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

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.

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

Patients consulting in participating units