Clinical trial NCT00822042: Corticosteroid-induced Lipodystrophy and Adipokines
Official title: Study of Histological and Adipokines Expression Variations in Lipodystrophic Adipose Tissue During Corticosteroids-induced Lipodystrophy
Study type: OBSERVATIONAL
Overall status: COMPLETED
Conditions: Lipodystrophy
Keywords: Lipodystrophy
Adipokines
Glucocorticoids
Patients with glucocorticoids
Lead sponsor: Assistance Publique - Hôpitaux de Paris
Sponsor class: OTHER
First posted: 2009-01-14
Enrollment: 32
Sex: ALL
Minimum age (years): 18
Standard ages: ADULT
OLDER_ADULT
Accepts healthy volunteers: no
Observational model: COHORT
Time perspective: PROSPECTIVE
Sampling method: NON_PROBABILITY_SAMPLE
Study population: Patients consulting in participating units

Brief summary: 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

Detailed description: Design: Monocentric, cross-sectional analytical study

Subjects: 32 HIV-free and Cushing disease-free adult patients for whom a prolonged treatment (³3months) with glucosteroids (³ 0.5 mg/kg/day) is initiated

Methods: At treatment initiation and 3 months after: comparison of fat sample mRNA expression of adipokines (adiponectin, leptin, IL6, TNFa), 11bHSD1, SREBP1c and PPARg, fat morphology and seric concentrations of adiponectin, leptin, IL6, sTNFR1 between patients LD+ and patients LD-. The diagnosis of LD will be performed by 3 experts using patients photographs

Aims of this study:

* To gain a better understanding of the pathophysiology of glucosteroids-induced LD
* To compare this pathophysiology to the one of HIV-associated LD for which the hypothesis of a local, cellular, hypercorticism has been put forward and for which related treatment have been prescribed.

Eligibility criteria: Inclusion Criteria:

* adult patient
* starting therapy with prednisone
* corticosteroid therapy lasting more than 3 months
* baseline prednisone dosage \>= 0.5 mg/kg/d

Exclusion Criteria:

* Cushing disease
* HIV +Pregnancy
* Recent weight lost (\> 5% of the usual weight)
* Therapy with glucocorticosteroids during the past 6 months

Primary outcomes:
measure: Expression of adiponectin in adipocytes
timeFrame: at the inclusion and M3 visits
Secondary outcomes:
measure: Plasma levels of adiponectin, leptin, sTNFR1, and IL6
timeFrame: at the inclusion and M3 visits
measure: Histological morphology of adipocytes
timeFrame: at the inclusion and M3 visits
measure: Expression of leptin, IL6, TNFa, 11bHSD1, SREBP1c and PPARg in adipocytes
timeFrame: at the inclusion and M3 visits
Other outcomes:
Locations:
city: Paris
country: France
facility: Hopital Saint-Antoine
Study officials:
affiliation: Assistance Publique - Hôpitaux de Paris
name: Laurence FARDET, MD PhD
role: PRINCIPAL_INVESTIGATOR
References: