Polycystic ovary syndrome pathophysiology: Difference between revisions
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===Increase in androgens=== | ===Increase in androgens=== | ||
*[[Insulin]] resistance leads to compensatory [[insulin]] hypersecretion by the [[pancreas]] in order to maintain normoglycemia. | *[[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 | *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]]. | *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 | *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]] | *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. | *The abnormal [[hormonal]] milieu also probably contributes to incomplete follicular development which results in polycystic ovarian morphology. | ||
===Formations of cysts=== | ===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 | *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 formation | *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. | ||
{{familytree/start |summary=Sample 1}} | {{familytree/start |summary=Sample 1}} | ||
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===Genetics=== | ===Genetics=== | ||
*Polycystic ovary syndrome may | *Polycystic ovary syndrome may have a [[Genetics|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. | *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 | *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=== | ||
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]
- Type 2 diabetes
- Endometrial hyperplasia and cancer
- Infertility
- Hypertension
- Gestational diabetes
- Preeclampsia
- Hirsutism
- Acne
References
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.