ESPE Abstracts (2015) 84 P-2-182

ESPE2015 Poster Category 2 Adrenals (38 abstracts)

Insulin Sensitivity and Adipocytokynes in Children with Classical Congenital Adrenal Hyperplasia

Nicola Improda , Manuela Cerbone , Andrea Esposito , Flavia Barbieri , Raffaella Di Mase , Donatella Capalbo & Mariacarolina Salerno


Federico II University, Department of Medical Traslational Sciences, Paediatric Endocrinology Section, Naples, Italy


Background: Recent studies demonstrate that children with Congenital Adrenal Hyperplasia (CAH) may develop visceral adiposity and insulin-resistance. Data on adipocytokines are scanty and contradictory.

Objective: To evaluate leptin and adiponectin concentrations in CAH adolescents and investigate their correlation with glucocorticoids and hormonal and metabolic profile.

Methods: Leptin, adiponectin, insulin and HOMA were evaluated in 21 classical CAH patients, aged 13.5±2.5 years, and 21 healthy subjects matched for age, sex and pubertal status. Anthropometric and hormonal parameters were also measured.

Results: CAH patients exhibited higher BMI SDS, waist circumference and waist-to-height ratio than controls (1±0.9 vs −0.2±1.4, P=0.002; 83.6±11 vs 73±13 cm, P=0.01; 0.55±0.07 vs 0.4±0.06 cm, P=0.008), thus suggesting a visceral pattern of adiposity. Compared to controls, CAH patients had higher fasting insulin (11.4±7.5 vs 9.4±14 uU/ml, P=0.01), HOMA (2.3±1.3 vs 1.2±0.9, P=0.05), leptin (15.06±8.9 vs 7.23±6 ng/ml, P=0.003) and leptin/adiponectin ratio (1.9±2.2 vs 0.76±0.74, P=0.03). This difference in leptin and leptin/adiponectin ratio did not persist after correction for waist circumference, but they were still significantly higher after correction for BMI SDS. Adiponectin levels and lipid profile were comparable between the two groups. Leptin and leptin/adiponectin ratio in CAH patients were positively correlated BMI SDS (r=0.5, P=0.03 and r=0.6, P=0.007, respectively) and weist-to-height ratio (r=0.67, P=0.001 and r=0.7, P=0.0009, respectively); and negatively correlated to the current hydrocortisone dosage (r=−0.5, P=0.02 and r=−0.6, P=0.003, respectively). No correlation was found between leptin or leptin/adiponectin ratio and androgens or cumulative hydrocortisone dosage in the last three years.

Conclusion: Children and adolescents with CAH may develop visceral adiposity, hyperinsulinism and insulin-resistance. Our results show that high leptin levels in CAH reflect increased adiposity; however the impact of sex and gender needs to be further investigated on larger cohorts. Finally, our data suggest that long-term hydrocortisone treatment does not affect leptin levels.

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