical proof. Intensive lipid-lowering with a statin in adequate dosage or a combination of a statin and a fibrate may be used to lower LDL-cholesterol levels to values < 2.6 mmol/l and triglyceride levels to < 1.7 mmol/l, a value at which few small dense LDL particles remain in circulation. Effective medication to raise HDL-cholesterol levels adequately are not yet available for clinical use. Treatment of diabetic dyslipidemia should be as simple as possible, given the polypharmacy that is often necessary for the patient with diabetes. Therefore, single treatment with a statin in adequate dosage is the first choice.
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PMID:Lipid-lowering therapy in diabetes mellitus. 1141 34

The metabolic syndrome consists of a cluster of metabolic disorders, many of which promote the development of atherosclerosis and increase the risk to develop cardiovascular disease. The metabolic syndrome is characterized by atherogenic dyslipidemia (elevated triglycerides, increased small dense low-density lipoproteins, and decreased high-density lipoproteins), hypertension, insulin resistance and obesity. To decrease the risk of cardiovascular disease events decreasing body weight by ingesting a healthy diet, increasing physical activity, cessation of smoking and managing dyslipidemia are recommended. Pharmacological treatment of dyslipidemia is based on different drug classes. For LDL-cholesterol-lowering mainly statins and for triglyceride-lowering mainly fibrates are used. In primary and secondary prevention trials of heart disease they have shown to reduce the incidence of coronary artery disease or coronary events by 25-60 percent. Statins reduce mainly LDL-cholesterol levels by competitive inhibition of HMG-CoA reductase but have also shown to reduce fasting and postprandial triglyceride levels. Fibrates effectively reduce fasting and postprandial lipemia, shift the distribution of LDL particles towards less dense particles and increase HDL-cholesterol. Thus fibrates particularly address components of the metabolic syndrome and features of diabetic dyslipidemia. However studies still are needed showing definite evidence on differential therapy in lipid lowering based on prospective controlled trials with endpoints of macro- and microangiopathy in diabetic patients.
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PMID:Treatment of dyslipoproteinemia in the metabolic syndrome. 1145 42

In 1999 WHO published the new recommendations for diagnostic criteria for diabetes. The same publication introduced several new categories including the first proposal for diagnostic criteria for the metabolic syndrome. Also, WHO established a new category labelled "impaired fasting glycaemia", and thereafter this new group and the already established impaired glucose tolerance was combined as a common entity labelled "impaired glucose regulation".--These recommendations from WHO followed a decision in the American Diabetes Association to lower the diagnostic plasma glucose threshold for diabetes in the fasting state from 7.8 to 7.0 mmol/l and to use fasting values as the diagnostic test for diabetes. The suggested changes in the diagnostic criteria will include a new group of individuals as having diabetes, while others may be left undiagnosed if fasting glucose values are used as the only diagnostic criteria. The consequence of this has been analysed by several groups including the collaborative European activity (the DECODE-study).--This review summarises the findings. One major problem is that if fasting glucose values are used as the only diagnostic criteria in screening for diabetes, approximately one third of the diabetic individuals will be left undiagnosed. Furthermore, this group is the group of diabetic patients that have the highest mortality from cardiovascular disease and stroke, and the group with the worst cardiovascular risk profile compared to individuals with elevated fasting glucose values alone. This observation raises the need for a continued use of the oral glucose tolerance test in selected groups.
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PMID:The new classification of diabetes mellitus and IGT: a critical approach. 1146 May 96

The triglyceride (TG) level is one of several lipid parameters that can aid prediction of coronary heart disease (CHD) risk. An elevated plasma TG level is strongly associated with an increased risk of CHD. Hypertriglyceridemia, the second most common dyslipidemic abnormality in hypertensive subjects after increased low-density lipoprotein cholesterol (LDL-C), is defined by the National Cholesterol Education Programme (NCEP) as a fasting TG level of > 2.26 mmol/l (> 200 mg/dl) and is recognised as a primary indicator for treatment in type IIb dyslipidemia. Raised TG levels can be present in individuals at risk for CHD when the total cholesterol is normal. However, not all individuals with raised TG levels have increased risk of CHD. Factors such as: diet, age, lifestyle, and a range of medical conditions, drug therapy and metabolic disorders, can all affect the TG level. In some of these circumstances, other factors protect against the risk of CHD, and can minimise or negate the effect of the risk factors present. Although TG reducing therapy has been shown to be associated with an improved clinical outcome, more research is needed to determine whether this is an independent effect of TG reduction or an effect of normalising the overall lipid profile in hypertriglyceridemic patients. Further trials are required to quantify the clinical benefits of lowering TG to 'target' levels and to confirm targets defined by NCEP-II (shown in Table 1). The role of TG in CHD pathogenesis is thought to involve several direct and indirect mechanisms, such as effects on the metabolism of other lipoproteins, transport proteins, enzymes, and on coagulation and endothelial dysfunction. More research is required to fully elucidate the role of TG, the ways in which it can influence other risk factors and the mechanism of its own more direct role in the atherogenic process. Patients with hypertriglyceridemia have been shown to respond well to dietary control and to the use of lipid lowering drugs such as 3-hydroxy-3-methylglutaryl-Coenzyme A (HMG CoA) reductase inhibitors (known as statins), fibrates and nicotinic acids. However, recent retrospective real-life clinical studies show that only 38% of patients receiving some form of lipid-lowering therapy achieved NCEP-defined LDL-C target levels, demonstrating the need for the use of more aggressive treatment. In hypertriglyceridemic patients, the newer statins, cerivastatin and atorvastatin, have shown comparable efficacy in reducing TG compared with the older statins. Achieving NCEP target lipid levels has been shown to reduce the risk of cardiovascular disease in dyslipidemic individuals, including high-risk patient groups such as those with additional risk factors, existing heart disease, diabetes mellitus and metabolic syndrome. Although the latest clinical studies investigating combination therapies, i.e. dual therapy with both a statin and a fibrate, have demonstrated them to be effective for overall control of lipid parameters and reducing coronary events, it is not yet clear whether this offers any significant advantage over monotherapy. Results from ongoing longer-term end-point clinical studies may provide further information in this area and consequent reviews of primary care management policies for dyslipidemia. Statin monotherapy may be a reliable option for primary care treatment of dyslipidemia (including hypertriglyceridemia).
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PMID:Hypertriglyceridemia: a review of clinical relevance and treatment options: focus on cerivastatin. 1146 48

For the care of an expanding segment of the US population with multiple coronary risk factors, combination lipid-altering therapy is emerging as a treatment imperative. The most recent National Cholesterol Education Program's consensus guidelines emphasize long-term global coronary heart disease (CHD) risk status, designate patients with CHD risk equivalents (eg, diabetes, peripheral arterial disease, 20% or more 10-year absolute CHD risk) for aggressive lipid-altering therapy, and deem the metabolic syndrome (eg, obesity, insulin resistance, hypertension, elevated triglycerides, low levels of high-density lipoprotein cholesterol, small dense low-density lipoprotein particles) as a secondary target for intervention. With the advancing age of the US population and the high prevalence of diabetes, the metabolic syndrome, and CHD, increasing numbers of patients will require a more balanced metabolic attack attainable only through combination lipid-altering regimens. Many of these patients, as well as persons at heightened risk for cardiovascular disease because of a range of heritable conditions (eg, familial hypercholesterolemia, familial combined hyperlipidemia), will undoubtedly require binary or ternary regimens involving statins in concert with niacin, fibric-acid derivatives, or bile acid resins. Such approaches enable the clinician to exploit the complementary effects of these agents, allowing them to be administered at low, optimally tolerable doses that are consistent with superior efficacy and a lower risk of adverse events as compared with escalating doses of monotherapy.
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PMID:Combination lipid-altering therapy: an emerging treatment paradigm for the 21st century. 1148 48

Insulin resistance, and the compensatory hyperinsulinemia that results, has been linked to a host of defects including glucose intolerance, diabetes, hypertension, dyslipidemia, endothelial dysfunction, impaired fibrinolysis, and subclinical inflammation. Patients with this metabolic syndrome have a markedly increased risk for the development of atherothrombotic cardiovascular disease. The characteristic dyslipidemia of insulin resistance consists of elevated triglyceride and triglyceride-rich lipoprotein levels, low levels of high-density lipoprotein cholesterol, and increased concentrations of small, dense low-density lipoprotein cholesterol. Management of this dyslipidemia typically involves a dual approach. Lifestyle modification is an essential component of any successful treatment plan, but alone is usually insufficient to correct these lipoprotein abnormalities. Medications that diminish insulin resistance and directly alter lipoproteins are also necessary in the majority of cases. Combinations of therapeutic agents are often required to optimize attainment of treatment goals.
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PMID:Pathophysiology and treatment of the dyslipidemia of insulin resistance. 1150 79

It is well recognized that aberrant fat localization such as visceral obesity rather than total body fat mass is a major risk factor for cardiovascular disease and type 2 diabetes mellitus. During recent decades, several studies have described a range of metabolic disturbances associated with abdominal obesity, including glucose intolerance, hyperinsulinaemia, insulin resistance, hypertension and dyslipoproteinaemia, now widely known as the metabolic syndrome. Several abnormalities in the hypothalamic-pituitary axis have been described associated with visceral obesity, suggesting a central neuroendocrine dysregulation including increased cortisol concentration and impaired gonadotropin and growth hormone (GH) secretion. Some steps in the chain of events in this theory still remain unclear, however, although these findings have introduced new therapeutic possibilities. These include therapy with sex steroids in both viscerally obese men and women, and several attempts to use GH to treat the endocrine abnormalities present in visceral obesity. The results of these studies are promising, but the therapies are still not recommended for general use.
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PMID:Visceral obesity and the role of the somatotropic axis in the development of metabolic complications. 1152 97


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