Polycystic ovary syndrome is the most prevalent endocrine-metabolic pathology in pre-menopausal women. Its etiopathogenesis is complex, multifactorial and heterogeneous, including the interaction of genetic, epigenetic and environmental factors. Androgenic excess constitutes the disease's main physiopathological mechanism and results in reproductive, metabolic and cosmetic alterations which negatively impact these patients' quality of life. The criteria established in the Rotterdam consensus and their correct application form the necessary basis for this syndrome's proper diagnosis. In the absence of an aetiological treatment, the aim is to improve the clinical signs and symptoms derived from hyperandrogenism, ovarian dysfunction and existing metabolic complications, and, therefore, they must be chronic and individualised.
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| http://dx.doi.org/10.1016/j.medcli.2018.11.019 | DOI Listing |
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Polycystic ovary syndrome (PCOS) is a complex polygenic endocrinopathy affecting 5-20% of reproductive-age women. Familial studies, candidate gene studies, and GWAS have identified multiple PCOS-associated genetic loci. This study aims to identify the functional variants associated with PCOS.
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The First College of Clinical Medical Science, China Three Gorges University, Yichang, China.
Introduction: The current study demonstrated that oxidative stress (OS) is closely related to the pathogenesis of polycystic ovary syndrome (PCOS). However, there are numerous factors that lead to OS, therefore, identifying the key genes associated with PCOS that contribute to OS is crucial for elucidating the pathogenesis of PCOS and selecting appropriate treatment strategies.
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Objective: With one in ten women globally suffering from it, polycystic ovarian syndrome (PCOS) has recently emerged as one of the most common endocrine multifactorial illnesses. Each patient may not experience all the potential symptoms of PCOS, which include insulin resistance, hirsutism, acanthosis nigricans, hyperandrogenism, weight gain, etc.
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