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Leptin and adiponectin in children and young persons with congenital adrenal hyperplasia
Irina Bacila1, Neil Richard Lawrence1, Sabah Alvi2
1Division of Clinical Medicine, School of Medicine and Population Health, University of Sheffield, Western Bank, Sheffield S10 2TH, United Kingdom.
Insights
Congenital adrenal hyperplasia (CAH) patients show decreased leptin with hydrocortisone dose, impacting hunger and satiety. Adiponectin levels in CAH correlate with androgen levels, indicating potential metabolic risk.
Area of Science:
- Endocrinology
- Pediatric Endocrinology
- Metabolic Disorders
Background:
- Congenital adrenal hyperplasia (CAH) is linked to metabolic complications.
- Adipokines like adiponectin, leptin, and resistin play roles in metabolic regulation.
- Understanding these hormones in CAH is crucial for managing associated risks.
Purpose of the Study:
- To investigate adiponectin, leptin, and resistin levels in children with CAH.
- To correlate adipokine levels with Body Mass Index (BMI), treatment, and hormonal/metabolic markers.
- To explore the relationship between hydrocortisone dosage and adipokine levels in CAH.
Main Methods:
- A cohort of 101 children with 21-hydroxylase deficiency CAH was studied.
- 83 sex- and age-matched healthy children served as controls.
- Fasted blood samples were analyzed for adipokines, hormonal, and metabolic markers after the first daily glucocorticoid dose.
Main Results:
- Leptin was higher in male CAH patients compared to controls.
- Leptin positively correlated with BMI-SDS in both groups; adiponectin negatively correlated with BMI only in CAH patients.
- Leptin decreased with increasing first daily hydrocortisone dose in CAH patients.
- Adiponectin levels decreased with higher concentrations of steroid precursors and androgens in CAH patients.
Conclusions:
- Decreased leptin with hydrocortisone dose suggests glucocorticoid effects on appetite regulation in CAH.
- Reduced adiponectin in CAH patients with elevated androgens may serve as a marker for poor hormonal control and metabolic risk.
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.
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