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

Apolipoprotein E2, which has an R158 for C substitution, has reduced affinity for the LDL receptor and is associated with type III hyperlipoproteinemia in humans. Consistent with these observations, we have found that following adenovirus-mediated gene transfer, full-length apoE2 aggravates the hypercholesterolemia and induces hypertriglyceridemia in E-deficient mice and induces combined hyperlipidemia in C57BL/6 mice. Unexpectedly, the truncated apoE2-202 form that has an R158 for C substitution when expressed at levels similar to those of the full-length apoE2 normalized the cholesterol levels of E-deficient mice without induction of hypertriglyceridemia. The apoE2 truncation increased the affinity of POPC-apoE particles for the LDL receptor, and the full-length apoE2 had a dominant effect in VLDL triglyceride secretion. Hyperlipidemia in normal C57BL/6 mice was prevented by coinfection with equal doses of each, the apoE2 and the apoE2-202-expressing adenoviruses, indicating that truncated apoE forms have a dominant effect in remnant clearance. Hypertriglyceridemia was completely corrected by coinfection of mice with an adenovirus-expressing wild-type lipoprotein lipase, whereas an inactive lipoprotein lipase had a smaller effect. The findings suggest that the apoE2-induced dyslipidemia is not merely the result of substitution of R158 for C but results from increased secretion of a triglyceride-enriched VLDL that cannot undergo lipolysis, inhibition of LpL activity, and impaired clearance of chylomicron remnants. Infection of E(-)(/)(-)xLDLr(-)(/)(-) double-deficient mice with apoE2-202 did not affect the plasma cholesterol levels, and also did not induce hypertriglyceridemia. In contrast, apoE2 exacerbated the hypercholesterolemia and induced hypertriglyceridemia, suggesting that the LDL receptor is the predominant receptor in remnant clearance.
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PMID:Molecular mechanisms of type III hyperlipoproteinemia: The contribution of the carboxy-terminal domain of ApoE can account for the dyslipidemia that is associated with the E2/E2 phenotype. 1292 33

The availability of highly active antiretroviral therapy (HAART) has resulted in dramatic declines in morbidity and mortality in patients infected with human immunodeficiency virus-1 (HIV-1). However, the success of HAART has been tempered by the recognition of adverse metabolic effects clearly associated with its use. These "metabolic complications" include dyslipidemia, changes in body fat distribution, insulin resistance and glucose intolerance, metabolic bone disease, and lactic acidosis. Guidelines to assist clinicians in the management of these complications have been put forth by various organizations, including the International AIDS Society, the HIV Medicine Association of the Infectious Disease Society of America, and the Adult AIDS Clinical Trials Group.
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PMID:Metabolic complications associated with the use of highly active antiretroviral therapy in HIV-1-infected adults. 1525 41

To determine the prevalence and clinical characteristics of lipodystrophy in HIV-infected Thai patients, a cross-sectional study was performed on 278 HIV-infected patients at Bamrasnaradura Infectious Disease Institute. Laboratory data related to lipid and glucose metabolism were obtained from both patients who self reported fat maldistribution or diagnosed by a physician. The history of antiretroviral treatment and HIV infection were recorded. Prevalence of lipodystrophy found in the present study was 17%. Lipodystrophy was reported mostly on the face, buttock, legs, arms, and abdomen respectively. Two-thirds of these patients had mixed syndromes of fat accumulation and fat wasting and the others had only fat wasting. Ninety-three percent of lipodystrophic patients had at least 1 abnormality in either lipid or glucose metabolism. Eighty-eight percent had dyslipidemia, 21% had impaired glucose tolerance, 30% had insulin resistance and 27% had diabetes mellitus. Lipodystrophic patients have a high rate of lipid and glucose metabolism abnormalities which are the major risk factors for cardiovascular events.
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PMID:Prevalence of lipodystrophy in Thai-HIV infected patients. 1527 36

Cardiovascular disease and its clinical sequelae remain the leading causes of morbidity and mortality in many regions of the world. Dyslipidemia is a critical risk factor to intercept in both the primary and secondary prevention of acute cardiovascular events. The prospective, placebo-controlled clinical trials conducted with statins over the course of the past 15 years have conclusively demonstrated that these drugs significantly reduce risk for fatal and nonfatal myocardial infarction, ischemic stroke, unstable angina, and frequency of myocardial ischemia, as well as cardiovascular and all-cause mortality. Of considerable interest is the fact that, even under the exquisitely controlled circumstances of a clinical trial, endpoint reductions in these trials typically occur in the range of 20% to 35%. Understandably, much attention is now being focused on deriving the pharmacologic means by which to further increase the magnitude of endpoint reduction. Epidemiologic investigation has demonstrated that the relationship between cholesterol and risk for atherosclerotic disease is a continuous one. Consequently, it is reasonable to assume that more aggressive reductions of low-density lipoprotein (LDL) cholesterol might result in even greater reductions of cardiovascular event rates and atheromatous plaque progression than heretofore observed. Two recent clinical trials, Reversal of Atherosclerosis with Aggressive Lipid Lowering (REVERSAL) and Pravastatin or Atorvastatin Evaluation and Infection Therapy (PROVE IT), prospectively tested and confirmed the validity of more aggressive LDL cholesterol lowering in high-risk patients with established coronary artery disease.
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PMID:Low-density lipoprotein reduction in high-risk patients: how low do you go? 1529

The metabolic effects of obesity have made this highly prevalent disease one of the most common risk factors for diabetes, hypertension, and atherosclerosis, the leading causes of end-stage renal failure. However, obesity per se, as defined by body mass index, is less predictive of the development of these diseases than is the presence of a constellation of obesity-related abnormalities now known as the metabolic syndrome. Recognition of this syndrome, which can readily be identified in clinical settings using defined threshold values for waist circumference, BP, fasting glucose, and dyslipidemia, allows for earlier intervention in these high-risk patients. Systemic insulin resistance has been implicated as one possible factor that links visceral obesity to adverse metabolic consequences; however, the mechanism whereby adipose tissue causes alterations in insulin sensitivity remains unclear. Infection and inflammation are commonly associated with insulin resistance, and visceral obesity is associated with a chronic, low-grade inflammatory state, suggesting that inflammation may be a potential mechanism whereby obesity leads to insulin resistance. Moreover, adipose tissue is now recognized as an immune organ that secretes numerous immunomodulatory factors and seems to be a significant source of inflammatory signals known to cause insulin resistance. Therefore, inflammation within white adipose tissue may be a crucial step contributing to the emergence of many of the pathologic features that characterize the metabolic syndrome and result in diabetes and atherosclerosis. This review describes the role of proinflammatory cytokines and hormones released by adipose tissue in generating the chronic inflammatory profile associated with visceral obesity.
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PMID:The inflammatory syndrome: the role of adipose tissue cytokines in metabolic disorders linked to obesity. 1550 32

Highly active antiretroviral therapy (HAART) improves the survival of patients with HIV infection; however, several observational studies have described associations between HIV infection, HAART, and cardiovascular disease. Important limitations of these studies included a low incidence of cardiovascular events, short duration of HAART exposure, and retrospective design. Nevertheless, the weight of evidence from observational and surrogate end point studies suggests that the dyslipidemia and other metabolic changes that are common in patients with HIV infection and those using HAART may be associated with increased cardiovascular risk. The Infectious Disease Society of America/Adults AIDS Clinical Trials Group guidelines for the evaluation and management of dyslipidemia recommend target lipid levels and treatment of dyslipidemia in patients with HIV infection. Although practitioners should consider dyslipidemia and cardiovascular risk when making plans for initiating or altering HAART therapy, maintaining viremic control should be the overriding factor, because short-term absolute rates of cardiovascular disease are significantly lower than death rates from AIDS in inadequately suppressed patients. This article reviews the cardiovascular risks in patients receiving HAART and discusses the implementation of the new guidelines.
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PMID:Managing cardiovascular risk in patients with HIV infection. 1567 95

Individuals with psychiatric disorders tend to have excessive morbidity. They typically have high rates of respiratory illnesses, infectious diseases, substance abuse (including smoking), obesity, diabetes mellitus, and cardiovascular disease (CVD). Persons with schizophrenia and affective disorders also have a high prevalence of risk factors for CVD, such as diabetes and obesity, which are on the order of 1.5 to 2.0 times higher than in the general population; this translates into increased mortality rates due to CVD. The use of certain psychotropics results in metabolic sequelae, such as obesity, dyslipidemia, glucose dysregulation, and the metabolic syndrome. These sequelae exacerbate the already elevated risk of CVD and diabetes in this group of people. Therefore, the use of psychotropic agents that result in, for example, excessive weight gain not only add another complication for physicians managing a patient with schizophrenia but also may have serious prognostic and cost implications with respect to treatment-related diabetes and coronary disease incidence. The recent American Diabetes Association (ADA) Consensus Panel concluded that some agents are associated with greater diabetes risk than others. The current review describes the prevalence of the metabolic syndrome in people with affective disorders and schizophrenic populations, its prognostic relevance, and its exacerbation among patients treated with particular psychotropic agents, including certain atypical antipsychotics, selective serotonin reuptake inhibitors, and mood stabilizers. The costs associated with the treatment of the metabolic syndrome, diabetes, and coronary heart disease in populations with schizophrenia are also described.
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PMID:Metabolic issues and cardiovascular disease in patients with psychiatric disorders. 1590 91

Secondary dyslipidemias may develop as a result of other diseases or some major exogenous influences. The most common are secondary dyslipidemias due to the following diseases: poorly controlled diabetes mellitus, hypothyreosis, hyperfunction of suprarenal glands, cholestasis, chronic renal diseases (chronic renal failure, nephrotic syndrome), acute infectious diseases. A very common cause of secondary dyslipidemia is abuse of alcohol. Also some drugs may induce dyslipidemias: corticosteroids, immunosuppressive drugs, less frequently also thiazide diuretics and non-selective beta-blockers. Secondary dyslipidemia is physiologic during pregnancy. If causal treatment of secondary dyslipidemia is possible, hypolipidemic drugs are not indicated. The decision to initiate treatment with hypolipidemic drugs depends on the degree of risk of a fatal cardiovascular event rather than on the blood lipids level. When hypolipidemic treatment is indicated, the choice of the drug and its dose also depends on the type of the primary disease and its severity.
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PMID:[Secondary dyslipidemias and their treatment]. 1757 73

This study aims at determining serum nitrite/nitrate (NO(x)) levels in healthy subjects within the framework of a population-based study. NO(x) concentration was measured in 3505 subjects aged > or =20 years. Subjects with diabetes, renal dysfunction, those undergoing treatment for dyslipidemia and hypertension, were excluded; also excluded were smokers, pregnant women, and subjects with cardiovascular and infectious diseases or cancer; leaving 1983 (667 men, 1316 women) asymptomatic non-smoking subjects for the analysis. NO(x) concentrations were determined in serum and compared in different age groups. Mean+/-SE of NO(x) concentration was 24.8+/-0.02 and 24.4+/-0.01 micromol/l in men and women respectively. Men aged 20-29 years had significantly higher NO(x) levels compared to corresponding women (25.1+/-0.03 vs. 22.7+/-0.02). Serum NO(x) concentration peaked at 50-59 years in both genders. Comparison between lower and upper quartiles of NO(x) levels was performed in both genders. Women with high serum NO(x) were older and had significantly higher body mass index and fasting plasma glucose. The results of this study determine the normal levels of serum NO(x) concentrations in asymptomatic non-smoker subjects; also show that serum NO(x) concentrations indicate sex and age differences in these subjects.
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PMID:Serum nitric oxide metabolite levels in a general healthy population: relation to sex and age. 1866 5


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