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Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

As the prevalence of the metabolic syndrome increases, 2 comorbid conditions--hepatic steatosis and human immunodeficiency virus (HIV) lipodystrophy--have become difficult clinical challenges. Dyslipidemia in patients with nonalcoholic fatty liver disease or nonalcoholic steatohepatitis may improve with use of statins, fibrates, niacin, and thiazolidinediones, but the data are presently very limited. HIV lipodystrophy is associated with a marked risk of coronary artery disease (CAD), and more aggressive management of the dyslipidemia is likely necessary to improve the prognosis.
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PMID:Management of dyslipidemia in patients with complicated metabolic syndrome. 1609 39

Studies published before the introduction of highly active antiretroviral therapy (HAART) have tracked the incidence and course of human immunodeficiency virus (HIV) infection in relation to cardiac disease.The introduction of HAART regimens, by preventing opportunistic infections and reducing the incidence of myocarditis, has reduced the prevalence of HIV-associated cardiomyopathy of about 30% and the prevalence of cardiac involvement of AIDS-associated malignancies of about 50%. However, HAART regimens, especially those including protease inhibitors have been shown to cause, in a high proportion of HIV-infected patients, a metabolic syndrome (lipodystrophy/lipoatrophy, dyslipidemia, type 2 diabetes mellitus, insulin resistance) that may be associated with an increased risk of cardiovascular disease (approximately 1.4 cardiac events per 1000 years of therapy according to the Framingham score). A careful stratification of the cardiovascular risk and cardiovascular monitoring of patients under HAART according to the most recent clinical guidelines is needed.
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PMID:Reviewing the cardiovascular complications of HIV infection after the introduction of highly active antiretroviral therapy. 1610 66

There is a paucity of information on the safety and efficacy of lipid-lowering therapy for dyslipidemia associated with human immunodeficiency virus (HIV) and antiretroviral therapy. Our objective was to determine whether fenofibrate and pravastatin were equivalent for the treatment of combined dyslipidemia in HIV as measured by a composite of the National Cholesterol Education Project (NCEP) goals based on absolute values for low-density lipoprotein (LDL), triglycerides (TG), and high-density lipoprotein (HDL) and to compare the safety of these agents through 48 weeks. This was a randomized, open-label trial with subjects assigned to fenofibrate 200 mg (n = 88) or pravastatin 40 mg (n = 86) daily. Subjects who failed to reach the NCEP composite goal on monotherapy by week 12 received both drugs. The composite goal at week 12 was achieved in 1% of fenofibrate and 5% of pravastatin subjects. At week 16, 69/88 subjects on fenofibrate added pravastatin (FP) and 67/86 subjects on pravastatin added fenofibrate (PF). At week 48, 7% FP subjects and 3% PF subjects achieved the composite goal. Median changes in LDL/HDL/TG/non-HDL were -8/+5/-144/+50 and -14/+2/-66/+34 mg/dl in subjects receiving FP and PF, respectively. There were few adverse events and no rhabdomyolysis reported. Combination therapy with fenofibrate and pravastatin for HIV-related dyslipidemia provides substantial improvements in lipid parameters and appears safe, but is unlikely to achieve all NCEP targets for lipid levels.
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PMID:A randomized trial of the efficacy and safety of fenofibrate versus pravastatin in HIV-infected subjects with lipid abnormalities: AIDS Clinical Trials Group Study 5087. 1621 99

Highly active antiretroviral therapy (HAART) has greatly extended the lives of people infected with the human immunodeficiency virus (HIV). This reduced risk of early death from opportunistic infections or other sequelae of HIV infection, however, means that other possible causes of death emerge. Myocardial infarction has become a matter of particular concern. Two of the main sources of cardiovascular disease in this population are believed to be vascular inflammation and dyslipidemia. We review the evidence for this hypothesis and discuss the relationship of HIV to vascular inflammation. Current treatment guidelines do not recommend the immediate initiation of HAART unless warranted, potentially allowing long-term, unchecked viral impact on the development of atherosclerosis. Finally, we consider the protease inhibitors traditionally included in HAART regimens and their relationship to the development of dyslipidemia, as well as other classes of antiretrovirals, such as the non-nucleoside reverse transcriptase inhibitors, which might be a better choice for patients with cardiovascular risks. Other strategies, such as pharmacologic, nutritional, and physical activity interventions are discussed. The patients who might benefit most are those in whom the precursors of vascular plaques, such as fatty streak, smooth muscle cell, macrophage, and T-lymphocyte aggregation not yet identified by echocardiographic and biopsy findings have already developed as a result of unchecked viral inflammation and replication.
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PMID:Impact of HIV and highly active antiretroviral therapy on leukocyte adhesion molecules, arterial inflammation, dyslipidemia, and atherosclerosis. 1629 90

Cardiovascular disease is increasingly recognised as a consequence of human immunodeficiency virus (HIV) infection in the era of highly active antiretroviral therapy (HAART). Dyslipidaemia is also a feature of HIV infection itself and the antiretroviral drugs from the protease inhibitor classes. Increased rates of atherosclerotic disease and diabetes have been associated with lipodystrophy and now from one of the major causes of morbidity in HIV and acquired immunodeficiency syndrome (AIDS).This review, based on a multi-database keyword search, summarises the lipid changes observed in the course of HIV infection and its treatment, and puts them into the context of other risk factors for cardiac disease, and other causes of cardiovascular disease in HIV.
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PMID:Dyslipidaemia and cardiovascular risk in HIV infection. 1630 91

Thanks to antiretroviral therapy, people with human immunodeficiency virus (HIV) infection are living longer, but as they do, non-HIV medical problems become more relevant. In particular, dyslipidemia, an important reversible risk factor for cardiovascular disease, has been linked to HIV infection and its treatment. Although controversy remains as to whether people with HIV infections will develop premature coronary heart disease, it seems prudent to manage dyslipidemia in these patients just as we do in our HIV-negative patients. Interactions between lipid-lowering drugs and antiretroviral drugs require special attention.
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PMID:Dyslipidemia in HIV patients. 1639 25

The Study of Fat Redistribution and Metabolic Change in HIV Infection (FRAM), initiated in 2000, investigates the prevalence and correlates of changes in fat distribution, insulin resistance, and dyslipidemia among human immunodeficiency virus (HIV)-infected men and women compared with a population-based group of control men and women. Between June 2000 and September 2002, 1,480 participants (1,183 HIV-infected persons and 297 controls) were enrolled in FRAM. Measurements taken included whole-body magnetic resonance imaging for quantification of regional fat, anthropometric measurements, central laboratory analysis of metabolites, and assessment of symptoms, sociodemographic factors, and lifestyle. Similar measurements were repeated among FRAM participants 4 years later (FRAM 2) for investigation of the progression of fat distribution changes, insulin resistance, and hyperlipidemia. In FRAM 2, which is ongoing, investigators are also determining the associations of subclinical cardiovascular disease, as measured by carotid intimal-medial wall thickness, with HIV infection, fat distribution changes, insulin resistance, and other proatherogenic changes in serum lipid levels. The demographic characteristics of HIV-infected FRAM men and women were comparable to those reported from a national random sampling of HIV-infected men and women receiving medical care in the United States. The representativeness of the FRAM sample increases its value as a resource for studies on fat distribution, metabolic changes, and atherosclerosis in HIV infection.
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PMID:The study of fat redistribution and metabolic change in HIV infection (FRAM): methods, design, and sample characteristics. 1652 55

The introduction of highly active antiretroviral therapy (HAART) has reduced morbidity and mortality in patients infected with the human immunodeficiency virus (HIV). However, prolonged treatment with combination regimens can be difficult to sustain because of problems with adherence and toxic effects. Treatment with antiretroviral agents--protease inhibitors in particular--has uncovered a syndrome of abnormal fat redistribution, impaired glucose metabolism, insulin resistance and dyslipidemia, collectively termed lipodystrophy syndrome (SLHIV). Nowadays, no clinical guidelines are available for the prevention or treatment of SLHIV, and its cause have yet to be totally elucidated. This review emphasizes the clinical features and the data from previous studies about the SLHIV taking into account that a better understanding of this syndrome for HIV specialists, cardiologists and endocrinologists is fundamental for the disease control.
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PMID:[Metabolic alterations in HIV-associated lipodystrophy syndrome]. 1654 8

To differentiate between the effects that antiretroviral drugs have on the endothelium and the secondary effects that they have on immune function, viral load, and dyslipidemia, 6 non-human immunodeficiency virus-infected human subjects were treated with lopinavir-ritonavir for 1 month and, on the basis of forearm blood flow, the treatment's effects on endothelial cell function were measured. Surprisingly, after exposure to lopinavir-ritonavir, absolute forearm blood-flow responses to the endothelium-dependent vasodilator, acetylcholine, increased significantly (P=.03), and forearm blood flow decreased to a greater extent during specific inhibition of NO synthase by N(G)-monomethyl-L-arginine. Thus, in this small cohort of subjects, short-term treatment with lopinavir-ritonavir does not appear to directly promote endothelial cell dysfunction.
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PMID:Lopinavir-ritonavir: effects on endothelial cell function in healthy subjects. 1665 79

The introduction of highly active antiretroviral therapy (HAART) has significantly modified the course of human immunodeficiency virus (HIV) disease, with longer survival and improved quality of life of HIV-infected subjects. However, HAART regimens, especially those including protease inhibitors, have been shown to cause in a high proportion of HIV-infected patients a metabolic syndrome (lipodystrophy/lipoatrophy, dyslipidemia, type 2 diabetes mellitus, insulin resistance) that may be associated with an increased risk of cardiovascular disease (coronary artery disease and stroke). A careful stratification of the cardiovascular risk and cardiovascular monitoring of patients under HAART is needed according to the most recent clinical guidelines.
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PMID:Highly active antiretroviral therapy-associated metabolic syndrome and cardiovascular risk. 1667


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