Polycystic ovary syndrome pathophysiology: Difference between revisions
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==Overview== | ==Overview== | ||
==Pathophysiology== | ==Pathophysiology== | ||
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. | 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. | ||
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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. | 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. | ||
===Genetics=== | ===Genetics=== | ||
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. | 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. | ||
===Associated Conditions=== | ===Associated Conditions=== | ||
PCOS may be associated with chronic [[inflammation]], with several investigators correlating inflammatory mediators with anovulation and other PCOS symptoms.<!-- | 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><!-- | ||
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[[Category:Endocrinology]] | [[Category:Endocrinology]] | ||
[[Category:Gynecology]] | [[Category:Gynecology]] | ||
[[Category:Obstetrics]] | [[Category:Obstetrics]] | ||
{{WikiDoc Help Menu}} | {{WikiDoc Help Menu}} | ||
{{WikiDoc Sources}} | {{WikiDoc Sources}} | ||
Revision as of 12:12, 21 July 2016
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Overview
Pathophysiology
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.
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.
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.
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.
Genetics
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.
Associated Conditions
PCOS may be associated with chronic inflammation, with several investigators correlating inflammatory mediators with anovulation and other PCOS symptoms.[1][2]
References
- ↑ 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.