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Endocrine Abstracts (2025) 110 P1030 | DOI: 10.1530/endoabs.110.P1030

1Istanbul University, Istanbul Faculty of Medicine, Department of Pediatric Endocrinology, Istanbul, Türkiye


JOINT2917

Background: Polycystic ovary syndrome (PCOS) is a complex endocrine disorder in adolescents, often linked to hyperandrogenemia, obesity, and insulin resistance. While metabolic dysfunction in PCOS is well-documented, the role of sleep disturbances remains underestimated. Emerging evidence suggests that poor sleep quality and increased obstructive sleep apnea (OSA) risk may worsen metabolic outcomes, independent of obesity. This study aims to explore the association between sleep disturbances, metabolic dysfunction, and obesity in adolescents with PCOS, with a particular focus on the independent contributions of hyperandrogenemia and insulin resistance.

Methods: A total of 74 adolescents and young adults diagnosed with PCOS (14-24 years) and 87 age-matched healthy controls were included in this cross-sectional study. Sleep quality was assessed using the Pittsburgh Sleep Quality Index (PSQI), Epworth Sleepiness Scale (ESS), and Berlin Questionnaire for OSA risk. Anthropometric measures included BMI, BMI-SDS. Biochemical analyses covered LH/FSH ratio, testosterone, SHBG, androstenedione, DHEAS, glucose, insulin, HOMA-IR, and lipid profile. Analysis was made between PCOS and control groups, as well as within the PCOS cohort based on obesity status.

Results: PCOS patients had significantly higher BMI (P < 0.001) and BMI-SDS (P < 0.001) than controls. Moreover, 57% of PCOS patients were obese, compared to only 11% in the control group. Compared to controls, PCOS patients had significantly higher ESS scores (P = 0.04) and an increased risk of OSA (P = 0.031), while overall sleep quality, as measured by PSQI scores, did not differ significantly. Among PCOS patients, obese individuals had significantly higher levels of testosterone (P = 0.017), androstenedione (P = 0.004), insulin (P < 0.001), HOMA-IR (P < 0.001), and LDL cholesterol (P = 0.018) compared to non-obese PCOS patients. Poor sleep quality (PSQI >5) was strongly associated with an increased risk of OSA (P < 0.001). Correlation analysis revealed a weak but positive association between HOMA-IR and Berlin Questionnaire scores (r = 0.272, P = 0.02), suggesting a potential link between HOMA-IR and OSA risk. Similarly, the triglyceride/glucose ratio showed a weak positive correlation with Berlin scores (r = 0.292, P = 0.015).

Conclusions: This study highlights that sleep disturbances in PCOS are not solely driven by obesity but are also influenced by metabolic status. Poor sleep quality is associated with increased OSA risk. Given the potential long-term cardiometabolic consequences, integrating sleep health into PCOS management may be crucial, especially in obese individuals. Further research with objective sleep assessments, like polysomnography, is crucial to gaining deeper insights into the complex relationship between PCOS, sleep disturbances, and metabolic dysfunction.

Key words: PCOS, adolescent, sleep quality, metabolic status, OSA.

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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