Polycystic ovary syndrome pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
Overview
There are several organ systems involved in the pathogenesis of Polycystic ovary syndrome like ovary, adrenal, hypothalamus, pituitary, or insulin-sensitive tissues.
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]
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 long term to high levels of LH.
- 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 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 follicles gets matured but were never released from the ovary because of abnormal hormone levels resulting in the formation of cysts and take on 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 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 poly cystic ovarian syndrome.
- 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.
- In rare instances, single-gene mutations can give rise to the phenotype of the syndrome.
Associated Conditions
Common conditions associated with Polycystic ovary syndrome are[2][3]
- 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.
- ↑ 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.