Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2025) 110 OC10.2 | DOI: 10.1530/endoabs.110.OC10.2

1Copenhagen University Hospital - Rigshospitalet, Department of Growth and Reproduction, Copenhagen, Denmark; 2Copenhagen University Hospital - Rigshospitalet, International Centre for Research and Research Training Centre in Endocrine Disruption of Male Reproduction and Child Health ((EDMaRC), Copenhagen, Denmark; 3Copenhagen University Hospital - Rigshospitalet, Clinical biochemistry, Copenhagen, Denmark; 4University of Copenhagen, Faculty of Health and Medical Sciences, Clinical Medicine, Copenhagen, Denmark


JOINT1276

Context: Prostate specific antigen (PSA) is an androgen-responsive biomarker regulated by testosterone (T) and dihydrotestosterone (DHT), with its expression tightly linked to androgen receptor activation. While PSA is primarily used in clinical practice for prostate cancer screening and monitoring, its physiological role as an androgen regulated protein suggests it may serve as a marker for androgen bioactivity in male pubertal development.

Objective: To evaluate PSA as an androgen-responsive biomarker in healthy boys during pubertal transition and to establish age-specific reference intervals for serum PSA concentrations.

Methods: This longitudinal study included 104 boys (corresponding to 890 serum samples) from The Copenhagen Puberty Study II conducted from 2006 to 2011. Serum PSA was measured using a commercially available assay with a limit of quantification (LOQ) of 0.014 µg/l. Age-specific RIs were developed using the generalized additive model for location, scale, and shape (GAMLSS). Total T was measured using a radioimmuno assay with a limit of detection (LOD) of 0.23 nmol/l. Free T was calculated using the Vermeulen equation. Pubertal onset was defined as a genital staging of G2.

Results: PSA concentrations were undetectable in prepubertal boys (G1) and at pubertal onset (G2). A significant increase in median PSA concentrations was observed from G2 to G3 (0.042 [0.009 - 0.104] µg/l, P<0.001). This upward trend continued into later stages (G4: 0.215 [0.116 - 0.357] µg/l, P=0.005; G5: 0.294 [0.204 - 0.447] µg/l, P=0.003). The increase between G3 and G5 was significant (P=0.003), whereas no significant difference was found between G3 and G4 (P=0.005).

Conclusion: Serum PSA concentrations increase progressively with pubertal development, mirroring the rise in bioactive androgens. While PSA remains undetectable in early puberty, its significant rise from G3 onward suggests a threshold effect, where androgen levels must reach a critical point before inducing measurable PSA production. These findings confirm PSA as an androgen-responsive biomarker, with its increase reflecting androgen receptor activation by testosterone and DHT. Our study provides clinically relevant reference intervals for PSA in the assessment of boys during pubertal transition.

Volume 110

Joint Congress of the European Society for Paediatric Endocrinology (ESPE) and the European Society of Endocrinology (ESE) 2025: Connecting Endocrinology Across the Life Course

European Society of Endocrinology 
European Society for Paediatric Endocrinology 

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