Polycystic ovary syndrome causes: Difference between revisions
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==Overview== | ==Overview== | ||
The underlying defect in patients with polycystic ovary syndrome (PCOS) remains unknown, but a [[ | The underlying defect in patients with polycystic ovary syndrome (PCOS) remains unknown, but a [[Esophageal stricture causes|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). | ||
==Causes== | ==Causes== | ||
Revision as of 20:13, 26 October 2017
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Polycystic ovary syndrome Microchapters |
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Differentiating Polycystic ovary syndrome from other Diseases |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]
Overview
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).
Causes
The underlying defect in patients with polycystic ovary syndrom (PCOS) remains unknown and is thought to be multifactorial, but abnormal gonadotropin dynamics are mainly responsible for the development of polycystic ovary syndrome. Most researchers think 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; multiple cysts form in the ovaries, largely without ovulation
- 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.
References
- ↑ Strauss JF (2003). "Some new thoughts on the pathophysiology and genetics of polycystic ovary syndrome". Ann. N. Y. Acad. Sci. 997: 42–8. PMID 14644808.
- ↑ Bednarska S, Siejka A (2017). "The pathogenesis and treatment of polycystic ovary syndrome: What's new?". Adv Clin Exp Med. 26 (2): 359–367. PMID 28791858.
- ↑ Kassi E, Diamanti-Kandarakis E (2008). "The effects of insulin sensitizers on the cardiovascular risk factors in women with polycystic ovary syndrome". J. Endocrinol. Invest. 31 (12): 1124–31. doi:10.1007/BF03345663. PMID 19246981.