4.7 Article

Persistent Body Fat Mass and Inflammatory Marker Increases after Long-Term Cure of Cushing's Syndrome

Journal

JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
Volume 94, Issue 9, Pages 3365-3371

Publisher

ENDOCRINE SOC
DOI: 10.1210/jc.2009-0766

Keywords

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Funding

  1. Instituto de Salud Carlos III (Fondo de Investigacion Sanitaria) [05/0448]
  2. Comissio Interdepartamental de Recera i Innovacio Tecnologica [2003FI00102]

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Objective: Although increased central fat mass is characteristic of active Cushing's syndrome (CS), little is known about body composition and secretion of adipokines after long-term recovery of CS. The aim of this study was to evaluate central fat mass and its correlation with adipokines and cardiovascular risk factors in patients after long-term remission of CS. Methods: Thirty-seven women with CS in remission (27 of pituitary and 10 of adrenal origin; mean age, 50 +/- 14 yr; mean time of hormonal cure, 11 +/- 6 yr) were enrolled and compared to 14 women with active CS and 85 gender-, age-, and body mass index-matched healthy controls. Total and trunk fat mass were measured by dual-energy x-ray absorptiometry scanning. Laboratory parameters and adipokine levels [including adiponectin, visfatin, soluble TNF alpha-receptor 1 (sTNF-R1), sTNF-R2, and IL-6] were measured. Results: Cured CS patients had more total and trunk fat mass than controls. Cured and active CS had higher levels of sTNF-R1 and IL-6 and lower adiponectin levels than controls. Higher insulin levels and blood pressure in both groups of CS patients and higher apolipoprotein B in cured CS were observed compared to controls. sTNF-R1 correlated positively with percentage of trunk fat mass and remained significant after adjusting for anthropometric parameters. Conclusion: Despite long-term cure, patients who have suffered CS exhibit persistent accumulation of central fat, as in active hypercortisolemia, with the consequent unfavorable adipokine profile, leading to a state of low-grade inflammation. This situation determines a persistent and increased cardiovascular risk in these patients. (J Clin Endocrinol Metab 94: 3365-3371, 2009)

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