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==Causes==
==Causes==
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. Most researchers think that more than one factor could play a role in developing PCOS.<ref name="pmid14644808">{{cite journal |vauthors=Strauss JF |title=Some new thoughts on the pathophysiology and genetics of polycystic ovary syndrome |journal=Ann. N. Y. Acad. Sci. |volume=997 |issue= |pages=42–8 |year=2003 |pmid=14644808 |doi= |url=}}</ref><ref name="pmid28791858">{{cite journal |vauthors=Bednarska S, Siejka A |title=The pathogenesis and treatment of polycystic ovary syndrome: What's new? |journal=Adv Clin Exp Med |volume=26 |issue=2 |pages=359–367 |year=2017 |pmid=28791858 |doi= |url=}}</ref><ref name="pmid19246981">{{cite journal |vauthors=Kassi E, Diamanti-Kandarakis E |title=The effects of insulin sensitizers on the cardiovascular risk factors in women with polycystic ovary syndrome |journal=J. Endocrinol. Invest. |volume=31 |issue=12 |pages=1124–31 |year=2008 |pmid=19246981 |doi=10.1007/BF03345663 |url=}}</ref>
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.<ref name="pmid14644808">{{cite journal |vauthors=Strauss JF |title=Some new thoughts on the pathophysiology and genetics of polycystic ovary syndrome |journal=Ann. N. Y. Acad. Sci. |volume=997 |issue= |pages=42–8 |year=2003 |pmid=14644808 |doi= |url=}}</ref><ref name="pmid28791858">{{cite journal |vauthors=Bednarska S, Siejka A |title=The pathogenesis and treatment of polycystic ovary syndrome: What's new? |journal=Adv Clin Exp Med |volume=26 |issue=2 |pages=359–367 |year=2017 |pmid=28791858 |doi= |url=}}</ref><ref name="pmid19246981">{{cite journal |vauthors=Kassi E, Diamanti-Kandarakis E |title=The effects of insulin sensitizers on the cardiovascular risk factors in women with polycystic ovary syndrome |journal=J. Endocrinol. Invest. |volume=31 |issue=12 |pages=1124–31 |year=2008 |pmid=19246981 |doi=10.1007/BF03345663 |url=}}</ref>
*Increased [[gonadotropin-releasing hormone]] secretion in the [[pituitary gland]] results in increased secretion of [[Luteinizing hormone|serum luteinizing hormone (LH)]] and an elevated [[LH]]/[[Follicle-stimulating hormone|follicle-stimulating hormone (FSH)]] ratio.
*Increased [[gonadotropin-releasing hormone]] secretion in the [[pituitary gland]] results in increased secretion of [[Luteinizing hormone|serum luteinizing hormone (LH)]] and an elevated [[LH]]/[[Follicle-stimulating hormone|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.
*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 [[Ovary|ovaries]], and anovulatory cycles.
*[[Gene]]s are thought to be another factor. The genetic component appears to be inherited in an [[Autosomal dominant inheritance|autosomal dominant]] fashion with high genetic [[penetrance]] but variable expressivity in females
*[[Gene]]s are thought to be another factor. The genetic component appears to be inherited in an [[Autosomal dominant inheritance|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 [[phenotype]] appears to manifest itself at least partially via heightened [[androgen]] levels secreted by ovarian follicle [[theca]] cells from women with the [[allele]].

Revision as of 18:54, 30 October 2017

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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 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]

References

  1. 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.
  2. 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.
  3. 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.


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