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PubMed2001

Clinical assessment of HIV-associated lipodystrophy syndrome: bioelectrical impedance analysis, anthropometry and clinical scores.

BACKGROUND: Diagnosis of the HIV-associated lipodystrophy syndrome is based on clinical assessment, in lack of a consensus about case definition and reference methods. Three bedside methods were compared in their diagnostic value for lipodystrophy. PATIENTS AND METHODS: Consecutive HIV-infected outpatients (n=278) were investigated, 128 of which also had data from 1997 available. Segmental bioelectrical impedance analysis (BIA) and waist, hip and thigh circumferences were performed. Changes in seven body regions were rated by physicians and patients using linear analogue scale assessment (LASA). Diagnostic cut-off values were searched by receiver operator characteristics. RESULTS: Lipodystrophy was diagnosed in 85 patients (31%). BIA demonstrated higher fat-free mass in patients with lipodystrophy but not after controlling for body mass index and sex. Segmental BIA was not superior to whole body BIA in detecting lipodystrophy. Fat-free mass increased from 1997 to 1999 independent from lipodystrophy. Waist-hip and waist-thigh ratios were higher in patients with lipodystrophy. BIA, anthropometry and LASA did not provide sufficient diagnostic cut-off values for lipodystrophy. Agreement between methods, and between patient and physician rating, was poor. CONCLUSION: These methods do not fulfil the urgent need for quantitative diagnostic tools for lipodystrophy. BIA estimates of fat free mass may be biased by lipodystrophy, indicating a need for re-calibration in HIV infected populations.

Adult↗
PubMed2000

Risk factors for the HIV-associated lipodystrophy syndrome in a cross-sectional single-centre study.

OBJECTIVE: Risk factors for the HIV-associated lipodystrophy syndrome (HALS) were studied in a single-centre, cross-sectional study. - PATIENTS AND METHODS: 278 consecutive HIV-infected outpatients at a German tertiary care centre were enrolled. Changes in body shape were quantified using linear analogue scales. Cumulative treatment duration for each antiretroviral drug, CD4 cells, viral load and age were investigated as potential risk factors for a clinical diagnosis of lipodystrophy syndrome by logistic regression. RESULTS: HALS was diagnosed in 88 patients. The risk of HALS increased significantly with longer protease inhibitor treatment (relative risk 1.61 (95% confidence interval, 1. 24 to 2.09, per year); older age and a history of low CD4 cell counts were cofactors in this multivariate model, but nucleoside analogues did not contribute significantly. Neither pattern nor severity of disease were predicted by these risk factors. Treatment durations and other risk factors were highly correlated with each other. CONCLUSIONS: These findings support a pathogenetic role for protease inhibitor toxicity, advanced HIV disease, and ageing. No evidence for an additional effect of nucleoside analogues was found. The high correlation of potential risk factors indicates that this and other available studies may be too small to detect multiple risk factors without major confounding.

Acquired Immunodeficiency Syndrome↗
PubMed2001

L-Carnitine in the treatment of HIV-associated lipodystrophy syndrome.

The objective of this pilot study was to assess the effect of L-carnitine on the course of the HIV-associated lipodystrophy syndrome. Twelve patients presenting with combined atrophic and hypertrophic changes of body fat were treated with L-carnitine 1000 mg bid for 3 months. No marked improvement of the body changes was observed. However a reduction in serum cholesterol levels, but not triglycerides, was noted. These preliminary data do not support the use of L-carnitine for the rapid reversal of advanced fat tissue alterations due to HIV-associated lipodystrophy.

Body Weight↗
PubMed2000

HIV-associated lipodystrophy syndrome.

Highly active antiretroviral therapy (HAART) for human immunodeficiency virus-1 (HIV-1) and prophylactic therapy for opportunistic infections have increased survival. Adverse effects of HAART include lipid profile alterations, diabetes mellitus, and fat redistribution. These metabolic and physical changes are called the HIV-associated lipodystrophy syndrome. A link to protease inhibitors has been suggested, and more recently to nucleoside reverse transcriptase inhibitors and factors related to duration of HIV-1 infection itself.

Anti-HIV Agents↗
PubMed2001

[HIV-lipodystrophy syndrome].

CLINICAL FINDINGS: The HIV-associated lipodystrophy syndrome is reported with an increasing incidence predominantly in HIV-seropositive patients on antiretroviral therapy. The core of the lipodystrophy syndrome consists of fat loss in face, extremities and buttocks with or without a visceral fat accumulation, hyperlipidemia and a disturbed glucose metabolism are considered essential parts of the syndrome too. Additional metabolic abnormalities are regarded as syndrome related. PATHOGENESIS: Currently identified risk factors associated with the development of lipodystrophy are antiretroviral treatment (duration, number and kind of drugs), low CD4 cell count, higher age and metabolic abnormalities. The currently favored hypotheses to explain the lipodystrophy syndrome are essentially based on the assumption that antiretroviral treatment is the cause of the disorder. TREATMENT: The short-term benefit of antiretroviral treatment is greater than the disadvantages of the lipodystrophy syndrome, in the long term, however, the cardiovascular risk associated with the metabolic disturbances may result in an increased mortality on its own. The current approach to treatment includes modification of antiretroviral therapy and specific treatment of symptoms.

Antiretroviral Therapy, Highly Active↗
PubMed2000

Pharmacology of nucleoside and nucleotide reverse transcriptase inhibitor-induced mitochondrial toxicity.

OBJECTIVE: This paper reviews the function of the mitochondria and the mechanisms by which nucleoside and nucleotide reverse transcriptase inhibitors (NRTIs) cause mitochondrial toxicity. BACKGROUND: Highly active antiretroviral therapy (HAART) reduces rates of morbidity and mortality due to HIV disease. However, long-term treatment with these drugs may be associated with adverse effects. Nucleoside and nucleotide analogues are potent inhibitors of HIV reverse transcriptase and have become the cornerstone of HAART. Unfortunately, these drugs have also been shown to inhibit cellular polymerases, most notably mitochondrial DNA polymerase gamma. RESULTS: Studies of the NRTIs in enzyme assays and cell cultures demonstrate the following hierarchy of mitochondrial DNA polymerase gamma inhibition: zalcitabine > didanosine > stavudine > lamivudine > zidovudine > abacavir. In vitro investigations have also documented impairment of the mitochondrial enzymes adenylate kinase and the adenosine diphosphate/adenosine triphosphate translocator. Inhibition of DNA polymerase gamma and other mitochondrial enzymes can gradually lead to mitochondrial dysfunction and cellular toxicity. The clinical manifestations of NRTI-induced mitochondrial toxicity resemble those of inherited mitochondrial diseases (ie, hepatic steatosis, lactic acidosis, myopathy, nephrotoxicity, peripheral neuropathy, and pancreatitis). Fat redistribution syndrome, or HIV-associated lipodystrophy, is another side effect attributed in part to NRTI therapy. The morphologic and metabolic complications of this syndrome are similar to those of the mitochondrial disorder known as multiple symmetric lipomatosis: suggesting that this too may be related to mitochondrial toxicity. The pathophysiology of less common adverse effects of nucleoside analogue therapy, such as diabetes, ototoxicity, and retinal lesions, may be related to mitochondrial dysfunction but have not been adequately studied. CONCLUSION: NRTls can block both HIV reverse transcriptase and mitochondrial DNA polymerase gamma. Inhibition of the latter enzyme is the most likely cause of the adverse effects associated with these drugs.

Animals↗
PubMed2000

Lipodystrophy syndrome in HIV infection: what is it, what causes it and how can it be managed?

Since the introduction of HIV-1 protease inhibitors as components of antiretroviral drug combination regimens, the clinical course of HIV disease and opportunistic infections has changed dramatically. Besides the favourable virological, immunological and clinical impact of highly active antiretroviral therapy (HAART), several adverse drug reactions have been observed in patients with HIV receiving therapy. Particularly, peripheral lipodystrophy, central adiposity, dyslipidaemia and insulin resistance have been described with a prevalence of up to 80% in patients infected with HIV, and attributed to almost all components of HAART. Hyperlipidaemia is characterised by an increase of low and very low density lipoprotein-cholesterol as well as apolipoproteins B and E. Several studies strongly suggest that there are either multiple syndromes or a variety of factors inducing different changes that influence the ultimate phenotype. Similarities between HIV-associated fat redistribution and metabolic abnormalities with both inherited lipodystrophies and benign symmetric lipomatosis suggest the pathophysiological involvement of, for example, nuclear factors like lamin A/C and drug-induced mitochondrial dysfunction. Moreover, there is some evidence that cytokines and hormones impair fat and glucose homeostasis in patients with HIV receiving HAART. Three years after the first description of HIV therapy-associated abnormal fat redistribution, there is still an ongoing discussion about the case definition, diagnostic procedure and treatment options for both body shape changes and metabolic disturbances. Regarding therapy, there is a major concern about possible complex pharmacological interactions and overlapping adverse effects between HAART and, for example, lipid-lowering therapy. In addition, the likely contribution of both nucleoside analogue reverse transcriptase inhibitors and protease inhibitors to the development of abnormal fat redistribution in patients with HIV limits options of changing to alternative effective antiretroviral drug combinations. Thus, the occurrence of hyperlipidaemia, maturity onset diabetes mellitus, and marked changes in body habitus resulted in important social and clinical consequences such as an increased risk of atherosclerosis. It also sheds new light on the use of protease inhibitors regarding risk factors for the initial treatment decision. In this article, we discuss the features, pathogenesis and treatment options for body fat redistribution and metabolic disturbances associated with HAART in HIV-1 infection.

Animals↗
PubMed2001

HIV-associated wasting in the HAART era: guidelines for assessment, diagnosis, and treatment.

Wasting (malnutrition) and lipodystrophy are the two major nutritional alterations in human immunodeficiency virus (HIV)-infected individuals. Both wasting and lipodystrophy may involve a decrease in body fat content, while wasting-but not lipodystrophy-also includes the loss of lean body mass. Lipodystrophy has made the identification of wasting increasingly more difficult. The diagnosis of wasting depends on a definition of the condition that takes into account sex and cultural differences, as well as measurements of body cell mass. Patient management involves a concurrent, comprehensive approach designed to restore lost body cell mass and weight. The authors make recommendations for defining, diagnosing, and treating HIV-associated wasting. Specific therapies include testosterone replacement, other anabolic steroids, and recombinant human growth hormone. Other adjunctive measures, such as progressive resistance exercise and cytokine modulation, may also be utilized. Expected outcomes from effective treatment include restored body cell mass, improvement in quality of life, and reduced rates of hospitalization. Future directions for research should address the need for optimal treatment strategies.

Anabolic Agents↗
PubMed1999

Altered body shape in HIV disease: a side effect of therapy?

An interactive teleconference on HIV-associated lipodystrophies and altered body habitus was held on January 20, 1999, part of a series known as HIV Treatment LIVE!. It was moderated by Ronald Baker, Ph.D., and sponsored by the AIDS Wasting Foundation (AWF). AWF, located at 15 East 26th Street, New York, NY 10010, was founded in 1997 as an education and advocacy organization, under the direction of Carola Burroughs, Executive Director. This tele-conference brought together three AIDS experts to address important issues concerning the etiology, diagnosis, and treatment of this novel and enigmatic syndrome. The resulting report is an edited, selected transcript of that discussion.

Anti-HIV Agents↗
PubMed2001

Clinical assessment of HIV-associated lipodystrophy in an ambulatory population.

OBJECTIVE: To identify clinical factors associated with prevalence of fat atrophy (lipoatrophy) and fat accumulation (lipoaccumulation) in HIV-1 infected patients. DESIGN: Evaluation of HIV-1 infected patients seen for routine care between 1 October and 31 December 1998 in the eight HIV Outpatient Study (HOPS) clinics. SETTING: Eight clinics specializing in the care of HIV-1 infected patients. PATIENTS: A total of 1077 patients were evaluated for signs of fat maldistribution. INTERVENTIONS: A standardized set of questions and specific clinical signs were assessed. Demographic, clinical and pharmacological data for each patient were also included in the analysis. MAIN OUTCOME MEASURES: Demographic, immunologic, virologic, clinical, laboratory, and drug treatment factors were assessed in stratified and multivariate analyses for their relationship to the presence and severity of fat accumulation and atrophy. RESULTS: Independent factors for moderate/severe lipoatrophy for 171 patients were increasing age, any use of stavudine, use of indinavir for longer than 2 years, body mass index (BMI) loss, and measures of duration and severity of HIV disease. Independent risk factors for moderate/severe fat accumulation for 104 patients were increasing age, BMI gain, measures of amount and duration of immune recovery, and duration of antiretroviral therapy (ART). The number of non-drug risk factors substantially increased the likelihood of lipoatrophy. If non-drug risk factors were absent, lipoatrophy was unusual regardless of the duration of drug use. CONCLUSIONS: HIV-associated lipodystrophy is associated with several host, disease, and drug factors. While prevalence of lipoatrophy increased with the use of stavudine and indinavir, and lipoaccumulation was associated with duration of ART, other non-drug factors were strongly associated with both fat atrophy and accumulation.

Acquired Immunodeficiency Syndrome↗
PubMed2000

Association of severe insulin resistance with both loss of limb fat and elevated serum tumor necrosis factor receptor levels in HIV lipodystrophy.

HIV-lipodystrophy (HIV-LD) is characterized by the loss of body fat from the limbs and face, an increase in truncal fat, insulin resistance, and hyperlipidemia, factors placing affected patients at increased risk for vascular disease. This study evaluated insulin sensitivity and inflammatory status associated with HIV-LD and provides suggestions about its etiology. Insulin sensitivity and immune activation markers were assessed in 12 control subjects and 2 HIV-positive groups, 14 without and 15 with LD syndrome. Peripheral insulin sensitivity (mostly skeletal muscle) was determined with the hyperinsulinemic-euglycemic clamp. Circulating insulin-like growth factor (IGF) binding protein-1 (IGFBP-1) and free fatty acid (FFA) levels, and their response to insulin infusion were indicative of insulin responsiveness of liver and adipose tissue, respectively. Serum levels of soluble type 2 tumor necrosis factor-alpha (TNF-alpha) receptor (sTNFR2) were used as an indicator of immune activation. HIV-LD study subjects had significantly reduced (twofold) peripheral insulin sensitivity, but normal levels of FFA and reduced levels of IGFBP-1, relative to the nonlipodystrophy groups, indicating that the loss of insulin sensitivity was more pronounced in skeletal muscle than in liver or fat. The significant loss of peripheral fat in the HIV-LD group (34%; p <.05) closely correlated with the reduced peripheral insulin sensitivity (p =. 0001). Levels of sTNFR2 were elevated in all HIV-infected study subjects, but they were significantly higher in those with lipodystrophy than without, and sTNFR2 levels strongly correlated with the reduction in insulin sensitivity (p =.0001). Loss of peripheral fat, normal levels of FFA, and reduced levels of IGFBP-1 indicate that insulin resistance in HIV-LD is distinct from type 2 diabetes and obesity. The relationship between the degree of insulin resistance and sTNFR2 levels suggests an inflammatory stimulus is contributing to the development of HIV-associated lipodystrophy.

Absorptiometry, Photon↗
PubMed2001

Gynecomastia associated with highly active antiretroviral therapy.

OBJECTIVE: To report four cases of HIV-associated gynecomastia diagnosed during treatment with nucleoside analogs with or without protease inhibitors. CASE SUMMARY: Four HIV-infected patients developed gynecomastia while taking two nucleoside analogs (stavudine combined with lamivudine in 3 patients, stavudine with didanosine in 1 patient) and protease inhibitors (indinavir, nelfinavir, ritonavir-saquinavir in 3 patients) all patients had received prior treatment with single or associated nucleoside analogs for > or = 21 months. Gynecomastia occurred three to seven months after the start of a triple regimen in the first three patients, and 17 months after initiating the last dual nucleoside analog therapy in the remaining patient. Liver, kidney, and thyroid function were normal; a routine endocrinologic workup showed slight follicle-stimulating hormone and luteinizing hormone abnormalities in one patient only. Other possible causes of drug- or disease-induced gynecomastia were excluded. A concurrent fat redistribution syndrome was present in three patients (including the patient who received nucleoside analogs only), while serum lipid and/or glucose concentration abnormalities were present in all patients. Gynecomastia remained unchanged during the subsequent seven- to 16-month follow-up, even after modification of antiretroviral therapy. DISCUSSION: Gynecomastia has been recently associated with antiretroviral therapy, and all reported cases but one occurred two to 17 months after the start of a protease inhibitor-based regimen. Our experience underlines the possible occurrence of gynecomastia in the absence of protease inhibitor administration, its persistence despite changes of antiretroviral regimen (thus resembling some signs related to lipodystrophy syndrome), and the apparently constant association with prolonged nucleoside analog administration (especially stavudine). CONCLUSIONS: Gynecomastia should be included among emerging adverse effects of antiretroviral therapy, although its etiopathogenesis deserves further investigation.

Adipose Tissue↗