Context: Glucocorticoid therapy may result in adipose tissue redistribution of unknown pathophysiology.
Objectives: To evaluate the effects of glucocorticoids on adipokine levels and adipose tissue inflammation. To compare the results in patients with or without glucocorticoid-induced lipodystrophy (GIL) after 3 months of therapy.
Design and setting: Prospective monocentric study.
Patients: Adult patients initiating systemic, high-dose prednisone therapy for at least 3 months. Blood samples and subcutaneous abdominal adipose tissue biopsies were collected at baseline and month 3. The presence of GIL after 3 months of therapy was assessed using standardized photography.
Results: Thirty-two patients were enrolled. Blood samples and subcutaneous abdominal adipose tissue were available at baseline and month 3 for 30 patients [median age: 61 (38-79) years, 77% women]. Among those 30 patients, 15 were classified as GIL+ and 15 were GIL- at month 3. Between baseline and month 3, adiponectin and leptin levels increased in the overall population while the level of resistin remained unchanged. At baseline, leptin level was higher [19.3 (8.3-31.1) vs 4.5 (2.4-11.3) μg/l, P = 0.006] and resistin level lower [7.1 (6.3-12.4) vs 10.4 (8.0-21.7) μg/l, P = 0.05] in GIL+ than in GIL- patients. Baseline leptin level was predictive of GIL occurrence. Receiver operating characteristic curve analysis demonstrated that the best diagnostic accuracy was obtained with a baseline leptin cut-off of 5.9 μg/l (sensitivity: 93%, specificity: 60%). At month 3, leptin and adiponectin levels increased more in the GIL+ than in the GIL- group, as did the number of anti-inflammatory M2 macrophages in subcutaneous abdominal fat.
Conclusion: Glucocorticoid-induced lipodystrophy is associated with a different adipokine profile both before and after glucocorticoid therapy. Serum leptin level prior to glucocorticoid therapy is highly predictive of GIL occurrence.
© 2012 Blackwell Publishing Ltd.