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Body weight, like cholesterol and blood pressure, are continuous variables. Overweight results when energy intake as food exceeds energy expenditure from exercise for a considerable period of time. When body weight becomes sufficiently high, it poses a risk to cardiovascular and metabolic health. The types of treatments considered by the physician and discussed with a patient should be based on this risk-benefit assessment. The body mass is the basic measurement for this assessment, and should be part of the "vital signs" when a patient is first evaluated by the medical staff. When the body mass index (BMI) is below 25 kg/m(2), there is little risk from the body weight, but because obesity is a "stigmatized" condition, many patients, particularly women, desire to lose weight even within the normal range. For this purpose, a high-quality diet like the Dietary Approaches to Stopping Hypertension (DASH) diet at a reduced-calorie intake would be our recommendation. When the BMI is above 25 kg/m(2), patients deserve dietary advice, but in addition to a reduced-calorie DASH-like diet, this is a place to consider using "portion-control" strategies, such as the nutrition labels that manufacturers provide on canned and frozen foods to guide patients in reducing calorie intake. In overweight individuals at high risk (ie, those with a BMI above 30 kg/m(2) or impaired glucose tolerance, hypertension, or the metabolic syndrome), the use of orlistat or sibutramine along with diet, exercise, lifestyle changes, and portion control should be considered. When the BMI is above 35 kg/m(2), bariatric surgery should also be discussed as an option for the "at-risk" individual. Evidence reviewed here shows that modest weight losses of 5% to 10% can reduce the risk of conversion from impaired glucose tolerance to diabetes and can maintain lower blood pressure over extended periods. All of the approaches described above can produce weight losses of this magnitude.
Curr Treat Options Cardiovasc Med 2003 Aug
PMID:Diet, Weight Loss, and Cardiovascular Disease Prevention. 1283 63

Cardiovascular 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) has prolonged many patients' lives, but many cardiac sequelae of HIV are not affected by HAART and continue to develop even with treatment. In addition, HAART itself causes in a high proportion of patients a metabolic syndrome, characterized by lipodystrophy/lipoatrophy, dyslipidemia and insulin resistance that may be associated with an increase in peripheral artery and coronary artery diseases. Careful cardiovascular evaluation in the course of HIV disease can identify cardiac complications early enough to treat. 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.
Cardiovasc Res 2003 Oct 15
PMID:HIV infection, highly active antiretroviral therapy and the cardiovascular system. 1452 10

The prognosis for patients who suffer myocardial infarctions (MIs) is poor, with 22% of male and 46% of female survivors being disabled by heart failure within 6 years. Many well-established risk factors for increased morbidity and mortality post-MI are closely linked to the metabolic syndrome and associated with over-activation of the renin-angiotensin-aldosterone and sympathetic nervous systems. Results from numerous large-scale clinical endpoint trials have shown that blocking the deleterious effects of these systems with either an angiotensin-converting enzyme inhibitor or a beta-adrenoceptor antagonist significantly reduces the risk of mortality and cardiovascular events in post-MI patients. Results from 1 recent study of the beta-blocker, carvedilol, have shown further that these benefits extend to high-risk patients with either diabetes or hypertension.
Rev Cardiovasc Med 2003
PMID:Diabetes, hypertension, and renal insufficiency in post-myocardial infarction cardiovascular risk. 1456 32

Several aspects of human eating behaviour may be relevant for identifying effective measures to treat or prevent diseases like obesity, diabetes, or the metabolic syndrome, whose natural history is strongly influenced by nutritional factors. Physiological factors determine hunger, satiety and satiation, and a biological learning mechanism supports the acquisition of food likes and dislikes. The paradigm of "conditioned taste aversion" refers to the acquisition of a strong rejection response after the intake of a food has been followed by digestive disorder. Food likes are acquired following the experience of the beneficial post-ingestive effects of intake. Physiological mechanisms reinforce the liking for energy-rich foods and both environmental and biological conditions facilitate "passive overconsumption". Sensory factors are important determinants of appetite and food choices from birth to old age. The human newborn exhibits an innate repertoire of acceptance or rejection for taste substances. The progressive change of sensory functions associated with ageing affects appetite and the pleasure of eating. Many individual psychological characteristics affect food intake behaviour in a significant way. These include chronic dietary restraint, disinhibition, etc. These psychological traits can be objectively assessed using validated psychometric instruments. Various stimuli present in the environment also affect ingestive behaviours in humans. Portion size is one potent environmental determinant of how much a person eats, regardless of hunger. The general increase in portion sizes observed in North America over the last decades might have played an important role in the rapid rise of obesity prevalence. Socio-economic factors also affect food selection and food intake in human societies. Factors such as education level and income determine food choices and behaviours in a way that does affect the risk of obesity. Behavioural science has provided many insights about crucial cause-and-effect relationships that affect nutrition and health. Therefore, clinicians and nutritionists cannot neglect this important area if they wish to effectively modify the habitual diet of individual patients or the general population.
Nutr Metab Cardiovasc Dis 2003 Aug
PMID:Why should we study human food intake behaviour? 1465 Mar 50

Plasma levels of high-density lipoprotein-cholesterol (HDL-C) are a powerful independent cardiovascular risk factor, bearing an inverse relationship with atherosclerotic cardiovascular disease (with risk rising sharply when levels are <1.04 mmol/L). Apart from its protective role in atherosclerosis, HDL-C increases fibrinolysis, is an antioxidant to low density lipoprotein-cholesterol (LDL-C), and decreases platelet aggregability. Up to a third of patients with atherosclerotic cardiovascular disease have 'desirable' plasma levels of total cholesterol but low HDL-C levels. Benefits of treating low plasma HDL-C levels were clearly demonstrated in the Veterans Affairs HDL Intervention Trial (VA-HIT) where gemfibrozil reduced nonfatal infarcts and coronary deaths by 22%. This was achieved by a 6% increase in plasma HDL-C levels, and a 24.5% decrease in plasma levels of triglycerides, without any significant decrease in LDL-C levels. Multivariate analyses revealed the rise in plasma HDL-C levels after treatment, but not decreases in plasma levels of triglycerides or LDL-C, predicted coronary artery disease events. The typical patient under consideration in this article is one with plasma levels of HDL-C <1 mmol/L, LDL-C <3.37 mmol/L [either receiving therapeutic lifestyle changes or or LDL-C-lowering therapy comprising a hydroxymethylglutaryl coenzyme-A (HMG-CoA) reductase inhibitor or bile acid sequestrant] and fasting triglycerides <2.26 mmol/L. We propose this dyslipidemia be classified as Type VI phenotype following the Frederickson and Lees classification. High-risk patients (with >/=2 risk factors for atherosclerotic cardiovascular disease, or 10-year cardiovascular risk >20%), patients with established atherosclerotic cardiovascular disease, or type 2 diabetes mellitus, or metabolic syndrome should receive pharmacotherapy. Plasma HDL-C levels >1.16 mmol/L may be considered optimal and between 1 and 1.16 mmol/L as desirable. Fibric acid derivatives, nicotinic acid, HMG-CoA reductase inhibitors, estrogens, and ethanol (not recommended as therapy) increase plasma HDL-C levels. Nicotinic acid is the most potent agent and recent reports indicate that, in contrast to gemfibrozil, it selectively increases antiatherogenic HDL subfraction, lipoprotein (Lp) AI (without apolipoprotein AII), in patients with low plasma HDL-C levels. An extended-release formulation, administered once daily, has improved the tolerability of nicotinic acid. Recent evidence also indicates that nicotinic acid may effectively correct dyslipidemia in patients with diabetes mellitus without significantly compromising glycemic control. Fibric acid derivatives and estrogen raise plasma HDL-C levels by different mechanisms of action, and these agents may be used with nicotinic acid. Combination therapy (especially HMG-CoA reductase inhibitor and nicotinic acid) should be considered in patients with atherosclerotic cardiovascular disease and low plasma HDL-C levels.
Am J Cardiovasc Drugs 2003
PMID:Optimal therapy of low levels of high density lipoprotein-cholesterol. 1472 46

In many industrialized nations, obesity is now considered an epidemic, resulting in accelerated morbidity and mortality. Obesity is associated with an increased risk of coronary artery disease as well as the metabolic syndrome comprising abdominal obesity, increased fasting blood glucose levels, dyslipidemia and hypertension, which are all recognized cardiovascular risk factors. Diet, exercise, and lifestyle changes constitute important recommendations for treatment. Unfortunately, although effective in some individuals, these recommendations have proven to be ineffective in adequately addressing the broad, enlarging scope of this public health problem. Drug treatment is often indicated but is somewhat limited by the minimal number of well tolerated drugs that have proven to have long-term efficacy in maintaining bodyweight loss. For example, phentermine may result in modest bodyweight loss through suppression of appetite, but potential cardiovascular adverse effects exist and the efficacy is mainly short-term. Sibutramine, an inhibitor of serotonin and norepinephrine (noradrenaline) reuptake, may increase satiety and result in modest bodyweight loss. However, cardiovascular adverse effects may occur in susceptible patients. Nonetheless, sibutramine is one of the few drugs that has been approved by the US Food and Drug Administration (FDA) for bodyweight loss. Orlistat, a lipase inhibitor, is also approved by the FDA for bodyweight loss but may have bothersome gastrointestinal adverse effects, especially among patients who do not adhere to the recommended low-fat diet. Ongoing studies continue to evaluate other drug treatments that may result in bodyweight reduction through a number of different mechanisms. It is anticipated that the development of effective and well tolerated antiobesity drugs will elevate the pharmacologic treatment of obesity to the status of other cardiovascular risk factors and metabolic disorders. This may be especially important given that dyslipidemia, hypertension and type 2 diabetes mellitus are often secondary to, or exacerbated by, obesity.
Am J Cardiovasc Drugs 2002
PMID:Pharmacotherapy of obesity: currently marketed and upcoming agents. 1472 70

Centrally acting imidazoline I(1)-receptor agonists such as moxonidine and rilmenidine induce peripheral sympathoinhibition via the stimulation of hypothetical I(1)-receptors in the rostral ventrolateral medulla. Because of a rather weak affinity for alpha(2)-adrenoceptors, the use of these agents is associated with a lower incidence of adverse reactions, such as sedation and dry mouth, compared with classic centrally acting alpha(2)-adrenoceptor agonists (clonidine, guanfacine, methyldopa). The antihypertensive efficacy of moxonidine and rilmenidine is well documented, and they display a favorable hemodynamic profile. Their tolerability is better than that of the aforementioned centrally acting antihypertensive agents. However, long-term outcome data for moxonidine and rilmenidine are not available, and neither is a quantitative evaluation of their adverse effects. There exists some uncertainty with respect to the identity of the imidazoline I(1)-receptor, which has so far not been cloned. Furthermore, it would be desirable to develop highly selective I(1)-receptor agonists as successor drugs to moxonidine and rilmenidine. Although available data indicate that I(1)-receptor agonists are effective in patients with hypertension, comparative data versus agents such as beta-blockers, diuretics, calcium channel antagonists and ACE inhibitors are required to establish their position in the treatment of hypertension. Finally, I(1)-receptor agonists have potential in the treatment of patients with CHF and those with the metabolic syndrome; syndrome X.
Am J Cardiovasc Drugs 2001
PMID:Centrally acting imidazoline I1-receptor agonists: do they have a place in the management of hypertension? 1472 14

Combined hyperlipidemia is increasing in frequency and is the most common lipid disorder associated with obesity, insulin resistance and diabetes mellitus. It is associated with other features of the metabolic syndrome including hypertension, hyperuricemia, hyperinsulinemia and highly atherogenic subfractions of lipoprotein remnant particles including small dense low density lipoprotein-cholesterol. This review examines the mechanisms by which combined hyperlipidemia arises and the various drugs including fibric acid derivatives, hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, and nicotinic acid which can be used either as monotherapy or in combination to manage it and to improve prognosis from atherosclerotic disease in diabetes mellitus, insulin resistant states and primary combined hyperlipidemia. The therapeutic approach to combined hyperlipidemia involves determination of whether the cause is hepatocyte damage or metabolic derangements. Combined hyperlipidemia due to hepatocyte damage should be treated by attention to the primary cause. In the case of metabolic dysfunction because of imbalance in glucose and fat metabolism, therapy of diabetes mellitus and obesity should be optimised prior to commencement of lipid lowering drugs. Both fibric acid derivatives and HMG-CoA reductase inhibitors can be used in the treatment of combined hyperlipidemia with fibric acid derivatives having greater effects on triglycerides and HMG-CoA reductase inhibitors on LDL-C though both have effects on the other cardiovascular risk factors. There is some evidence of benefit with both interventions in mild combined hyperlipidemias and large scale trials are underway. Fibric acid derivatives and HMG-CoA reductase inhibitor therapy can be combined with care, provided that gemfibrozil is avoided, fibric acid derivatives are given in the mornings and shorter half -life HMG-CoA reductase inhibitors are used at night. Combined hyperlipidemia emergencies occur with predominant hypertriglyceridemia in pregnancy or as a cause of pancreatitis. Therapy in the former should aim to reduce chylomicron production by a low fat diet and intervention to suppress VLDL-C secretion using omega-3 fatty acids. In the latter case, fluid therapy alone and medium chain plasma triglyceride infusions usually reduce levels satisfactorily though apheresis may be required. Blood glucose levels also need aggressive management in these conditions. Combined hyperlipidemia is likely to become an increasing problem with the increase in the prevalence of obesity and diabetes mellitus and needs aggressive management to reduce cardiovascular risk.
Am J Cardiovasc Drugs 2001
PMID:Drug treatment of combined hyperlipidemia. 1472 15

The metabolic syndrome is a compilation of factors characterized by insulin resistance and the identification of 3 of the 5 criteria of abdominal obesity, elevated triglycerides, decreased high-density lipoprotein (HDL) level, elevated blood pressure, and elevated fasting plasma glucose. According to census data from 2000, these criteria have lead to the diagnosis of approximately 47 million Americans with the metabolic syndrome, correlating with the 61% increase in the incidence of obesity between 1991 and 2000. Insulin resistance occurs when target tissues cannot respond properly to normal concentrations of insulin. The results are hypercoagulability, endothelial dysfunction, inflammation, and eventually coronary artery disease. Treatment involves lifestyle modification, including diet and exercise, to treat obesity and prevent the development of diabetes. Patients who meet the criteria for the metabolic syndrome may also be treated with insulin-sparing and insulin-sensitizing medications that help to improve endothelial function, vascular reactivity, and vascular inflammation. Ultimately, treatment goals are to prevent cardiovascular disease by both altering the risk factors that are components of the syndrome, and treating the lifestyle issues inherent to the disease process, such as caloric restriction and increased physical activity. There are 2 million more women than men in the United States categorized as being obese, with the trend of obesity and diabetes increasing. In the last decade there has been a 74% increase in obesity, mostly in women. This epidemic needs to be understood and managed to prevent further morbidity and mortality owing to diabetes and cardiovascular disease.
Prog Cardiovasc Dis
PMID:The metabolic syndrome: an emerging health epidemic in women. 1496 55

Rosuvastatin (Crestor, AstraZeneca) is a synthetic statin that represents an advance on the pharmacologic and clinical properties of other agents in this class. Relative to other statins, rosuvastatin possesses a greater number of binding interactions with HMG-CoA reductase and has a high affinity for the active site of the enzyme. Rosuvastatin is relatively hydrophilic and is selectively taken up by, and active in, hepatic cells. Rosuvastatin has the longest terminal half-life of the statins and is only minimally metabolized by the cytochrome P450 (CYP 450) enzyme system with no significant involvement of the 3A4 enzyme. Consistent with this finding is the absence of clinically significant drug interactions between rosuvastatin and other drugs known to inhibit CYP 450 enzymes. In patients with hypercholesterolemia, rosuvastatin 10-40 mg has been shown to reduce low-density lipoprotein cholesterol (LDL-C) levels by 52-63%, as well as increase high-density lipoprotein cholesterol (HDL-C) levels by up to 14% and reduce triglycerides (TG) by up to 28%. Studies have shown that rosuvastatin is superior to atorvastatin, simvastatin and pravastatin in reducing LDL-C and favorably modifying other components of the atherogenic lipid profile. The significant decreases in LDL-C with rosuvastatin treatment should help to improve attainment of lipid goals and reduce the requirement for dose titration. In addition, the effects of rosuvastatin on HDL-C and TG levels will be of benefit in treating patients with abnormalities such as mixed dyslipidemia and the metabolic syndrome. Rosuvastatin is well tolerated, with a safety profile comparable with that of other currently available statins.
Expert Rev Cardiovasc Ther 2003 Nov
PMID:Rosuvastatin: a new inhibitor of HMG-coA reductase for the treatment of dyslipidemia. 1503 Feb 49


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