UMLS:C0042373 - FACTA Search

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Query: UMLS:C0042373 (vascular disease)
17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Approximately 1% of the population have a dominantly inherited lipid disorder predisposing to premature vascular disease. Apolipoproteins (Apo) B, and A1, the carrier proteins for the atherogenic low density lipoprotein (LDL) and the protective high density lipoprotein (HDL) cholesterol respectively are markers for these disorders, as is Apo(a), the unique carrier protein for lipoprotein(a). We assessed changes in these apolipoproteins during the first 12 years of life, aiming to detect young families with inherited dyslipidaemia and implement early prevention. Among 1032 consecutively born babies in whom levels were measured within their first week and at a mean age of 8.5 months, the Apo B/A1 ratio and Apo(a) both tracked closely (p < 0.01 and < 0.0001). High B/A1 ratios (> 95 percentile) identified two families with familial hypercholesterolaemia, and infants with high Apo B identified two families with hyperapolipoprotein B. Apo(a) levels increased twofold between the first week and 8.5 months and were highly correlated (r = 0.73, p < 0.0001). Levels at 8.5 months were not different from parental values and were closely correlated with them. We then assessed school children aged eight to 12 years. In a pilot study (n = 1400) we have established normal apolipoprotein values and distribution patterns and defined the 95th percentile for each. This study is continuing and parents of children with high levels are being recalled (with their children) for lipid measurements. Our findings indicate that our approach is feasible and has wide acceptance, and that measuring Apo B/A1 and Apo(a) in childhood identifies families at increased cardiovascular risk. We have yet to assess the efficacy of our family-based coronary prevention programme.
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PMID:The Apo A, B, a of coronary risk: back to kindergarten. 144 41

To study the effect of renal function on the development of lipid and apolipoprotein abnormalities in human renal disease, we have investigated 75 patients at different stages of renal insufficiency. The patient population consisted of 19 patients with less advanced renal failure (CRF:1) characterized by a mean glomerular filtration rate (GFR) of 37.4 +/- 14 ml/min, 31 patients with advanced renal failure (CRF:2) having a mean GFR value of 7.9 +/- 7.3 ml/min and 25 patients on maintenance hemodialysis (CRF:HD). Patients in the CRF:1 group had normal plasma triglyceride (TG) and total cholesterol (TC) levels. In the CRF:2 and CRF:HD group, TG levels were increased two- to threefold, together with a moderate elevation of TC levels. All patient groups had elevated levels of VLDL cholesterol and slightly decreased levels of HDL cholesterol. The apolipoprotein profile of all patient groups was characterized by significantly reduced levels of apolipoprotein (Apo)A-I and ApoA-II and significantly increased levels of ApoC-III. CRF:2 and CRF:HD patients had also moderately elevated levels of ApoB, ApoC-I and ApoC-II. Levels of ApoE were only elevated in CRF:HD patients. All patients, regardless of TG levels, had significantly lower ApoA-I/ApoC-III ratios than controls. GFR was positively correlated with ApoA-I and inversely correlated with TC, TG and ApoC-III. CRF:HD patients had slightly higher ApoA-I and ApoA-II and lower ApoB levels compared to CRF:2 patients. Patients with vascular disease had higher TC, TG, ApoB, ApoC-II and ApoE than patients without vascular disease. These results demonstrate that the dyslipoproteinemia with CRF is already manifested at the early stages of disease through its abnormal apolipoprotein rather than lipid profile.
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PMID:Lipid and apolipoprotein profiles of uremic dyslipoproteinemia--relation to renal function and dialysis. 204 21

Apolipoprotein (apo) E deficiency is a rare genetic disease characterized by palmar and tuberoeruptive xanthomas, type III hyperlipoproteinemia, and premature atherosclerotic vascular disease. The plasma level of apoE in apoE deficiency is less than 0.05 mg/dl by radioimmunoassay, and no structural variants of apoE were detected by immunoblot of plasma or VLDL separated by two-dimensional gel electrophoresis. The apoE gene is present in the apoE deficient patient, and there are no major insertions or deletions in the gene by Southern blot analysis. Blood monocyte-macrophages isolated from a patient with apoE deficiency contain 1-3% of the level of apoE mRNA present in monocyte-macrophages isolated from normal subjects. The apoE mRNA in the monocyte-macrophages of the apoE deficient patient is similar in size to normal apoE mRNA. The deficiency of plasma apoE in the patient with apoE deficiency is due to a markedly decreased level of apoE mRNA and decreased production of the E apolipoprotein. The decreased apoE mRNA may be due to a defect in transcription or processing of the primary transcript of the apoE gene or to instability of the apoE mRNA. The decreased plasma level of apoE results in delayed clearance of remnants of triglyceride rich lipoproteins, hyperlipidemia, and a type III phenotype.
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PMID:ApoE deficiency: markedly decreased levels of cellular ApoE mRNA. 300 75

Coronary artery disease (CAD) is the leading cause of death among whites with non-insulin-dependent diabetes mellitus (NIDDM). Several risk factors--dyslipidemia induced by NIDDM, obesity, hypertension and hyperglycemia--likely contribute to accelerated atherosclerosis. The dyslipidemia in NIDDM is characterized by abnormalities in composition and metabolism of very low density lipoproteins, low-density lipoproteins (LDL) and high-density lipoproteins (HDL). However, because of the lack of long-term prospective epidemiologic studies, the relative importance of lipoprotein risk factors in the causation of CAD in diabetic patients is not clear. The World Health Organization Multinational Study of vascular disease in diabetics observed increased prevalence of CAD in diabetic populations with relatively high levels of plasma cholesterol and supports the concept that lowering cholesterol levels may significantly reduce coronary risk in NIDDM. To determine the effectiveness of lovastatin, an inhibitor of HMG CoA reductase, for lowering cholesterol levels, 16 patients with NIDDM and mild to moderate increases in plasma cholesterol were given lovastatin (20 mg twice daily) in a randomized, double-blind, placebo-controlled manner for 4 weeks. Compared with the placebo, lovastatin reduced concentrations of total cholesterol (233 +/- 10 vs 172 +/- 7 mg/dl [standard error of the mean], p less than 0.001), LDL cholesterol (140 +/- 9 vs 101 +/- 6 mg/dl, p less than 0.001), and LDL apolipoprotein-B (108 +/- 16 vs 80 +/- 16 mg/dl, p less than 0.001). Plasma triglycerides and very low density lipoprotein cholesterol levels also decreased by 31 and 42%, respectively. Although HDL cholesterol levels did not increase, the total cholesterol/HDL cholesterol ratio decreased significantly with lovastatin therapy. No adverse effects were noted and glycemic control was well-maintained.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Treatment of dyslipidemia in non-insulin-dependent diabetes mellitus with lovastatin. 305 23

Carriers of the apolipoprotein A-IMilano (apo A-IM) variant represent a selected group of subjects showing low levels of high density lipoprotein (HDL), variable hypertriglyceridemia, and low prevalence of atherosclerotic vascular disease. The distribution of HDL subfractions and the correlation with abnormalities in triglyceride transport were determined in these subjects. Sera from 24 apo A-IM carriers (A-IM+ and from age- and sex-matched normolipidemic controls (A-IM-) were analyzed by rate zonal ultracentrifugation. The A-IM+ subjects showed a marked decrease of HDL3 mass with reduced flotation rates and major compositional alterations; the HDL2 were nearly absent. The HDL subclasses from 10 A-IM+ subjects were resolved according to particle size by gradient gel electrophoresis (GGE). The HDL patterns detected in the carriers were unique in exhibiting a distinct peak in the (HDL3b)gge interval, undetectable in the controls. Three patterns reflecting the relative contributions of smaller (HDL3b)gge and larger (HDL3a)gge particles could be distinguished in the carriers, and these were clearly related to different triglyceride and HDL cholesterol levels in plasma. These findings in a highly selected group of subjects with generally low HDL levels and quite variable triglyceridemia confirmed the existence of relationships between alterations in triglyceride transport and abnormalities in the HDL subclass distribution, possibly reflecting the variable atherosclerotic risk in hypertriglyceridemic subjects.
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PMID:Apolipoprotein A-IMilano. Correlation between high density lipoprotein subclass distribution and triglyceridemia. 311 56

In the past years, the structure and function of the plasma lipoproteins and apolipoproteins have been elucidated. The biochemical defect of several genetic lipoprotein disorders and their role in the development of atherosclerosis are now well understood. Electrophoretic separation of lipoproteins in polyacrylamide gradient gel gives an acurate characterization of the different lipoproteins and allows the phenotyping of hyperlipoproteinemia. Abnormal concentrations of plasma lipoproteins have been known for many years to be a major risk factor in the development of premature ischemic heart disease. Although large-scale epidemiological studies have focused attention on the association between above-normal concentrations of plasma lipids and coronary atherosclerosis, recent findings have shown that quantitative lipoprotein and apoprotein determination may be a more nearly accurate predictor in the recognition of atherosclerosis. The risk for vascular disease seems to be particularly associated with an increase in the concentrations of apolipoprotein B (apo B), the major protein moiety of low density lipoproteins and a decrease in apolipoprotein Al, the major polypeptide of high-density lipoproteins.
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PMID:[Methods of biochemical analysis in hyperliproproteinemias]. 640 90

With sensitive methods, the lipoprotein Lp(a) can be demonstrated in the serum of all human subjects, except patients with abetalipoproteinaemia. A high serum level of Lp(a) is considered as a risk factor for atherosclerotic vascular disease (coronary heart disease). The chemical and physical properties of Lp(a) are very similar to those of low density lipoproteins (LDL, Lp-B). In contrast to LDL, Lp(a) has an additional apolipoprotein, the specific Lp(a) antigen. From in vivo studies with 125I-labeled lipoproteins, the following conclusions can be drawn: 1. Lp(a) is not a metabolic product of other apolipoprotein B-containing lipoproteins. Apparently, Lp(a) is synthesized as a separate lipoprotein. 2. Lp(a) is not catabolized to other lipoproteins. Lp(a) leaves the plasma as an intact particle. 3. The fractional catabolic rate and the distribution between the intra- and extravascular compartment are similar for Lp(a) and LDL. 4. The serum level of Lp(a) is primarily determined by the synthetic rate and not by the catabolic rate.
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PMID:[Metabolism and clinical significance of lipoprotein Lp(a) (author's transl)]. 645 20

Advances in the study of cerebrovascular disease suggest that many risk factors for stroke are under genetic influence. Epidemiologic studies show that parental and sibling histories of cerebral ischemic events are associated with an increased risk of stroke. Explanations for familial stroke aggregation include differential phenotypic expression of apolipoprotein (a) and apolipoprotein E, racial variations in the distribution of vascular disease, identification of the autosomal-dominant disorder cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy, specific point mutations in the mitochondrial-related disorders, and identification of the clinical significance of hereditable coagulopathies. Greater understanding of these factors may lead to early recognition of and intervention in stroke.
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PMID:Genetics of ischemic stroke. 774 12

Increased morbidity and mortality from atherosclerotic vascular disease were observed in subjects with slightly elevated urinary albumin excretion rate (UAER), known as microalbuminuria. Therefore, the association between microalbuminuria and established atherogenic risk factors was studied in clinically healthy subjects. All healthy 40-65 year-old participants with microalbuminuria, examined within the first 21 months of The Copenhagen City Heart Study, were invited, and 28 were studied. An age- and sex-matched group of 60 randomly chosen subjects with normoalbuminuria served as control. Microalbuminuria was defined as a UAER of 6.6-150 micrograms/min, and normoalbuminuria as a UAER < or = 6.6 micrograms/min. In the microalbuminuric group, systolic and diastolic blood pressures were both elevated (mean (95% C.I.) 128 (123-134) vs. 119 (116-122) mmHg; P = 0.005, and 75 (71-78) vs. 69 (67-71) mmHg; P = 0.008, respectively), and serum apolipoprotein (apo) A-1 concentration was lower (1.30 (1.20-1.37) vs. 1.42 (1.36-1.47) milligrams; P = 0.02) in comparison with the normoalbuminuric group. Furthermore, serum HDL-cholesterol concentration tended to be lower, whereas body weight, body mass index and fasting serum insulin concentration were slightly elevated in the microalbuminuric group but not statistically significant. It is concluded that microalbuminuria in clinically healthy subjects is associated with increased levels of atherogenic risk factors. This may contribute to the increased vascular morbidity and mortality observed in these individuals.
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PMID:Atherosclerotic risk factors are increased in clinically healthy subjects with microalbuminuria. 777 83

The effect of variation at the cholesteryl ester transfer protein (CETP) gene locus and in the apolipoprotein (apo) AI-CIII-AIV gene cluster on the susceptibility of individuals with non-insulin-dependent diabetes mellitus (NIDDM) to atherosclerotic vascular disease was studied in 136 male and 122 female patients with NIDDM. The prevalence of myocardial infarction was high (38%) in patients with the EcoNI genotype 2-2 of the CETP gene locus (= 2-2; subjects homozygous for the absence of the restriction site) compared with patients with the genotype 1-1 (= 1-1; subjects homozygous for the presence of the restriction site) (18%, p < 0.02). The prevalence of any evidence of coronary heart disease (CHD) (presence of ischaemic ECG changes or definite myocardial infarction) was high in 2-2 (73%) compared with the genotype 1-2 (= 1-2; heterozygous for the presence of the restriction site) (52%, p < 0.02) and genotype 1-1 (p = 0.06). CHD was more prevalent in men with 2-2 (70%) than in those with 1-1 (42%, p < 0.05), but in women no significant differences were found in the prevalences of CHD between the EcoNI genotypes. Neuropathy was more often present in the patients with 2-2 (31%) than in those with 1-1 (12%, p < 0.02) or 1-2 (14%, p < 0.01). Plasma total cholesterol and total- and VLDL-triglycerides were higher in women with the EcoNI genotype 1-1 than in those with the genotype 1-2. In men no significant differences in plasma lipids were found. In addition, the prevalence of cerebrovascular disease was high (21%) in the patients with the genotype 1-1 of the TaqIB polymorphism compared with the genotype 2-2 (6%, p < 0.02). None of the alleles defined by four polymorphisms in the apo AI-CIII-AIV gene region were associated with an increased risk for macroangiopathy. The PstI polymorphism had an effect on plasma triglyceride levels. At the CETP locus one pair of loci (TaqIB and EcoNI) and three pairs of loci at the apo AI-CIII-AIV gene cluster (SacI and MspI, SacI and PvuII and MspI and PvuII) showed significant allelic association. In conclusion, the variation of CETP locus modulates the risk for diabetic complications in patients with NIDDM and the effect seems to be different between men and women. In contrast, the AI-CIII-AIV gene cluster polymorphisms seem not to be related to the risk of CHD in NIDDM.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:DNA polymorphisms at the locus for human cholesteryl ester transfer protein (CETP) are associated with macro- and microangiopathy in non-insulin-dependent diabetes mellitus. 782 Sep 35

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