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PubMed2003

4th International Workshop on Adverse Drug Reactions and Lipodystrophy in HIV. San Diego, California, USA 22-25 September 2002.

Highlights are presented from this annual workshop, which was devoted to the investigation of adverse effects associated with antiretroviral therapy for HIV infection. Topics covered included the lipodystrophy syndrome, which encompasses body composition changes (subcutaneous fat wasting, visceral fat accumulation) and metabolic abnormalities (insulin resistance and dyslipidaemia). The relevance of HIV protease inhibitor-induced metabolic abnormalities to cardiovascular disease is discussed. Research in the areas of hyperlactataemia, abacavir hypersensitivity, and bone mineral density in the context of HIV infection is also briefly reviewed.

Acidosis, Lactic↗

PubMed1975

Lipoatrophy produced in mice and rabbits by a fraction prepared from the urine from patients with congenital generalized lipodystrophy.

Urine from 5 patients with congenital generalized lipodystrophy has been fractionated by protein precipitation and Sephadex gel filtration. A fraction with a molecular weight in the range of 1000 was observed to be metabolically active in mice, rats, and rabbits. Hypophysectomized rats got hypoglycaemia following an injection, and the lipolytic-hyperglycaemic effect of ACTH was reduced after injection into intact mice. This effect was probably due to insulin release, because no insulin-like activity was observed on isolated fat cells in vitro. Persistant changes were observed in the animals after 3 weeks of daily injections of the urinary fraction. Adult mice and rabbits developed lipoatrophy with decrease of body weight in spite of a doubling of the food consumption. The metabolic rate and the body temperature were raised. Infantile animals developed a lipodystrophic state with increased growth velocity, and 50 per cent increase of the body weight, although no fat depots were observed. The treated animals got hyperglycaemia, hypertriglyceridaemia, hyperinsulinaemia, and insulin resistance. The rabbits developed manifest diabetes. The corresponding fraction prepared from the urine from the lipoatrophic rabbits produced lipoatrophy after injection into the mice. It is suggested that the lipodystrophic urinary fraction is of hypothalamic origin, and that it acts through the pituitary gland. The fraction is still heterogenous, and was observed to contain thyrotrophin releasing activity.

Adolescent↗

PubMed1978

Fat cell size and lipid content of subcutaneous tissue in congenital generalized lipodystrophy.

Fat cell size and lipid composition of subcutaneous tissue from 3 patients with congenital generalized lipodystrophy have been measured before and after treatment with either pimozide, fenfluramine or hypophysectomy. The fat cell volume before treatment ranged between 9.8 x 10(4) and 17.7 x 10(4) micron 3, compared to 9.0 x 10(4) and 85.3 x 10(4) micron 3 in 15 controls. The amount of lipids was only 1/10 to 1/50 of normal, triglycerides being the most heavily reduced lipid component. Neither the fat cell size nor the lipid content were affected by treatment with hypophysectomy, pimozide or fenfluramine.

Adipose Tissue↗

PubMed2006

[Metabolic alterations in HIV-associated lipodystrophy syndrome].

The introduction of highly active antiretroviral therapy (HAART) has reduced morbidity and mortality in patients infected with the human immunodeficiency virus (HIV). However, prolonged treatment with combination regimens can be difficult to sustain because of problems with adherence and toxic effects. Treatment with antiretroviral agents--protease inhibitors in particular--has uncovered a syndrome of abnormal fat redistribution, impaired glucose metabolism, insulin resistance and dyslipidemia, collectively termed lipodystrophy syndrome (SLHIV). Nowadays, no clinical guidelines are available for the prevention or treatment of SLHIV, and its cause have yet to be totally elucidated. This review emphasizes the clinical features and the data from previous studies about the SLHIV taking into account that a better understanding of this syndrome for HIV specialists, cardiologists and endocrinologists is fundamental for the disease control.

Anti-HIV Agents↗

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

Lipodystrophy syndrome in children infected with human immunodeficiency virus.

Lipodystrophy syndrome (LDS), a fat-wasting condition commonly reported in adults infected with human immunodeficiency virus (HIV), has been linked to the use of antiretroviral agents. Recently, LDS was observed in children infected with HIV Little is known about the pathophysiology of this condition, although it is believed that LDS has many causes and modes of presentation. Even less is known about what long-term effects LDS will have on HIV-infected patients. Three patients who developed LDS were observed in a pediatric HIV clinic. Due to the lack of knowledge about the condition's natural course and the benefits versus risks of treatment, they were not treated specifically for LDS. Their lipid profiles, however, continue to be monitored closely twice/year.

Antiretroviral Therapy, Highly Active↗

PubMed2003

AIDS-related insulin resistance and lipodystrophy syndrome.

The recent development of highly active antiretroviral therapy (HAART) has drastically improved the life expectancy of AIDS patients, by reducing infection-related mortality. However, the prolongation of the lives of HIV-1-infected patients and/or the long-term use of novel, potent antiviral agents have generated a score of new problems and complications. Among them is the AIDS-related insulin resistance and lipodystrophy syndrome, which is observed in 30-80% of AIDS patients who are well controlled by HAART. This syndrome is associated with severe metabolic disturbances, such as carbohydrate intolerance/diabetes mellitus and dyslipidemia, which cause atherosclerotic cardiovascular disease. The etiology of this syndrome appears to be multi-factorial; other than the anti-viral drugs, hypercytokinemia and the HIV-1 infection itself, including the virally encoded molecules Vpr and Tat, could contribute to the development of these pathologic changes or increase the vulnerability of patients to the adverse effect of the therapeutic compounds. In this article, we review our current understanding of the pathogenesis and therapeutic approach of this newly emerging AIDS-associated metabolic syndrome.

Acquired Immunodeficiency Syndrome↗

PubMed2005

Regional body fat distribution in HIV-infected patients with lipodystrophy.

BACKGROUND: Objective criteria for the assessment of patients with lipodystrophy syndrome in human immunodeficiency virus infection (LDHIV) have not emerged. METHODS: We compared regional body fat changes in 13 men with severe LDHIV on protease inhibitor-inclusive antiretroviral therapy with 13 control HIV-infected men using anthropometry, dual-energy X-ray absorptiometry (DEXA), and whole-body magnetic resonance imaging (MRI). RESULTS: LDHIV patients, compared with control subjects, had thinner gluteal, suprailiac, and triceps skinfolds (p < .01) and increased waist circumference (98 +/- 5 cm vs 86 +/- 9 cm, respectively; p = .0008). DEXA studies revealed reduced lower extremity fat (12 +/- 5% vs 22 +/- 9%; p = .0006), increased head and neck fat (18 +/- 3% vs 16 +/- 1%; p = .01), and increased proportion of total body fat in the trunk (65 +/- 7% vs 53 +/- 8%; p = .0005). MRI analysis revealed reduced thigh fat (12 +/- 5% vs 22 +/- 12%; p = .01), increased dorsocervical fat depth (47 +/- 24 mm vs 19 +/- 7 mm; p = .0009), and nearly significant increase in intra-abdominal fat (218 +/- 90 cm2 vs 157 +/- 70 cm2; p = .057). Interestingly, control subjects showed a positive relationship between intra-abdominal and dorsocervical fat (r= .57, p = .04), but the LDHIV patients showed a negative relationship (r= -.55, p = .05), suggesting a novel split phenotype among LDHIV patients of either dorsocervical or intra-abdominal fat accumulation. CONCLUSIONS: We conclude that MRI provides the best tools for definition of LDHIV syndrome and reveals variable phenotypes among LDHIV patients.

Absorptiometry, Photon↗

PubMed2000

Conjugated linoleic acid supplementation reduces adipose tissue by apoptosis and develops lipodystrophy in mice.

Conjugated linoleic acid (CLA) is a naturally occurring group of dienoic derivatives of linoleic acid found in beef and dairy products. CLA has been reported to reduce body fat. To examine the mechanism(s) of CLA reduction of fat mass, female C57BL/6J mice were fed standard semipurified diets (10% fat of total energy) with or without CLA (1% wt/wt). Terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick endlabeling (TUNEL) and DNA fragmentation analysis revealed that fat-mass decrease by CLA was mainly due to apoptosis. Tumor necrosis factor (TNF)-alpha and uncoupling protein (UCP)-2 mRNA levels increased 12- and 6-fold, respectively, in isolated adipocytes from CLA-fed mice compared with control mice. Because it is known that TNF-alpha induces apoptosis of adipocytes and upregulates UCP2 mRNA, a marked increase of TNF-alpha mRNA with an increase of UCP2 in adipocytes caused CLA-induced apoptosis. However, with a decrease of fat mass, CLA supplementation resulted in a state resembling lipoatrophic diabetes: ablation of brown adipose tissue, a marked reduction of white adipose tissue, marked hepatomegaly, and marked insulin resistance. CLA supplementation decreased blood leptin levels, but continuous leptin infusion reversed hyperinsulinemia, indicating that leptin depletion contributes to the development of insulin resistance. These results demonstrate that intake of CLA reduces adipose tissue by apoptosis and results in lipodystrophy, but hyperinsulinemia by CLA can be normalized by leptin administration.

Adipose Tissue↗

PubMed2003

Insulin resistance and lipodystrophy in mice lacking ribosomal S6 kinase 2.

The p90 ribosomal S6 kinase 2 (RSK2) is a serine/threonine kinase with high expression levels in adipose tissue. Numerous in vitro studies show that RSK2 is activated by a broad number of cellular stimuli and suggest that RSK2 is involved in the regulation of a variety of cellular processes. However, the physiological role of RSK2 still remains elusive. We therefore generated rsk2 knockout (KO) mice to better understand the function of RSK2 in vivo. Birth weights of RSK2 KO mice are normal, but the body weight is reduced with age, as compared with wild-type littermates. We found that the difference in body weight was largely caused by a specific loss of white adipose tissue that is accompanied by reduced serum levels of the adipocyte-derived peptide, leptin. KO mice also have impaired glucose tolerance and elevated fasting insulin and glucose levels that are restored following administration of low amounts of leptin, which do not affect food intake. We conclude that RSK2 plays a novel and an important role in regulation of adipose mass in mice and speculate that the reduction in fat tissue may negatively affect insulin sensitivity, as observed in human lipodystrophy, through reduced levels of adipocyte-derived factors, such as leptin.

Adipose Tissue↗

PubMed2000

Skeletal muscle morphology and exercise response in congenital generalized lipodystrophy.

OBJECTIVE: Congenital generalized lipodystrophy (CGL) is an autosomal recessive genetic disorder characterized by almost complete absence of adipose tissue, muscular appearance, and severe insulin resistance since birth. We investigated whether insulin resistance in CGL patients is associated with abnormal muscle morphology and whether increased muscularity imparts increased muscle strength and exercise capacity RESEARCH DESIGN AND METHODS: We obtained quadriceps muscle biopsies to study muscle fiber types and capillary density in three African-American women (aged 17-20 years) with CGL. We also assessed quadriceps muscle strength, muscle metabolism, and maximal O2 consumption in the patients. RESULTS: Quadriceps muscle biopsies revealed a markedly higher percentage of type II (fast-twitch glycolytic) muscle fibers in patients with CGL versus sedentary young women (75-78 vs. 47-57%, respectively). The capillary-to-fiber ratio (2.7-3.0), however, was normal. Cross-sectional areas of type I (slow-twitch oxidative) (1,262-2,685 microm2) and type II (2,304-3,594 microm2) fibers were far below the normal values (3,811-4,310 and 3,115-4,193 microm2, respectively), suggesting muscle hyperplasia but not hypertrophy The quadriceps muscle strength, as measured by Cybex, was below average; the maximal O2 consumption (23-32 ml x kg(-1) x min(-1)) was also below average. 31P nuclear magnetic resonance spectroscopy of the forearm muscles revealed normal pH and metabolic responses to static and dynamic exercises. CONCLUSIONS: We conclude that insulin resistance in patients with CGL is associated with an increased proportion of type II muscle fibers but not reduced capillary density. Increased muscularity in CGL is due to muscle hyperplasia and is not associated with increased muscle strength.

Adipose Tissue↗

PubMed2003

Risk factors for diabetes in familial partial lipodystrophy, Dunnigan variety.

OBJECTIVES: Familial partial lipodystrophy, Dunnigan variety (FPLD), is an autosomal dominant disorder due to missense mutations in the lamin A/C (LMNA) gene encoding nuclear lamina proteins. It is characterized by loss of subcutaneous fat from the extremities and trunk and accumulation of fat in the head and neck region beginning at puberty. Patients with FPLD are predisposed to metabolic complications of insulin resistance such as diabetes. We sought to identify risk factors for diabetes in patients with FPLD. RESEARCH DESIGN AND METHODS: A cross-sectional study comparing clinical, biochemical, and anthropometric variables and LMNA genotypes in FPLD patients with and without diabetes. RESULTS: We studied 52 women and 24 men with FPLD from 18 different families. Twenty-eight women (54%) but only four men (17%) had diabetes (P < 0.001); therefore further comparisons were mostly limited to women. Compared with women without diabetes, those with diabetes had higher BMI (median values 23 vs. 24 kg/m(2), respectively; P = 0.03), increased chin skinfold thickness (10 vs. 20 mm; P = 0.001), lower rates of nulliparity (60% vs. 28%; P = 0.04), and higher levels of fasting serum triglycerides (2.4 vs. 3.5 mmol/l; P < 0.001) but similar serum leptin levels (3.4 vs. 3.6 ng/ml; P = 0.9). The prevalence of diabetes was not related to age, menopausal status, family history of type 2 diabetes in unaffected relatives, or LMNA genotype. CONCLUSIONS: We conclude that increased adiposity as reflected by excess subcutaneous fat accumulation in the chin region and parity may predispose women with FPLD to develop diabetes.

Adipose Tissue↗

PubMedDate not supplied

Hepatic ultrastructure in congenital total lipodystrophy with special reference to peroxisomes.

The liver of an 8-year-old boy with congenital total lipodystrophy was investigated by means of catalase cytochemistry and morphometry. Comparison was made with eight human control livers. Light microscopy revealed cirrhosis and steatosis. Ultrastructural changes included lipid droplets with lamellae in the periphery, cup-shaped mitochondria, and nuclear pseudoinclusions. Peroxisomes were significantly increased in number but were not enlarged; they displayed various shapes and showed a moderate heterogeneity in catalase activity. A correlation between increased lipids and peroxisomal proliferation is suggested.

Child↗

PubMed2000

Efficacy and safety of troglitazone in the treatment of lipodystrophy syndromes.

BACKGROUND: Troglitazone promotes adipocyte differentiation in vitro and increases insulin sensitivity in vivo. Therefore, troglitazone may have therapeutic benefit in lipoatrophic diabetes. OBJECTIVE: To determine whether troglitazone ameliorates hyperglycemia and hypertriglyceridemia or increases fat mass in lipoatrophic patients. DESIGN: Open-labeled prospective study. SETTING: United States and Canada. PATIENTS: 20 patients with various syndromes associated with lipoatrophy or lipodystrophy. INTERVENTION: 6 months of therapy with troglitazone, 200 to 600 mg/d. MEASUREMENTS: Levels of hemoglobin A1c triglycerides, free fatty acids, and insulin; respiratory quotient; percentage of body fat; liver volume; and regional fat mass. RESULTS: In the 13 patients with diabetes who completed 6 months of troglitazone therapy, hemoglobin A1c levels decreased by a mean of 2.8% (95% CI, 1.9% to 3.7%; P < 0.001). In all 19 study patients, fasting triglyceride levels decreased by 2.6 mmol/L (230 mg/dL) (CI, 0.7 to 4.5 mmol/L [62 to 398 mg/dL]; P = 0.019) and free fatty acid levels decreased by 325 micromol/L (CI, 135 to 515 micromol/L; P = 0.035). The respiratory quotient decreased by a mean of 0.12 (CI, 0.08 to 0.16; P < 0.001), suggesting that troglitazone promoted oxidation of fat. Body fat increased by a mean of 2.4 percentage points (CI, 1.3 to 4.5 percentage points; P = 0.044). Magnetic resonance imaging showed an increase in subcutaneous adipose tissue but not in visceral fat. In one patient, the serum alanine aminotransferase level increased eightfold during the 10th months of troglitazone treatment but normalized 3 months after discontinuation of treatment Liver biopsy revealed an eosinophilic infiltrate, suggesting hypersensitivity reaction as a cause of hepatotoxicity. CONCLUSION: Troglitazone therapy improved metabolic control and increased body fat in patients with lipoatrophic diabetes. The substantial benefits of troglitazone must be balanced against the risk for hepatotoxicity, which can occur relatively late in the treatment course.

Adipose Tissue↗

PubMed1976

[Dermolipectomy for the reduction of redundant skin and local lipodystrophy].

Operative techniques by Pitanguy for abdominoplasty and fat reduction in trochanteric lipodystrophy and their results are presented. In comparison to most other procedures this technique shows the following advantages: low and horizontal final scar; the possibility to remove periumbilical fat and skin by transposition of the umbilicus; a diastasis of the mm.recti can be corrected and infraumbilical scars can be removed. The technique of excision described by Pitanguy for reduction of trochanteric fat is a simple and safe procedure leading to satisfying cosmetic results. During the past 18 months we treated 20 patients using Pitanguys technique. The results are definitely better than those achieved with other methods.

Abdomen↗

PubMed1976

The myopahtology of congenital generalized lipodystrophy light and electron microscopic observations.

The light and electron microscopic myopathology in five patients with congenital generalized lipodystrophy consist of variation in fiber size, ringbenden, various degrees of fiber degeneration and fragmentation, accumulation of glycogen, aggregation of mitochondria. streaming of Z line, myofilamentous inclusions and dilatation of sarcoplasmic reticulum profiles. The light microscopic myopathology in the five patients is compared with the few available observations in the literature. No reports of electron microscopy of muscle in this syndrome are available in the literature. No reports of electron microscopy of muscle in this syndrome are available in the literature. It is concluded that the myopathologic features are nonspecific in nature and may be secondary to the diencephalic disturbance which is known to occur in this syndrome.

Adolescent↗

PubMed1999

[Lipodystrophy: a complication of protease inhibitors in HIV seropositive patients].

Indinavir-induced lipodystrophy constitutes a new complication of this therapeutic category. It is characterized by loss of fat from the face and limbs and accumulation of fat in the abdominal wall (possibly simulating an abdominal mass), but also in the abdominal cavity (retroperitoneum, greater omentum, mesocolon, mesentery). This complication, whose frequency is currently assessed to be between 24 to 64%, occurs an average of 10 months after starting treatment. It is often accompanied by laboratory abnormalities, such as hypertriglyceridaemia, hypercholesterolaemia or insulin resistance. The pathophysiology and long-term consequences of this complication are still poorly understood.

Anti-HIV Agents↗

PubMed1999

Suction-assisted lipectomy for lipodystrophy syndromes attributed to HIV-protease inhibitor use.

The addition of HIV-protease inhibitors to the arsenal of therapies for the treatment of HIV infection has resulted in significant suppression of viral load such that HIV-positive individuals experience reduced morbidity and extended life expectancy. Recently, a number of syndromes have been described involving abnormal fat distribution that may be associated with prolonged HIV-protease inhibitor therapy. These syndromes include hypertrophy of the cervicodorsal fat pad ("buffalo hump"); a tendency toward increased central adiposity ("protease paunch"); adiposity in the submental, mandibular, and lateral cheek regions of the face; and hypertrophy of adipose tissue in the breast in women. A peripheral lipodystrophy, or fat-wasting, in the extremities and face (particularly the malar and nasolabial fold regions) has also been observed. As these patients live longer and healthier lives, many are beginning to seek surgical correction of the disfigurements. In this regard, we present a review of the literature regarding these recently described syndromes to familiarize plastic and reconstructive surgeons with the unique deformities encountered in this ever-increasing patient population. We also present our results with suction-assisted lipectomy for treatment of these deformities. Physical findings, pathogenesis, and surgical management are discussed.

Adult↗