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PubMed2006

Use of a biopolymer polyalkylimide filler for facial lipodystrophy in HIV-positive patients undergoing treatment with antiretroviral drugs.

OBJECTIVES: To evaluate the efficacy, overall esthetic effect, and safety of a new permanent, polyalkylimide dermal filler in HIV-infected patients with severe facial lipodystrophy. METHODS: Eleven subjects with severe facial lipodystrophy secondary to HIV infection were injected bilaterally with 15 and 30 cm3 of a polyalkylimide gel into the buccal, malar, and temporal areas of the face in an attempt to restore their facial contour. The youngest treated subject was 31 years of age and the oldest 73 years of age. RESULTS: All 11 subjects received an immediately acceptable therapeutic esthetic effect. Injections were generally well tolerated, with only three adverse events (swelling and bruising) recorded. Subjects, assessed at 3 and 18 months after treatment, continued to show improvement. CONCLUSIONS: The immediate benefits of a polyalkylimide gel in the correction and restoration of facial contour in subjects having severe HIV-related facial lipodystrophy were demonstrated. This improvement was still noted at 18 months. The efficacy, ease of injection, and safety profile of polyalkylimide gel make this filling material a potentially attractive treatment for lipodystrophy. These data must be tempered with the need for significant further safety studies to determine whether this long-term filler has a safety profile consistent with other currently popular fillers.

Adult↗
PubMed1996

Generalized lipodystrophy, congenital and acquired (lipoatrophy).

This review is based on longitudinal studies on our seven patients with congenital generalized lipodystrophy, our patient with acquired generalized lipodystrophy, and published papers on these subjects. An inability to store energy in adipose tissue is of pathogenetic importance. In congenital lipodystrophy, insulin resistance is present from birth, resulting in hyperinsulinaemia, dyslipidaemia. and insulin-resistant diabetes with an anabolic syndrome worsened by a voracious appetite. Clinically, we observed increased height velocity in pre-school age children, and organomegaly with hypertrophic cardiomyopathy, which seems to be lethal in early adulthood: three of our patients died at the ages of 24, 32 and 37 years. The oldest alive, 39 years, suffers from stenocardia. Regarding treatment, it is most important to reduce energy consumption. The congenital form is recessively inherited. The aetiology may be related to insulin receptor or postreceptor mechanisms. Acquired generalized lipodystrophy seems to be an autoimmune disorder with secondary destruction of the adipose organ: the anabolic syndrome with insulin-resistant diabetes is secondary. Our patient died when 24 years old from pneumonia.

Carbohydrate Metabolism↗
PubMed2002

High concentrations of nelfinavir as an independent risk factor for lipodystrophy in human immunodeficiency virus-infected patients.

To assess the relationship between antiretroviral drug exposure and lipodystrophy, 69 human immunodeficiency virus type 1-infected patients receiving nelfinavir were investigated cross-sectionally. Lipodystrophy was defined by patients' self-report. Nelfinavir trough concentrations in plasma were significantly related to overall lipodystrophy and peripheral fat wasting scores and appeared to be an independent risk factor for lipodystrophy

Body Composition↗
PubMed1990

Partial lipodystrophy in coeliac disease.

The association of coeliac disease and partial lipodystrophy is described. The patient also had deficiencies of serum IgA and C3 complement (the latter associated with partial lipodystrophy). In addition, there was subclinical dermatitis herpetiformis confirmed by skin biopsy. The facial wasting of fully developed partial lipodystrophy may be misinterpreted as a sign of malabsorption but the facial, upper limb, and truncal lipodystrophy contrasts with normal pelvic and lower limb appearances.

Adolescent↗
PubMed2003

Increased systemic and adipose tissue cytokines in patients with HIV-associated lipodystrophy.

The lipodystrophy syndrome (adipose tissue redistribution and metabolic abnormalities) observed with highly active antiretroviral therapy (HAART) during human immunodeficiency virus (HIV) infection may be related to increased proinflammatory cytokine activity. We measured acute cytokine (TNF-alpha, IL-6, leptin), glycerol, and lactate secretion from abdominal subcutaneous adipose tissue (SAT), and systemic cytokine levels, in HIV-infected subjects with and without lipodystrophy (HIVL+ and HIVL-, respectively) and healthy non-HIV controls. Lipodystrophy was confirmed and characterized as adipose tissue redistribution in HIVL+ compared with HIVL- and controls, by dual-energy X-ray absorptiometry and by whole body MRI. TNF-alpha secretion from abdominal SAT and circulating levels of IL-6, soluble TNF receptors I and II, and insulin were elevated in HIVL+ relative to HIVL- and/or controls, particularly in HIVL+ undergoing HAART. In the HIV-infected group as a whole, IL-6 secretion from abdominal SAT and serum IL-6 were positively associated with visceral fat and were negatively associated with the relative amount of lower limb adipose tissue (P < 0.01). Decreased leptin and increased lactate secretion from abdominal SAT were specifically associated with HAART. In conclusion, increased cytokine secretion from adipose tissue and increased systemic proinflammatory cytokine activity may play a significant role in the adipose tissue remodeling and/or the metabolic abnormalities associated with the HIV-lipodystrophy syndrome in patients undergoing HAART.

Abdomen↗
PubMed2002

Partial lipodystrophy in a patient with systemic lupus erythematosus.

A 54-year-old woman developed partial lipodystrophy on the left side of her face. She had been suffering from systemic lupus erythematosus (SLE) since 1985 when she was 45 years old, and she had been treated with 30 mg/day of oral prednisolone as an initial dose. Partial lipodystrophy appeared on her left lower jaw in 1994 when the SLE was inactive, and the dose of prednisolone was reduced to 5 mg/ 3 days. Gradually, the lipodystrophy spread toward her left cheek and her left forehead without any preceding skin symptoms. Histological examination showed a loss of fat tissue and mild lymphocytic infiltrations mainly around cutaneous appendages and vessels in the dermis and subcutaneous tissue. The dose of prednisolone was increased to 10 mg/day and the lesions stopped spreading. Such partial lipodystrophy is distinct from lipoatrophy of lupus profundus.

Female↗
PubMed2002

Clinical review 153: Lipodystrophy in human immunodeficiency virus-infected patients.

Human immunodeficiency virus (HIV) infection is a major global health problem. Recently, combination therapy including HIV-1 protease inhibitors (PIs) has dramatically improved the long-term survival of HIV-infected patients. However, such therapy is associated with a lipodystrophy syndrome characterized by selective loss of sc fat from the face and extremities and, in some patients, accumulation of fat around the neck, dorsocervical region, abdomen, and trunk. Lipodystrophy in HIV-infected patients (LDHIV) is associated with insulin resistance and its metabolic complications such as impaired glucose tolerance, diabetes, hypertriglyceridemia and low serum high density lipoprotein cholesterol levels. PIs appear to be the strongest link to LDHIV; however, fat loss has been reported in some patients taking non-PI antiretroviral drugs. Other factors, such as duration of HIV infection, age, and gender, may also contribute to the risk of development of LDHIV. The molecular basis of LDHIV remains unknown. There is no specific therapy for LDHIV. Avoiding weight gain by reducing energy intake and increasing physical activity may be beneficial in reducing fat accumulation as well as improving metabolic complications. Antihyperglycemic drugs may be used to treat diabetes. Management of dyslipidemia may require lipid-lowering drugs; however, the safety and efficacy of such intervention require further studies. Substitution of PIs with other antiretroviral drugs can mitigate dyslipidemia and glucose intolerance, but whether reversal of lipodystrophy occurs remains unknown. Future research is needed to discover the biochemical and molecular markers of lipodystrophy in HIV patients and develop PIs or other antiretroviral agents that are free of metabolic toxicity.

Adipose Tissue↗
PubMed2005

In vivo evidence of impaired peripheral fatty acid trapping in patients with human immunodeficiency virus-associated lipodystrophy.

The use of antiretroviral combination therapy in HIV has been associated with lipodystrophy and several metabolic risk factors. We postulated that patients with HIV-lipodystrophy have impaired adipose tissue free fatty acid (FFA) trapping and, consequently, increased hepatic FFA delivery. We investigated FFA, hydroxybutyric acid (HBA; reflecting hepatic FFA oxidation), and triglyceride (TG) changes after a high fat meal in HIV-infected males with (LIPO; n = 26) and without (NONLIPO; n = 12) lipodystrophy and in healthy males (n = 35). Because defective peripheral FFA trapping has been associated with impaired action of complement component 3 (C3), we also determined postprandial C3 concentrations. The LIPO group had higher homeostasis model assessment scores compared with the other groups. Areas under the curve (AUCs) for FFA, HBA, and TG were higher in the LIPO group than in the NONLIPO group or the controls. No differences in TG-AUC, FFA-AUC, and HBA-AUC were observed between the NONLIPO group and controls. In HIV-infected patients, FFA-AUC and HBA-AUC were inversely related to sc adipose tissue area. Plasma C3 showed a postprandial increase in healthy controls, but not in the HIV-infected groups. C3 was not related to body fat distribution, postprandial FFA, or HBA. The present data suggest disturbed postprandial FFA metabolism in patients with HIV-lipodystrophy, most likely due to inadequate incorporation of FFA into TG in sc adipose tissue, but do not support a major role for C3 in these patients. The higher postprandial HBA levels reflect increased hepatic FFA delivery and may aggravate insulin resistance and dyslipidemia, leading to increased cardiovascular risk.

Adolescent↗
PubMed2005

Role of CD95-mediated adipocyte loss in autoimmune lipodystrophy.

CONTEXT: Lipodystrophies are rare disorders characterized by the selective loss of adipose tissue. Metabolic complications increase in severity with the extent of fat loss. In some forms of acquired lipodystrophy, the loss of fat is suggested to be a result of autoimmune destruction of adipocytes. Here, the pathogenic mechanism is still poorly understood. OBJECTIVE: We have analyzed sc adipose tissue from a 5-yr-old girl with ongoing fat loss by immunohistochemistry. Using cultured human preadipocytes and adipocytes, we elucidated a possible mechanism leading to adipocyte loss in this patient. RESULTS: Analysis of adipose tissue samples of the patient with acquired lipodystrophy obtained from skin areas affected by panniculitis suggested that loss of adipocytes was mediated by CD95-induced apoptosis. Regression of adipose tissue was accompanied by lymphohistiocytic infiltration/inflammation and increased serum levels of inflammatory cytokines interferon-gamma and TNF-alpha. In vitro studies with human adipocytes demonstrated that interferon-gamma and TNF-alpha are able to up-regulate CD95 expression and enhance CD95-death-inducing signaling complex formation resulting in a robust sensitization for CD95-mediated apoptosis. CONCLUSION: We have identified here a possible mechanism responsible for the loss of adipocytes by apoptosis in autoimmune lipodystrophy.

Adipocytes↗
PubMed2006

Efficacy and safety of leptin-replacement therapy and possible mechanisms of leptin actions in patients with generalized lipodystrophy.

BACKGROUND: Lack of leptin is implicated in insulin resistance and other metabolic abnormalities in generalized lipodystrophy; however, the efficacy, safety, and underlying mechanisms of leptin-replacement therapy in patients with generalized lipodystrophy remain unclear. METHODS: Seven Japanese patients with generalized lipodystrophy, two acquired and five congenital type, were treated with the physiological replacement dose of recombinant leptin during an initial 4-month hospitalization followed by outpatient follow-up for up to 36 months. RESULTS: The leptin-replacement therapy with the twice-daily injection dramatically improved fasting glucose (mean +/- SE, 172 +/- 20 to 120 +/- 12 mg/dl, P < 0.05) and triglyceride levels (mean +/- SE, 700 +/- 272 to 260 +/- 98 mg/dl, P < 0.05) within 1 wk. The leptin-replacement therapy reduced insulin resistance evaluated by euglycemic clamp method and augmented insulin secretion at glucose tolerance test with different responses between acquired and congenital types. Improvement of the fatty liver was also observed. The efficacy and safety of the once-daily injection were comparable to those of the twice-daily injection. The leptin-replacement therapy ameliorated macro- and microalbuminuria and showed no deterioration of neuropathy and retinopathy of these patients. The leptin-replacement therapy is beneficial to diabetic complications and lipodystrophic ones. Two patients developed antileptin antibodies but not neutralizing antibodies. The therapy was well tolerated, and its effects were maintained for up to 36 months without any notable adverse effects such as hypoglycemia, high blood pressure, or reduction of bone mineral density. CONCLUSIONS: The present study demonstrates the efficacy and safety of the long-term leptin-replacement therapy and possible mechanisms of leptin actions in patients with generalized lipodystrophy.

Adolescent↗
PubMed2000

Hyperandrogenemia in human immunodeficiency virus-infected women with the lipodystrophy syndrome.

A novel lipodystrophy syndrome characterized by insulin resistance, hypertriglyceridemia, and fat redistribution has recently been described in human immunodeficiency virus (HIV)-infected men and women. Women with the HIV lipodystrophy syndrome exhibit a marked increase in waist-to-hip ratio and truncal adiposity; however, it is unknown whether androgen levels are increased in these patients. In this study, we assessed androgen levels in female patients with clinical lipodystrophy based on evidence of significant fat redistribution in the trunk, extremities, neck and/or face (LIPO: n = 9; age, 35.7+/-1.7 yr; BMI, 24.7+/-0.8 kg/m2) in comparison with age- and BMI-matched nonlipodystrophic HIV-infected females (NONLIPO: n = 14; age, 37.6+/-1.1 yr; BMI, 23.4+/-0.6 kg/m2) and healthy non-HIV-infected control subjects (C: n = 16; age, 35.8+/-0.9 yr; BMI, 23.1+/-0.4 kg/m2). Fasting insulin, lipid levels, virologic parameters, and regional body composition using dual energy x-ray absorptiometry were also assessed. Total testosterone [ LIPO, 33+/-6 ng/dL (1.1+/-0.2 nmol/L); NONLIPO, 17+/-2 ng/dL (0.6+/-0.1 nmol/L); C, 23+/-2 ng/dL (0.8+/-0.1 nmol/L); P < 0.05 LIPO vs. C and LIPO vs. NONLIPO] and free testosterone determined by equilibrium dialysis [LIPO, 4.5+/-0.9 pg/mL (16+/-3 pmol/L); NONLIPO, 1.7+/-0.2 pg/mL (6+/-1 pmol/L); C, 2.4+/-0.2 pg/mL (8+/-1 pmol/L); P < 0.05 LIPO vs. C and LIPO vs. NONLIPO] were increased in the lipodystrophic patients. Sex hormone-binding globulin levels were not significantly different between LIPO and C, but were significantly lower in the LIPO vs. NONLIPO patients (LIPO 84+/-7 vs. NONLIPO 149+/-17 nmol/L, P < 0.05). The LH/FSH ratio was significantly increased in the LIPO group compared with the NONLIPO and C subjects (LIPO, 2.0+/-0.6; NONLIPO, 1.1+/-0.1; C, 0.8+/-0.1; P < 0.05 LIPO vs. NONLIPO and LIPO vs. C). Body fat distribution was significantly different between LIPO and C subjects. Trunk to extremity fat ratio (1.46+/-0.17 vs. 0.75+/-0.05, LIPO vs. C, P < 0.05) was increased and extremity to total fat ratio decreased (0.40+/-0.03 vs. 0.55+/-0.01, LIPO vs. C, P < 0.05). In contrast, fat distribution was not different in the NONLIPO group vs. control subjects. Among the HIV-infected patients, free testosterone correlated with percent truncal fat (trunk fat/trunk mass) (r = 0.43, P = 0.04). These data suggest that hyperandrogenemia is another potentially important feature of the HIV-lipodystrophy syndrome in women. Additional studies are necessary to determine the clinical significance of increased androgen levels and the relationship of hyperandrogenism to fat redistribution and insulin resistance in this population of patients.

Adult↗
PubMed2001

Apoprotein c-III and E-containing lipoparticles are markedly increased in HIV-infected patients treated with protease inhibitors: association with the development of lipodystrophy.

Long-term therapy with protease inhibitors (PIs) can induce hypertriglyceridemia and development of a lipodystrophy. To better understand these metabolic alterations, the apoprotein and lipoparticle profile was investigated in male HIV patients under antiretroviral therapy: 49 received PIs, and 14 were given only two reverse transcriptase inhibitors. As controls, 63 male subjects were selected from a population study carried out in the Toulouse, France, area. Fasting glucose, insulin, and C-peptide were also determined. All patients under PIs displayed low levels of plasma glucose and increased insulin. PI administration was associated with moderate hypertriglyceridemia, low high-density cholesterol and apolipoprotein (apo) A-I levels. The most striking changes were a 2- to 3-fold increase in apo E and apo C-III, essentially recovered as associated to apo B-containing lipoparticles. Levels of those lipoparticles were two to eight times above control values. About 50% of PI-treated patients had developed a patent lipodystrophy. Multivariate analysis revealed that, among the investigated parameters, apo C-III was the only one found strongly associated with the occurrence of lipodystrophy (odds ratio, 5.5; P: < 0.015). Finally, 13 PI-receiving subjects with patent hypertriglyceridemia were given fenofibrate and were reevaluated 2 months later. Triglycerides, apo E, apo C-III, and the corresponding lipoparticles had returned to nearly normal levels. These results document the accumulation of potentially atherogenic lipoparticles under PIs. Apo C-III may play a pivotal role in the development of hypertriglyceridemia and lipodystrophy.

Adult↗
PubMed2002

Effect of leptin replacement on pituitary hormone regulation in patients with severe lipodystrophy.

Leptin is important in regulating energy homeostasis. Severe lipodystrophy is associated with leptin deficiency and insulin resistance, hypertriglyceridemia, and hepatic steatosis. Leptin deficiency is also associated with abnormalities of the pituitary hormones in rodent models and patients with congenital absence of leptin. We inquired whether similar abnormalities are seen in patients with lipodystrophy and whether replacement of leptin will make an impact on the regulation of pituitary hormones. Seven female patients (aged 15-42 yr, all diabetic) with lipodystrophy and serum leptin levels less than 4 mg/liter were treated with recombinant methionyl-human leptin (recombinant leptin) in physiological doses in an open-labeled study. The following parameters were evaluated before and at 4 months of leptin treatment: menstrual history, pelvic ultrasonogram, LHRH, TRH, and CRH tests. While on recombinant leptin, mean serum leptin concentration increased from 1.3 +/- 0.3 mg/liter to 11.1 +/- 2.5 mg/liter. Only one of five patients who had intact reproductive systems was cycling normally before leptin therapy, and all five had normal menses by the fourth month of leptin therapy. Serum E2 concentrations increased (110 +/- 44 pmol/liter vs. 546 +/- 247 pmol/liter, P = 0.002), serum T concentrations decreased (3.5 +/- 3.0 nmol/liter vs. 1.3 +/- 0.7 nmol/liter, P = 0.055), and the attenuated LH response to LHRH was corrected with therapy. Serum T(3) and free T(4) were in the normal range before leptin therapy and did not change. However, serum TSH concentrations fell from 2.2 +/- 1.1 microU/ml to 1.2 +/- 0.7 microU/ml (P < 0.001). The percent increase in TSH following TRH administration was similar before (560%) and at 4 months (580%) of leptin therapy. The mean nonstimulated ACTH and cortisol concentrations were, respectively, 6.0 +/- 3.4 pmol/liter and 680 +/- 280 nmol/liter before leptin and did not change after 4 months of therapy (4.2 +/- 1.2 pmol/liter, P = 0.11 and 453 +/- 142 nmol/liter, P = 0.13, respectively). The ACTH and cortisol responses to CRH stimulation were normal both before and after therapy. Leptin replacement improved menstrual abnormalities and low E2 levels and corrected the attenuated LH response to LHRH in a group of young women with lipodystrophy and leptin deficiency. These results add to the growing body of evidence that metabolic signals such as leptin play a role in neuroendocrine regulation.

Adolescent↗
PubMed2002

Familial lipodystrophy associated with neurodegeneration and congenital cataracts.

BACKGROUND: The lipodystrophies are characterized by loss of body fat and metabolic disturbances, but the CNS is seldom affected. METHODS: An investigation of a family with partial lipodystrophy and neurologic abnormalities included lipid analysis, dual-energy x-ray absorbtiometry (DEXA) for adiposity, insulin resistance, karyotype and other genetic analyses, peroxisomal function, glycosylation pattern of transferrin and thyroglobulin, and muscle biopsy. RESULTS: The propositus, a 28-year-old woman with congenital partial lipodystrophy and cataracts, presented with a spastic-ataxic gait and lower extremity paresthesiae at age 18. Laboratory investigation revealed a type V hyperlipidemia pattern, insulin resistance, and high alpha-tocopherol levels. A similar syndrome in other family members suggested an autosomal dominant pattern of inheritance. DISCUSSION: The progressive neurologic degenerative condition associated with this autosomal dominant, partial lipodystrophy may be misdiagnosed as MS or spinocerebellar degeneration. Search for a few relevant candidate genes was unrevealing. A genome-wide search to determine the molecular etiology can be undertaken if other similar cases are identified.

Adult↗
PubMed2006

Exercise training in HIV-1-infected individuals with dyslipidemia and lipodystrophy.

PURPOSE: Highly active antiretroviral therapy has improved the prognosis of human immuno deficiency virus type 1 (HIV-1)-infected individuals, but it has been associated with the development of metabolic and fat distribution abnormalities known as the lipodystrophy syndrome. This study tested the hypothesis that aerobic exercise training added to a low-lipid diet may have favorable effects in HIV-1-infected individuals with dyslipidemia and lipodystrophy. METHODS: Thirty healthy subjects, carriers of HIV-1, with dyslipidemia and lipodystrophy, all of whom were using protease inhibitors and/or non-nucleoside reverse transcriptase inhibitors, were randomly assigned to participate in either a 12-wk program of aerobic exercise or a 12-wk stretching and relaxation program. All subjects received recommendations for a low-lipid diet. Before and after intervention, peak oxygen uptake, body composition, CD4, viral load, lipid profile, and plasma endothelin-1 levels were measured. RESULTS: Peak oxygen uptake increased significantly in the diet and exercise group (mean +/- SD: 32 +/- 5 mL x kg(-1) x min(-1) before; 40 +/- 8 mL x kg(-1) x min(-1) after) but not in the diet only group (34 +/- 7 mL x kg(-1) x min(-1) before; 35 +/- 8 mL x kg(-1) x min(-1) after). Body weight, body fat, and waist-to-hip ratio decreased significantly and similarly in the two groups. There were no significant changes in immunologic variables in either group. Likewise, plasma triglycerides, total cholesterol, and HDL cholesterol levels did not change significantly in either group. Plasma endothelin-1 levels were elevated in both groups and presented no significant changes during the study. CONCLUSION: HIV-seropositive individuals with lipodystrophy and dyslipidemia submitted to a short-term intervention of low-lipid diet and aerobic exercise training are able to increase their functional capacity without any consistent changes in plasma lipid levels.

Adult↗
PubMed2002

Self-reported signs of lipodystrophy by persons living with HIV infection.

OBJECTIVE: To identify risk factors for the development of lipodystrophy in HIV infected patients on highly active antiretroviral therapy. METHODS: A survey among patients with HIV infection using an anonymous questionnaire was conducted in 10 European countries between December 1998 and December 1999. Nine hundred and four people receiving antiretrovirals, were included in the analyses. RESULTS: 368 (41%) people reported an increase in abdominal girth since commencing current antiretroviral treatment. Breast enlargement was reported by 106 people (12%). Lipoatrophy signs were reported by approximately one-third of the people: 291 (32%) complained about decrease in facial fat and 300 (33%) reported decrease in buttock fat. One hundred and thirty-one (15%) people reported both lipoatrophy signs and an increase in abdominal girth (mixed lipodystrophy syndrome). In multivariate analysis, the development of the mixed lipodystrophy syndrome was associated with a longer use of indinavir (OR=1.03, 95% CI: 1.00-1.06), ritonavir (OR=1.06, 1.02-1.09) and stavudine (OR=1.05, 1.02-1.08) and also with age, a longer duration of HIV seropositivity and an advanced stage of HIV infection. CONCLUSIONS: This study suggests that multiple factors are associated with the occurrence of lipodystrophy, including the prolonged use of protease inhibitors.

Adult↗
PubMed2005

Total body composition by DXA of 241 HIV-negative men and 162 HIV-infected men: proposal of reference values for defining lipodystrophy.

The aim of this study was to define standard values for fat mass distribution by dual-energy X-ray absorptiometry in human immunodeficiency virus (HIV)-negative men and to analyze factors associated with lipodystrophy in HIV-infected men. Total-body composition was analyzed in 241 HIV-negative men (controls) and 162 HIV-infected men. We created a fat mass ratio (FMR) as the ratio of the percentage of the trunk fat mass to the percentage of the lower limbs fat mass. We defined the FMR standard values as the mean value+/-standard deviation. We compared body mass index (BMI), fat mass percentage (%FM), lean mass (LM), bone mineral density (BMD), and FMR between the control group and HIV-infected men, by age range, according to prescription of treatment and presence of clinical lipodystrophy. The FMR standard value is equal to 1.3+/-0.2. The FMR was higher in treated HIV-infected men with or without clinical lipodystrophy. The FMR was similar for naïve HIV-infected men and controls. It was positively correlated with age, cumulative time on treatment, zidovudine, stavudine, or indinavir. BMD and fat mass were lower for treated and naïve HIV-infected men than for HIV-negative men. The FMR seems to be a valuable index for measuring fat mass distribution. We defined FMR standard values from the largest group of HIV-negative men to our knowledge. Applying FMR to HIV patients could help physicians to diagnose lipodystrophy earlier.

Absorptiometry, Photon↗
PubMed2001

Strategies for treating HIV-related lipodystrophy.

HIV-related lipodystrophy has emerged as one of the most prevalent problems for patients with HIV, since this infection can now be seen as a chronic disease. Despite its growing importance, crucial issues such as aetiopathogenesis, diagnosis, prevention and therapy remain largely unknown and unexplored. Current evidence suggests that aetiology is multifactorial. HIV infection, antiretroviral therapy and patient-related factors probably all contribute to the development of lipodystrophy. The lack of a formal definition and the nature of wasting syndromes that affect HIV-infected patients can hinder the diagnosis and treatment of lipodystrophy. Body fat changes have a major negative impact on the quality of life of patients. Metabolic abnormalities are also well known cardiovascular risk factors that can increase the morbidity and mortality due to cardiovascular disorders in a relatively young population. As yet, we do not know whether lipodystrophy is preventable or reversible. Several therapeutic approaches have been tested with limited success, however potential complications must be considered. These therapeutic approaches include general health measures (diet, exercise and discontinuation of smoking), switching antiretrovirals (from protease inhibitors to non-nucleoside reverse transcriptase inhibitors or abacavir, or from stavudine to other nucleoside reverse transcriptase inhibitors) and use of drugs with metabolic effects (metformin, thiazolidinediones, recombinant growth hormone and anabolic steroids). A judicious use of available data, and opting for an individualised approach seems the best option for management of this problem at present.

Animals↗