Leptin and adiponectin in children and young persons with congenital adrenal hyperplasia.

OBJECTIVES

Patients with congenital adrenal hyperplasia (CAH) have increased prevalence of metabolic problems. We studied adiponectin, leptin and resistin in children with CAH, in relation to BMI, treatment, hormonal and metabolic biomarkers.

DESIGN AND METHODS

We analysed 101 patients with 21-hydroxylase deficiency (54 females, 13.0 ± 2.92 years) from 13 centres in the United Kingdom, and 83 sex- and age-matched controls. Blood parameters (leptin, adiponectin, resistin, metabolic and hormonal markers) were measured in fasted state, between 09:00 and 11:00, after the first glucocorticoid (GC) dose.

RESULTS

A difference in adipokines between patients and controls was only found for leptin in males (patients > control, P = .033). In patients and controls, leptin had a positive relationship with BMI-SDS (P < .001). However, adiponectin decreased with the BMI only in patients (P  <  .001). Contrary to published evidence on the effect of synthetic steroids on leptin, in our cohort, leptin decreased with the increasing first daily hydrocortisone (HC) dose (Log10Leptin  =  4.1- 0.08xfirstGCdose (mg/m2), P  =  .009) but not with the total daily dose. When correcting for BMI, a positive relationship between leptin and insulin was only found in controls (P  <  .001). Adiponectin decreased with steroid precursor and androgen concentrations (17-hydroxyprogesterone, androstenedione, testosterone, 11-hydroxyandrostenedione, 11-ketotestosterone) in patients.

CONCLUSION

Our findings indicate a decrease in leptin with the HC dose, consistent with a detrimental effect of glucocorticoid on satiety and hunger pathways in CAH. Adiponectin was decreased in patients with increased androgens concentrations, suggesting it may be used as an indicator of metabolic risk associated with poor hormonal CAH control.