ECE2008 Poster Presentations Neuroendocrinology (107 abstracts)
1Endocrinology Department and Center for Biomedical Research on Rare Diseases (CIBERER Unit 747), Hospital Sant Pau, Autonomous University of Barcelona, Barcelona, Spain; 2Endocrinology Department, Hospital J Trueta, Girona, Spain.
Metabolic syndrome and insulin resistance persist 5 years after remission of Cushings syndrome (CS). Adiponectin and visfatin are two adipokines highly expressed in adipose tissue. Adiponectin is reduced in obesity and insulin-resistant states; visfatin has been shown in some studies to be reduced in obesity. The aim was to evaluate visfatin and adiponectin levels, body composition, insulin resistance and prevalence of metabolic syndrome in a cohort of women with long-term remission of CS, and compare it with that of controls matched for sex, age and BMI.
Methods: We report 37 women in long-term remission of CS and 72 controls, in whom body composition was measured by dual-energy X-ray absorptiometry scanning. Circulating adiponectin, visfatin, insulin and lipid profile were measured. Insulin resistance was calculated using the formula of the homeostasis model assessment (HOMA). Metabolic syndrome was evaluated using the NCEP ATP III criteria.
Results: Patients had been cured of hypercortisolism for 11±6 years and their current age was 50±14 years. When compared with the controls, cured CS patients had more total fat mass (39.7±7.4 vs 35.7±6.5, P<0.05) and trunk fat mass percentage (40.8±9 vs 34.3±8.3, P<0.05) and less visfatin (15.57 (8.524.5) vs 19.9 (11.259.3) μg/ml, P<0.05) and adiponectin levels (12.48 (5.0232.4) vs 18.1 (4.556.5) μg/ml, P<0.05). There were no differences in insulin, HOMA-IR and prevalence of metabolic syndrome (9%) between both groups. Visfatin negatively correlated with fat mass. No correlation between adiponectin and body composition were found.
Conclusions: Despite long-term control of hypercortisolism, patients who have suffered CS have a persistent increase in total and trunk fat mass and a reduction in circulating visfatin and adiponectin levels, which may contribute to their increased cardiovascular risk. These alterations are not related to metabolic syndrome or insulin resistance.