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

Lipodystrophy, a change in body composition and metabolic processes, may result from drugs used to treat HIV. Some reports suggest that lipodystrophy occurs at a higher frequency in women than in men. Several studies examining these differences are described. It is noted that there is a need for larger and more precise studies of lipodystrophy on men and women before conclusions can be made on the role of gender.
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PMID:Body composition changes in women. 1136 53

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

A satellite symposium was held at the 12th World AIDS Conference to address issues related to wasting, metabolic changes, and altered body shapes in persons with HIV/AIDS. Wasting, which is defined as severe weight loss, is a serious problem for people with HIV, who can lose an average of 20 percent of their body weight. Wasting is associated with changes in metabolism and increases in viral load. In addition, a syndrome called peripheral lipodystrophy has been identified, and can be recognized by many different symptoms, such as an accumulation of fat in the stomach or on the back of the neck. Peripheral lipodystrophy may be strongly associated with protease inhibitor use. Also discussed were micronutrient deficiencies, abnormalities in testosterone levels, and the links of these to wasting and lipodystrophy.
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PMID:Wasting and body changes: what do we know so far? 1136 89

Clear advantages in HIV therapy can be shown since 5 years. Questions arise concerning possible reductions of drug exposure per unit of time. These questions have become important in the light of possible development of lipodystrophy, hepatotoxicity and other side effects. Eradication at this point is not possible. Control of virus may be possible even when therapy is started later than recommended so far. 200 CD4 cells in asymptomatic patients and 100,000 copies of virus may be new starting points. There is a potential of decreasing drug exposure to 70% or 50% of the actual amount by structured or supervised therapy interruptions. Especially for the largest group of chronically infected patients no clear results concerning immunologic or virologic outcomes can be presented at this moment. If no harm is done, reduced amounts of drug exposure may be considered as an advantage.
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PMID:[New trend in HIV therapy. Later treatment onset and structured pauses]. 1137 73

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

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

We report a case of gynaecomastia developed in a HIV-seropositive man, associated with a severe lipodystrophy. We hypothesize the responsibility of stavudine and didanosine in the development of these 2 complications. If many reports suggest that the protease inhibitors may promote gynaecomastia, long-term nucleoside analogue therapy may also cause this side effect.
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PMID:Gynaecomastia in a male patient during stavudine and didanosine treatment for HIV infection. 1139 87

Alterations in regional fat, often associated with abnormalities in lipid and insulin metabolism, have been reported in HIV-infected adults. To determine whether similar abnormalities occur in children with HIV, patterns of change in regional body fat distribution were determined by dual energy x-ray absorptiometry in 28 prepubertal HIV-infected children. Eight (29%) children experienced lipodystrophy (LD), defined as extremity lipoatrophy together with trunk fat accumulation. Despite a mean body weight increase of 2.9 +/- 2.4 kg, children with LD experienced a mean loss of total fat in contrast to children without LD who increased total fat (-0.151 +/- 0.324 versus 0.981 +/- 1.041 kg; p <.01). Children with LD had significantly higher levels of HIV RNA and lower CD4 count and percentage at baseline. LD was associated with use of protease inhibitors or stavudine, (odds ratio [OR], 7.0, 95% confidence interval [CI], 1.1-45.2, p =.04; OR, 9.0, 95% CI, 1.4-59.8, p =.03, respectively). This observational study suggests that during a time in childhood when accumulation of extremity and trunk fat is expected, some HIV-infected children experience changes in fat distribution that are similar to HIV-associated LD reported in adults. Studies to determine whether HIV-infected children with changes in regional fat also experience increases in "atherogenic" lipids and insulin resistance as described in adults with HIV-associated LD are warranted.
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PMID:Lipodystrophy in HIV-infected children is associated with high viral load and low CD4+ -lymphocyte count and CD4+ -lymphocyte percentage at baseline and use of protease inhibitors and stavudine. 1140 17

Infection with human immunodeficiency virus (HIV) is associated with marked disturbance of metabolism affecting the metabolism of carbohydrates, fats and proteins. In the first decade of clinical experience of HIV, the primary clinical manifestation of such disturbed metabolism was wasting. Such wasting was often severe and contributed significantly to the morbidity and mortality of AIDS. Mechanistic studies demonstrated that in addition to the effects of altered intermediary metabolism, reduced food intake played a major role in the causation of AIDS-related wasting. More recently, potent anti-retroviral drugs have dramatically changed the clinical consequences of HIV infection. Wasting has become far less frequent among infected patients and occurs in only a small percentage of subjects on effective anti-retroviral therapy. However, a new constellation of metabolic syndromes has become apparent characterized by altered body fat distribution ('lipodystrophy'), lactic acidosis and evidence of mitochondrial dysfunction. The mechanistic basis for such syndromes is currently unclear, but is the subject of ongoing research.
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PMID:Metabolic syndromes in human immunodeficiency virus infection. 1140 60

'Lipodystrophy syndrome' in the setting of HIV infection has come to encompass a collection of morphological and metabolic abnormalities linked with the use of antiretroviral therapy and other risk factors. We review the clinical literature on this subject as it has evolved historically, taking pertinent methodological issues into account.
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PMID:Antiretroviral therapy and the lipodystrophy syndrome. 1141 66


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