Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0948265 (metabolic syndrome)
 24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The metabolic syndrome represents a constellation of interrelated risk factors that identify individuals at increased risk for the development of type 2 diabetes mellitus and cardiovascular events. Currently, the major cardiovascular risk factors and validated risk-assessment tools do not adequately account for the increased cardiovascular risk that accompanies the metabolic syndrome. In prospective population studies, cardiovascular risk assessment in individuals with the metabolic syndrome is improved by measures of low-density lipoprotein (LDL) particle number, C-reactive protein, and plasminogen activator inhibitor-1 levels. Although adiponectin and soluble tumor necrosis factor receptor-2 may be more integrally involved in insulin resistance, the studies with these biomarkers are less extensive. Risk assessment models for patients with the metabolic syndrome should consider inclusion of LDL particle number, inflammatory markers, and levels of plasminogen activator inhibitor-1.
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PMID:Assessing risk across the spectrum of patients with the metabolic syndrome. 1609 36

Recent studies have suggested the insulin resistance might be accompanied by enhanced erythropoiesis. We have examined this association in individuals with the metabolic syndrome (MS) who in addition to insulin resistance harbor a chronic low grade inflammation. This study is relevant because chronic inflammation might have a suppressive effect on erythropoiesis. 280 and 554 non-smoking women and men with respective age of 46.4+/-9.3 (mean+/-S.D.) and 44.0+/-11.0 years are included. A significant correlation was noted between the numbers of the components of the MS and the inflammatory biomarkers including the white blood cell count, high sensitivity C-reactive protein, fibrinogen concentrations and the erythrocyte sedimentation rate. In addition, a significant correlation (r=0.157, p=0.008) was noted between the number of components of the MS and the number of red blood cells in the peripheral blood in women. The same was true for men (r=0.192, p<0.0005). We conclude that enhanced erythropoiesis could be a new, hitherto unrecognized component of the MS. The enhanced erythropoiesis could give an erroneous impression of general "good" health in these individuals.
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PMID:Increased erythropoiesis and subclinical inflammation as part of the metabolic syndrome. 1609 21

Peripheral vascular disease (PVD) is very prevalent in the United States and is part of a global vascular problem. PVD patients have a heightened inflammatory state and are at high risk of death from acute cardiovascular problems rather than from progression of PVD. Modifiable risk factors for PVD include smoking, hypertension, diabetes, hyperlipidemia, elevated high sensitivity C-reactive protein, obesity, and the metabolic syndrome. Symptomatic treatment of claudication includes smoking cessation, exercise, cilostazol, statins, and revascularization with percutaneous or surgical therapy. Antithrombotic therapy with aspirin or clopidogrel is important to reduce cardiovascular events but does not affect symptoms of claudication. Patients with rest limb ischemia or ulceration should be revascularized to minimize the chance of limb loss. Percutaneous revascularization is not without significant complications, however, and future research needs to focus on inflammation, thrombosis, and restenosis in the PVD patient. Finally, new devices that tackle difficult lesions, drug-eluting stents, and pharmacologic agents that reduce global atherosclerosis are on the horizon and are likely to become critical components in the management of the PVD patient.
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PMID:Evidence-based management of peripheral vascular disease. 1610 78

We sought to determine, in United States (US) patients with the metabolic syndrome (MS), diabetes mellitus (DM), or preexisting cardiovascular disease, whether higher levels of C-reactive protein (CRP) would identify those with an increased likelihood of peripheral arterial disease (PAD). In a cross-sectional evaluation of the National Health and Nutrition Examination Survey (NHANES), 1999 to 2000, of 1,600 adults (representing a US population of 62.9 million) aged > or =40 years who had valid ankle-brachial index measurements available, subjects were categorized as having MS (without DM), DM, preexisting cardiovascular disease, or none of these conditions. The presence of PAD was defined as an ankle-brachial index <0.9. Subjects were also divided into groups according to CRP levels that were low (<1 mg/L), intermediate (1 to 3 mg/L), and elevated (>3.0 mg/L). Weighted multiple logistic regression analysis examined the odds of PAD by CRP group and disease category compared with the reference group of subjects who did not have MS, DM, or cardiovascular disease and had a CRP level of <1 mg/L. Those with MS (including DM) had an increased likelihood of PAD (odds ratio 4.8, 95% confidence interval 1.4 to 16.1, p = 0.01) as did those with MS without diabetes and an elevated CRP level (odds ratio 3.9, 95% confidence interval 1.1 to 14.6, p = 0.04); those with DM and an elevated CRP had the highest likelihood of PAD (odds ratio 8.6, 95% confidence interval 2.2 to 34.0, p = 0.001). In conclusion, the likelihood of PAD in US adults with MS and DM is enhanced by elevated CRP levels.
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PMID:Impact of C-reactive protein on the likelihood of peripheral arterial disease in United States adults with the metabolic syndrome, diabetes mellitus, and preexisting cardiovascular disease. 1612 89

Metabolic syndrome (MetS) is associated with increased risk of cardiovascular disease (CVD). The relation of MetS with early stages of atherosclerosis, more important from a prevention perspective, has not been evaluated extensively. We examined the association of MetS, using WHO and NCEP definitions, with number of carotid and femoral plaques; carotid intima-media thickness (IMT); pulse wave velocity (PWV) in a random population-based sample of 1153 French adults (35-65 year). Impact of inflammatory factors (C-reactive protein and soluble intercellular adhesion molecule-1) on these parameters was also evaluated. Prevalence of MetS was 14.5 (CI: 12.3-16.0) and 17.5 (CI: 15.1-20.2)%, using NCEP and WHO definitions, respectively. MetS significantly predicted number of plaques, IMT, and PWV after adjustment for traditional risk factors (P<0.05). Inflammatory factors predicted peripheral plaques only. The risk of subclinical atherosclerosis was considerably increased with MetS (P<0.05); odds ratios ranged 1.80-2.15 with NCEP definition, and 1.48-1.97 with WHO definition. Individuals meeting both NCEP and WHO definitions had slightly greater risk of increased plaques, IMT, and PWV. MetS was strongly associated with subclinical atherosclerosis and aortic stiffness, and can be used as a surrogate marker for high CVD risk, deserving aggressive treatment.
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PMID:Metabolic syndrome is associated with markers of subclinical atherosclerosis in a French population-based sample. 1612 41

Menopause-related oestrogen deficiency increases the risk of cardiovascular disease (CVD). The presence of abdominal obesity, dyslipidemia, hypertension, fasting hyperglycaemia or impaired glucose tolerance further aggravates the CVD risk imposed by menopause. A detailed personal history should be recorded, covering PCOS, gestational diabetes mellitus, alcohol intake and smoking, as well as a family history of cardiovascular disease. Screening of the a-symptomatic post-menopausal woman should include fasting lipid profile, plasma glucose and liver, renal and thyroid function tests. Serum low-density lipoprotein cholesterol (LDL-c)>130 mg/dL is associated with an increased risk of CVD. Levels of triglycerides (TG)>or=150 mg/dL and high-density lipoprotein cholesterol (HDL-c)<or=50 mg/dL coupled with an increase in small dense LDL and very low-density lipoprotein (VLDL) particles constitute the atherogenic dyslipidemia, which characterizes the metabolic syndrome. In women with previous VTE episodes, screening for thrombophilia is advisable, as well as an estimation of baseline homocysteine and C-reactive protein (CRP). Non-pharmacological intervention should be targeted towards smoking cessation, a low-salt, low-fat, high-fibre diet and increased physical activity.
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PMID:Cardiovascular disease: screening and management of the a-symptomatic high-risk post-menopausal woman. 1614 Apr 82

C-reactive protein (CRP) and urinary albumin excretion are both determinants of cardiovascular risk. The first is closely related to systemic and vascular low-grade inflammation, the latter is considered to be a marker of endothelial dysfunction. Because of these properties, one might presume them to be closely interrelated. In this article, we review the available evidence concerning the relationships of CRP and urinary albumin excretion, with each other and with other cardiovascular risk markers and factors. Should they be considered as dependent or independent risk markers, and which risk markers might be present in the cardiovascular risk estimation formula of the near future? The reasons that this formula might or should include CRP and urinary albumin excretion, rather than diabetes mellitus and the metabolic syndrome, are discussed.
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PMID:Microalbuminuria and C-reactive protein: similar messengers of cardiovascular risk? 1615 83

Cytokines mediate and control immune and inflammatory responses. Complex interactions exist between cytokines, inflammation and the adaptive responses in maintaining homeostasis, health, and well-being. Like the stress response, the inflammatory reaction is crucial for survival and is meant to be tailored to the stimulus and time. A full-fledged systemic inflammatory reaction results in stimulation of four major programs: the acute-phase reaction, the sickness syndrome, the pain program, and the stress response, mediated by the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system. Common human diseases such as atopy/allergy, autoimmunity, chronic infections and sepsis are characterized by a dysregulation of the pro- versus anti-inflammatory and T helper (Th)1 versus Th2 cytokine balance. Recent evidence also indicates the involvement of pro-inflammatory cytokines in the pathogenesis of atherosclerosis and major depression, and conditions such as visceral-type obesity, metabolic syndrome and sleep disturbances. During inflammation, the activation of the stress system, through induction of a Th2 shift, protects the organism from systemic 'overshooting' with Th1/pro-inflammatory cytokines. Under certain conditions, however, stress hormones may actually facilitate inflammation through induction of interleukin (IL)-1, IL-6, IL-8, IL-18, tumor necrosis factor-alpha and C-reactive protein production and through activation of the corticotropin-releasing hormone/substance P-histamine axis. Thus, a dysfunctional neuroendocrine-immune interface associated with abnormalities of the 'systemic anti-inflammatory feedback' and/or 'hyperactivity' of the local pro-inflammatory factors may play a role in the pathogenesis of atopic/allergic and autoimmune diseases, obesity, depression, and atherosclerosis. These abnormalities and the failure of the adaptive systems to resolve inflammation affect the well-being of the individual, including behavioral parameters, quality of life and sleep, as well as indices of metabolic and cardiovascular health. These hypotheses require further investigation, but the answers should provide critical insights into mechanisms underlying a variety of common human immune-related diseases.
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PMID:Cytokine dysregulation, inflammation and well-being. 1616 5

Peroxisome proliferator-activated receptor-gamma (PPARgamma) is a nuclear transcription factor that comprises the primary molecular target for thiazolidinedione (TZD) insulin-sensitizing drugs. Whilst expressed in many tissues in humans, its abundant expression in adipose tissue is believed to be the focal point through which TZDs regulate genes involved in glucose and lipid metabolism and via which these agents ultimately improve the hyperglycemia of type 2 diabetes. However, TZDs exhibit many additional properties, not least an array of effects which suggest a broad attack on the inflammatory process. Thus, TZDs have been shown to reduce plasma levels of the chemokine, monocyte chemotactic protein-1 (MCP-1), the anti-fibrinolytic protein, plasminogen activator inhibitor-1 (PAI-1), the endothelial cell adhesion molecules, e-selectin and inter-cellular adhesion molecule-1 (ICAM-1), the leucocyte-activating molecule, CD40L, and the tissue-remodeling enzyme, matrix metalloproteinase-9 (MMP-9). Further tangible evidence of a reduction by TZDs of systemic inflammation in patients with the classical metabolic syndrome stems from falls in the white blood cell count, P-selectin-positive platelets and in the acute-phase inflammatory proteins, C-reactive protein, serum amyloid A and fibrinogen. At the tissue level, TZDs improve vascular endothelial function, and reduce the rate of progression of intimal-medial thickening of the carotid artery and the microalbuminuria of type 2 diabetes. Further, TZDs have been shown to be efficacious in inflammatory diseases as wide-ranging as psoriasis, ulcerative colitis and non-alcoholic steatohepatitis (NASH). In the case of the latter, a broad spectrum of TZD-related properties is visible. Here, these drugs improve insulin sensitivity for glucose metabolism, reduce hyperinsulinemia, hepatic steatosis, inflammation and fibrosis, and lower the circulating levels of liver transaminases (ALT, AST), alkaline phosphatase and gamma glutamyl transferase. These effects in humans are also well-supported by investigative animal and in vitro studies. The ameliorative effects on liver fibrosis are of particular interest since they suggest that TZDs are able to activate a program of corrective tissue-remodeling. The basis for this action may be partly an ability to inhibit matrix protein secretion by hepatic stellate cells. An analogous action has also been seen in kidney mesangial cells. In conclusion, TZDs are important new drugs, presently indicated for the treatment of type 2 diabetes but with a spectrum of properties which suggests their potential for treating a number of degenerative inflammatory diseases, including NASH. However, full-scale, long-term clinical trials are needed with TZDs to test their potential to treat NASH, not least because of the (hepatotoxic) legacy of the prototype TZD, troglitazone, but also in view of the escalating burden of liver disease which is accompanying the increasing global prevalence of clinical obesity and type 2 diabetes.
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PMID:Thiazolidinediones: Pleiotropic drugs with potent anti-inflammatory properties for tissue protection. 1619 19

The prevalence of diabetes is increasing worldwide. Insulin resistance and diabetes mellitus are major predictors of cardiovascular ischaemic disease. Other risk factors for cardiovascular death including hypertension, dyslipidaemia, smoking and visceral obesity are especially lethal in diabetics. C-reactive protein, plasminogen activator inhibitor-1, matrix metalloproteinases and other emerging risk factors and their roles are continually being researched and discovered. Treatment of this syndrome must be aimed at lifestyle modification, glycaemic control and management of concomitant risk factors. Diet and exercise play a vital role in the treatment of diabetes and the metabolic syndrome. Weight reduction and increased physical activity will improve insulin resistance, hyperglycaemia, hypertension and dyslipidaemia. Hypertension management has been shown to be especially important in diabetics to prevent cardiovascular events. Likewise, multiple clinical trials show that reduction of cholesterol is even more vital in diabetics than the general population for risk reduction of coronary disease. There is a great deal of evidence that tight control of glycaemia is essential to treatment of this condition. There are a variety of available pharmacological agents available including metformin, insulin secretagogues, alpha-glucosidase inhibitors, thiazolidinediones and insulin. The mechanisms and side effects of these medications are discussed. As macrovascular disease is the major cause of morbidity and mortality, an early, aggressive, multi-factorial approach to treatment of the metabolic syndrome and diabetes is vital to prevent adverse cardiac outcomes.
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PMID:Insulin resistance, diabetes and cardiovascular risk: approaches to treatment. 1621 8


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