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)

Concomitant arterial hypertension and metabolic disorders is a frequent finding raising the risk of micro- and macrovascular complications. While prevalence of stroke and myocardial infarction is going down in hypertensives, end-stage renal disease (ESRD) becomes a bigger problem especially in diabetic hypertensives. The metabolic abnormalities are linked to the hypertension by the sympathoadrenal system mediated by insulin resistance (IR); subjects with hyperinsulinemia and increased sympathetic activity tend to have higher blood pressure, typical dyslipidemia, reduced fibrinolytic activity and other risk factors (RF) called metabolic syndrome of IR. Albuminuria (AUR) is considered as an important RF for the development of nephropathy, ESRD, cardiovascular diseases. AUR is a marker of cardiovascular and total mortality in diabetic and/or non-diabetic hypertensives. AUR reflects the endothelial dysfunction not only in glomerulus but also in the other arteries. Tissue Renin-Angiotensin System plays a significant role in the pathogenesis of hypertension and metabolic disorders; it affects the arterial wall, kidneys and heart longitudinally. Life style is very essential in the treatment of hypertension and metabolic disorders: rational diet with reduced amount of salt and animal proteins, non-smoking and sufficient physical activity. Antihypertensive drugs without any metabolic side effects and with the renal protection are necessary for the patients with hypertension and metabolic disturbances. ACE-inhibitors and/or some of the Ca-antagonists seems to be valuable especially as combined therapy.
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PMID:[New approaches in the treatment of hypertension in metabolic diseases]. 972 74

Despite the decrease in coronary heart disease (CHD) mortality in the US in the past 30 years, CHD is the leading cause of death in men and women. Cardiovascular disease, including CHD, kills nearly 500,000 American women each year. In women, the development of CHD can be delayed by an average of 10 years compared with men, and, on average, women can experience a first myocardial infarction 20 years later than men. While CHD prevalence rates are similar in black men and white men, heart disease is not color-blind in women. Black women generally have a higher prevalence of CHD risk factors and a higher death rate at a younger age than white women. A strong family history of early onset of heart disease, increasing age, and race are unalterable factors that raise the risk of CHD. The major factors that can be modified include cigarette smoking, hypertension, diabetes mellitus, physical inactivity, obesity, dyslipidemia, estrogen level changes after menopause, and psychosocial stressors. CHD is a multifactorial process; the hazard posed by one particular risk factor is significantly influenced by other risk factors that are present, and no individual risk factor is essential or sufficient to cause CHD.
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PMID:What Can Be Done to Prevent Coronary Heart Disease in Women? 974 63

In Taiwan over the past decades there has been enormous economic growth and rapid westernization of people's life style, as well as a concomitant rise in coronary heart disease (CHD) mortality and morbidity. Studying the effects of such a degree of socioeconomic development on the coronary risk factors of the Chinese population, an ethnic group long regarded as having a low incidence of CHD, may provide some insight into the etiology of coronary atherosclerosis. Coronary risk factors among 1,449 patients (759 with CHD) were retrospectively studied. Diagnosis was established by angiography or a definite history of myocardial infarction in approximately 60% of the patients, and for the remainder, at least by noninvasive testing. The frequencies of dyslipidemia and nonlipid risk factors in patients with and without CHD were determined and compared. The lipid levels of subjects with or without CHD were close to or approaching those reported from the United States. Socioeconomic development and changes in dietary patterns seem influential in this regard. Among risk factors, high-density lipoprotein cholesterol (HDL-C), smoking, diabetes mellitus, hypertension and family history in males and, in females, total cholesterol, HDL-C, diabetes mellitus and hypertension, were significantly and independently correlated with CHD. These risk factors are similar to those found in the West; however, there is an important association of serum HDL-C concentrations with CHD, irrespective of gender. This issue requires further study in Chinese populations in other Asian countries.
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PMID:A retrospective hospital-based study of coronary risk factors in Taiwan. Analysis of patients with established diagnoses. 981 Feb 94

It has been suggested that the postprandial elevation of plasma triglycerides is more closely linked to coronary heart disease (CHD) than the fasting triglyceride level. However, the postprandial situation is complex, as hepatogenous triglyceride-rich lipoprotein (TRL) particles (apolipoprotein [apo]B-100 and very-low-density lipoprotein [VLDL]) are mixed in the blood with apoB-48-containing lipoproteins secreted from the intestine. To analyze the relative proportion of liver-derived and intestinal apoB-containing TRL in subjects with and without CHD, we performed standardized oral fat-loading tests in young survivors of myocardial infarction, a large proportion of whom are hypertriglyceridemic (HTG), as well as sex- and population-matched healthy control subjects. A special effort was made to recruit healthy HTG subjects as controls for the HTG patients. Fasting plasma triglycerides (3.74+/-1.35 v3.01+/-0.83, NS), low-density lipoprotein (LDL) cholesterol, and VLDL lipids, and apoB-100 and apoB-48 content at Svedberg flotation rate (Sf) 60-400, Sf 20-60, and Sf 12-20 did not differ between HTG patients (n = 10) and HTG controls (n = 14). Normotriglyceridemic (NTG) patients (n = 15) had higher fasting plasma triglycerides (1.44+/-0.39 v 0.98+/-0.33 mmol/L, P < .05) and LDL cholesterol (4.07+/-0.71 v 3.43+/-0.64, P < .05) than NTG controls (n = 34). The triglyceride elevation was accounted for by a higher level of small VLDL (apoB-100 in the Sf 20-60 fraction, 52+/-17 v29+/-20 mg/L, P < .05). HTG patients responded with clearly elevated plasma triglycerides in the late postprandial phase, ie, 7, 8, and 9 hours after fat intake. Essentially, this was explained by a retention of large VLDL particles, since HTG patients exhibited no major differences in apoB-48 concentrations in the Sf > 400, Sf 60-400, and Sf 20-60 fractions but showed marked differences in the level of apoB-100 at Sf 60-400 (large VLDL) 9 hours after fat intake when compared with HTG controls (101+/-13 v 57+/-5 mg/L, P < .01). NTG patients were characterized by a more rapid increase of large VLDL in the early postprandial state, ie, 3 hours after fat intake, with a mean increase from baseline to 3 hours of 24.1+/-6.7 mg/L for NTG patients and 11.8+/-2.0 mg/L for controls (P < .05). ApoB-48 levels were also slightly higher, but all TRL parameters returned to baseline within 9 hours after fat intake. In conclusion, elevated triglyceride levels in the postprandial state in CHD patients are explained to a large extent by the accumulation of endogenous TRL. This suggests that the postprandial dyslipidemia encountered in CHD is more dependent on a failure of regulation of endogenous TRL versus the exogenous TRL species.
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PMID:Differences in postprandial concentrations of very-low-density lipoprotein and chylomicron remnants between normotriglyceridemic and hypertriglyceridemic men with and without coronary heart disease. 1009 4

The metabolic syndrome X, characterized by insulin resistance, dyslipidemia, hypertension, and a male, visceral distribution of adipose tissue, is associated with increased morbidity and mortality from several prevalent diseases, such as diabetes, cancers, myocardial infarction, and stroke. Because the liver has a central role in carbohydrate, lipid, and steroid metabolism, we investigated the relationships between liver pathology and the metabolic syndrome. Blood chemistry, anthropometry (waist/hip circumference ratio), and intraoperative routine knife biopsies of the liver were obtained in 551 (112 men) severely obese patients (body mass index, 47 +/- 9; mean +/- SD) undergoing antiobesity surgery. Steatosis was found in 86%, fibrosis in 74%, mild inflammation or steatohepatitis in 24%, and unexpected cirrhosis in 2% (n = 11) of the patients. The risk of steatosis was 2.6 times greater in men than in women (P < 0.0001). With each addition of 1 of the 4 components of the metabolic syndrome, elevated waist/hip ratio, impaired glucose tolerance, hypertension, and dyslipidemia, the risk of steatosis increased exponentially from 1- to 99-fold (P < 0.001). Fibrosis correlated with steatosis (r = 0.56; P < 0.0001), whereas patients with diabetes or impaired glucose tolerance had a 7-fold increased risk of fibrosis (P < 0.0001). Diabetes, steatosis, and age were all significant indicators of cirrhosis, whereas inflammation was only associated with age. We conclude that the metabolic syndrome via impaired glucose tolerance is strongly correlated with steatosis, fibrosis, and cirrhosis of the liver.
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PMID:Liver pathology and the metabolic syndrome X in severe obesity. 1056 91

The Polycystic Ovary Disease (PCOD) is one of the most common endocrine disorders in women with a prevalence of 5%. Affected women often consult a gynecologist because of menstrual irregularities, fertility problems or problems of androgen excess. However, PCOD is a metabolic disorder affecting multiple organs. Studies suggest that those women are at risk for developing several complications such as type II diabetes mellitus, hypertension, dyslipidemia and myocardial infarction. The risk to develop endometrial carcinoma is also elevated. To give adequate treatment to women with PCOD, an interdisciplinary approach of gynecologists together with endocrinologists specialized in metabolic and nutritional disorders at the University of Basel is presented. The work-up for diagnosis and assessment of risk factors is outlined. Goal of this interdisciplinary approach is an adequate evaluation of affected patients and their long-term follow-up to test if proposed interventions as weight loss, treatment of hyperinsulinemia, regulation of menstrual cycle and others can avoid long-term sequelae.
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PMID:[Polycystic ovary syndrome--only relevant in reproductive medicine?]. 1040 2

The differences in direct health care costs and use between HMO enrollees with both diabetes mellitus and hypertension and enrollees with either disease alone were studied. Two years' worth of medical and pharmacy claims data from a hybrid (independent practice association and group)-model HMO were evaluated. Diagnoses were determined from medical claims data and cross-referenced with prescription information from pharmacy claims data. Aggregate costs associated with each disease, including pharmacy costs, costs of physician office visits, and laboratory costs, were compiled. Comparisons were made of all costs (any cost incurred by the health plan for the member, regardless of disease) and disease-specific costs. The frequency of comorbid conditions was identified. A total of 6195 patients (670 with diabetes and hypertension, 1756 with diabetes alone, and 3769 with hypertension alone) were assessed. Patients with both diseases incurred much higher costs per year than patients with diabetes or hypertension alone (mean costs, $13,446, $8,493, and $8,424, respectively). Hospitalization costs contributed the greatest amount to total costs, while emergency room costs contributed the least. Disease-specific costs for diabetes and hypertension represented less than one quarter of total health care costs per patient. Average disease-specific costs were highest for patients with both diseases ($2,955), followed by costs for patients with hypertension alone ($1,803) and patients with diabetes alone ($689). The percentage spent on prescriptions was much higher for disease-specific costs than for total costs. The three most common comorbid conditions were dyslipidemia, coronary artery disease, and chronic obstructive pulmonary disease, with the frequency of cerebrovascular disease and myocardial infarction more than double in patients with diabetes and hypertension compared with patients with either disease alone. The cost of care for a patient with both diabetes and hypertension, although not double that for a patient with diabetes or hypertension alone, was higher than the cost of treating either disease.
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PMID:Direct health care costs for treatment of diabetes mellitus and hypertension in an IPA-group-model HMO. 1047 88

We sought to evaluate the potential interactions between systemic hypertension and blood lipids on the risk of myocardial infarction (MI). Recent evidence suggests that hypertension may interact with other risk factors such as dyslipidemia in the development of coronary heart disease. However, the precise nature of that interrelation remains unclear. We selected 340 cases of first MI and an equal number of age-, sex-, and community-matched controls. Data were collected on a large number of coronary risk factors, and fasting blood samples were obtained. Logistic regression was used to calculate the odds ratio (OR) of nonfatal MI. The age- and sex-adjusted OR of MI was 1.61 (95% confidence interval [CI] 1.15 to 2.25) among treated hypertensives compared with nonhypertensives. Further adjustment for coronary risk factors did not materially alter the results (OR 1.67, 95% CI 1.16 to 2.41). To explore the interrelations among hypertension, lipids, and risk of MI, each lipoprotein parameter was individually added to the risk factor-adjusted multivariate model. The apparent risk associated with hypertension was substantially attenuated by the addition of either high-density lipoprotein cholesterol (OR 1.25, 95% CI 0.82 to 1.90) or triglycerides (OR 1.37, 95% CI 0.91 to 2.05). No significant interactions were found between hypertension and any lipoprotein parameter. These data indicate that the risk of MI associated with treated hypertension may have a lipid mechanism involving high-density lipoprotein cholesterol and/or triglycerides.
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PMID:Relation between systemic hypertension and blood lipids on the risk of myocardial infarction. 1051 71

The management of dyslipidemia after myocardial infarction (MI) is an important aspect of post-myocardial infarction care. However, acute changes in the lipid profile immediately following myocardial infarction have resulted in uncertainty regarding the clinical utility of lipid levels assessed during hospitalization for MI. We studied the effect of the timing of plasma lipid assessment among 294 patients who presented with MI to determine whether the differences between the serum lipid values in-hospital when compared with post-discharge values (generally 2-3 months after MI) would have a substantial impact on the decision to initiate lipid-lowering therapy. We found that the mean total and LDL cholesterol levels were significantly lower in-hospital when compared with generally 2-3 months later. However, patients whose lipids were measured within 48 h of presentation did not have significantly different values compared with generally 2-3 months post-discharge. Moreover, despite slightly lower in-hospital levels, 83.7% of patients were above the National Cholesterol Education Program target LDL for secondary prevention and 57.6% met the criteria for drug therapy based on in-hospital assessment. Total and LDL cholesterol levels fall modestly after an acute MI; however, from a clinical perspective, in-hospital levels can be used to guide decisions regarding lipid-lowering therapy which can begin in the immediate post-MI setting. In-hospital levels approximate post-MI levels, particularly if drawn within 48 h of presentation. All patients with acute myocardial infarction should have complete lipid profiles measured prior to discharge.
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PMID:Clinical utility of lipid and lipoprotein levels during hospitalization for acute myocardial infarction. 1061 26

Metabolic insulin resistance syndrome is a critical factor in the pathogenesis of atherosclerosis and coronary heart disease in Indians. In a preliminary case-control study, 44 young patients (age < 40 years) with coronary heart disease (angina, myocardial infarction), not previously diagnosed to have diabetes mellitus, were recruited seven days to six weeks after the cardiac event (group I), and compared to 20 healthy subjects (group II). After recording history and anthropometric data, they were subjected to oral glucose tolerance test. Each group was divided into A and B subgroups according to the magnitude of impaired glucose tolerance. Hypertension was recorded in 11 (25%) patients in group I, while all the subjects in group II were normotensive (p < 0.05). Groups IB and IIB, consisting of subjects with impaired glucose tolerance displayed significantly high post-load blood glucose values. After excluding patients with the family history of diabetes mellitus, there were 13 (39%) and 3 (17%) patients with impaired glucose tolerance in groups I and II, respectively. Total cholesterol and low-density lipoprotein cholesterol levels were higher in group I as compared to group II (p < 0.01). Group IB showed highest mean values of total cholesterol, triglycerides, low-density lipoprotein cholesterol and lowest level of high-density lipoprotein cholesterol as compared to other subgroups. Serum insulin levels at 30 and 90 minutes were significantly higher in group I (p < 0.05). Group IB and IIB showed higher insulin values at 90 minutes when compared to group IA (p < 0.05) and IIA (p < 0.05). Elevated serum insulin values at 90 minutes during oral glucose tolerance test could differentiate among both groups and subgroups, except IB versus IIB. The study demonstrates significantly high prevalence of hypertension, obesity, impaired glucose tolerance, hyperinsulinemia and dyslipidemia, suggesting fully developed metabolic insulin resistance syndrome in young north Indian patients with manifest coronary heart disease.
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PMID:Clustering of impaired glucose tolerance, hyperinsulinemia and dyslipidemia in young north Indian patients with coronary heart disease: a preliminary case-control study. 1062 65


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