The underlying defect in patients with polycystic ovary syndrome (PCOS) remains unknown, but a hormonal imbalance between LH/FSH and estrogen is mainly responsible for the development of polycystic ovary syndrome. Most studies suggest that more than one factor could play a role in developing Polycystic ovary syndrome (PCOS).

The underlying defect in patients with polycystic ovary syndrome (PCOS) remains unknown and is thought to be multifactorial, but abnormal gonadotropin dynamics are mainly responsible for the development of polycystic ovary syndrome. It is suggested that more than one factor could play a role in developing PCOS.^[1][2][3]

• Increased gonadotropin-releasing hormone secretion in the pituitary gland results in increased secretion of serum luteinizing hormone (LH) and an elevated LH/follicle-stimulating hormone (FSH) ratio.
• Hypersecretion of LH results in increased ovarian androgen production, leading to arrest of follicular development with follicular atresia which may result in multiple cysts formation in the ovaries, and anovulatory cycles.
• Genes are thought to be another factor. The genetic component appears to be inherited in an autosomal dominant fashion with high genetic penetrance but variable expressivity in females
• The phenotype appears to manifest itself at least partially via heightened androgen levels secreted by ovarian follicle theca cells from women with the allele.
• The exact gene affected has not yet been identified.
• In rare instances, single-gene mutations can give rise to the phenotype of the syndrome.

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