Corticosteroid-induced Lipodystrophy and Adipokines

Lipodystrophy Clinical Trial

— ADIPOKINES  

Official title:

Study of Histological and Adipokines Expression Variations in Lipodystrophic Adipose Tissue During Corticosteroids-induced Lipodystrophy

Clinical Trial Details — Status: Completed

Administrative data

• NCT number: NCT00822042
• Other study ID #: P 051037
• Secondary ID: CIRC 05147
• Status: Completed
• Phase: N/A
• First received: January 13, 2009
• Last updated: February 26, 2014
• Start date: August 2006
• Est. completion date: November 2008

Study information

• Verified date: January 2009
• Source: Assistance Publique - Hôpitaux de Paris
• Contact: n/a
• Is FDA regulated: No
• Health authority: France: Ministry of Health
• Study type: Observational

Clinical Trial 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

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.

Recruitment information / eligibility

• Status: Completed
• Enrollment: 32
• Est. completion date: November 2008
• Est. primary completion date: October 2008
• Accepts healthy volunteers: No
• Gender: Both
• Age group: 18 Years and older

Eligibility

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

Study Design

Observational Model: Cohort, Time Perspective: Prospective

Related Conditions & MeSH terms

• Lipodystrophy

Intervention

Other:
• Samples and procedures
Scanner, histomorphometry : at the inclusion and M3 visits whole blood samples, cytoponction : at the inclusion and M3 visits

Locations

Country	Name	City	State
France	Hopital Saint-Antoine	Paris

Sponsors (1)

Lead Sponsor	Collaborator
Assistance Publique - Hôpitaux de Paris

Country where clinical trial is conducted

France, 

Outcome

Type	Measure	Description	Time frame	Safety issue
Primary	Expression of adiponectin in adipocytes		at the inclusion and M3 visits	No
Secondary	Plasma levels of adiponectin, leptin, sTNFR1, and IL6		at the inclusion and M3 visits	No
Secondary	Histological morphology of adipocytes		at the inclusion and M3 visits	No
Secondary	Expression of leptin, IL6, TNFa, 11bHSD1, SREBP1c and PPARg in adipocytes		at the inclusion and M3 visits	No