Active clinical trials for "Lipodystrophy"

To evaluate the prevalence of lipodystrophy syndrome in patients receiving currently available antiretroviral drugs, and the prevalence of associated metabolic syndrome in HIV-infected patients with a previous diagnosis of lipodystrophy syndrome, according to the severity of fat accumulation and antiretroviral drug use.

Cardiac steatosis is increased among individuals with HIV, and may predispose to cardiac mechanical dysfunction and subsequent heart failure. The pathogenesis and treatment of cardiac steatosis is not well understood. The investigators have previously shown that perturbed growth hormone (GH) secretion in HIV contributes to ectopic fat accumulation in the viscera and the liver. Moreover, the investigators have found that augmentation of endogenous GH secretion with the FDA-approved medication tesamorelin reduces visceral and hepatic fat. In this longitudinal observational study, the investigators will examine patients with HIV and abdominal fat accumulation who either plan or do not plan to initiate tesamorelin prescribed clinically. The investigators hypothesize that blunted GH secretion in HIV is associated with cardiac steatosis. The investigators also hypothesize that use of tesamorelin for 6 months is associated with a reduction in intramyocardial fat and preserved cardiac function.

The hypotheses of this study were that: HIV lipodystrophy is associated with psychological morbidity relating to body image, anxiety and depression. Treatment of HIV lipodystrophy using autologous fat transfer, polylactic acid or Bio-alcamid, is associated with an improvement in psychological morbidity and anatomical volume of treated areas. The DI3D system is a valid and reproducible method of recording and measuring facial 3-D volume.

The purpose of this study is to assess the prevalence of metabolic and physical abnormalities in HIV infected (via mother-to-child transmission) and uninfected children and youth. Metabolism, body composition, bone density, and other factors will be assessed in relationship to participants' exposure to highly active antiretroviral therapy (HAART).

Familial Partial Lipodystrophy type 2 (FPLD2) is a heterogeneous group of rare lipodystrophy due to autosomal dominant mutation in LMNA encoding Lamin A/C. Lamins A and C form with the B-type lamins the lamina network underlying the nuclear envelope. Lamins are major components that provide structural and mechanical stability for the nucleus ubiquitously. Lamins are also key epigenetic regulator. Mutations in LMNA are involved in different inherited pathologies as Emery-Dreifuss muscular Dystrophy, Limb Girdle muscular dystrophy, dilated cardiomyopathy and conduction system disease, Charcot Marie Tooth Disorder type 2, mandibuloacral dysplasia, Hutchinson Gilford progeria and Dunnigan-type-familial partial lipodystrophy (FPLD2). Inherited lipodystrophy prevalence is reported around 1.3 to 10 cases per million worldwide and FPLD2 is the most frequent of all. Nevertheless, recent reports with systematic screening in all non-obese patients with type 2 diabetes or metabolic syndrome found higher prevalence of lipodystrophy up to 1/7000 subjects. FPLD2 remain a rare group of disease and only relatively small and heterogeneous cohorts of patients are reported. For this reason it is difficult to fully decipher all aspects of this rare group of diseases. The "typical" FPLD2 is associated with missense mutation affecting the arginin residue in position 482 (p.R482Q,p.R482W,p.R482L). Patients harbouring mutation in other spot are considered to have "atypical" lipodystrophy. The "typical" FPLD2 start around puberty with progressive subcutaneous fat loss in upper limbs, gluteo-femoral adipose tissue and trunk and fat accumulation in the cervicofacial area, neck, upper trunk, labia majora and visceral fat. Resulting from the inability to store fat, patients affected by inherited lipodystrophy develop severe metabolic syndrome and its complications: type 2 diabetes (DT2), dyslipidaemia, nonalcoholic fatty liver disease (NAFLD) and premature cardiovascular disease (CVD). In 2006 a specific mutation of LMNA has been described in a patient originated from La Réunion living in France mainland. To date this mutation have only been reported in patient native from La Réunion and is called 'Reunionese' mutation and consist in a G insertion after nucleotide 5670 (codon 654) in the prelamin-A-specific exon 11 (g.5670_5671insG) p.T655fsX49 that lead to a longer and non farnelysated prelamin A lacking the C-terminal CSIM motif. As a result, nonfarnelysated mutated prelamin A accumulated in the cells leading to oxidative stress and premature cell senescence. The 'Reunionese' mutation is expressed in 2 forms either homozygous or heterozygous. Homozygous patients present with more severe phenotype and cardiac laminopathy. The aim of our study is to update the characterization of the patients diagnosed with the 'Reunionese' mutation. The investigators report here the largest cohort of patient with FPLD2 due to one single LMNA mutation either homozygous or heterozygous.

Metreleptin was approved in the United States as adjunct to diet as replacement therapy to treat the complications of leptin deficiency in patients with congenital or acquired generalized lipodystrophy in February 2014. The approval was based on results obtained in 2 open-label, investigator-sponsored studies (Studies 991265 and 20010769) conducted at the National Institutes of Health (NIH) to evaluate the safety and efficacy of metreleptin treatment in patients with lipodystrophy and 1 treatment IND (FHA101/MB002-002/MB002-002) conducted by Bristol-Myers Squibb on behalf of AstraZeneca (BMS/AZ) in patients with diabetes mellitus and/or hypertriglyceridemia related to lipodystrophy. These studies enrolled patients with lipodystrophy including both generalized and partial lipodystrophy. Although the marketing authorization restricted the indication to patients with generalized lipodystrophy, meaningful clinical benefit was achieved in a subset of patients with partial lipodystrophy, and these patients from FHA101/MB002-002 form the basis of the request for ongoing treatment under expanded access.

Background: Several studies have reported increased resting energy expenditure (REE) in people living with HIV/AIDS possibly due to changes in body composition that occurs in HIV lipodystrophy syndrome. The aim of this study was to evaluate the influence of the use of lipid-lowering drugs in resting energy expenditure (REE) and total energy expenditure (TEE) in patients seropositive for HIV in treatment of lipodystrophy.

HIV infected subjects receiving antiretroviral treatment for greater than 6 years with be evaluated for clinical lipoatrophy and mitochondrial function after switching nucleoside analogues from stavudine (d4T) to tenofovir treatment and after 4. Hypothesis: Tenofovir therapy will increase peripheral fat content as assessed by DEXA and mitochondrial function at 48 weeks.

The purpose of this study is to learn how changes in body build affect the lives of people taking anti-HIV medications. By learning this, a set of questions can be created to help understand how changes in body build and image affect people living with HIV infection. A set of questions used to measure body image might be useful in future HIV studies. It may help doctors understand patient concerns about their body image and why some patients stop taking their anti-HIV medications.

What is Impact of Amount Versus Surface Area of Liposuction on Haematological Parameters, Coagulopathy Profile and Electrolyte Balance? Liposuction involves the creation of extensive subsurface trauma, comparable in many respects to the massive injury of an internal burn. Liposuction commences with cannula aspiration of several liters of fluid-engorged adipose tissue, during which small feeder vessels are inevitably torn. Operating on multiple areas increases the area of injury regardless of whether just small amounts of fat are removed. Because many of the complications associated with large volume liposuction are related to fluid shifts and fluid balance, classifying the procedure based on the total volume removed from the patient, including fat, wetting solution, and blood, makes more sense to evaluate the damage made by the procedure. Safety and aesthetic issues define large-volume liposuction as having a 5,000-ml aspirate, mega-volume liposuction as having an 8,000-ml aspirate, and giganto-volume liposuction as having an aspirate of 12,000 ml or more.