Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Widespread utilization of highly active antiretroviral therapy (HAART) for HIV-infection, primarily protease inhibitors in combination with nucleoside analogue reverse transcriptase inhibitors, has recently led to a sustained reduction in the morbidity and mortality of this disease. However, administration of HAART is frequently associated with the development of lipid disorders. The severity and prevalence of dyslipidaemia vary, depending on the type of HAART, nutritional status, HIV disease stage, and concomitant presence of lipodystrophy and insulin resistance (two additional adverse effects of HAART). The mechanism that is responsible for HAART-associated dyslipidaemia remains incompletely understood. Recent data indicate that this effect may be, at least in part, accounted for by protease inhibitor-mediated inhibition of the proteasome activity and accumulation of the active portion of sterol regulatory element-binding protein-1c in liver cells and adipocytes. Whether lipid disorders in HIV-infected patients receiving HAART translate into an increased cardiovascular risk, and the indications for lipid-lowering interventions in this population, remain to be established.
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PMID:Antiretroviral therapy-associated hyperlipidaemia in HIV disease. 1135 35

The authors report an 18-year-old girl with HIV infection who developed new-onset insulin-dependent diabetes mellitus (IDDM) in association with anemia. IDDM among patients with HIV infection has been infrequently reported and suggested to be caused by different etiologies. Susceptibility to autoimmune diseases, such as IDDM, has been associated functionally with two members of a newly described multigene family called PERB11. In this patient, the progression of hyperglycemia associated with a rapid increase in insulin requirement is suggestive of insulin resistance.
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PMID:New onset diabetes mellitus in an HIV-positive adolescent. 1136 30

The New York Supreme Court's Appellate Division reversed a January 1995 decision of the State Workers' Compensation Board which had awarded benefits to a nurse's aide who claimed she contracted HIV from a needlestick injury in March 1989. According to the panel, contracting HIV is not an occupational disease for nurse's aids under the State Workers' Compensation Law because the aides are not authorized to give injections. The claim was brought by [name removed], a nurse's aide at the Kingsbrook Jewish Medical Center in New York. [Name removed] accidentally stuck herself with a needle that a registered nurse had handed her after injecting insulin into a patient. She tested positive for HIV 4 months later. Hospital officials contend that none of the patients in the nursing home in March 1989 were HIV-positive to their knowledge, although the patient in question had never been tested for HIV infection. Bill Borwegen, health and safety director for the Service Employees International Union, wonders how an injury that occurs in the workplace cannot be called an occupational injury. [Name removed] died of AIDS-related causes 2 years ago.
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PMID:HIV not seen as 'occupational disease' for nurse's aides. 1136 36

The Immune Restoration Think Tank addressed research questions on issues relating to the immune environment, advances in tools to measure immune response, and therapies for treating advanced HIV. A study of the thymus, which is where cells grow, concluded that there was some thymus regeneration in people with CD4 cell counts between 300 - 500. Thymus transplants can be considered if no regeneration can be detected. Use of thymic compounds such as Thymic Humoral Factor, Interleukin-2 (IL-2) and Insulin-like Growth Factor (IGF-1) are thought to boost growth of thymic cells. To gain more information about the immune system, additional research will be developed on bone marrow in people with HIV. Also, in order to gauge the level of immune response and monitor cell development and migration, a new measuring device, called cell labeling, is being studied. A working group, in conjunction with the National Institutes of Health, was established to investigate cell labeling and other possible tools. Immune-based therapies are also under investigation to elevate immune responses for people in advanced stages of HIV.
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PMID:Report from the Seventh Immune Restoration Think Tank. 1136 48

Reports indicate some people on anti-HIV drugs experience changes in metabolism and body shape. Metabolic changes include increased levels of lipids and glucose in the blood, and insulin resistance. Body shape changes seem to be caused by fat moving from the extremities and face to areas such as the abdomen, shoulders, and neck. These changes are believed to be attributed to one or all of the following: the direct effects of anti-HIV drugs, the indirect effects of anti-HIV drugs, and/or the role of HIV and its effect on hormone production. PIs were thought to be responsible, but these changes have also been seen in patients who have not taken this class of drug.
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PMID:Are changes in body shape due to drug side effects? 1136 90

A study by doctors in Germany found that HIV-infected people who received PI therapy were more likely to have problems with their body's ability to use glucose. PI use was associated with reduced insulin sensitivity, and the development of diabetes in severe cases. In addition, PI treated subjects had increased levels of lipids in the blood, specifically triglycerides and cholesterol. These levels were not linked to the amount of time people used PIs.
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PMID:Protease therapy and changes to insulin and glucose. 1136 92

Research groups from different countries created a case definition for lipodystrophy at a lipodystrophy workshop held in San Diego, CA. According to the definition, symptoms of lipodystrophy may include prominent veins in the legs, breast enlargement, and accumulation of fat on the face and on the back of the neck. Results of several foreign studies on lipodystrophy are presented. The results of two studies suggest that using nucleoside analogue reverse transcriptase inhibitors (NARTIs) may increase the risk for developing lipodystrophy. The incidence of decreased insulin sensitivity and its correlation to anti-HIV drug use was also discussed at the workshop.
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PMID:Recent lipodystrophy findings. 1136 68

Protease inhibitors used in the treatment of HIV infection have been causally associated with lipodystrophy and insulin resistance and were shown to alter adipocyte differentiation in cultured cells. We aimed to delineate the mechanism by which indinavir impaired adipocyte function. We report that indinavir altered neither the growth nor insulin sensitivity of 3T3-F442A preadipocytes, nor did it alter the initial step of their differentiation, i.e., clonal proliferation. However, adipose conversion was inhibited by indinavir (by 50-60%), as shown by 1) the decrease in the number of newly formed adipocytes; 2) the lower level of the adipogenic protein markers, sterol regulatory element-binding protein-1 (SREBP-1), peroxisome proliferator-activated receptor-gamma (PPAR-gamma), and the insulin receptor (IR); and 3) the lack of SREBP-1 and PPAR-gamma immunoreactivity in the nucleus of most indinavir-treated cells. Partial adipose conversion also correlated with an accumulation of SREBP-1 at the nuclear periphery and an alteration in its electrophoretic mobility. Defective expression and nuclear localization of PPAR-gamma probably resulted from the decreased level of nuclear SREBP-1. Indinavir also rendered 3T3-F442A adipocytes resistant to insulin for mitogen-activated protein kinase activation at a step distal to IR substrate-1 tyrosine phosphorylation. Hence, indinavir impairs differentiation at an early step of adipose conversion probably involving the process controlling SREBP-1 intranuclear localization.
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PMID:The HIV protease inhibitor indinavir impairs sterol regulatory element-binding protein-1 intranuclear localization, inhibits preadipocyte differentiation, and induces insulin resistance. 1137 39

HIV protease inhibitors (HPIs) are potent antiretroviral agents clinically used in the management of HIV infection. Recently, HPI therapy has been linked to the development of a metabolic syndrome in which adipocyte insulin resistance appears to play a major role. In this study, we assessed the effect of nelfinavir on glucose uptake and lipolysis in differentiated 3T3-L1 adipocytes. An 18-h exposure to nelfinavir resulted in an impaired insulin-stimulated glucose uptake and activation of basal lipolysis. Impaired insulin stimulation of glucose up take occurred at nelfinavir concentrations >10 micromol/l (EC(50) = 20 micromol/l) and could be attributed to impaired GLUT4 translocation. Basal glycerol and free fatty acid (FFA) release were significantly enhanced with as low as 5 micromol/l nelfinavir, displaying fivefold stimulation of FFA release at 10 micromol/l. Yet, the antilipolytic action of insulin was preserved at this concentration. Potential underlying mechanisms for these metabolic effects included both impaired insulin stimulation of protein kinase B Ser 473 phosphorylation with preserved insulin receptor substrate tyrosine phosphorylation and decreased expression of the lipolysis regulator perilipin. Troglitazone pre- and cotreatment with nelfinavir partly protected the cells from the increase in basal lipolysis, but it had no effect on the impairment in insulin-stimulated glucose uptake induced by this HPI. This study demonstrates that nelfinavir induces insulin resistance and activates basal lipolysis in differentiated 3T3-L1 adipocytes, providing potential cellular mechanisms that may contribute to altered adipocyte metabolism in treated HIV patients.
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PMID:The HIV protease inhibitor nelfinavir induces insulin resistance and increases basal lipolysis in 3T3-L1 adipocytes. 1137 44

Highly active antiretroviral therapy in HIV-1 infected patients is associated with a lipodystrophy syndrome, characterized by wasting of peripheral fat, central adiposity, hyperlipidaemia and insulin resistance. The CT findings are presented and the differential diagnosis is discussed.
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PMID:CT appearances of HIV-related lipodystrophy syndrome. 1138 59


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