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

Authors analysed the cardiovascular risk factors, their relationship to each other, the rate of multiple appearance in 1476 patients (774 men, 702 women) with essential hypertension. They produced a special questionnaire and risk factor analysing program for performing static and dynamic investigations on the base of international and domestic experiences. The data of their investigations verified, that the occurrence of obesity is very frequent and is associated with abnormal cholesterol and triglyceride values. The appearance of glucose metabolism disorder was in 44% of patients. The rate of metabolic syndrome can be estimated on 25-30% in the hypertensive population.
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PMID:[Cardiovascular risk factors in essential hypertension]. 1134 Sep 43

The essential arterial hypertension is the second (after diabetes mellitus) cause of chronic renal failure which means a great social and economic burden to the society. It is well known that hypertension is a metabolic syndrome resulting in tissue injury. We tried to investigate the possible influence of some metabolic disturbances on renal function in nontreated essential hypertension. We have compared 25 patients with nontreated essential hypertension (11 women, 14 men) with 14 healthy volunteers (7 women, 7 men) matched for age. The patients' group was characterized by significantly higher urine excretion of NAG (N-acetyl-beta-D-glucosaminidase) (2.75 +/- 1.69 vs 1.82 +/- 1.46 p < 0.05) and a tendency to significantly higher urine fractional sodium excretion without significant difference in albumin excretion. These findings suggest that the tubular damage is present. We noticed the negative linear correlation between mean arterial pressure and (MAP) and NAG urine excretion in the group of hypertensive patients which may reflect the renal ischemia in tubulo-interstitial pathology. Our data suggests that in nontreated arterial hypertension the renal blood flow disturbances are the important cause of the deterioration of tubular function (which are earlier to glomerular damage).
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PMID:[Does any relationship exist between metabolic disturbances and some markers of renal damage in patients with untreated essential hypertension?]. 1139 62

In essential hypertension (EHT) the presence of a metabolic syndrome increases the risk of cardiovascular disease. A cell membrane abnormality is implicated but its role in cardiovascular disease is unclear. Neutrophil accumulation, which occurs by beta2-integrin (CD11b/CD18) expression, followed by release of proinflammatory factors from primary vesicles is an important factor in vascular damage. CD11b and CD69 expression on neutrophils from normal controls and EHT patients was determined by fluorescence-activated cell scanning. Neutrophils were activated with phorbol myristate acetate (PMA). Protein kinase C (PKC) and calpain were inhibited with bisindolylmaleimide and E64d, respectively. In EHT patients CD11b was not increased on neutrophils at rest. However, EHT neutrophils more readily expressed CD11b on incubation in phosphate-buffered saline and more cells went on to exocytose primary granules indicated by expression of CD69. Stimulation with PMA caused more rapid activation in EHT neutrophils with expression of CD11b, followed rapidly by exocytosis of primary granules. Bisindolylmaleimide slowed but did not prevent CD11b expression, which, together with primary granule exocytosis, continued to be faster in EHT neutrophils. E64d also slowed but did not prevent either CD11b expression or primary granule exocytosis, but this inhibitor did abolish the difference between NC and EHT neutrophils. The membrane abnormality in EHT may contribute to cardiovascular risk by increasing the rate of vesicle fusion with the cell membrane to increase neutrophil accumulation and release of inflammatory agents at sites of vascular damage. Calpain activation may be the rate-limiting component that is abnormal.
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PMID:Rapid fusion of granules with neutrophil cell membranes in hypertensive patients may increase vascular damage. 1158 60

Studies on the role of parental history on the risk of developing metabolic syndrome (MS) show inconsistent data that may depend on misclassification of the parental history. Confirming carefully the parental phenotype (PF) of type 2 diabetes mellitus (DM) and essential hypertension (EH) of participants' parents, we determined the relationship between PF of either DM or EH and the risk of developing MS in Mexican individuals. A case-control study of 210 subjects randomly recruited from Durango, Mexico was carried out. Subjects with MS (cases) were compared with a control group of subjects without MS matched by age and gender. MS was defined by the presence of two or more of the following: fasting glucose > or =7.0 mmol/l; blood pressure > or =160/90 mmHg; fasting triglycerides > or =1.7 mmol/l and/or HDL-cholesterol <1.0 mmol/l; and obesity (body mass index > or =30 kg/m2 and/or waist-to-hip ratio > or =0.85). The PF of DM and EH was confirmed by direct clinical examination and/or review of certificates of death of each of the participants' parents. Incomplete or unclear data about PH were exclusion criteria. Multivariate analysis showed that PF of DM without EH (odds ratio (OR) 2.6; 95% CI, 1.3-7.8, p=0.044) and PF of both DM and EH (OR, 3.1; 95% CI, 1.5-9.1, p=0.0001), but not the PF of EH without DM are independent predictors for developing MS in Mexican individuals. In the offspring generation of Mexican subjects, the PF of DM seems to increase the risk of developing MS, whereas PF of EH does not.
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PMID:The parental phenotype of diabetes, but not of essential hypertension, is linked to the development of metabolic syndrome in Mexican individuals. 1175 7

Human hypertension is a common and complex disease and is associated with diabetes, cardiovascular, and renal disease. Therefore, it is important to understand the genetic basis of this disease. Specific genetic mutations leading to monogenic forms of hypertension have been identified in Liddle's syndrome and glucocorticoid-remediable hypertension and in some syndromes in which blood pressure is lowered. Because essential hypertension is a polygenic disease, elucidating a genotype that is causally related to essential hypertension will be difficult. To date, no genotype has been conclusively linked to essential hypertension except in certain populations. However, there has been progress in finding genetic variations that are associated with hypertension in patients with components of the metabolic syndrome (or Syndrome X). Future discoveries in this area should enhance our ability to intervene earlier and more effectively and therefore lessen the complications of this common disease.
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PMID:The genetics of human hypertension. 1178 66

Insulin resistance and compensatory hyperinsulinemia are recognized not only in type 2 diabetes mellitus(DM) but also in essential hypertension(EHT), hyperlipidemia and obesity; these are known as the components of metabolic syndrome and accumulation of these components increase risk of cardiovascular diseases(CVD). When coronary angiographic findings were evaluated in patients with coronary artery disease(CAD), the severity was higher in CAD with DM than that without DM. Even in CAD without DM, the severity of coronary angiographic findings was higher in CAD with insulin resistance than that without insulin resistance. When residents of rural communities in Japan were followed 8 years, the incidence of CVD was 3.5 times higher in subjects with insulin resistance than those without insulin resistance. One of the intracellular signal transduction of insulin receptor; MAP kinase may be concerned atherosclerotic mechanisms of insulin resistance. These findings suggest that insulin resistance is a significant background of atherosclerosis, and insulin resistance is one of the major facilitation factors of genesis and progression of CVD.
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PMID:[Significance of insulin resistance to atherosclerotic complications in essential hypertension]. 1473 36

Metabolic syndrome represents a cluster of clinical, biochemical and humoral abnormalities associated with impaired insulin action in glucose metabolism. In the literature also the term syndrome of insulin resistance, dysmetabolic syndrome X, Reaven syndrome or Kaplans dead quartet can be found. Hyperinsulinaemia, central obesity, essential hypertension, dyslipidaemia, impaired glucose homeostasis or type 2 diabetes, hyperuricaemia, hypercoagulable state, endothelial dysfunction and increased markers of inflammation such as C-reactive protein, selectines, adhesion molecules, pro-inflammatory cytokines are the typical components of metabolic syndrome increasing the risk of cardiovascular complications. List of currently recognized clinical and biochemical manifestations continues to expand and include also non-alcoholic steatohepatitis, polycystic ovaric syndrome (PCOS), hyperhomocysteinaemia and others. No standard definition of metabolic syndrome has been routinely used. The WHO initially proposed a definition of metabolic syndrome in 1998, and more recently NCEP-ATP III provided a new working definition in 2001, which is more suitable for clinical practice. Prevalence of metabolic syndrome is very high, about 25-30% in Caucasians, depending on diagnostic criteria used. The clinical significance of metabolic syndrome is augmented by its association with increased and accelerated atherosclerosis. Whether IR predicts cardiovascular disease (CVD) independently of diabetes and other CVD risk factors is still a matter of controversy. Recently there is a growing evidence that metabolic syndrome increases also the risk of all-cause mortality and risk of certain tumors.
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PMID:[The metabolic syndrome]. 1504 Jan 52

Hyperinsulinemia and insulin resistance are commonly observed in essential hypertension, which is part of the metabolic syndrome. The aim of this study was to examine whether insulin secretion abnormalities or alterations in insulin sensitivity and glucose tolerance are also present in healthy men, offspring of patients with essential hypertension. Twelve young (27 +/- 3.6 years), lean normotensive offspring were compared with 14 age-, sex-, and body mass index (BMI)-matched controls without a family history of hypertension, diabetes mellitus, and coronary heart disease. We studied glucose tolerance, insulin secretion, and sensitivity using 10-hour hyperglycemic and 10-hour hyperinsulinemic-euglycemic clamps (HIC). Glucose tolerance was comparable in the offspring and controls. However, the offspring had higher insulin and C-peptide levels during the hyperglycemic clamp (HGC) compared with controls (P <.05). There was no difference in the early phase of insulin secretion between the groups. The insulin sensitivity index (glucose infusion rate/serum insulin) was significantly lower in the offspring during both clamps. Moreover, the offspring had higher systolic (P <.001) and diastolic (P <.001) blood pressure and had higher serum cholesterol (P <.01) and triglyceride (P <.05) levels. Apparently healthy, young, lean individuals with a genetic predisposition to essential hypertension and with normal glucose tolerance had higher insulin secretion and lower insulin sensitivity than controls. These abnormalities, together with higher blood pressure and altered lipid metabolism, may play a role in the development of hypertension and an increased risk of cardiovascular morbidity and mortality in these individuals.
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PMID:Insulin secretion, sensitivity, and metabolic profile of young healthy offspring of hypertensive parents. 1504 94

Changes in renal function related with essential hypertension are associated with an elevated cardiovascular morbidity and mortality. Indices of altered renal function (e.g., microalbuminuria, increased serum creatinine concentrations, decrease in estimated creatinine clearance or GFR, and overt proteinuria) are independent predictors of cardiovascular morbidity and mortality. The Framingham Heart Study documented the relevance of proteinuria for cardiovascular prognosis in the community. The INSIGHT Study assessed the role of proteinuria as a risk factor in essential hypertension. The presence of proteinuria at baseline turned out to be a very potent predictor for the development of cardiovascular events and death in patients with essential hypertension and one or more associated cardiovascular risk factors. Recent data indicate that minor derangements of renal function, including proteinuria, are associated, both in the community and in the hypertensive population, with the clustering of cardiovascular risk factors observed in metabolic syndrome that promote progression of atherosclerosis. Renal function has to be routinely evaluated in every hypertensive patient, and the presence of minor alterations considered in the stratification of cardiovascular risk in hypertensive patients.
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PMID:Effect of proteinuria and glomerular filtration rate on cardiovascular risk in essential hypertension. 1548 17

There is increasing evidence that primary hypertension, coronary heart disease, and other aspects of the so-called metabolic syndrome that develop in adulthood are primed in fetal life or early postnatally. The identification of this phenomenon, also known as prenatal or fetal programming, and the detailed characterization of the underlying pathomechanisms will greatly influence the understanding of these diseases. The present paper reviews recent experimental and clinical evidence that low nephron number, found in patients with renal dysplasia and low birth weight, is a risk factor for cardiovascular disease in later life. Therefore, it is important to identify children at risk as early as possible in order to treat them early and to prevent the development of end-organ damage. This could be an important goal for pediatrics in the near future.
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PMID:Low nephron number--a new cardiovascular risk factor in children? 1549 Feb 50


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