Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dyslipidemia is a major risk factor for atherosclerosis in adults and children. This study investigated the levels of lipoproteins in a northern Italian pediatric population, in relation to nutritional and familial factors. We studied 650 children on the basis of a 3-day dietary record; 361 of these children had their lipid levels [total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), and triglycerides] measured by a dry, multilayer method and apoprotein A-I and B by an immunonephelometric method. Familial history of cardiovascular disease and dyslipidemia was recorded. Anthropometric variables were taken for each child. Mean TC and low-density lipoprotein cholesterol (LDL-C) were high compared with southern Italian data, but similar to those of other Western countries. Family history of cardiovascular disease could not identify children with higher levels of atherogenic lipoprotein. Nutritional factors affected lipoprotein levels. The most important finding was a higher TC/HDL-C ratio in the lower quartile of polyunsaturated fatty acid intake. Obese children had higher levels of ApoB, triglycerides, TC and LDL-C, and lower levels of HDL-C; figures were higher for obese boys than for obese girls. Our study confirms a high prevalence of elevated levels of atherogenic lipoproteins among the northern Italian pediatric population and an association with nutritional factors and weight.
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PMID:Cholesterol and lipoprotein levels in Milanese children: relation to nutritional and familial factors. 161 95

A 17-year-old male was admitted with an acute myocardial infarction. A coronarography showed 90% occlusion in of the descendent anterior artery. A coronary angioplasty was done with excellent response. As coronary risk factors he had diabetes mellitus for 5 years and dyslipidemia with a phenotype IIb and hypo-alpha-lipoproteinemia. The case is discussed in regard to the possible etiopathogenic causes for his premature atherosclerosis.
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PMID:[Premature atherosclerosis in a 17-year-old male with diabetes mellitus and familial dyslipoproteinemia]. 163 17

Recent studies suggest that circulating blood monocytes may serve as a lipid clearance system in early atherosclerotic lesions. To evaluate the influence of moderate hyperlipoproteinemia on monocyte lipid concentrations, we measured fasting serum and monocyte lipid levels in 7 healthy individuals, in 7 patients with primary hypercholesterolemia and in 17 patients with secondary dyslipidemia due to chronic renal failure; 10 of these patients were treated by hemodialysis (HD) and 7 patients by continuous ambulatory peritoneal dialysis (CAPD). The hypercholesterolemic patients had elevated serum levels of total cholesterol, LDL-cholesterol and apolipoprotein (apo) B, but normal plasma triglycerides. Patients on dialysis had elevated serum levels of triglycerides, serum cholesterol (CAPD only) and VLDL- and LDL-cholesterol (CAPD only) and apo B (CAPD only), whereas HDL-cholesterol and apo A-I levels (HD only) were decreased. In monocytes, we measured the content of free cholesterol (FC), cholesteryl esters (CE) and triglycerides (TG). The normal mean intracellular concentrations of FC, CE and TG were 48.3, 1.7 and 2.4 micrograms/mg cell protein, respectively. All monocyte lipid levels were similar in patients and controls, with the exception of a decreased content of FC (30.8 micrograms/mg) in monocytes of HD patients. We conclude that moderate increases in serum lipoprotein lipid levels are not associated with lipid accumulation in monocytes.
Atherosclerosis 1992 Jun
PMID:Lipid levels in monocytes of patients with moderate hyperlipoproteinemia. 163 66

Hypertension is only one component of a multifaceted metabolic-hemodynamic complex that also includes obesity, subtle and overt glucose intolerance, dyslipidemia, enhanced vascular resistance and accelerated atherosclerosis. Results of a number of studies in the past 5 years have shown that even nonobese, nondiabetic individuals with hypertension display insulin resistance, which is located in peripheral tissues (primarily skeletal muscle), is limited to nonoxidative pathways of glucose disposal, and appears to be directly correlated with the severity of hypertension. Insulin resistance and associated hyperinsulinemia in hypertensive individuals are also associated with increased plasma triglyceride levels and decreased high-density lipoprotein concentrations, which likely contributes to enhanced atherosclerosis. Hyperinsulinemia may directly promote atherosclerosis by enhancing LDL-cholesterol accumulation in vessel walls, vascular smooth muscle migration, and proliferation, augmenting connective tissue synthesis in the vascular wall, and decreasing the regression of lipid plaques. The enhanced peripheral vascular resistance that characterizes insulin resistance/hyperinsulinemic states may be related to decreased vascular smooth muscle responses to insulin, which normally modulates (attenuates) vascular contractile responses to vasoactive agents.
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PMID:Insulin resistance, hyperinsulinemia, dyslipidemia, hypertension, and accelerated atherosclerosis. 163 39

Chronic renal failure is associated with abnormalities in lipoprotein metabolism that may contribute to premature atherosclerosis and early mortality in patients on dialysis. In previous studies, we found that plasma clearance of radiolabelled low density lipoprotein (LDL) was retarded in nephrectomized guinea pigs left with one-sixth of normal functioning renal mass. To elucidate potential mechanisms of delayed LDL clearance, we compared binding of LDL to hepatic membranes from both normal and uremic guinea pigs. One hundred micrograms of the 8000-100,000 X g hepatic microsomal protein was incubated with 125I-labelled normal guinea pig LDL (10-150 micrograms/mL) for 1 h at 37 degrees C, and the membrane washed and pelleted by centrifugation in a Beckman Ti 42.2 rotor. Parallel incubations with excess unlabelled LDL were done to determine specific binding. LDL specific binding to uremic hepatic membranes was significantly impaired compared with normal ones. The major abnormality, as determined by Scatchard transformation of the binding data, was a reduction of the apparent maximal binding of LDL to uremic membranes, with an average Bmax of 4.1 micrograms/mg protein compared with 6.6 micrograms/mg protein for normal hepatic microsomes. The affinity of LDL for uremic liver membranes was only slightly diminished with a mean apparent Kd of 35.2 micrograms/mL in comparison with 21.8 micrograms/mL for normal liver membranes. These results provide a biochemical explanation for the diminished LDL clearance in uremia and may account for the dyslipidemia of renal failure.
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PMID:Impaired binding of low density lipoprotein to hepatic membranes from uremic guinea pigs. 166 54

The objective of treating patients with hypertension is not simply to reduce blood pressure but rather to prevent the associated morbidity and mortality. Recent assessments of clinical trials have shown that while the risk of stroke is consistently lower with antihypertensive therapy, the same degree of success has not been demonstrated for coronary artery disease (CAD). Although there are many explanations of why we have not done as well in preventing CAD, one possibility is that the therapy used in clinical trials, primarily thiazide diuretics and beta-adrenoreceptor blockers, has increased the patient's risk of developing coronary atherosclerosis or lethal arrhythmias. Four classes of antihypertensive agents are recommended for initial therapy--thiazide diuretics, beta-adrenoreceptor blockers, angiotensin-converting enzyme (ACE) inhibitors, and calcium entry blockers. The metabolic effects of thiazide diuretics include electrolyte disturbances (hypokalemia, hypomagnesemia, and hyponatremia), dyslipidemia (increased triglycerides), abnormalities of glucose metabolism (hyperglycemia, hyperinsulinemia, and peripheral insulin resistance), and hyperuricemia. beta-Adrenoreceptor blockers have many of the same metabolic adverse reactions. beta-Adrenoreceptor blockers without intrinsic sympathomimetic activity (ISA) also cause dyslipidemias (lowered high-density lipoprotein cholesterol and increased triglycerides) and abnormalities of glucose metabolism (hyperglycemia, hyperinsulinemia, and peripheral insulin resistance). beta-Adrenoreceptor blockers with ISA and third-generation beta-blockers with selective partial agonist activity (celiprolol and dilevalol) do not cause dyslipidemia and to date do not appear to induce abnormalities in glucose metabolism. ACE inhibitors may decrease triglycerides and increase high-density lipoprotein cholesterol, and captopril may improve insulin sensitivity. Calcium entry blockers are metabolically neutral.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Metabolic considerations in the choice of therapy for the patient with hypertension. 167 Nov 90

Absent hepatic lipase (HL) activity results in dyslipidemia and premature atherosclerosis. DNA sequencing of the HL gene from subjects with heritable HL deficiency identified a new C to T substitution within exon 8 that in the mature enzyme caused a threonine to methionine change at position 383 (T383M). With a rapid DNA detection method we observed that all 6 individuals with complete HL deficiency from 2 families had the T383M mutation. None of 50 random unrelated unaffected subjects had this mutation. We propose that T383M is specific to families with heritable HL deficiency. Furthermore, structural variation at the HL gene, possibly in combination with other factors, appears to be etiologic in HL deficiency.
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PMID:A hepatic lipase gene mutation associated with heritable lipolytic deficiency. 167 86

Hypertension, dyslipidemia, and glucose intolerance cocluster in the population and act synergistically in increasing coronary artery disease risk. The mechanisms by which these risk factors interact in atherosclerosis are complex. First, hypertension, dyslipidemia, and altered insulin sensitivity may have a common pathophysiological basis. Activation of neurohormonal mechanisms may be implicated in many or all of these processes. In addition, underlying these processes may be common genetic and environmental influences. Second, these risk factors ultimately act on the blood vessel, thereby leading to atherosclerosis. Elevated serum lipids lead to vessel wall responses, including endothelial dysfunction, smooth muscle cell proliferation, lipid accumulation, foam cell formation, and, eventually, necrosis and plaque development. Hypertension may induce shear-related injury to the vessel. Endothelial injury (caused by hypertension) and vascular cell proliferation (induced by increased pressure and/or vasoactive substances) are effects that amplify the atherosclerotic process. In addition, diabetes and hyperinsulinemia can increase vascular tone, impair endothelial function, and stimulate vascular smooth muscle cell proliferation. Control of these risk factors should prevent or attenuate the vessel wall responses. Emphasis is now being placed on pharmacological therapeutic modalities that decrease blood pressure and improve insulin sensitivity and lipid metabolism. Identification of common links between risk factors, such as neurohormonal mechanisms (e.g., angiotensin), should lead to better therapeutic strategies.
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PMID:Atherosclerosis and hypertension: mechanisms and interrelationships. 169 33

Atherosclerosis is the main cause of mortality in diabetic patients, and the incidence of coronary heart disease is increased in the presence of microalbuminuria. The mechanisms of this association are not known and could involve genetic factors (predisposition to hypertension), renal disease and dyslipidemia. An increase in plasma triglyceride and apoprotein B levels, a decrease in plasma HDL cholesterol, qualitative abnormalities of VLDL and HDL are related to cardiovascular risk in diabetic patients. All these factors are worsened by nephropathy. Lipoproteins abnormalities could be involved in the progression of renal injury. In microalbuminuric patients, it seems important to reduce glomerular hyperfiltration and to normalize glycemia and blood pressure in order to prevent impairment of renal injury and dyslipidemia induced by nephropathy. Early treatment of lipoprotein abnormalities could decrease the incidence of cardiovascular complications.
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PMID:[Association of atherosclerosis and nephropathy in diabetes mellitus. Role of lipid anomalies]. 183 72

HMG-CoA reductase inhibitors have been proven effective in decreasing the plasma cholesterol levels in patients affected with various forms of hypercholesterolemia, familial dysbetalipoproteinemia, familial combined hyperlipidemia and in nephrotic and diabetic dyslipidemia. The purpose of this study was to monitor and evaluate the efficiency and safety of the therapy with simvastatin, an HMG-CoA reductase inhibitor, in a group of patients treated by continuous ambulatory peritoneal dialysis (CAPD) with severe hypercholesterolemia. Monitoring of the changes occurring in the various lipids and apolipoproteins in these patients included the measurements of the plasma lipids and apolipoproteins A-I, A-II, B, C-II, A-IV and Lp(a). Lipoproteins were separated by gel filtration, on a Superose 6HR column, before and after 24 weeks of treatment. The patterns were compared to those observed in a group of primary hyperlipidemic patients treated with Lovastatin, a compound of the same class. The drug was well tolerated by the CAPD patients and no adverse reaction was observed. In addition to the decrease of the total and LDL cholesterol, similar to that reported in other groups of patients, we further observed a decrease of the apo E concentration in both the CAPD and the hyperlipidemic patients. This decrease was especially pronounced in the HDLE fraction and could involve an upregulation of the apo B-E and/or apo E receptor. These results should provide information about the mechanism of action of this drug in patients with end-stage renal disease.
Atherosclerosis 1991 Feb
PMID:Effect of simvastatin treatment on the dyslipoproteinemia in CAPD patients. 187 12


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