Polycystic ovary syndrome causes: Difference between revisions
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==Overview== | ==Overview== | ||
The underlying defect in patients with 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 | The underlying defect in patients with polycystic ovary syndrome (PCOS) remains unknown, but a [[Hormone|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== | ||
The underlying defect in patients with PCOS remains unknown and is thought to be multifactorial, but abnormal gonadotropin dynamics are mainly responsible for the development of polycystic ovary syndrome. | 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 serum luteinizing hormone (LH) and an elevated LH/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 | *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 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]]. | ||
*The exact gene affected has not yet been identified. | *The exact [[gene]] affected has not yet been identified. | ||
*In rare instances, single-gene mutations can give rise to the phenotype of the syndrome. | *In rare instances, single-gene mutations can give rise to the [[phenotype]] of the syndrome. | ||
==References== | ==References== | ||
Latest revision as of 20:20, 3 August 2020
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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]
- 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.
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.