Introduction: Higher cortisol levels and, in particular, hyperactivity of the HPA axis might play a role in the development of MS at least in adults. Data on the pediatric age are scanty.
Aim of our study was to evaluate ACTH and cortisol association with MS, its components, phenotypic parameters, family history of metabolic derangements in pediatric obesity.
Methods: Cross-sectional study. 271 Caucasian overweight or obese children and adolescents (age range: 1.818.0 years) were evaluated for: family history, detailed clinical examinations, fasting morning ACTH, cortisol, glucose, insulin, lipid profile and OGTT test; HOMA, ISI and QUICKI were calculated. We divided patients according to pediatric NCEP criteria for MS.
Results: 62.4% of the subjects had MS (73.9% had hypertension, 58.4% HDL-cholesterol <10th percentile, 23.1% triglycerides >90th percentile, and 8.2% IFG, IGT or type 2 diabetes). Children and adolescents with MS presented higher ACTH (P<0.0001) and cortisol levels (P<0.03) than those without MS. Increasing numbers of features of MS were associated with higher ACTH, but not cortisol, also when adjusted for confounding factors (P<0.001). Subjects with IFG, IGT or type 2 diabetes, or altered HDL-cholesterol or triglycerides respect to the MS cut-offs had higher ACTH, but not cortisol levels (P<0.01). Subjects with hypertension had increased levels of both ACTH and cortisol levels (P<0.02) if the cut-off was 95th percentile, and only cortisol (P<0.05) if the cut-off was reduced to 90th percentile as suggested by MS criteria. ACTH and cortisol levels were associated with insulin resistance. Subjects with a family history of hypertension (P<0.003) had higher cortisol levels.
Conclusions: In obese pediatric subjects, MS is associated with higher ACTH and cortisol levels. The features of MS could be differently modulated by ACTH and cortisol. Cortisol secretion seems mainly involved in hypertension and its family history.
Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.
Funding: This research did not receive any specific grant from any funding agency in the public, commercial or not-for-profit sector.
05 - 09 May 2012
European Society of Endocrinology