Polycystic ovary syndrome pathophysiology
|
Polycystic ovary syndrome Microchapters |
|
Differentiating Polycystic ovary syndrome from other Diseases |
|---|
|
Diagnosis |
|
Treatment |
|
Case Studies |
|
Polycystic ovary syndrome pathophysiology On the Web |
|
American Roentgen Ray Society Images of Polycystic ovary syndrome pathophysiology |
|
Risk calculators and risk factors for Polycystic ovary syndrome pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
Overview
Pathophysiology
The pathophysiology of PCOS is not well understood. There are several organ systems involved in the pathogenesis of PCOS like ovary, adrenal, hypothalamus, pituitary, or insulin-sensitive tissues.
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 PCOS 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
- 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 poly cystic ovarian syndrome.
Associated Conditions
Common conditions associated with PCOS are[1][2]
- Type 2 diabetes
- Endometrial hyperplasia and cancer
- Infertility
- Hypertension
- Gestational diabetes
- Preeclampsia
- Hirsutism
- Acne
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.