Active clinical trials for "Lipodystrophy"

SHARE: Simple HAART with Abacavir, Reyataz, and Epivir

The sample will be divided into two groups:- - Control group which will include 60 adult individuals between 18 and 35 years old who have BMI between 19 and 25, not complaining of any thigh contour deformities or skin redundancy with no history of body weight fluctuations. This group will be divided into two subgroups, 30 males and 30 females. The following measurements will be recorded :- Weight, height, thigh length, hip circumference, maximum buttocks circumference, upper thigh, middle thigh and lower thigh circumferences. - Patient group which will include 40 patients suffering from thigh lipodystrophy and contour deformities who will undergo surgical intervention after their assessment. After assessment, one of the following techniques will be selected:- Liposuction only. thigh lift. Liposuction assisted thigh lift.

Randomized controlled parallel open-label study in persons living with HIV. The aim is to study weight changes in patients switching from a dolutegravir and tenofovir disoproxil containing regimen to either a dolutegravir or tenofovir disoproxil free regimen.

5 year, open-label study to evaluate safety of SCULPTRA on the signs of lipoatrophy of the face in at least 100 evaluable subjects with human immunodeficiency virus.

In this study, eligible patients with the medical indications (facial lipoatrophy, morphological asymmetry of the face, or debilitating scars) will be treated with Princess® FILLER, and then will return for follow-up assessments 2, 4 and 24 weeks after the treatment. A touch-up treatment may be done 2 weeks after the treatment.

In this study, eligible patients with the medical indications (facial lipoatrophy, morphological asymmetry of the face, or debilitating scars) will be treated with Princess® VOLUME, and then will return for follow-up assessments 2, 4, 24, and 36 weeks after the treatment. A touch-up treatment may be done 2 weeks after the treatment if deemed appropriate by the Investigator.

This proposal will evaluate the glucocorticoid mediated changes in body fat distribution and metabolism that occur in patients with Cushing's disease. The objective is to identify the mechanisms that influence both the accumulation of lipodystrophic fat and also the changes in energy expenditure and metabolism that accompany them. The study is designed to determine if the high cortisol and AgRP levels in the blood of people living with Cushing's syndrome, either from taking steroid medications or from tumors, impact body fat and metabolism by turning off brown fat, which is a type of fat that increases one's metabolism.

White adipose tissue-related diseases spread from excess (obesity) to lack (lipoatrophies) through aberrant distribution (lipodystrophies), these 3 different disorders being paradoxically able to induce a metabolic insulin resistance syndrome. The respective part of quantitative and qualitative anomalies of adipose tissue, gluco- and lipo-toxicity, liver and muscle insulin resistance, low-grade fat inflammation and immune alterations are not perfectly understood in the metabolic syndrome yet. Therefore, the aim of this study is to assess different cytokines, especially interleukin 7, and metabolic parameters as well as fat mass distribution with DEXA and RMN, in different models of fat distribution, including normal-weight, obese and lipodystrophic patients. A plasma serum, gene and adipose tissue bank will be constituted at the same time to improve our knowledge in disorders linking fat mass, insulin resistance and immunity, especially in lipodystrophies, a rare monogenic model of insulin resistance.

Lipodystrophy Connect is an online survey tool designed to collect demographic data and health information from individuals with Lipodystrophy.

Hypothesis: systemic therapy with corticosteroid induces morphological changes (e.g., moon face, buffalo neck) called lipodystrophy (LD). We hypothesize that this LD is associated with variation of adipocytokines (e.g., adiponectin, leptine, IL6) levels Primary objective: To show a 50% decrease in adipocytes adiponectin's expression in patients who developed LD versus those who did not developed LD during the first 3 months of a systemic therapy with corticosteroids Secondary objectives: To look for differences in the mRNA expression of 11bHSD1, SREBP1c and PPARg in fat samples of patients before and after treatment with systemic corticosteroids and between LD+ and LD-patients To compare the fat morphology before and after treatment with glucosteroids