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

The metabolic syndrome is a highly prevalent clinical entity, which is often overlooked and may have far-reaching health implications for the patient. Up to 80% of patients with the metabolic syndrome die as a result of cardiovascular complications. Insulin resistance is the central component of this complex syndrome and should be appropriately addressed to ensure the best possible outcome for our patients. Recent advances in the pathogenesis and management of this syndrome is discussed in this article.
Cardiovasc J S Afr
PMID:The metabolic syndrome--pathogenesis, clinical features and management. 1238 60

In westernised societies the metabolic syndrome (MS) is common and primarily a lifestyle disease with significant morbidity and premature mortality. The main endpoints are related to cardiovascular disease (CVD), especially affecting the heart. Although insulin resistance (and hyperinsulinaemia) is an early marker of MS and future adverse cardiovascular outcomes, it is not known if on its own this is sufficient. The issue is further clouded in prospective studies by the development in study subjects of some, or all of the components of MS, each of which is an independent risk factor for CVD! Therefore, in spite of a number of appropriate long-term observational studies, we are unable to tease out the exact contribution of the individual components of MS, which together are unequivocally responsible for this present-day epidemic of CVD.
Cardiovasc J S Afr
PMID:The metabolic syndrome, insulin resistance and cardiovascular disease. 1238 61

Metabolic syndrome, insulin resistance, prediabetes, and overt type 2 diabetes mellitus are associated with an accelerated atherosclerosis (atheroscleropathy). This quartet is also associated with multiple metabolic toxicities resulting in the production of reactive oxygen species. The redox stress associated with these reactive oxygen species contribute to the development, progression, and the final fate of the arterial vessel wall in prediabetic and diabetic atheroscleropathy. The prevention of morbidity and mortality of these intersecting metabolic diseases can be approached through comprehensive global risk reduction.
Cardiovasc Diabetol 2002 Sep 27
PMID:Intimal redox stress: accelerated atherosclerosis in metabolic syndrome and type 2 diabetes mellitus. Atheroscleropathy. 1239

Vascular complications in the course of human immunodeficiency virus (HIV) infection are multifactorial and may be caused by the virus itself or by the related opportunistic infections and neoplasms. Highly active antiretroviral therapy (HAART), which dramatically modifies the natural history of HIV disease, causes in a high proportion of patients a metabolic syndrome that includes body fat redistribution, hypercholesterolaemia, hypertriglyceridaemia and insulin resistance. These effects are particularly evident in patients treated with protease inhibitors (PIs). However, studies on the cardiovascular risk among HIV-infected individuals receiving PIs have not shown a consistent association. The pathogenesis of the HAART-associated metabolic syndrome has not been completely elucidated, but there is growing evidence that a synergistic effect between PIs and nucleoside reverse transcriptase inhibitors might play a significant role. All HIV-infected patients candidate to antiretroviral therapy and patients already under treatment should undergo an assessment that includes the evaluation of the cardiovascular risk with the available guidelines.
J Cardiovasc Risk 2002 Oct
PMID:HIV infection, antiretroviral therapy and cardiovascular risk. 1239 24

Cardiovascular complications are frequently encountered in the HIV-infected population. Cardiac care providers should implement appropriate preventive, screening, and therapeutic strategies to maximize survival and quality of life in this increasingly treatable, chronic disease. All HIV-infected individuals should undergo periodic cardiac evaluation, including echocardiography, in order to identify subclinical cardiac dysfunction. Left ventricular (LV) dysfunction can result from, or be exacerbated by, a variety of treatable infectious, endocrine, nutritional, and immunologic disorders. Aggressive diagnosis and treatment of these conditions may lead to improvement or even normalization of myocardial function. Endomyocardial biopsy should be considered to direct etiology-specific therapy. Standard measures for the prevention and treatment of congestive heart failure are recommended for HIV-infected patients. Afterload reduction with angiotensin-converting enzyme inhibitors may be indicated for patients with elevated afterload and preclinical LV dysfunction diagnosed by echocardiogram. However, judicious drug selection and titration are necessary in this cohort of patients with frequent autonomic dysfunction, at risk for a number of potentially lethal drug interactions. Carnitine, selenium, and multivitamin supplementation should be considered, especially in those with wasting or diarrhea syndromes. Monthly intravenous immunoglobulin (IVIG) infusions have been demonstrated to preserve LV parameters in HIV-infected children; ventricular recovery has been documented in some children with recalcitrant HIV-related cardiomyopathy following IVIG infusion. We support the use of immunomodulatory therapy in the pediatric population, and look forward to further study into the efficacy and broader application of this approach. Highly active antiretroviral therapy (HAART) may be associated with dyslipidemia and the metabolic syndrome. This should be treated with dietary and possibly with pharmacologic interventions. Drug interactions need to be considered when instituting pharmacologic therapies. Pericardial effusions are often seen in patients with advanced HIV infection. Asymptomatic effusions are most often nonspecific in nature, related to the proinflammatory milieu found in advanced AIDS. Nonspecific effusions are a marker of advanced disease and do not require exhaustive etiologic evaluation. In contrast, large or symptomatic effusions are often associated with infection or malignancy, and warrant thorough investigation and etiology-specific treatment.
Curr Treat Options Cardiovasc Med 2002 Dec
PMID:Myocardial and Pericardial Disease in HIV. 1240 91

Rosuvastatin, a new statin, has been shown to possess a number of advantageous pharmacological properties, including enhanced HMG-CoA reductase binding characteristics, relative hydrophilicity, and selective uptake into/activity in hepatic cells. Cytochrome p450 (CYP) metabolism of rosuvastatin appears to be minimal and is principally mediated by the 2C9 enzyme, with little involvement of 3A4; this finding is consistent with the absence of clinically significant pharmacokinetic drug-drug interactions between rosuvastatin and other drugs known to inhibit CYP enzymes. Dose-ranging studies in hypercholesterolemic patients demonstrated dose-dependent effects in reducing low-density lipoprotein cholesterol (LDL-C) (up to 63%), total cholesterol, and apolipoprotein (apo) B across a 1- to 40-mg dose range and a significant 8.4% additional reduction in LDL-C, compared with atorvastatin, across the dose ranges of the two agents. Rosuvastatin has also been shown to be highly effective in reducing LDL-C, increasing high-density lipoprotein cholesterol (HDL-C), and producing favorable modifications of other elements of the atherogenic lipid profile in a wide range of dyslipidemic patients. In patients with mild to moderate hypercholesterolemia, rosuvastatin has been shown to produce large decreases in LDL-C at starting doses, thus reducing the need for subsequent dose titration, and to allow greater percentages of patients to attain lipid goals, compared with available statins. The substantial LDL-C reductions and improvements in other lipid measures with rosuvastatin treatment should facilitate achievement of lipid goals and reduce the requirement for combination therapy in patients with severe hypercholesterolemia. In addition, rosuvastatin's effects in reducing triglycerides, triglyceride-containing lipoproteins, non-HDL-C, and LDL-C and increasing HDL-C in patients with mixed dyslipidemia or elevated triglycerides should be of considerable value in enabling achievement of LDL-C and non-HDL-C goals in the numerous patients with combined dyslipidemias or metabolic syndrome who require lipid-lowering therapy. Rosuvastatin is well tolerated alone, and in combination with fenofibrate, extended-release niacin, and cholestyramine, and has a safety profile similar to that of currently marketed statins. A large, long-term clinical trials program is under way to investigate the effects of rosuvastatin on atherosclerosis and cardiovascular morbidity and mortality.
Cardiovasc Drug Rev 2002
PMID:Rosuvastatin: a highly effective new HMG-CoA reductase inhibitor. 1248 Dec 2

The metabolic syndrome is a complex constellation of disorders, each one a significant risk factor for the development of cardiovascular disease (CVD). The increasing prevalence of this condition is a major concern for healthcare providers both in Europe and North America. The concern surrounding the prevalence of the metabolic syndrome is reflected in the recently published National Cholesterol Education Program Adult Treatment Panel III guidelines. Although complex in nature, the individual components of the metabolic syndrome appear to be linked by the presence of insulin resistance. Concurrently treating the underlying insulin resistance along with the complex array of other disorders should form the core of any management strategy. Treatment of atherogenic dyslipidaemia should be a major aim, since it is associated with a significant risk of CVD. While lifestyle modifications form the cornerstone of any dyslipidaemia management strategy, many patients require the addition of lipid-modifying drugs. Several agents are available for the treatment of lipid abnormalities, including fibrates, bile acid sequestrants, niacin and hydroxymethyl glutaryl coenzyme A reductase inhibitors (statins). Of these, statins should be used as the first treatment option in the majority of patients because they are efficacious for reducing low-density lipoprotein cholesterol, are effective across the lipid profile and are well tolerated in the majority of cases. Furthermore, the American Diabetes Association (ADA) recommends statins as first-line pharmacological treatment of dyslipidaemia in patients with diabetes mellitus. This review discusses the diagnosis and management of the metabolic syndrome and examines the potential of future treatment options.
J Cardiovasc Risk 2003 Apr
PMID:The metabolic syndrome: targeting dyslipidaemia to reduce coronary risk. 1266 9

Between January 1993 and December 2001, we employed percutaneous cardiopulmonary support (PCPS) in 35 patients. PCPS was used for postcardiotomy in 25 of these patients who could not be weaned from cardiopulmonary bypass (CPB) because of severe cardiogenic shock. In the other 10 patients, PCPS was used for a non-surgical disease. Twenty-nine patients (82.9%) were weaned from PCPS, and 28 (80.0%) survived. The other 7 patients (20.0%) died due to postoperative complications. The causes of death were multiple organ failure (MOF) due to wound bleeding, low cardiac output syndrome (LOS), myonephropathic metabolic syndrome (MNMS) with severe lower limbs ischemia, cerebrovascular accident (CVA), and sepsis. The first cause for the complications was postoperative sustained severe heart failure. To improve the survival rate, it was necessary to prevent bleeding and begin PCPS at an earlier stage.
Ann Thorac Cardiovasc Surg 2003 Apr
PMID:Clinical effects of percutaneous cardiopulmonary support in severe heart failure: early results and analysis of complications. 1273 87

Insulin resistance and hyperinsulinemia are the critical characteristics of the metabolic syndrome that is associated with abdominal obesity and are the early manifestations of its progression to type 2 diabetes. These metabolic abnormalities are becoming recognized as a major contributor to cardiovascular disease. The experimental studies required to elucidate the underlying mechanisms and to develop effective preventative strategies will require the use of appropriate animal models and these are available. The evidence from such research indicates that a wide range of interventions (including peroxisome proliferator activator receptor agonists, insulin-sensitizing agents, statins, fibrates, angiotensin-converting enzyme inhibitors, estrogen receptor modulators, lipid-based nutriceuticals, and ethanol) can markedly reduce or prevent vasculopathy and ischemic cardiac lesions in animal models. Overall, the results suggest that early damage to the vascular wall, both in function and presenting as atherosclerotic lesions, is secondary to long-term hyperinsulinemia and, especially, to postprandial peaks in plasma insulin levels, and is exacerbated by the accompanying hyperlipidemia. Effective treatment will, of necessity, be preventative and will necessitate diagnostic approaches that can identify asymptomatic individuals at high risk for vascular damage and eventual progression to type 2 diabetes. Therapeutic targets in this population include insulin sensitivity and the associated signal transduction pathways, the peroxisome proliferator activator receptor-alpha and -gamma systems, and the complex pathways leading from acetyl CoA and the citric acid cycle to the synthesis of fatty acid and the storage of triglyceride. These pharmacological approaches offer the prospect of preventing a significant proportion of cardiovascular disease.
Curr Drug Targets Cardiovasc Haematol Disord 2001 Dec
PMID:Reduction and prevention of the cardiovascular sequelae of the insulin resistance syndrome. 1276 60

The metabolic syndrome is a highly prevalent clinical entity. The recent Adult Treatment Panel (ATP III) guidelines have called specific attention to the importance of targeting the cardiovascular risk factors of the metabolic syndrome as a method of risk reduction therapy. The main factors characteristic of this syndrome are abdominal obesity, atherogenic dyslipidemia, elevated blood pressure, insulin resistance (with or without glucose intolerance), prothrombotic and proinflammatory states. An insulin resistance following nuclear peroxisome proliferator activated receptors (PPAR) deactivation (mainly obesity-related) is the key phase of metabolic syndrome initiation. Afterwards, there are 2 principal pathways of metabolic syndrome development: 1) with preserved pancreatic beta cells function and insulin hypersecretion which can compensate for insulin resistance. This pathway leads mainly to the macrovascular complications of metabolic syndrome; 2) with massive damage of pancreatic beta cells leading to progressively decrease of insulin secretion and to hyperglycemia (e.g. overt type 2 diabetes). This pathway leads to both microvascular and macrovascular complications. We suggest that a PPAR-based appraisal of metabolic syndrome and type 2 diabetes may improve our understanding of these diseases and set a basis for a comprehensive approach in their treatment.
Cardiovasc Diabetol 2003 Mar 23
PMID:Metabolic syndrome and type 2 diabetes mellitus: focus on peroxisome proliferator activated receptors (PPAR). 1283 41


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>