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Endocrine Abstracts (2026) 117 OC1.6 | DOI: 10.1530/endoabs.117.OC1.6

SFEBES2026 Oral Communications Adrenal and Cardiovascular (6 abstracts)

Childhood Androgen Excess and Metabolic Risk: A Case-Control Study in Premature Adrenarche and Adolescent Polycystic Ovary Syndrome

wogud Ben Said 1,2,3,4 , Asha Marichetty Rameshbabu 3,5 , Angela E Taylor 3 , Joshua Bain 3 , Lucy Cooper 4,5 , Shakila Thangaratinam 6 , Wiebke Arlt 7,8 & Jan Idkowiak 1,2,3,4


1Department of Endocrinology and Diabetes, Birmingham Women’s and Children’s NHS Foundation Trust, Birmingham, United Kingdom; 2Department of Metabolism and Systems Science, University of Birmingham, Birmingham, United Kingdom; 3NIHR Birmingham Biomedical Research Centre, Women’s Metabolic Health Theme, University of Birmingham, Birmingham, United Kingdom; 4Birmingham Health Partners, University of Birmingham, Birmingham, United Kingdom; 5NIHR/Wellcome Trust Clinical Research Facility, Birmingham Women’s and Children’s NHS Foundation Trust, Birmingham, United Kingdom; 6Institute of Life Course and Medical Sciences, Faculty of Health and Life Sciences, University of Liverpool, Liverpool, United Kingdom; 7Medical Research Council Laboratory of Medical Sciences, London, United Kingdom; 8Institute of Clinical Sciences, Imperial College London, London, United Kingdom


Background: Idiopathic early onset androgen excess often presents in pre-pubertal children as premature adrenarche (PA) and in teenagers as adolescent Polycystic Ovary Syndrome (PCOS). There is inconclusive evidence on whether younger children with PA have higher risk of developing metabolic complications or progressing to PCOS in later life.

Aim: To describe the clinical, hormonal and biochemical phenotype of children with PA and adolescents with PCOS compared to healthy controls.

Design and Methods: Single-centre cross-sectional study (DUCHESS study). We report on auxology and body composition measured by dual-x-ray absorptiometry (DXA), fasting serum hormone profiles (DHEAS, androstenedione, testosterone, SHBG, prolactin, IGF-1), biochemical surrogate markers of metabolic risk (lipid profile, HbA1c, glucose) and 24-hour urinary steroid profiling (gas-chromatography/mass spectrometry; in PA only).

Results: We recruited 68 children with PA (59 girls, 9 boys) and 39 healthy controls (21 girls, 18 boys), and 30 adolescent girls with PCOS and 16 controls; there were no significant age differences between cases and controls. Other causes of androgen excess were excluded. PA children, characterised by increased serum DHEAS, had higher weight, height, BMI z-score, total fat mass, IGF-1, and HDL cholesterol and lower SHBG than controls (median 61nmol/l [IQR 45.5] vs 88.6 [67.8]; P = 0.002). Adolescent girls with PCOS, characterised by increased serum androstenedione and DHEAS, had higher weight, BMI, and total fat mass and fasting triglycerides (1.06 mmol/l [0.46] vs. 0.65 [0.24]; P = 0.0006) and lower SHBG than controls. Urinary steroid profiling in PA revealed significantly higher excretion of DHEAS and 17-hydroxypregnenolone metabolites.

Summary and Conclusion: Children with early-onset androgen exposure have multiple differences from matched controls including higher stature, weight and BMI, lower SHBG, and altered urinary steroidogenesis. Ongoing work includes further recruitment and expanded biochemical characterisation, including fasting insulin and HOMA-IR assessments, serum multi-steroid profiling, and untargeted metabolomic analyses to identify metabolic risk signatures.

Volume 117

Society for Endocrinology BES 2026

Harrogate, United Kingdom
02 Mar 2026 - 04 Mar 2026

Society for Endocrinology 

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