BSPED2024 Poster Presentations Adrenal 1 (7 abstracts)
Adipokine analysis in relation to the glucocorticoid dose and androgen concentrations in the paediatric CAH-UK cohort
Irina A Bacila 1,2 , Neil R. Lawrence 1,2 , Sabah Alvi 3 , Timothy D. Cheetham 4 , Elizabeth Crowne 5 , Urmi Das 6 , Mehul T. Dattani 7 , Justin H. Davies 8,9 , Evelien Gevers 10 , Brian Keevil 11 , Ruth E. Krone 12 , Allan Lawrie 13 , Leena Patel 14 , Tabitha Randell 15 , Fiona J. Ryan 16 , Ajay Thankamony 17 , S Faisal. Ahmed 18 & Nils P. Krone 1,2
1The University of Sheffield, Sheffield, United Kingdom; 2Sheffield Children’s Hospital, Sheffield, United Kingdom; 3Leeds General Infirmary, Leeds, United Kingdom; 4Great North Children’s Hospital, University of Newcastle, Newcastle, United Kingdom; 5Bristol Royal Hospital for Children, University Hospitals Bristol Foundation Trust, Bristol, United Kingdom; 6Alder Hey Children’s Hospital, Liverpool, United Kingdom; 7Great Ormond Street Hospital, London, United Kingdom; 8University Hospital Southampton, Southampton, United Kingdom; 9University of Southampton, Southampton, United Kingdom; 10Centre for Endocrinology, William Harvey Research Institute, Queen Mary University London, London and Barts Health NHS Trust - The Royal London Hospital, London, United Kingdom; 11Department of Biochemistry, Manchester University NHS Foundation Trust, Manchester, United Kingdom; 12Birmingham Women’s & Children’s Hospital, Birmingham, United Kingdom; 13Faculty of Medicine, National Heart & Lung Institute, Imperial College London, London, United Kingdom; 14Paediatric Endocrine Service, Royal Manchester Children’s Hospital, Manchester University NHS Foundation Trust, Manchester, United Kingdom; 15Nottingham Children’s Hospital, Nottingham, United Kingdom; 16Oxford Children’s Hospital, Oxford University Hospitals NHS Foundation Trust, Oxford, United Kingdom; 17Department of Paediatrics, University of Cambridge, Cambridge, United Kingdom; 18Developmental Endocrinology Research Group, University of Glasgow, Glasgow, United Kingdom
Introduction: Patients with congenital adrenal hyperplasia (CAH) have increased prevalence of obesity and metabolic problems, however, their mechanisms are not clearly known. We aimed to understand the roles of adiponectin and leptin in the development of metabolic problems in CAH.
Methods: In a national multicentre cohort of 102 patients with 21-hydroxylase deficiency (54 females, age 13.0±2.92 years) and 83 sex- and age-matched controls, we analysed plasma adiponectin and leptin in relation to anthropometric parameters, medication doses, and biochemical markers (17-hydroxyprogesterone, androstenedione, testosterone, 11-hydroxyandrostenedione, 11-ketotestosterone, metabolic profiles). Blood samples were collected between 9:00-11:00, after the morning hydrocortisone dose.
Results: Leptin and adiponectin had a significant relationship with the BMI, regression analysis showing that CAH patients with higher BMI had increased leptin (leptin(ng/dl) = 4810 + 3939 x BMI-SDS, P < 0.01), and decreased adiponectin (adiponectin(pg/dl) = 98 – 11 x BMI-SDS, P < 0.01). Although patients had higher prevalence of overweight (26.4% vs 10.8%) and obesity (22.6% vs 10.8%) compared to controls (P < 0.001), there was no significant difference in adiponectin or leptin between groups, except for leptin being higher in male patients (P = 0.033). Leptin increased with the insulin level and decreased with the morning relative hydrocortisone dose in patients (regression analysis: leptin(ng/dl) = 11846 + 250 x insulin – 1316 x dose, P < 0.01), but had no significant relationship with the daily dose. Adiponectin had negative correlation with all the plasma androgens in patients: 17-hydroxyprogesterone (r<sub>s</sub> = -0.34, P < 0.00), androstenedione (r<sub>s</sub> = -0.34, P < 0.01), testosterone (r<sub>s</sub> = -0.33, P < 0.01), 11-hydroxyandrostenedione (r<sub>s</sub> = -0.32, P < 0.01) and 11-ketotestosterone (r<sub>s</sub> = -0.28, p = 0.01), which was not found in controls. Leptin was only found to correlate with testosterone (r<sub>s</sub> = -0.29, p = 0.01).
Conclusion: Our results indicate that glucocorticoid replacement may inhibit leptin response, which could contribute to the weight gain and the development of metabolic problems in patients with CAH. A high adiponectin was found to be associated with more effective androgen suppression indicating its potential use as a marker of metabolic and androgen control in CAH.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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