Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 275 neonates mean cord blood cholesterol level was 70 +/- 17 (SD) mg/dl, with a range from 30 to 153 mg/dl. Mean cord blood triglyceride level was 33 +/- 26 (SD) mg/dl, with a range of 5-192 mg/dl. In an attempt to correlate perinatal problems and hypercholesterolemia in neonates we compared 15 hypercholesterolemic neonates who had cord blood cholesterol levels above 95 mg/dl, range 100-153 mg/dl, and triglyceride levels less than 65 mg/dl, with 65 normal neonates whose cord blood cholesterol levels were less than 95 mg/dl and triglyceride values were less than 65 mg/dl. We also compared 19 hypertriglyceridemic neonates who had cord blood triglyceride levels greater than 65 mg/dl, range 66-192 mg/dl, and cholesterol levels less than 95 mg/dl with the 65 normal neonates. Elevated cord blood cholesterol values greater than 95 mg/dl or triglyceride values greater than 65 mg/dl were associated with maternal-fetal problems related to unfavorable intralterine environment, fetal distress, and fetal anoxia. There was a significant correlation between post-term delivery and hypercholesterolemic neonates, and low Apgar scores and maternal hypertension were more often associated with hypertriglyceridemic infants. There was no association between serum cholesterol or triglyceride levels and prolonged ruptured membranes, cesarean section, maternal diabetes, or maternal hypothyroidism. Consequently, we think that when neonates are identified who have elevated cholesterol or triglyceride levels, the possible influence of maternal-fetal perinatal complications should be considered. Speculation Infants with familial hypercholesterolemia may be identified by increases in cord blood cholesterol concentrations. Elevated cord blood cholesterol or triglyceride values of some neonates, however, may represent hyperlipoproteinemia related to neonatal stress associated with maternal-fetal perinatal problems.
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PMID:Cord blood hyperlipoproteinemia and perinatal stress. 83 Dec 15

High density lipoproteins (HDLs; d = 1.063 - 1.21 g/ml) were isolated by ultracentrifugation and radiolabeled with 111In. The in vitro binding onto platelets from healthy volunteers (n = 15) and patients (n = 36) with heterozygous familial hypercholesterolemia (FH) was investigated. Binding was saturable and indicated high-affinity binding sites, which bound 1,882 +/- 361 ng protein of 111In-HDL/10(9) platelets (dissociation constant [Kd] = 7 +/- 3 micrograms protein/ml) in healthy volunteers and significantly (p less than 0.01) lower amounts in the FH patients (1,012 +/- 439 ng protein of 111In-HDL/10(9) platelets [Kd = 12 +/- 4 micrograms protein/ml]; p less than 0.01). The capacity to displace one half of the bound ligand (IC50) amounted to 14 +/- 3 micrograms protein/ml in healthy volunteers and 22 +/- 9 micrograms protein/ml in FH patients (p less than 0.001). Treatment with lipid-lowering drugs (gemfibrozil, alone or in combination with cholestyramine) in 10 patients resulted in an increased HDL binding capacity: before treatment, 1,280 +/- 883; after 2 months of treatment, 2,052 +/- 873 (p less than 0.05); and after 6 months of treatment, 2,127 +/- 812 ng protein/10(9) platelets (p less than 0.01). There was a significant (p less than 0.001) correlation between 111In-HDL binding data and plasmatic lipid and lipoprotein values. Furthermore, those FH patients with the additional risk factors of smoking (p less than 0.05) and hypertension (p less than 0.01) showed significantly lower 111In-HDL binding onto platelets. The findings indicate specific 111In-HDL binding sites for human platelets, which may be decreased in patients with heterozygous FH. Upregulation of HDL binding sites during lipid-lowering medication therapy supports the hypothesis that high-affinity HDL binding is involved in hyperlipemic disorders and is possibly related to the reactivity of platelets.
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PMID:Binding of 111In-labeled HDL to platelets from normolipemic volunteers and patients with heterozygous familial hypercholesterolemia. 131 36

The primary and secondary prevention of cardiovascular diseases and, therefore, the therapy of hyperlipidemia is essential in strategies to lower morbidity and mortality from coronary heart disease (CHD), the most relevant atherosclerosis-associated disease. These programs imply not only a medical but also an economic challenge to our health system. That is why all therapeutic measures have to be evaluated regarding their cost-effectiveness. A cost-effectiveness profile was calculated for all the therapies of hyperlipidemia (nutritional therapy, dietetic nutritionals, drugs and LDL-apheresis) with respect to the following parameters: total cholesterol, LDL-cholesterol, HDL-cholesterol and triglycerides. The daily costs of all interventional measures are compared to the success rate, whereby an index of daily therapy costs and 1% change per lipid parameter was calculated. Nutritional therapy is by far the cheapest, and LDL-apheresis the most expensive but also the most effective and reliable therapeutic measure. It has to be considered, however, that dietary intervention can be very successful in overnutrition while in rare cases of severe homozygous familial hypercholesterolemia there is no therapeutic alternative to LDL-apheresis. Life-style modifications, such as changing nutritional habits, may contribute towards reducing or removing one or more risk factor(s) (e.g. malnutrition is associated with overweight, hyperlipoproteinemia (HLP), hyperinsulinemia (syndrome X), hyperfibrinogenemia and hypertension). But neither health politicians nor the population seem to be conscious of the fact that life-style changes help to reduce medical expenditure. Considering the fact that nearly every medical service is getting more and more expensive, the need to introduce financial regulations is evident.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Economic aspects of therapy for lipid metabolism disorders]. 150 39

The goal of antihypertensive treatment must be not only the reduction of high blood pressure, but also the effective management of elevated cholesterol levels and other risk factors of coronary heart disease (CHD). In controlled clinical trials, doxazosin has been shown to have antihypertensive efficacy comparable with other classes of antihypertensive agents and to lower the levels of total cholesterol, low-density lipoprotein (LDL) cholesterol, and triglycerides while increasing the levels of high-density lipoprotein cholesterol. Doxazosin appears to inhibit the development of CHD on two fronts. First, doxazosin binds to the alpha 1-adrenoreceptor and inhibits the receptor-mediated responses to epinephrine and norepinephrine. Second, doxazosin has direct and indirect effects on lipid metabolism by increasing LDL receptor activity, decreasing intracellular LDL synthesis, reducing the synthesis and secretion of very low-density lipoprotein cholesterol, and stimulating lipoprotein lipase activity. Doxazosin may also inhibit platelet aggregation. Long-term studies will determine how these actions translate into reductions in the morbidity and mortality rates of CHD. First-year results from the Treatment of Mild Hypertension Study (TOMHS) have demonstrated expected reductions in blood pressure for all antihypertensive agents studied. The lipid changes have varied with the type of antihypertensive treatment and have been favorable for doxazosin.
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PMID:Effects of doxazosin on serum lipids: a review of the clinical data and molecular basis for altered lipid metabolism. 182 47

This study explores the influence of selected genetic and environmental factors on the clinical expression of heterozygous familial hypercholesterolemia (FH). A detailed examination of the physical and biochemical features of FH was performed in a large cohort of 208 females and 156 males. Females with FH had higher levels of total, low density lipoprotein (LDL), and high density lipoprotein (HDL) cholesterol when compared with males, although the concentration of HDL cholesterol was significantly lower for both sexes when compared with normals. The reported incidence of coronary artery disease (CAD) was 31% for men and 13% for women, which was lower when compared with figures from previous studies. The average age of onset of coronary symptoms was delayed in females, with a mean age of 55 years compared with 48 years for males (p less than 0.05). A greater risk of developing CAD in men was associated with lower levels of HDL cholesterol and a history of smoking. In women, however, CAD was associated with elevated triglycerides and the presence of hypertension. The frequencies of the epsilon 2, epsilon 3, and epsilon 4 alleles of apolipoprotein E in 125 unrelated FH subjects did not differ significantly from the normal population. In addition, there was no apparent relation between apo E4 and the concentration of any of the parameters in the plasma lipid profile; however, the presence of the E2 isoform was associated with significantly elevated triglycerides in both sexes. This study has allowed us to identify those factors, which, in addition to total cholesterol levels, are associated with the development of premature coronary atherosclerosis in heterozygous FH.
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PMID:Genetic and environmental factors affecting the incidence of coronary artery disease in heterozygous familial hypercholesterolemia. 199 46

Coronary heart disease (CHD) is an imprecise, inappropriate monitor of atherosclerosis severity and by inapplicable extrapolation CHD risk factors are incorrectly assumed to be causes of atherosclerosis. Taking into account (1) the misuse and substantial diagnostic error of CHD, (2) errors in determining the prevalence of risk factors, (3) the use of a young non-representative minority of sufferers of CHD, (4) bias posed by inclusion of familial hypercholesterolemia (FH) in clinical studies and (5) mutual inter-relationships, genetic influence and age dependence of hypercholesterolemia, hypertension, diabetes mellitus and body mass or obesity, it is unlikely that multivariate statistical analyses can adequately differentiate between their effects. These factors are age dependent and so are CHD and atherosclerosis. The importance of hypercholesterolemia in atherogenesis is suspect particularly since the vascular pathology of familial hypercholesterolemia and of cholesterol-fed animals has been misrepresented and does not provide support for the role of hypercholesterolemia in atherogenesis.
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PMID:The epidemiological relationship of hypercholesterolemia, hypertension, diabetes mellitus and obesity to coronary heart disease and atherogenesis. 220 Aug 50

The prevalence of mild and moderate hypercholesterolemia among the middle-aged population of the G.D.R. is about 30%. Thus, this is the most important risk factor for coronary heart diseases. Primary therapeutic techniques are elimination of overweight, low-fat diet, rich in monoenic and polyenic acids, and increase of physical activity. When by these measures a decrease of cholesterol to 5.2-5.5 mmol/l is not achieved the introduction of lipid drugs is to be considered in dependence on the individual risk (associated risk factors like smoking, hypertension, diabetes, low HDL-cholesterol). In case of mild to moderate polygenic hypercholesterolemia cholestyramine, nicotinic acid and modern fibrates have the priority. Familial hypercholesterolemia demands as a rule the introduction of statins (e.g. lovastatin) or combinations of the above mentioned lipid drugs or the combination of cholestyramine and lovastatin, resp. In this way the prognosis even of patients with severe familial hypercholesterolemia can be improved decisively. Considering the fact that this would be a life-accompanying therapy a thorough consideration of the risk/benefit ratio and an adequate medical supervision are necessary.
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PMID:[Guidelines for the treatment of hypercholesterolemia]. 224 95

The frequency of familial dyslipidemia syndromes was determined from blood tests in 33 objectively ascertained families with early coronary heart disease (CHD) (two or more siblings with CHD by the age of 55 years). Three fourths of persons with early CHD in these families had 90th percentile lipid abnormalities (cholesterol level at or above the 90th percentile, triglyceride level at or above the 90th percentile, and/or high-density lipoprotein cholesterol (HDL-C) level at or less than the 10th percentile). The HDL-C and triglyceride abnormalities were twice as common as low-density lipoprotein-cholesterol abnormalities. The most common syndromes found were familial combined hyperlipidemia (36% to 48% of families with CHD), familial dyslipidemic hypertension (21% to 54% of families with CHD), and isolated low levels of HDL-C (15%), with overlapping familial dyslipidemic hypertension with familial combined hyperlipidemia and low-level HDL-C. Well-defined monogenic syndromes were uncommon: familial hypercholesterolemia being 3% and familial type III hyperlipidemia, 3%. Another 15% of families with CHD had no lipid abnormalities at the 90th percentile. Physicians should learn to recognize and treat these common familial syndromes before the onset of CHD by evaluating family history and all three standard blood lipid determinations. Failure to recognize and treat them leaves affected family members at high risk of premature CHD.
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PMID:Population-based frequency of dyslipidemia syndromes in coronary-prone families in Utah. 231 Feb 76

There is good epidemiologic evidence that hypertension is associated with a high risk of cardiovascular disease. However, primary intervention trials have failed to demonstrate that a reduction in blood pressure in hypertensive patients reduces morbidity and mortality from cardiac events. Since various antihypertensive drugs adversely affect lipoprotein metabolism, these drugs may increase associated coronary risk and offset the beneficial effects of lowering blood pressure. This article reviews the effects of various antihypertensive drugs on plasma lipids, lipoproteins, and apolipoproteins. They can be summarized as follows: thiazide-type diuretics cause a marked elevation of plasma triglycerides and very low-density lipoprotein (VLDL) and minor increases in total cholesterol and low-density lipoprotein (LDL), but have little effects on high-density lipoprotein (HDL). The nonselective beta-blockers do not significantly affect total cholesterol and LDL, but increase total triglycerides and VLDL and decrease HDL. The changes in plasma lipids and lipoproteins caused by cardioselective beta-blockers and beta-blockers with intrinsic sympathomimetic activity are qualitatively similar but less pronounced. Calcium antagonists and angiotensin-converting enzyme inhibitors appear to have no significant effects on plasma lipids. alpha 1-Inhibitors reduce total triglycerides, total cholesterol, VLDL, and LDL and increase HDL. The possible mechanisms by which antihypertensive drugs affect cellular lipid metabolism (e.g., LDL receptor, lipid synthesis, lipoprotein lipase, lecithin cholesteryl acyltransferase, acylcholesteryl acyltransferase, and cholesteryl ester hydrolase) are described. The clinical significance of changes in blood lipids and cellular lipid metabolism caused by antihypertensive drugs is not yet totally clear. Nevertheless, before antihypertensive drug treatment is initiated, blood lipid levels should be measured to identify preexisting hyperlipidemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of antihypertensives on plasma lipids and lipoprotein metabolism. 305 88

The purpose of this study was to elucidate the relationship between two genetic factors associated with raised blood cholesterol, i.e. familial hypercholesterolemia (FH) and apolipoprotein (apo) E4. A group of 50 unrelated heterozygous FH patients aged 33-71 years were studied together with 129 normolipidemic subjects. A significantly higher frequency of apo E4 phenotypes was found in FH patients (30.0%) than in normolipidemic subjects (15.5%). FH patients were divided into two groups with and without apo E4. Plasma total cholesterol (Chol) and triglyceride (TG) levels were significantly higher, and plasma low density lipoprotein-cholesterol (LDL-Chol) level tended to be higher in FH patients with apo E4 than in those without apo E4. In addition, the prevalence of ischemic heart disease (IHD) was significantly higher in FH patients with apo E4 (73.3%) than in those without apo E4 (31.4%). No significant difference was noted in age and in the prevalence of obesity, diabetes, hypertension and smoking between the FH groups with and without apo E4. These results suggest that apo E4 is associated with higher levels of total Chol and TG and, at least in part, contributes to the predisposition to IHD in FH.
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PMID:Familial hypercholesterolemia and apolipoprotein E4. 321 64


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