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The metabolic syndrome is a constellation of interrelated abnormalities that increase the risk for cardiovascular disease and progression to type 2 diabetes. The prevalence of this syndrome is increasing because of the 'obesity epidemic'. The National Cholesterol Education Program Adult Treatment Panel III defined practical criteria for the diagnosis of the metabolic syndrome and established the basic principles for its management. Also, the International Diabetes Federation recently proposed another definition. The metabolic syndrome is a secondary target for cardiovascular risk reduction. Clinicians should identify individuals with this condition, assess their cardiovascular risk and treat them by an aggressive and multifaceted approach. The most effective therapeutic intervention in patients with the metabolic syndrome should focus on modest weight reduction and regular physical activity. Adoption of a healthier diet and smoking cessation are necessary. Drug therapy may be needed to achieve recommended goals if therapeutic lifestyle changes are not sufficient. Low-density lipoprotein cholesterol is the primary target of therapy (new aggressive goals should be achieved). Statins are probably the drugs of choice. Fibrates and nicotinic acid are also useful options. Hypertension should be managed aggressively probably starting with an inhibitor of the renin-angiotensin system or a calcium channel blocker and adding a low dose of a thiazide diuretic if necessary. Aspirin should be administered if the cardiovascular risk is high. In the future acarbose, metformin, meglitinides and thiazolidinediones may be used in patients with the metabolic syndrome to delay the onset of type 2 diabetes and reduce cardiovascular risk. Such an intense and multifactorial approach is likely to reverse the bad prognosis associated with the metabolic syndrome.
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PMID:Diagnosis and management of the metabolic syndrome in obesity. 1624 14

The metabolic syndrome is a common disorder characterized by central obesity, impaired glucose tolerance, hypertension, and atherogenic dyslipidemia (including the combination of hypertriglyceridemia, low levels of high-density lipoprotein cholesterol, and a preponderance of small, dense low-density lipoprotein particles). In this manuscript, we review the pathogenesis and significance of dyslipidemia in the metabolic syndrome, the role of nonpharmacologic therapy with therapeutic lifestyle changes, and drug therapies, including statins, fibrates, nicotinic acid, and omega-3 fatty acids or fish oils, alone or in drug combinations, to improve lipids and reduce the chance of subsequent cardiovascular disease events.
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PMID:Importance and management of dyslipidemia in the metabolic syndrome. 1635 14

Type 2 diabetes and atherosclerotic vascular disease develop in parallel. Prospective epidemiologic studies have shown a striking communality of major risk factors for both diseases. This raises the question of a "common soil". The traits of the metabolic syndrome including dyslipidemia, visceral obesity and hypertension are predictors of type 2 diabetes as well as coronary heart disease. The same applies to the environmental factors: overnutrition, physical inertia and smoking. Visceral obesity, insulin resistance and low-grade inflammation are known as major components of the common soil for metabolic syndrome and coronary heart disease. Depending on the quality of metabolic control diabetes will accelerate the progression of atherosclerosis via unstable plaque formation. The "common soil" concept provides a paradigm for an integrated therapeutic approach. This applies to a lifestyle intervention as well as a rational use of drugs in diseases of the metabolic syndrome. The medication should consider coexisting disorders of the metabolic syndrome to use pleiotropic effects. On the other hand, side effect such as the worsening of blood glucose levels caused by beta-blockers and diuretics should be avoided. The following medication should be preferred in context of the metabolic syndrome: oral antidiabetics such as acarbose, metformin and thiazolidinediones, antihypertensives such as ACE inhibitors and ARBs (angiotensin receptor blockers) and lipid-lowering drugs such as atorvastatin, rosuvastatin, and the modern nicotinic acid derivative Niaspan, respectively. The strategy using synergies in drug treatment can reduce polypharmacy and costs and improve the patients' compliance.
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PMID:[Metabolic syndrome: "common soil" for diabetes and atherosclerosis. Novel approaches to an integrated therapy]. 1677 May 62

Statins are effective drugs for lowering low-density lipoprotein cholesterol, and their use has been associated with a significant decrease in cardiovascular morbidity and mortality. However, statins are ineffective in lowering plasma triglycerides and lipoprotein(a), or increasing low high-density lipoprotein cholesterol (HDL-C) plasma levels, which are independent risk factors for coronary heart disease. Niacin, on the other hand, is the most potent drug available for lowering plasma levels of triglycerides and lipoprotein(a) and raising HDL-C levels. It follows, then, that a combination of niacin with a statin might be an effective combination in improving all components of the lipid profile. Previous studies have shown that the use of long-acting niacin with a statin, in dose combinations of niacin-ER/lovastatin 1,000/20 mg or 2,000/40 mg once daily, has been effective in favorably modifying low-density lipoprotein cholesterol, triglycerides, lipoprotein(a), and HDL-C plasma levels. Dyslipidemias often predate the onset of hypertension, and HDL-C has been found to be inversely related to the incidence of hypertension. Normalization of lipid components, including the total cholesterol/HDL-C ratio, is important in the management of hypertensive individuals and patients with the metabolic syndrome or diabetes. Thus, the long-term treatment of dyslipidemias with these two agents may help to modify risk and reduce cardiovascular morbidity and mortality in these patients over and above benefits achieved by lowering blood pressure.
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PMID:Niacin-ER/statin combination for the treatment of dyslipidemia: focus on low high-density lipoprotein cholesterol. 1684 3

The metabolic syndrome or cardiovascular dysmetabolic syndrome is characterized by obesity, central obesity, insulin resistance, atherogenic dyslipidemia, and hypertension. The major risk factors leading to this syndrome are physical inactivity and an atherogenic diet and cornerstone clinical feature is abdominal obesity or adiposity. In addition, patients usually have elevated triglycerides, low HDL cholesterol, elevated LDL cholesterol, other abnormal lipid parameters, hypertension, and elevated fasting blood glucose. Impaired fibrinolysis, increased susceptibility to thrombotic events, and raised inflammatory markers are also observed. Given that India has the largest number of subjects with type-2 diabetes in the world it can be extrapolated that this country also has the largest number of patients with the metabolic syndrome. Epidemiological studies confirm a high prevalence. Therapeutic approach involves intervention at a macro-level and control of multiple risk factors using therapeutic lifestyle approaches (diet control and increased physical activity, pharmacotherapy - anti-obesity agents) for control of obesity and visceral obesity, and targeted approach for control of individual risk factors. Pharmacological therapy is a critical step in the management of patients with metabolic syndrome when lifestyle modifications fail to achieve the therapeutic goals. Anti-obesity drugs such as sibutramine and orlistat can be tried to reduce weight and central obesity and jointly control the metabolic syndrome components. Other than weight loss, there is no single best therapy and treatment should consist of treatment of individual components of the metabolic syndrome. Newer drugs such as the endocannabinoid receptor blocker,rimonabant, appear promising in this regard. Atherogenic dyslipidemia should be controlled initially with statins if there is an increase in LDL cholesterol. If there are other lipid abnormalities then combination therapy of statin with fibrates, nicotinic acid, or ezetimibe should be considered. For insulin resistance, drugs such as thiazolidinediones and renin-angiotensin system blockers are available. Available evidence suggests that angiotensin converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBS) may be more beneficial for treatment of hypertension in patients with metabolic syndrome compared to others as these drugs also prevent development of diabetes. Patients with metabolic syndrome also have elevations in fibrinogen and other coagulation factors leading to prothrombotic state and aspirin may be beneficial for primary prevention in these patients. The new developments in the treatment of metabolic syndrome with drugs, such as peroxisome proliferator-activated receptor (PPAR) agonists and cannabinoid receptor-1 antagonists, will broaden the horizons of the current treatment options. Fixed-dose combination polypharmacy using a single pill is an interesting concept that needs to be evaluated in long-term prospective trials in such patients.
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PMID:Management issues in the metabolic syndrome. 1721 77

The patient introduced in the case history had a myocardial infarction in 2001 and a coronary two-vessel disease (extensive subtotal proximal stenosis of the left anterior descending [LAD] and proximal subtotal stenosis of the right coronary artery) which was diagnosed via coronary angiography at the age of 39 years. Besides smoking and obesity an important coronary risk factor was hyperlipoproteinemia with an especially massive increase in lipoprotein (a) level. The lipoprotein (a) level in January 2002 was massively elevated with 273.7 mg/dl (2 737 mg/l; Table 1). Despite invasive therapy with percutaneous transluminal coronary angioplasty (PTCA) and stent implantation in LAD and immediate therapy with atorvastatin, a restenosis in LAD was detected in April 2002 (Figure 1). Re-PTCA and intracoronary brachytherapy were performed (Figure 2). After presentation of unstable angina pectoris symptoms in November 2003, again a new in-stent restenosis in LAD could be detected via coronary angiography (Figure 3a), so that a single-bypass operation became necessary (Figure 3b). Since December 2001, an intensified treatment in a specialized polyclinic for lipid metabolism has been carried out, in which LDL-C values of 104 mg/dl (2.7 mmol/l) were targeted under aggressive lipid-lowering therapy with atorvastatin 80 mg/d and ezetimibe 10 mg/d (Table 1). Since 1998, the patient has quitted smoking. Blood pressure values are now in the therapeutic range, but the obesity could not be overcome.A distinctly elevated lipoprotein (a) level is an important risk factor for an early-onset and badly progressive arteriosclerosis. Thus, once in lifetime in the scope of risk factor management one should measure the lipoprotein (a) level. In case of elevated values the crucial treatment options include a very good management of all other risk factors, whereas an LDL-C level < 100 mg/dl (< 2.6 mmol/l), optionally < 70 mg/dl (< 1.8 mmol/l), is of vital importance. Nicotinic acid derivatives lower lipoprotein (a) levels by about 20-30%. All other risk factors, e.g., diabetes or hypertension, should be strictly managed as well. Cardiologic and angiologic examinations have to be an integral part of the treatment of these patients.
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PMID:[Severe progression of coronary heart disease in a patient with elevated lipoprotein (a) level in spite of optimal LDL-C decrease]. 1797 32

A study of prescription patterns by office-based physicians was conducted to analyse the use of lipid lowering drugs (LLD) in a Germany area of 1,768,874 inhabitants during a 1-year period. The prescription database consisted of health insurance files from a random sampling of persons (n=7490) belonging to a large statutory health insurance organization during 1993-1994. During the study period LLD were prescribed to about 2.8% of the study population. Fibrates (43.7%) were the most frequently prescribed drugs followed by HMG-CoA reductase inhibitors (29.5%) and nicotinic acid with derivatives (21.7%). The prevalence of treatment rose with increasing age peaking among 60- to 69-year-olds (7.5%). More than two-thirds of the patients were not treated continuously, receiving LLD for less than 6 months. Thus, in patients being treated with LLD, the therapy seems to be ineffective due to the short episodes of drug administration. The presence of hyperlipidaemia plus additional risk factors such as hypertension led to a higher rate of LLD prescriptions than that for hyperlipidaemia alone. Only half of the patients with a history of previous myocardial infarction and hyperlipidaemia received LLD. Furthermore, patients with hyperlipidaemia and additional risk factors such as arterial hypertension, diabetes mellitus and coronary heart disease (CHD), in whom administration of LLD has often been shown to be effective, were by far too infrequently treated with these drugs. Copyright (c) 2000 John Wiley & Sons, Ltd.
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PMID:The prescribing of lipid lowering drugs during a 1-year period: analysis of 7490 health insurance files. 1902 11

Significant reduction of renal mass causes progressive deterioration of renal function and structure which is mediated by systemic and glomerular hypertension, hyperfiltration, oxidative stress, inflammation, and dyslipidemia. Niacin is known to improve lipid metabolism and exert antioxidant/anti-inflammatory actions. Therefore, we considered that niacin supplementation may attenuate oxidative stress, inflammation, and tissue injury in the remnant kidney. To this end, 56 nephrectomized [chronic kidney disease (CKD)] rats were randomly assigned to niacin-treated (50 mg x kg(-1) x day(-1) in the drinking water for 12 wk) and untreated groups. Sham-operated rats served as controls. The untreated CKD rats exhibited azotemia, hypertension, hypertriglyceridemia, proteinuria, glomerulosclerosis, tubulointerstitial damage, upregulation of MCP-1, plasminogen activator inhibitor-1 (PAI-1), transforming growth factor (TGF)-beta, cyclooxygenase (COX)-1, COX-2, and NAD(P)H oxidase (NOX-4, gp91(phox), p47(phox) and p22(phox) subunits) and activation of NF-kappaB (IkappaB phosphorylation). Niacin administration reduced MCP-1, PAI-1, TGF-beta, p47(phox), p22(phox), COX-1, and NF-kappaB activation, ameliorated hypertension, proteinuria, glomerulosclerosis, and tubulointerstitial injury. Although niacin lowered serum creatinine and raised creatinine clearance, the differences did not reach statistical significance. Thus niacin supplementation helps to attenuate histological injury and mitigate upregulation of oxidative and inflammatory systems in the remnant kidney.
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PMID:Niacin ameliorates oxidative stress, inflammation, proteinuria, and hypertension in rats with chronic renal failure. 1942 Jan 10

Niacin has profound and unique effects on lipid metabolism. In addition to increasing high-density lipoprotein cholesterol, it is also known to decrease total cholesterol, low-density lipoprotein cholesterol, and triglyceride. Interestingly, the plasma concentration of lipoprotein(a) [Lp(a)], which has been suggested to play a role as an independent risk factor for coronary heart disease, is also decreased by niacin. Therefore, it is not surprising that in the literature it was given unique description as broad-spectrum lipid drug. Its impact is referred to as desirable normalization of a range of cardiovascular risk factors. However, its clinical use is limited due to harmless but unpleasant unique side effect of cutaneous flushing. Interestingly, recent experimental and clinical studies suggest the potential benefit of niacin as a treatment of dyslipidemia and high plasma phosphate associated with chronic kidney disease (CKD). Both dyslipidemia and high serum phosphate levels are shown to be associated with higher cardiovascular mortality. Furthermore, niacin administration improves renal tissue lipid metabolism, renal function and structure, hypertension, proteinuria, and histological tubulointerstitial injury. Further studies are required before the use of niacin for the treatment of both dyslipidemia and hyperphosphatemia with CKD advocated.
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PMID:Niacin as potential treatment for dyslipidemia and hyperphosphatemia associated with chronic renal failure: the need for clinical trials. 2048 51

Elevated Triglyceride levels are associated with increased risk for atherosclerotic disease and additional vascular risk factors such as obesity, hypertension and impaired glucose tolerance. To estimate the individual cardiovascular risk of a patient with elevated triglycerides LDL- and HDL-cholesterol levels, concomitant diseases, composition of triglyceride rich lipoproteins and a family history for premature coronary heart disease are important. Primary goals for the management of hypertriglyceridemia are a reduction of cardiovascular risk and prevention of triglyceride associated complications such as the chylomicronemia syndrome. The basis of treatment are lifestyle changes: dietary intervention, alcohol avoidance, regular physical activity, weight loss and smoking cessation to modify risk factors. If triglyceride levels can not be sufficiently reduced by lifestyle intervention pharmacotherapy (nicotinic acid, fibrates and omega-3-acid ethyl esters) is indicated. Beyond reduction of triglyceride levels optimization of non-HDL-cholesterol by statin treatment is warranted to reduce vascular risk.
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PMID:[Hypertricglyceridemia: prognostic impact and treatment options]. 2178 52

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