A Review of Hyperandrogenism State in Polycystic Ovarian Syndrome

    Mohamed Shabi M., P. S. Nivya, C Devika, Madhavi Reddy, Nair Poornima, K. Roopesh, Joel P. Joseph, Shivanand Kolageri
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    Studysummary This review discusses the hypotheses surrounding the developmental origins of polycystic ovary syndrome, particularly the role of prenatal androgen exposure, and reports no new experimental results. Our plain-language summary of this paper — not a Tressless recommendation.
    Polycystic ovary syndrome (PCOS) is a prevalent endocrine disorder in premenopausal women, caused by disturbances in the hypothalamic-pituitary-ovarian axis, abnormal steroidogenesis, and a combination of genetic and environmental factors. The disorder is characterized by the overexpression of the CYP11A, CYP17, and CYP19 genes, which disrupts the steroidogenic pathway and leads to a state of hyperandrogenism. This excess of androgen hampers folliculogenesis, leading to symptoms such as hirsutism, acne, and androgenic alopecia. The study also suggests that women with PCOS may have an excess of androgen during fetal life due to elevated expression of P450c17a throughout pregnancy, which could influence gene expression in adolescence and adulthood, potentially inducing PCOS. The disorder is also associated with anovulation due to the presence of many small follicles in the ovaries and irregularities in early stages of folliculogenesis.
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