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Background <p>Polycystic ovary syndrome (PCOS) is characterized by hyperandrogenism, ovulatory dysfunction, and a polycystic ovarian morphology. Emerging evidence suggests that autoimmunity may contribute to PCOS pathogenesis.</p> Methodology <p> In this cross-sectional study, 100 women with PCOS and 78 age-matched healthy controls underwent clinical assessment, hormonal profiling (FSH, LH, LH/FSH ratio, total testosterone, AMH, prolactin, and thyroid hormones), and autoantibody measurement (anti‐ovarian (AoA), anti‐thyroid peroxidase (anti‐TPO), anti‐thrombopoietin [anti‐THPO], and anti‐GAD) using validated immunoassays.</p> Results <p>PCOS participants demonstrated higher BMI, hyperandrogenism, elevated LH/FSH ratio, increased AMH and prolactin levels, and mild thyroid hormone elevation. The autoantibody levels (anti-TPO, anti-THPO, anti-GAD, and AoA) were significantly higher in the PCOS (<i>p</i> &lt; 0.05). ROC curve analysis identified anti-TPO (AUC = 0.90) and anti-GAD (AUC = 0.86) as strong discriminators. In the multivariate logistic regression, anti‐THPO (OR = 1.97 per ng/mL, <i>p</i> = 0.0052), anti‐TPO (OR = 1.48 per IU/mL, <i>p</i> = 0.048), and anti‐GAD (OR = 1.52 per ng/mL, <i>p</i> = 0.0046) remained independent predictors of PCOS. Correlation analysis revealed significant associations between the LH/FSH ratio and AMH (<i>r</i> = 0.300, <i>p</i> = 0.002), testosterone and anti‐TPO (<i>r</i> = 0.385, <i>p</i> &lt; 0.001), and anti‐GAD and AMH (<i>r</i> =  − 0.251, <i>p</i> = 0.012).</p> Conclusions <p>Autoimmune markers coexist with classical endocrine abnormalities in PCOS patients. Incorporating targeted autoantibody screening may improve PCOS characterization and guide personalized management.</p>

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Concurrent autoimmune and endocrine dysregulation in polycystic ovary syndrome

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年7月12日

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  • Abduljabbar Halah Amer,
  • Majid Mohammed Mahmood,
  • Methaq J. Al-Jbooriay,
  • Manal Taha Al-obaidi

摘要

Background

Polycystic ovary syndrome (PCOS) is characterized by hyperandrogenism, ovulatory dysfunction, and a polycystic ovarian morphology. Emerging evidence suggests that autoimmunity may contribute to PCOS pathogenesis.

Methodology

In this cross-sectional study, 100 women with PCOS and 78 age-matched healthy controls underwent clinical assessment, hormonal profiling (FSH, LH, LH/FSH ratio, total testosterone, AMH, prolactin, and thyroid hormones), and autoantibody measurement (anti‐ovarian (AoA), anti‐thyroid peroxidase (anti‐TPO), anti‐thrombopoietin [anti‐THPO], and anti‐GAD) using validated immunoassays.

Results

PCOS participants demonstrated higher BMI, hyperandrogenism, elevated LH/FSH ratio, increased AMH and prolactin levels, and mild thyroid hormone elevation. The autoantibody levels (anti-TPO, anti-THPO, anti-GAD, and AoA) were significantly higher in the PCOS (p < 0.05). ROC curve analysis identified anti-TPO (AUC = 0.90) and anti-GAD (AUC = 0.86) as strong discriminators. In the multivariate logistic regression, anti‐THPO (OR = 1.97 per ng/mL, p = 0.0052), anti‐TPO (OR = 1.48 per IU/mL, p = 0.048), and anti‐GAD (OR = 1.52 per ng/mL, p = 0.0046) remained independent predictors of PCOS. Correlation analysis revealed significant associations between the LH/FSH ratio and AMH (r = 0.300, p = 0.002), testosterone and anti‐TPO (r = 0.385, p < 0.001), and anti‐GAD and AMH (r =  − 0.251, p = 0.012).

Conclusions

Autoimmune markers coexist with classical endocrine abnormalities in PCOS patients. Incorporating targeted autoantibody screening may improve PCOS characterization and guide personalized management.