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)

Elevated plasma levels of total cholesterol and increase in the hepatic synthesis of some apo B-containing lipoproteins have been noted in the nephrotic syndrome. Apoprotein (a), the apolipoprotein distinguishing lipoprotein (a) [Lp(a)] from low-density lipoprotein, is equally of hepatic origin, and Lp(a) recently has been shown to possess both atherogenic and thrombogenic activities. However, little is known of Lp(a) levels in nephrotic patients. We measured plasma Lp(a) concentrations in 11 patients with primary nephrotic syndrome in the absence of hematuria, hypertension, and renal insufficiency. Histologic lesions were minimal-change disease in five cases, membranous glomerulopathy in four cases, and focal and segmental glomerulosclerosis in two cases. Mean levels of Lp(a) (98 +/- 92 mg/dL [mean +/- SD]) were markedly elevated in the nephrotic patients as compared with the controls (14 +/- 13 mg/dL). No correlation was noted between plasma Lp(a) and proteinuria, albuminemia, total cholesterolemia, low-density lipoprotein cholesterol, apoprotein B100, or plasminogen. Furthermore, there was no correlation between Lp(a) levels and apoprotein (a) isoform size. In four patients, the level of Lp(a) decreased approximately fourfold after remission of the nephrotic syndrome under corticosteroid treatment. Our observation that Lp(a) levels are elevated in the nephrotic syndrome is consistent with the hypothesis that these patients may be at an increased risk of cardiovascular and thrombotic complications.
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PMID:Elevated lipoprotein (a) levels in primary nephrotic syndrome. 825 27

The effects of long-term monotherapy with felodipine, a calcium antagonist, on blood pressure, glucose tolerance, and serum lipid profiles were prospectively investigated in 51 hypertensive patients: 13 with normal glucose tolerance and 38 with glucose intolerance. The levels of plasma glucose, serum lipids, and glycosylated hemoglobin A1c were determined before and during long-term (7.5 +/- 0.5 months; range, 6 to 9 months) therapy with felodipine. A 75-g oral glucose tolerance test was performed before and during long-term felodipine therapy. Significant decreases in both systolic and diastolic blood pressures in both patient groups were maintained during the therapy. Neither fasting nor post-glucose load venous plasma glucose levels were altered in either group of patients, and no patients with normal glucose tolerance developed diabetes mellitus during the study. Serum lipid levels did not change significantly in either group of patients except for significant decreases in high-density lipoprotein cholesterol and apolipoprotein A-I in the group with normal glucose tolerance tests, but those changes remained within the normal range. Furthermore, neither serum lipid nor apolipoprotein levels were altered, even in patients with hypercholesterolemia (total cholesterol levels, > 5.69 mmol/L = 220 mg/dL). These results suggest that long-term therapy with felodipine may not alter glucose and lipid metabolism in hypertensive patients, and felodipine appears to be useful as an antihypertensive agent for hypertensive patients with either dyslipidemia or impaired glucose metabolism.
Hypertension 1994 Jan
PMID:Felodipine therapy may not alter glucose and lipid metabolism in hypertensives. Felodipine Multicenter Prospective Study Group in Japan. 828 62

The genetic and environmental determinants of hypertension, lipid abnormalities, and coronary artery disease (CAD) have been studied for 15 years in Utah in population-based multigenerational pedigrees (2500 subjects among 98 pedigrees), twin pairs (74 monozygous and 78 dizygous), hypertensive siblings (131 sibships), siblings with CAD before age 55 (45 sibships), and anecdotally ascertained pedigrees with type II diabetes (271 subjects among 16 pedigrees), lipoprotein lipase deficiency (106 subjects in a single pedigree), and familial hypercholesterolemia (502 heterozygotes among 50 pedigrees). Estimates of heritability ranged from 20 to 75% for blood pressures and blood lipids. A strong positive family history predicts a future occurrence of hypertension (relative risk [RR] = 3.8) and CAD (RR = 12.7). Segregating single-gene effects were found for several 'intermediate phenotypes' associated with hypertension (erythrocyte sodium-lithium countertransport, intraerythrocytic sodium, a relative fat pattern, total urinary kallikrein excretion, and fasting insulin levels). Strong single-gene effects in segregation analysis were also found for low-density lipoprotein (LDL) cholesterol, lipoprotein (a) (Lp[a]), low high-density lipoprotein (HDL) cholesterol, and high apolipoprotein (apo) B. Deoxyribonucleic acid (DNA) markers of lipid abnormalities or hypertension have included LDL-receptor defects, lipoprotein lipase deficiency, high Lp(a), familial defective apo B, decreased quantitative levels of apo B, apo E phenotype, angiotensinogen, and 'glucocorticoid remediable aldosteronism (GRA) hypertension.' Also tested in Utah studies, but not found to be DNA markers for hypertension, were the genetic loci for the structural genes for renin and angiotensin-converting enzyme, and the sodium antiport system. In addition, important gene-gene interactions (LDL receptor with apo E2) and gene-environment interactions (kallikrein with potassium intake) were found.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Genetic basis of familial dyslipidemia and hypertension: 15-year results from Utah. 829 39

Peripheral vascular diseases, both symptomatic and asymptomatic, are strong predictors of total and cardiovascular mortality. The commonly used Rose questionnaire, although highly specific, has a low sensitivity to detecting peripheral vascular disease and is not adequate for asymptomatic subjects. Doppler ultrasound measurement of the ankle/brachial systolic blood pressure ratio is a non-invasive, reproducible and accurate method of assessment of peripheral vascular disease and has been validated by angiography. METHODS. Five hundred and ten subjects, corresponding to fifty percent of the people working as civil servants in the Catanzaro city hall, were invited to join the study by a letter. Three hundred and eighty four participated. Exclusion criterion was claudicatio intermittens as detected by Rose questionnaire. All the subjects filled a questionnaire to assess coronary heart disease risk factors and underwent a full clinical examination. Brachial blood pressure was measured on both arms with participants in supine position, just before ECG. The systolic ankle blood pressure was measured with ultrasonic technique. The blood pressure cuff was placed just proximal to the medial malleolus. The ankle-brachial systolic pressure index (Winsor Index) was determined by dividing the highest of the posterior tibial or dorsalis pedis pressures by the highest brachial pressure. A limit of 0.95 was chosen to identify subjects with peripheral arterial disease. Venous blood for serum cholesterol and triglycerides, apolipoprotein AI and B and blood glucose, was collected after an overnight fasting, into Vacutainer Tubes (Becton & Dickinson). RESULTS. No subject had claudicatio intermittens. Sixteen subjects were excluded from the statistical analysis because of missing data. Two hundred and sixty-three were males and 105 females. Twenty-one (5.7%) out of 368 participants had a Winsor Index < 0.95 in at least one leg. These subjects had higher values of systolic and diastolic blood pressure compared to normal subjects whereas no differences were observed with regard to age, BMI, lipid profile and blood glucose. Furthermore the prevalence of hypertension was higher in the group of subjects with asymptomatic peripheral arterial disease. The prevalence of other risk factors for atherosclerosis (cigarette smoking, hyperlipidemia, diabetes mellitus, obesity) was similar in subjects with or without peripheral arterial disease. DISCUSSION. In the present study the prevalence of Winsor Index < 0.95 was 5.7%, similar to that reported by other authors. Hypertension was the only risk factor for atherosclerosis associated with peripheral arterial disease. Other authors also reported a higher prevalence of cigarette smoking among subjects with peripheral disease. In our population this association was not found but the participants were younger and consequently the exposure to this risk factor was shorter. CONCLUSION. The measurement of systolic ankle blood pressure by Doppler ultrasounds is a non-invasive, well accepted, highly specific and sensitive method to detect asymptomatic peripheral arterial disease. It might be of value in better defining the cardiovascular risk profile both in epidemiologic studies and clinical practice, especially in subjects with hypertension.
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PMID:[Asymptomatic arteriopathy of the lower limbs. Prevalence and risk factors in a population of southern Italy]. 833 69

The familial lipoprotein disorder type III hyperlipoproteinemia (HPL) carries a marked increase in the risk of accelerated and premature atherosclerosis, but there is considerable variation among affected individuals in susceptibility to cardiovascular disease (CVD). We studied the influence of independent risk factors for atherosclerosis in 67 patients with clinically overt type III HPL and homozygosity for apolipoprotein (apo) E2. Among the different risk factors (lipid and lipoprotein levels, age, sex, body mass index, smoking status, hypertension, and diabetes mellitus) there was only a statistically significant difference in age between 25 patients with atherosclerosis and 42 patients without atherosclerosis. Serum lipoprotein (a), [Lp, (a)], levels were 30.6% higher in the atherosclerosis group, but this was not statistically significant. We conclude that (in contrast to familial hypercholesterolemia) elevated Lp (a) concentrations may not be regarded as a component of the clinical syndrome of type III HPL.
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PMID:Relation of cardiovascular risk factors to atherosclerosis in type III hyperlipoproteinemia. 837 May 76

The objective of the present study was to determine whether information about a biometrically inferred single gene with large effects on erythrocyte sodium-lithium countertransport is useful in predicting the probability of having hypertension. We used multivariate logistic regression to model the relationship between the probability of having hypertension and predictor traits in a sample of 382 unrelated adult women and 347 unrelated adult men from Rochester, Minn. First, we identified a set of demographic, biochemical, and physiological predictors. Second, we analyzed whether the relationship between the probability of having hypertension and the identified predictor traits was heterogeneous between the biometrically inferred single locus genotypes with large effects on sodium-lithium countertransport level. Third, if there was no heterogeneity, we assessed whether sodium-lithium countertransport genotypes made an additional contribution to predicting the probability of having hypertension after other predictors were considered. In women, the predictors of the probability of having hypertension were age, plasma apolipoprotein CIII, body mass index, and an interaction term involving age and body mass index. The relationship between the probability of having hypertension and the identified predictors was not heterogeneous between sodium-lithium countertransport genotypes, and genotype did not contribute to the prediction of the probability of having hypertension after the identified predictors were considered. In men, predictors of the probability of having hypertension were age, plasma levels of high-density lipoprotein cholesterol, apolipoproteins AI and CII, sodium-lithium countertransport level, and sodium-lithium countertransport genotype. The relationship between the probability of having hypertension and sodium-lithium countertransport level and age were heterogeneous between biometrically inferred sodium-lithium countertransport genotypes.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1993 Oct
PMID:Sodium-lithium countertransport genotype and the probability of hypertension in adults. 840 61

In an attempt to discern biological (such as thrombotic or fibrinolytic) risk factors in patients developing restenosis after percutaneous transluminal coronary angioplasty, the following factors were measured prior to angiography in a population of 23 patients (20 men, 3 women, mean age 57 +/- 5 yr) treated by a successful angioplasty (gain > 20% and residual stenosis < 50%) for stable angina pectoris and who had a routine angiographic restudy. The following factors were thus assessed: lipid factors: cholesterol, triglycerides, high density lipoprotein cholesterol, low density lipoprotein cholesterol, apolipoprotein AI, apolipoprotein B; coagulation factors: fibrinogen, antithrombin III, fibrinopeptide A, factor VIII coagulant, factor VIII antigen, protein C; factors of physiological fibrinolysis: plasminogen, alpha 2-antiplasmin, tissue plasminogen activator and euglobulin clot lysis time before and after venous occlusion, plasminogen activator inhibitor before venous occlusion; and factors of platelet release: beta-thromboglobulin, platelet factor 4. Also studied were clinical characteristics: age, gender, diabetes, hypertension, smoking habits, previous myocardial infarction; angiographic data: global extent of coronary artery disease, location of the stenosis in a bend or branch point, complexity of the lesion, initial and residual stenosis and treatment during follow-up. The coronary angiograms were analyzed by a computer-assisted method with automatic edge detection. On angiographic criteria, 6 patients (restenosis group) were judged to have developed a restenosis (30% decrease in diameter and/or return to a 50% stenosis). The other 17 patients (those without restenosis) were considered to have a persistent success. Apart from age (group without restenosis: 55 +/- 6; restenosis group 61 +/- 5, p < 0.04), there were no differences in clinical, angiographic or treatment variables. There were no differences in lipid factors, but significant differences were observed in hemostatic variables: fibrinogen (without restenosis: 3.18 +/- 0.83; restenosis: 3.83 +/- 0.51 milligrams, p = 0.05), tissue plasminogen activator before venous occlusion (without restenosis: 10.9 +/- 26.8; restenosis: 232.5 +/- 371.2 IU, p < 0.04), euglobulin clot lysis time after venous occlusion (without restenosis: 176.5 +/- 100.5; restenosis: 78.6 +/- 40.2 min, p < 0.05) and for marker of the platelet release: platelet factor 4 (without restenosis: 10.8 +/- 7.9; restenosis: 20.5 +/- 7.5 ng/l, p < 0.04). These findings indicate that patients developing restenosis after coronary angioplasty tend to have an imbalance in the prothrombotic-antithrombotic equilibrium prior to the procedure.
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PMID:Biological risk factors for restenosis after percutaneous transluminal coronary angioplasty. 844 4

In this study, the authors examined relations between coronary and carotid atherosclerosis and between coronary atherosclerosis and silent cerebral infarction. They ascertained the risk factors for carotid atherosclerosis and silent cerebral infarction complicating coronary heart disease (CHD) in 77 Japanese subjects. As coronary atherosclerosis progressed, the carotid ultrasonographic score and the brain computed tomographic score increased. Multivariate analyses showed that the significant and independent risk factors for carotid atherosclerosis in patients with CHD were age (p < 0.01) and apolipoprotein (apo) B (p < 0.05) and the factors for silent cerebral infarction were age (p < 0.05) and hypertension (p < 0.05). Their study confirms a positive relation between coronary atherosclerosis and carotid atherosclerosis and between coronary atherosclerosis and silent cerebral infarction in patients with CHD. Their data suggest that carotid atherosclerosis should be looked for in patients with CHD who are old and have a high value of apo B, and silent cerebral infarction should be looked for in those who are old and have hypertension, to prevent complicating symptomatic cerebral vascular disease (CVD). If severe carotid atherosclerosis or silent cerebral infarction are detected, antithrombotic medication should be given.
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PMID:Risk factors for carotid atherosclerosis and silent cerebral infarction in patients with coronary heart disease. 850 8

Genetic variation at the apolipoprotein (apo) A-I/C-III/A-IV gene cluster on chromosome 11 has been associated with differences in occurrence of atherosclerosis and with variability in lipid levels among hypercholesterolemic-hypertriglyceridemic individuals. The functional cause of the association is not known, but polymorphisms of the apo A-IV gene are of interest because apo A-IV is involved in both triglyceride and cholesterol metabolism. Two mutations in the apo A-IV gene, 347T->S and 360Q->H, are known to cause amino acid substitutions in the mature protein. These polymorphisms were typed in a sample of 119 subjects with high cholesterol and high triglycerides in whom carotid artery wall thickness was previously shown to be strongly associated with silent polymorphic variation in the A-I/C-III/A-IV gene cluster. The relative allele frequencies were 0.83 and 0.17 for codon 347T->, and 0.95 and 0.05 for codon 360Q-> H. These polymorphisms did not show a statistically significant relationship with prevalent hypertension, diabetes, or cardiovascular disease or with plasma lipid levels. Most importantly, these amino acids substitutions in apo A-IV were not associated with carotid artery wall thickness. Therefore, the genetic cause of disease variability in a sample of mixed hyperlipidemics is not amino acid substitutions in codons 347 or 360 of the apoliproteins A-IV gene.
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PMID:No association of apolipoprotein A-IV codon 347 and 360 variation with atherosclerosis and lipid transport in a sample of mixed hyperlipidemics. 853 54

The apolipoprotein epsilon4 allele and homozygous deletion allele (DD) of the angiotensin-converting enzyme gene are reported to be associated with an increase in the incidence of ischemic heart disease. In this study, we examined whether the apolipoprotein epsilon4 genotype and angiotensin-converting enzyme/DD allele are associated with silent myocardial ischemia. We screened 3920 subjects undergoing general checkups who no symptoms of ischemic heart disease. Seventy subjects (2 percent) showed ischemic ST-segment depression during the double two-step exercise test. One hundred and twenty control subjects without ischemic ST-segment depression were recruited from the same population and matched for sex, age, and blood pressure. We performed genotyping of the apolipoprotein E gene (epsilon2, epsilon3, and epsilon4) and angiotensin-converting enzyme gene (I and D) using polymerase chain reaction-restriction fragment length polymorphism and polymerase chain reaction, respectively. Allele frequently of epsilon4 of the apolipoprotein E gene was higher in the ischemic group (11 percent) than the nonischemic group (5 percent) (chi2 = 5.35, P < .05), but there was no significant association between the allele or the genotype frequency of the angiotensin-converting enzyme gene and the incidence of ischemic ST-segment depression. Furthermore, stepwise multiple regression analysis also revealed that total cholesterol level and epsilon4 genotype were predictors of ischemic change in the exercise tolerance test (chi2 = 12.8, P < .005, R(2) = .051). These results suggest that the apolipoprotein epsilon4 allele is an independent genetic risk factor for silent myocardial ischemia in Japanese subjects.
Hypertension 1996 Jun
PMID:Polymorphism of the apolipoprotein E and angiotensin-converting enzyme genes in Japanese subjects with silent myocardial ischemia. 864 25


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