Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Risk factors for primary cerebral hemorrhage remain uncertain. The population-based Stroke Registry of Dijon provides data on the risk factors. Among residents of Dijon (France), 130 cases of primary cerebral hemorrhage hospitalized from 1985 to 1992 were matched with 130 controls by age and sex. The following data were collected: history of hypertension, alcohol consumption, tobacco consumption, history of coagulation disorder, diabetes mellitus, dyslipidemia, and infectious disease in the 7 days before admission. The following parameters were measured on admission: blood pressure, blood glucose, cholesterol, triglycerides, hematocrit, fibrinogen, prothrombin levels, platelet counts, prothrombin time, bilirubin, transaminases, gamma-glutamyltransferase, and alkaline phosphatase. Electrocardiogram and Doppler ultrasound examination of cervical arteries were performed. Statistical analysis was performed by means of relative risk ratio for paired samples when dealing with proportions, and Student's t test for quantitative variables. A stepwise discriminant analysis was carried out to establish the relative weight of the different risk factors and their discriminant values. Among the qualitative data, the significant factors were history of hypertension, alcohol consumption, cardiac arrhythmia, atherosclerosis of carotid arteries and a previous infectious disease in the 7 days before admission. Among the quantitative data, the significant factors were early hypertension, high blood glucose levels, high hematocrit, and low cholesterol levels, in the acute stage of the stroke. After multifactorial analysis, only two factors were significant: hypertension and low cholesterol levels. Our population-based case-control study showed that hypertension and low cholesterol levels are the two discriminant risk factors for both lobar and basal ganglia primary cerebral hemorrhage. Therefore, treatment of hypercholesterolemia may increase risk of cerebral hemorrhage.
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PMID:Risk factors for primary cerebral hemorrhage: a population-based study--the Stroke Registry of Dijon. 789 3

Herpes ophthalmicus (HO) patients were examined for lipid spectrum of the serum. The tests revealed dyslipidemia (DLE) with a distinctive rise in the levels of total cholesterol (CS), alpha-CS and beta-CS. The severity of the lipidemic shifts correlated with that of the infection. DLE was more marked in recurrent HO. Clinical evidence was consistent with experimental findings. In rabbit models, herpetic keratoconjunctivitis was characterized by pronounced lipidemic alterations correctable with antiherpetic drug furavir. The results are discussed in terms of herpetic infection pathogenesis and its role in the development of atherosclerosis.
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PMID:[Dyslipidemia in herpetic infection]. 790 19

Coronary artery disease (CAD) patients (n = 235), comprising minimal (CAD-, n = 124) and severe (CAD+, n = 111) CAD, were recruited on the basis of their angiographic scores. Male control subjects (n = 123) were selected randomly from the Caerphilly Heart Study cohort. Subjects were genotyped for the Ser447-Ter mutation and HindIII/Pvu II restriction fragment length polymorphisms of the lipoprotein lipase gene and investigated for associations with severity and development of CAD and lipid and lipoprotein levels. The Ser447-Ter mutation showed no significant associations with CAD or dyslipidemia but was related to favorable lipid and lipoprotein profiles. The H2H2 genotype (P < .05) and H2 allele (P = .05) were significantly more frequent in CAD+ versus CAD- and control subjects versus CAD-. H2H2 subjects, among the entire male cohort, had significantly higher levels of apolipoprotein B (P = .0002), total cholesterol (P < .004), and triglycerides (P < .04) than alternative genotypes. P2P2 associated with significantly lower high-density lipoprotein cholesterol levels (P < .01). The H2 allele had most significant associations with raised apolipoprotein B levels compared with other biochemical parameters. Our data suggest that the H2 allele may be a linkage marker for an etiologic mutation for dyslipidemia and the severity and development of atherosclerosis; this is not the Ser447-Ter mutation.
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PMID:DNA variants at the LPL gene locus associate with angiographically defined severity of atherosclerosis and serum lipoprotein levels in a Welsh population. 791 49

Dyslipidemia is commonly observed in nephrotic syndrome, in chronic renal failure, and after renal transplantation. The patterns of dyslipidemia, however, differ among these three conditions, and the origins and mechanisms responsible for abnormalities in lipoprotein metabolism in each are not well understood. Whether these dyslipidemias contribute to the development of atherosclerosis and coronary heart disease is uncertain, but it is probable that they do. Important questions are whether an attempt should be made to treat the various renal dyslipidemias, and if so, by what means. Also of current interest are dyslipidemias in the nephrotic syndrome, chronic renal failure (uremia), and the post-renal transplantation state.
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PMID:Mechanisms and treatment of dyslipidemia of renal diseases. 792 19

Atherosclerosis develops rapidly in patients with diabetes or renal insufficiency. Plasma lipoprotein profiles are frequently abnormal in these conditions and reflect an elevation in the level of the apoprotein B (ApoB)-containing components very low density lipoprotein (VLDL) and low density lipoprotein (LDL). High levels of circulating advanced glycation end products (AGEs) also occur in diabetes and end-stage renal disease (ESRD). These products arise from glucose-derived Amadori products and include AGE-modified peptides (AGE-peptides) which result from the catabolism of AGE-modified tissue proteins. AGE-peptides have been shown to crosslink protein amino groups and to accumulate in plasma as a consequence of renal insufficiency. To address potential mechanisms for the dyslipidemia of diabetes and ESRD, we investigated the possibility that circulating AGEs react directly with plasma lipoproteins to prevent their recognition by tissue LDL receptors. AGE-specific ELISA showed a significantly increased level of AGE-modified LDL in the plasma of diabetic or ESRD patients compared with normal controls. AGE-LDL formed readily in vitro when native LDL was incubated with either synthetic AGE-peptides or AGE-peptides isolated directly from patient plasma. LDL which had been modified by AGE-peptides in vitro to the same level of modification as that present in the plasma of diabetics with renal insufficiency exhibited markedly impaired clearance kinetics when injected into transgenic mice expressing the human LDL receptor. These data indicate that AGE modification significantly impairs LDL-receptor-mediated clearance mechanisms and may contribute to elevated LDL levels in patients with diabetes or renal insufficiency. This hypothesis was further supported by the observation that the administration of the advanced glycation inhibitor aminoguanidine to diabetic patients decreased circulating LDL levels by 28%.
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PMID:Modification of low density lipoprotein by advanced glycation end products contributes to the dyslipidemia of diabetes and renal insufficiency. 793 86

Chronic hemodialysis (CHD) patients have a high incidence and prevalence of atherosclerotic disease which may be related to numerous atherosclerotic risk factors. Among them dyslipidemia plays a significant role. Elevated Lp(a) levels, which are strongly associated with atherosclerosis, have been reported recently in uremic patients. The aim of our study was the determination of the levels of lipid parameters including Lp(a) in 151 CHD patients (76 male) aged 57 (12-81) years, who were on hemodialysis for a mean of 44.3 (range 1 to 189) months. Eighty-four normal individuals age and sex matched were used as controls. The median serum Lp(a) concentration in hemodialysis patients was 13 mg/dL compared with 6.5 mg/dL in healthy controls, p < 0.001 by distribution-free Mann-Whitney test. The prevalence of subjects with Lp(a) levels above 25 mg/dL was significantly higher in CHD patients compared to normal subjects (30% vs. 8%, p < 0.001). Even if CHD patients were matched for fasting lipid levels, they showed Lp(a) levels significantly higher than controls. No significant correlation was found between Lp(a) levels and either the age of the patients or the duration of hemodialysis. The etiology of primary renal disease did not influence the Lp(a) levels.
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PMID:Lipid parameters including Lp(a) in hemodialysis patients. 793 58

To characterize acute myocardial infarction (AMI) in young adults and octogenarians, 475 AMI patients, in age subsets, were examined. The clinical features, risk factors and in-hospital mortality were compared among 17 young patients (< 40 years), 426 patients of common age (40-79 years), and 32 very elderly patients (> or = 80 years). The octogenarian patients were mainly female (male/female ratio, 0.9 vs. 4.7 in other subgroups, P < 0.005), and had more frequent atypical presentation and postinfarctional congestive heart failure; whereas infarct size, location and development of Q-wave, major arrhythmias and cardiac wall rupture were not different among these age subsets. The most common risk factors in the young group were dyslipidemia (67%) and cigarette smoking (65%), and in the octogenarian group were dyslipidemia (52%) and hypertension (50%). Among age subsets, however, the prevalence of risk factors was not significantly different except for a relatively lower smoking rate in the octogenarians. Compared with 40- to 79-year-old patients who had predominantly multi-vessel diseases, the young patients had milder coronary atherosclerosis and were more likely to have normal coronaries (27% vs. 5%, P < 0.01). Significantly more octogenarians than young patients succumbed to AMI in the hospital (44% vs. 18%, P < 0.005), usually because of a cardiogenic complication (93%). Also, the octogenarians were less likely than the younger patients to have received thrombolytic therapy, mostly because of delayed diagnosis and arrival at the hospital, or because of old age itself.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acute myocardial infarction in young and very old Chinese adults: clinical characteristics and therapeutic implications. 802 Oct 47

Asymptomatic or silent myocardial ischemia (SI) is frequent in coronary heart disease and its prognostic value is controversial. The aim of our study is to compare coronary atherosclerosis, left ventricular function and clinical out come of 110 patients with S.I. (A group) and 210 patients with stable angina (B group). The 320 patients were submitted: to symptom limited exercise stress-test with permanent electrocardiographic control by a Case 12-15 digitalized system with ST segment depression interpretation. A test was considered positive for ischemia if there was ST depression of > 1 mv in magnitude from baseline, persisting for 0.08 sec or exercise angina and ischemia: to selective coronarography by Seldinger technic, with left ventricular cineangiography in 2 incidences. A significant coronary stenosis was defined as > 50% reduction of luminal diameter; to medical treatment with betablockers (87.5% of patients), calcium inhibitors (12.5%), aspirin (90%) and nitrates; to regular medical surveillance. During the follow-up (42.4 +/- 5 months in mean) the number of deaths, myocardial infarctions, heart failure, unstable angina and revascularizations were analyzed. Patients of A group with S.I. had a high percentage of risks factors (diabetes mellitus 55%, nicotinism 85%, dyslipidemia 22.5%) and history of previous myocardial infarction in 33% of cases. There are not significant differences between severity and extension of coronary disease, or ventricular dysfunction in patients of A group or B. The percentages of deaths (2.10 versus 3%), acute myocardial infarctions (9.5 versus 8.5%), heart failures (2.72 versus 3%), surgical indications (14.7 versus 15.7%) are not significantly different between the 2 groups. In A group, 34% of patients were treated by angioplasty versus 40% of patients in group B (p < 0.02). S.I. has a bad prognostic and the clinical out come of coronary heart disease is not dependent of presence of angina during exercise testing and daily activities.
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PMID:[Prognosis of silent myocardial ischemia]. 803 89

The pathophysiology of various stages of hypertension is different. In early hyperkinetic borderline hypertension, the sympathetic drive to the heart and blood vessels is increased while the parasympathetic cardiac inhibition is decreased. The elevated cardiac output, vascular resistance, and blood pressure at that stage can be fully normalized by autonomic blockade. As hypertension advances, a hyperkinetic circulation is less evident, since beta-adrenergic responsiveness and cardiac compliance tend to decrease. Simultaneously hypertrophy of the resistance vessels increases the baseline vascular resistance and the vessels' responsiveness to constrictive stimuli. Eventually a picture of a normal cardiac output/high vascular resistance typical for established essential hypertension emerges. As the blood vessels become hyperreactive, the same degree of vasoconstriction/blood pressure elevation can be achieved with less sympathetic tone. In that phase the sympathetic overactivity is less evident, as the brain resets itself to maintain the same blood pressure elevation with a small amount of sympathetic discharge. While sympathetic overactivity may be less evident in established hypertension, it remains an important pathophysiologic factor, not only for the maintenance of blood pressure, but also for a number of other abnormalities in hypertension. Hypertension is intimately associated with higher levels of pressure-unrelated risk for development of atherosclerosis: dyslipidemia, overweight, and hyperinsulinemia. Furthermore, a number of factors in hypertension favor a poorer outcome from coronary heart disease. These pressure-independent factors increase the risk of coronary thrombosis, arrhythmic deaths, and coronary spasms. Sympathetic overreactivity appears to be crucially implicated in the evolution of this added coronary risk in hypertension. Understanding the pathophysiology of coronary risk and its relationship to sympathetic overreactivity in hypertension is helpful in seeking further improvements in clinical practice. At present antihypertensive treatment is less efficacious in reducing coronary events in hypertension than would be expected. Judicious use of appropriate drugs promises to further improve the efficacy of antihypertensive treatment in those patients who, in addition to high blood pressure, also have other associated risk factors.
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PMID:Abnormalities of autonomic nervous control in human hypertension. 806 76

Insulin resistance is associated with a number of risk factors for atherosclerosis, including glucose intolerance, hypertension, and dyslipidemia. Management of these disorders should include an attempt to reduce insulin resistance and certainly not to increase it. For example, when possible, thiazide diuretics and beta blockers should be avoided for treating hypertension, because they increase insulin resistance and, in diabetic patients, adversely affect glycemic control. Since exercise, weight loss, and cessation of smoking reduce insulin resistance, they are often helpful components of a treatment regimen for patients who have chronic medical disorders that are associated with insulin resistance.
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PMID:Insulin resistance. An often unrecognized problem accompanying chronic medical disorders. 809 25


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