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{{Polycystic ovary syndrome}}
{{Polycystic ovary syndrome}}
 
{{CMG}}; {{AE}} {{ADG}}
{{CMG}}
 
==Overview==
==Overview==
There are several organ systems involved in the [[pathogenesis]] of polycystic ovary syndrome like [[ovary]], [[adrenal]], [[hypothalamus]], [[pituitary]], or [[insulin]]-sensitive tissues. The [[pathophysiology]] of Polycystic ovary syndrome is not well understood. [[Insulin resistance]] leads to compensatory insulin hypersecretion by the [[pancreas]] in order to maintain [[Blood sugar regulation|normoglycemia]]. The resulting [[hyperinsulinemia]] promotes [[ovarian]] [[androgen]] output and may also promote [[adrenal]] [[androgen]] output.


==Pathophysiology==
==Pathophysiology==
The pathophysiology of polycystic ovary syndrome is not well understood. There are several organ systems involved in the [[pathogenesis]] of polycystic ovary syndrome like [[ovary]], [[adrenal]], [[hypothalamus]], [[pituitary]], or [[insulin]]-sensitive tissues.<ref name="pmid27459230">{{cite journal |vauthors=Rosenfield RL, Ehrmann DA |title=The Pathogenesis of Polycystic Ovary Syndrome (PCOS): The Hypothesis of PCOS as Functional Ovarian Hyperandrogenism Revisited |journal=Endocr. Rev. |volume=37 |issue=5 |pages=467–520 |year=2016 |pmid=27459230 |doi=10.1210/er.2015-1104 |url=}}</ref><ref name="pmid28930378">{{cite journal |vauthors=Behboudi-Gandevani S, Amiri M, Bidhendi Yarandi R, Noroozzadeh M, Farahmand M, Rostami Dovom M, Ramezani Tehrani F |title=The risk of metabolic syndrome in polycystic ovary syndrome: A systematic review and meta-analysis |journal=Clin. Endocrinol. (Oxf) |volume= |issue= |pages= |year=2017 |pmid=28930378 |doi=10.1111/cen.13477 |url=}}</ref><ref name="pmid28919160">{{cite journal |vauthors=Rothenberg SS, Beverley R, Barnard E, Baradaran-Shoraka M, Sanfilippo JS |title=Polycystic ovary syndrome in adolescents |journal=Best Pract Res Clin Obstet Gynaecol |volume= |issue= |pages= |year=2017 |pmid=28919160 |doi=10.1016/j.bpobgyn.2017.08.008 |url=}}</ref>
===Increase in androgens===
*[[Insulin]] resistance leads to compensatory [[insulin]] hypersecretion by the [[pancreas]] in order to maintain normoglycemia.
*The resulting hyperinsulinemia promotes [[ovarian]] [[androgen]] output and may also promote [[Adrenal|adrena<nowiki/>l]] androgen output.
*High insulin levels also suppress [[hepatic]] production of [[Sex hormone binding globulin|sex hormone binding globulin (SHBG)]], which exacerbates hyperandrogenemia by increasing the proportion of free circulating [[androgens]].
*Another factor that promotes [[ovarian]] [[androgen]] output is the fact that women with polycystic ovary syndrome are exposed to high levels of [[LH]] for long term.
*This [[LH]] excess seems to be a result of an increased frequency of [[Gonadotropin-releasing hormone|gonadotropin releasing hormone]] pulses from the [[hypothalamus]].
*The abnormal [[hormonal]] milieu also probably contributes to incomplete follicular development which results in polycystic ovarian morphology.
===Formations of cysts===
*Polycystic ovaries develop when the [[Ovary|ovaries]] are stimulated to produce excessive amounts of male hormones ([[androgens]]), particularly [[testosterone]], either through the release of an excessive [[luteinizing hormone]] (LH) by the [[anterior pituitary gland]] or through high levels of [[insulin]] in blood (hyperinsulinemia) of women whose [[ovaries]] are sensitive to this stimulus.
*These follicles get matured but were never released from the [[ovary]] because of abnormal hormone levels resulting in the cyst formation and make a '''string of pearls''' appearance.


Polycystic Ovaries develop when the ovaries are stimulated to produce excessive amounts of male hormones ([[androgens]]), particularly [[testosterone]], either through the release of excessive [[luteinizing hormone]] (LH) by the [[anterior pituitary gland]] or through high levels of [[insulin]] in the blood ([[hyperinsulinaemia]]) in women whose ovaries are sensitive to this stimulus.
{{familytree/start |summary=Sample 1}}
 
{{familytree | | | B01 | | | | | | | | | | |B02| | |B01=↑ 5α-reductase<br>reductivity|B02=↓ Hβ-HSD1<br>activity }}
These form where egg follicles matured but were never released from the [[ovary]] because of abnormal hormone levels. These generally take on a 'string of pearls' appearance.
{{familytree | | | |`|-|-|-|-|-|v|-|-|-|-|-|'| | | | }}
 
{{familytree | | | | | | | | | B01 | | | | | |B01=↑ Cortisol<br>metabolism}}
A majority of patients with PCOS have insulin resistance. Their elevated insulin levels contribute to or cause the abnormalities seen in the [[hypothalamic-pituitary-ovarian axis]] that lead to PCOS.  
{{familytree | | | | | | | | | |!| | | | | |}}
 
{{familytree | | | | | | | | | B01 | | | | | |B01=↑ ACTH}}
Specifically, hyperinsulinemia increases [[GnRH]] pulse frequency, LH over FSH dominance, increased ovarian androgen production, decreased follicular maturation, and decreased [[SHBG]] binding; all these steps lead to the development of PCOS. Insulin resistance is a common finding among both normal weight and overweight PCOS patients.
{{familytree | | | | | |,|-|-|-|^|-|-|-|-|.| | | }}
 
{{familytree | | | | | B01 | | | | | | | B02 |B01=↑ Adrenal <br>androgens|B02=Normal serum<br>cortisol}}
{{familytree | | | | | |!| | | | | | | | | |}}
{{familytree | | | | | B01 | | | | | | | | | |B01=PCOS}}
{{familytree/end}}
===Genetics===
===Genetics===
 
*Polycystic ovary syndrome may have a [[Genetics|genetic]] predisposition.  
PCOS is characterized by a complex set of symptoms, and the cause cannot be determined for all patients.  However, research to date suggests that insulin resistance could be a leading cause. PCOS may also have a genetic predisposition, and further research into this possibility is taking place. No specific [[gene]] has been identified, and it is thought that many genes could contribute to the development of PCOS.
*No specific [[gene]] has been identified, and it is thought that many genes could contribute to the development of the polycystic ovarian syndrome.
*The genetic component appears to be inherited in an [[Autosomal dominant inheritance|autosomal dominant fashion]] with high genetic [[penetrance]] but variable expressivity in females.


===Associated Conditions===
===Associated Conditions===
 
Common conditions associated with polycystic ovary syndrome are:<!--
PCOS may be associated with chronic [[inflammation]], with several investigators correlating inflammatory mediators with anovulation and other PCOS symptoms.<!--
   --><ref>{{cite journal | author = Fukuoka M, Yasuda K, Fujiwara H, Kanzaki H, Mori T | title = Interactions between interferon gamma, tumour necrosis factor alpha, and interleukin-1 in modulating progesterone and oestradiol production by human luteinized granulosa cells in culture. | journal = Hum Reprod | volume = 7 | issue = 10 | pages = 1361-4 | year = 1992 | id = PMID 1291559}}</ref><!--
   --><ref>{{cite journal | author = Fukuoka M, Yasuda K, Fujiwara H, Kanzaki H, Mori T | title = Interactions between interferon gamma, tumour necrosis factor alpha, and interleukin-1 in modulating progesterone and oestradiol production by human luteinized granulosa cells in culture. | journal = Hum Reprod | volume = 7 | issue = 10 | pages = 1361-4 | year = 1992 | id = PMID 1291559}}</ref><!--
   --><ref>{{cite journal | author = González F, Rote N, Minium J, Kirwan J | title = Reactive oxygen species-induced oxidative stress in the development of insulin resistance and hyperandrogenism in polycystic ovary syndrome. | journal = J Clin Endocrinol Metab | volume = 91 | issue = 1 | pages = 336-40 | year = 2006 | id = PMID 16249279}}</ref>
   --><ref>{{cite journal | author = González F, Rote N, Minium J, Kirwan J | title = Reactive oxygen species-induced oxidative stress in the development of insulin resistance and hyperandrogenism in polycystic ovary syndrome. | journal = J Clin Endocrinol Metab | volume = 91 | issue = 1 | pages = 336-40 | year = 2006 | id = PMID 16249279}}</ref>
*[[Type 2 diabetes]]
*[[Endometrial hyperplasia|Endometrial hyperplasia and cancer]]
*[[Infertility]]
*[[Hypertension]]
*[[Gestational diabetes]]
*[[Preeclampsia]]
*[[Hirsutism]]
*[[Acne]]


==References==
==References==
{{Reflist|2}}
{{Reflist|2}}
[[Category:Endocrinology]]
[[Category:Gynecology]]
[[Category:Obstetrics]]
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Latest revision as of 18:44, 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

There are several organ systems involved in the pathogenesis of polycystic ovary syndrome like ovary, adrenal, hypothalamus, pituitary, or insulin-sensitive tissues. The pathophysiology of Polycystic ovary syndrome is not well understood. Insulin resistance leads to compensatory insulin hypersecretion by the pancreas in order to maintain normoglycemia. The resulting hyperinsulinemia promotes ovarian androgen output and may also promote adrenal androgen output.

Pathophysiology

The pathophysiology of polycystic ovary syndrome is not well understood. There are several organ systems involved in the pathogenesis of polycystic ovary syndrome like ovary, adrenal, hypothalamus, pituitary, or insulin-sensitive tissues.[1][2][3]

Increase in androgens

  • Insulin resistance leads to compensatory insulin hypersecretion by the pancreas in order to maintain normoglycemia.
  • The resulting hyperinsulinemia promotes ovarian androgen output and may also promote adrenal androgen output.
  • High insulin levels also suppress hepatic production of sex hormone binding globulin (SHBG), which exacerbates hyperandrogenemia by increasing the proportion of free circulating androgens.
  • Another factor that promotes ovarian androgen output is the fact that women with polycystic ovary syndrome are exposed to high levels of LH for long term.
  • This LH excess seems to be a result of an increased frequency of gonadotropin releasing hormone pulses from the hypothalamus.
  • The abnormal hormonal milieu also probably contributes to incomplete follicular development which results in polycystic ovarian morphology.

Formations of cysts

  • Polycystic ovaries develop when the ovaries are stimulated to produce excessive amounts of male hormones (androgens), particularly testosterone, either through the release of an excessive luteinizing hormone (LH) by the anterior pituitary gland or through high levels of insulin in blood (hyperinsulinemia) of women whose ovaries are sensitive to this stimulus.
  • These follicles get matured but were never released from the ovary because of abnormal hormone levels resulting in the cyst formation and make a string of pearls appearance.
 
 
↑ 5α-reductase
reductivity
 
 
 
 
 
 
 
 
 
 
↓ Hβ-HSD1
activity
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
↑ Cortisol
metabolism
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
↑ ACTH
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
↑ Adrenal
androgens
 
 
 
 
 
 
Normal serum
cortisol
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
PCOS
 
 
 
 
 
 
 
 
 

Genetics

  • Polycystic ovary syndrome may have a genetic predisposition.
  • No specific gene has been identified, and it is thought that many genes could contribute to the development of the polycystic ovarian syndrome.
  • The genetic component appears to be inherited in an autosomal dominant fashion with high genetic penetrance but variable expressivity in females.

Associated Conditions

Common conditions associated with polycystic ovary syndrome are:[4][5]

References

  1. ↑ Rosenfield RL, Ehrmann DA (2016). "The Pathogenesis of Polycystic Ovary Syndrome (PCOS): The Hypothesis of PCOS as Functional Ovarian Hyperandrogenism Revisited". Endocr. Rev. 37 (5): 467–520. doi:10.1210/er.2015-1104. PMID 27459230.
  2. ↑ Behboudi-Gandevani S, Amiri M, Bidhendi Yarandi R, Noroozzadeh M, Farahmand M, Rostami Dovom M, Ramezani Tehrani F (2017). "The risk of metabolic syndrome in polycystic ovary syndrome: A systematic review and meta-analysis". Clin. Endocrinol. (Oxf). doi:10.1111/cen.13477. PMID 28930378.
  3. ↑ Rothenberg SS, Beverley R, Barnard E, Baradaran-Shoraka M, Sanfilippo JS (2017). "Polycystic ovary syndrome in adolescents". Best Pract Res Clin Obstet Gynaecol. doi:10.1016/j.bpobgyn.2017.08.008. PMID 28919160.
  4. ↑ Fukuoka M, Yasuda K, Fujiwara H, Kanzaki H, Mori T (1992). "Interactions between interferon gamma, tumour necrosis factor alpha, and interleukin-1 in modulating progesterone and oestradiol production by human luteinized granulosa cells in culture". Hum Reprod. 7 (10): 1361–4. PMID 1291559.
  5. ↑ González F, Rote N, Minium J, Kirwan J (2006). "Reactive oxygen species-induced oxidative stress in the development of insulin resistance and hyperandrogenism in polycystic ovary syndrome". J Clin Endocrinol Metab. 91 (1): 336–40. PMID 16249279.


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