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Corticosteroid-induced Lipodystrophy and Adipokines

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

Status
Completed
Phases
Unknown
Study type
Observational
Source
ClinicalTrials.gov
Registry ID
NCT00822042
Acronym
ADIPOKINES
Enrollment
32
Registered
2009-01-14
Start date
2006-08-31
Completion date
2008-11-30
Last updated
2014-02-27

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

Lipodystrophy

Keywords

Lipodystrophy, Adipokines, Glucocorticoids, Patients with glucocorticoids

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.

Interventions

OTHERSamples and procedures

* Scanner, histomorphometry : at the inclusion and M3 visits * whole blood samples, cytoponction : at the inclusion and M3 visits

Sponsors

Assistance Publique - Hôpitaux de Paris
Lead SponsorOTHER

Study design

Observational model
COHORT
Time perspective
PROSPECTIVE

Eligibility

Sex/Gender
ALL
Age
18 Years to No maximum
Healthy volunteers
No

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

Design outcomes

Primary

MeasureTime frame
Expression of adiponectin in adipocytesat the inclusion and M3 visits

Secondary

MeasureTime frame
Plasma levels of adiponectin, leptin, sTNFR1, and IL6at the inclusion and M3 visits
Histological morphology of adipocytesat the inclusion and M3 visits
Expression of leptin, IL6, TNFa, 11bHSD1, SREBP1c and PPARg in adipocytesat the inclusion and M3 visits

Countries

France

Outcome results

None listed

Source: ClinicalTrials.gov · Data processed: Feb 4, 2026