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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The HIV associated lipodystrophy syndrome is characterized by fat loss from the periphery, fat accumulation in the abdominal, dorsocervical regions and breasts, and hyperlipidaemia, insulin resistance and lactic acidaemia. Although several mechanisms have been proposed to explain these abnormalities, the exact aetiology of the condition remains unclear and will likely prove to be complex. The principal clinical concerns that arise from this disorder are possible increased risks of premature atherosclerosis and cardiovascular disease. A variety of therapeutic interventions, designed to limit these risks, are under evaluation.
HIV Med 2001 Jul
PMID:HIV-associated lipodystrophy. 1173 97

Since the introduction of highly active antiretroviral therapy (HAART), AIDS has become a treatable disease. A steep decline in morbidity and mortality has been observed in most western countries. The HIV epidemic is now moving into middle-aged populations which are already at increased risk for cardiovascular disease. Since the cardiovascular system is frequently affected in HIV infection, reflections on traditional cardiovascular risk factors is a pressing issue. Moreover, during the last few years, complex lipodystrophic body changes in association with metabolic abnormalities such as dyslipidemia and insulin resistance have become a common feature in HIV+ patients on HAART. Although the precise mechanisms are not fully understood, early reports on myocardial infarctions and vascular changes have raised concern about the possibility of an epidemic of cardiovascular events among HAART patients within the next decade. Not only more data on lipid-lowering drugs in the context of HAART, on switching strategies, and treatment interruptions, but also from intervention studies on traditional risk factors such as smoking, are urgently needed. In this review the key issues concerning cardiovascular aspects of HIV infection in the era of HAART and possible preventive strategies are discussed.
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PMID:Cardiology and AIDS--HAART and the consequences. 1176 82

HIV infection is accompanied by disturbances in lipid and glucose metabolism, which are further compounded by changes induced by antiretroviral drugs. There is increasing concern that these changes will lead to an epidemic of cardiovascular disease. Cardiovascular disease will no doubt increase, but current data indicate that the average absolute levels are likely to remain low, although patients with additional risks (smoking, hypertension, diabetes, age, family history, etc.) are certainly more susceptible. The complications of therapy need to be taken into account when deciding on the time of treatment, and reducing risk factors should become a routine aspect of the care of an HIV population that now lives longer as a result of highly active antiretroviral therapy.
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PMID:Cardiovascular disease risk factors in HIV-infected patients in the HAART era. 1176 87

Cardiovascular complications are important contributors to morbidity and mortality in HIV-infected patients. These complications can usually be detected at subclinical levels with monitoring, which can help guide targeted interventions. This article reviews available data on types and frequency of cardiovascular manifestations in HIV+ patients and proposes monitoring strategies aimed at early subclinical detection. In particular, we recommend routine echocardiography for HIV+ patients, even those with no evidence of cardiovascular disease. We also review preventive and therapeutic cardiovascular interventions. For procedures that have not been studied in HIV+ patients, we extrapolate from evidence-based guidelines for the general population.
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PMID:Cardiovascular monitoring and therapy for HIV-infected patients. 1176 91

We recently reported that treatment with a pharmacologic dose of recombinant human growth hormone (GH) resulted in a significant loss of body fat and gain in lean tissue in HIV-infected patients with syndromes of fat accumulation. However, insulin-mediated glucose disposal decreased transiently after one month of GH therapy. The present paper focuses on the changes of hepatic carbohydrate and fat metabolism associated with GH treatment in the same subjects. We assessed hepatic insulin sensitivity under both fasting and hyperinsulinemic-euglycemic clamp conditions prior to and after one and six months of GH treatment (3 mg/day) in five patients using stable isotope tracer techniques. Indirect calorimetry, and measurements of lipid concentrations. Fasting endogenous glucose production (EGP) increased significantly at one month (12.0 +/- 0.7 to 14.9 +/- 0.9 micromol/kg/min, P < 0.03), and the increase was sustained at six months of GH treatment (14.0 +/- 1.1 micromol/kg/min, NS). This increase in EGP was driven in part by increased glucogenesis (GNG) (3.5 +/- 0.9 to 5.2 +/- 0.9 and 5.8 +/-1.2 micromol/kg/min, n = 4, P < 0.01 and P < 0.01 at one and six months, respectively); small changes in hepatic glycogenolysis also contributed. Sustained increases in lipolysis and progressive decreases in hepatic fractional de novo lipogenesis (DNL) and triglyceride concentrations occurred with GH treatment. These changes were accompanied by an improved lipid profile with a significant increase in HDL cholesterol and significant decreases in total and LDL cholesterol and triglyceride levels, the latter consistent with the decrease in hepatic DNL. During a hyperinsulinemic-euglycemic glucose clamp, EGP and GNG were markedly suppressed compared to the corresponding time points under fasting conditions, albeit less so when measured after one month of GH treatment. Thus, in HIV-infected patients with abnormal fat distribution, pharmacologic doses of GH improved the overall lipid profile, but worsened glucose homeostasis under both fasting and hyperinsulinemic conditions. The combined implications of these positive and negative metabolic effects for cardiovascular disease risk remain unknown.
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PMID:Effects of recombinant human growth hormone on hepatic lipid and carbohydrate metabolism in HIV-infected patients with fat accumulation. 1183 45

Although disparities in outcomes among African Americans compared with whites with respect to cardiovascular disease, cancer, diabetes, infant mortality, and other health standards have been well-described, these disparities are most dramatic with respect to kidney diseases. End-stage renal disease (ESRD) occurs almost 4 times more commonly in African Americans than in their white counterparts. These disparate rates of kidney disease may be caused by the complex interplay of genetic, environmental, cultural, and socioeconomic factors. African Americans are particularly vulnerable to the deleterious renal effects of hypertension and may require more aggressive blood pressure control than whites to accrue benefit with respect to preservation of renal function. Diabetes, the leading cause of ESRD in the United States, is another important factor in the excess renal morbidity and mortality of African Americans because of its prevalence in this population. Other renal diseases, especially those associated with HIV/AIDS, are also much more likely to affect African Americans than other American population subgroups. A more thorough understanding of the epidemiology of renal diseases in African Americans and the cultural, social, and biological differences that underlie racial disparities in prevalence of renal disease will be essential to the design of effective public health strategies for prevention and treatment of this burdensome problem.
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PMID:The epidemiology of end-stage renal disease among African Americans. 1186 81

Much published research documents continuing racial and ethnic disparities in health, particularly for African Americans, which apply to both oral and systemic diseases. Current research suggests biologically plausible associations between oral and systemic diseases; however, clear cause-and-effect relationships have not been substantiated. Some researchers and health care providers have noted anecdotal associations between oral and systemic health, as well as compounding adverse effects of oral and systemic diseases and dysfunctions. Historically, African American physicians, dentists, and pharmacists have bonded together under one organizational umbrella to combat discrimination, prejudice, and racism directed at them and their patient populations. This coming together has resulted in a more comprehensive clinical, behavioral, economic, and public health decision-making process related to the general health and well-being of their patient populations, such as maximizing health care visits, treatment plans, reimbursements, and oral and systemic health care follow-ups. According to the 1985 Secretary's Task Force Report, the six causes of excess deaths among African Americans were: cardiovascular disease and stroke; cancer; diabetes; cirrhosis; homicide and accidents; and infant mortality. In 1991, HIV/AIDS became the seventh cause of excess deaths. This article summarizes salient information about cardiovascular diseases, diabetes, cancer, and the social and behavioral factors related to oral and systemic health.
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PMID:Enhancing oral and systemic health. 1191 51

Decreased insulin sensitivity, hyperlipidemia, and body fat changes are considered as risk factors for coronary heart disease (CHD). A clustering of such factors (metabolic syndrome [MSDR]) exponentially increases the risk. Impaired fibrinolysis and increased coagulation are additional independent risk factors for CHD. We studied the effects of protease inhibitor (PI)-containing highly active antiretroviral therapy (HAART) on metabolic and hemostatic parameters in 363 HIV-infected individuals, of whom 266 were receiving PI-containing HAART and 97 were treatment naive. The fasting plasma levels of insulin, glucose, triglycerides, cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, plasminogen activator inhibitor type 1 (PAI-1), and fibrinogen were evaluated together with the areas of visceral adipose tissue and the visceral adipose tissue/subcutaneous adipose tissue area ratio. The levels of insulin, triglycerides, cholesterol, and low-density lipoprotein cholesterol; visceral adipose tissue area; low-density lipoprotein/high-density lipoprotein ratio; and visceral adipose tissue/subcutaneous adipose tissue area ratio were significantly increased in patients receiving PI-containing HAART compared with treatment-naive patients. The levels of PAI-1 and fibrinogen were significantly higher in patients receiving PI-containing HAART. PAI-1 levels were higher in individuals with MSDR but also in patients without MSDR who were receiving PI-containing HAART. PAI-1 was independently correlated to use of PI-containing HAART, triglyceride level, insulin level, and body mass index (p <.001). These findings suggest that patients receiving PI-containing HAART have decreased fibrinolysis and increased coagulability, which may thus represent additional risk factors for cardiovascular disease in this patient group.
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PMID:Hypofibrinolytic state in HIV-1-infected patients treated with protease inhibitor-containing highly active antiretroviral therapy. 1198 59

Chronic infection with HIV type 1 is associated with alterations in macronutrient metabolism, specifically elevated plasma lipids, glucose and reduced insulin sensitivity. These alterations are most severe in patients at the later stages of AIDS, indicating a relationship with disease progression. Recently, a metabolic syndrome, termed lipodystrophy, has been described in successfully-treated HIV patients in whom the altered macronutrient metabolism of HIV infection appears to be amplified markedly, with concurrent alterations in adipose tissue patterning. This syndrome presents a paradox, as before the development of highly-active antiretroviral therapy (HAART) the most severe perturbations in metabolism were observed in the sickest patients. Now, the patients that respond well to therapy are showing metabolic perturbations much greater than those seen before. The implications of this syndrome are that, whilst life expectancy may be increased by reducing viral load, there are concomitant increases in the risk of cardiovascular disease, diabetes and pancreatitis within this patient population. The aetiology of the syndrome remains unclear. In a collaborative trial with the Chelsea and Westminster Hospital in London we have used stable-isotope-labelled fatty acids to examine the hypothesis that treatment with HAART causes a delayed clearance of dietary lipid from the circulation, resulting in the retention of lipid within plasma and the downstream changes in insulin and glucose homeostasis. This hypothesis would indicate a role for low-fat diets, exercise and drugs that reduce plasma lipid or insulin resistance, in modulating the response to antiretroviral therapy in HIV infection.
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PMID:The paradox of improved antiretroviral therapy in HIV: potential for nutritional modulation? 1200 87

Changes in lipid and carbohydrate metabolism and in body composition associated with the most potent and effective therapies available are being reported with increasing frequency. These changes could potentially lead to increased risks of cardiovascular disease. Clinical trials set up to investigate new antiretroviral therapies need to explore the therapies' impact on these potentially serious adverse outcomes, at least in a subset of patients. The measurements that are feasible to include for all patients clearly differ from those required by a metabolic substudy. We propose the following: firstly, a minimal set of parameters that should be included in all trials; secondly, a desirable set of parameters that should be included whenever possible; and thirdly, a list of exploratory measures that should be considered. These exploratory measures are classified by the different mechanisms for changes in body composition or weight: endocrinal, cardiovascular, sterol and chemokine/cytokine pathways. Standardized instruments for evaluating patients' reports of body changes and potential methods for assessing the risk of cardiovascular disease are described. Minimum and desirable standards for methods of measurement are also proposed. The choice of parameters is based on expert clinical opinion. The experts consulted include investigators from four large ongoing clinical trials with substudies specifically designed to investigate lipid and carbohydrate metabolism and changes in body composition, together with standard parameters for measurement within individual mechanistic pathways. The parameters proposed should be kept under review as the body of knowledge about metabolic function and fat redistribution in HIV infection increases.
HIV Med 2002 Jan
PMID:The evaluation of metabolic function and fat redistribution in clinical trials. 1205 54


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