Development and risk factors of type 2 diabetes in a nationwide population of women with polycystic ovary syndrome

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Abstract

Objective: Polycystic ovary syndrome (PCOS) is associated with insulin resistance and obesity. Prospective population-based data regarding development and possible predictors of type 2 diabetes (T2D) in PCOS are limited. Design: National Patient Register–based study. Methods: Patients with PCOS [PCOS Denmark and embedded cohort, PCOS Odense University Hospital (OUH)] and a control population with no previous diagnosis of T2D. PCOS OUH (N = 1,162) included premenopausal women with PCOS and standardized clinical and biochemical examination. PCOS Denmark (N = 18,477) included women with PCOS in the Danish National Patient Register. Three age-matched controls were included per patient (N = 54,680). Main outcome: T2D events according to diagnosis codes and filled medicine prescriptions. Results: The median (quartiles) follow-up was 11.1 (6.9 to 16.0) years. The hazard ratio (HR) with 95% confidence interval (CI) for development of T2D in PCOS Denmark was HR = 4.0 (95% CI, 3.7 to 4.3; P, 0.001), and the total event rate of T2D was 8.0 per 1000 person years in PCOS Denmark vs 2.0 per 1000 person years in controls (P, 0.001). The median age at diagnosis of T2D was 31 (26 to 37) years in PCOS Denmark vs 35 (27 to 44) years in controls (P, 0.001). In multiple regression analyses, body mass index, glycated hemoglobin, fasting blood glucose, 2-hour blood glucose, homeostasis model assessment of insulin resistance, and triglycerides were positively associated with development of T2D, whereas higher number of births was negatively associated with development of T2D. Conclusion: The event rate of T2D was higher in PCOS compared with controls, and T2D was diagnosed at a younger age.

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Rubin, K. H., Glintborg, D., Nybo, M., Abrahamsen, B., & Andersen, M. (2017). Development and risk factors of type 2 diabetes in a nationwide population of women with polycystic ovary syndrome. Journal of Clinical Endocrinology and Metabolism, 102(10), 3848–3857. https://doi.org/10.1210/jc.2017-01354

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