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  • Print publication year: 2014
  • Online publication date: June 2014

12 - Polycystic ovary syndrome

Summary

Management of excessive menstrual bleeding has changed over the past two decades with the promotion of effective medical treatments and in particular the use of the levonorgestrel-releasing intrauterine device. The aims of therapy are to reduce blood loss, reduce the risk of anaemia and improve quality of life. Non-hormonal treatment options for excessive menstrual bleeding are non-steroidal anti-inflammatory drugs, antifibrinolytics, and etamsylate. Intrauterine administration of levonorgestrel, oral and intramuscular progestogens, oestrogen/progestogen combinations, and antiprogestogens are used as hormonal treatments for excessive menstrual bleeding. Plasminogen activator inhibitors have been promoted as a treatment for excessive menstrual bleeding because of increased endometrial fibrinolytic activity in women. The use of progestogens is based on the erroneous concept that women with excessive menstrual bleeding principally have anovulatory cycles and require progestogen supplementation. From clinical experience, combined oral contraceptives (COCs) are generally considered to be effective in the management of dysfunctional menstrual bleeding.

References

1. The Rotterdam ESHRE/ARSM-Sponsored PCOS consensus workshop group. Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome (PCOS). Hum Reprod 2004;19:41–7.
2. MoralesAJ, LaughlinGA, BützowT, MaheshwariH, BaumannG, YenSS. Insulin, somatotropic, and luteinizing hormone axes in lean and obese women with polycystic ovary syndrome: common and distinct features. J Clin Endocrinol Metab 1996;81:2854–64.
3. TarlatzisBC, GrimbizisG, PournaropoulosF, et al. The prognostic value of basal luteinizing hormone:follicle-stimulating hormone ratio in the treatment of patients with PCOS by assisted reproduction techniques. Hum Reprod 1995;10:2545–9.
4. Huber-BuchholzMM, CareyDG, NormanRJ. Restoration of reproductive potential by lifestyle modification in obese polycystic ovary syndrome: role of insulin sensitivity and luteinizing hormone. J Clin Endocrinol Metab 1999;84:1470–4.
5. TsilchorozidouT, OvertonC, ConwayG. The pathophysiology of polycystic ovary syndrome. Clin Endocrinol (Oxf) 2004;60:1–17.
6. VelazquezEM, MendozaSG, WangP, GlueckCJ. Metformin therapy is associated with a decrease in plasma plasminogen activator inhibitor-1, lipoprotein(a), and immunoreactive insulin levels in patients with the polycystic ovary syndrome. Metabolism 1997;46:454–7.
7. CrosignaniPG, ColomboM, VegettiW, SomiglianaE, GessatiA, RagniG. Overweight and obese anovulatory patients with polycystic ovaries: parallel improvements in anthropometric indices, ovarian physiology and fertility rate induced by diet. Hum Reprod 2003;18:1928–32.
8. KoustaE, WhiteDM, FranksS. Modern use of clomiphene citrate in induction of ovulation. Hum Reprod Update 1997;3:359–65.

Further reading

Royal College of Obstetricians and Gynaecologists. Long-term Consequences of Polycystic Ovary Syndrome. Green-top Guideline no. 33. London: RCOG; 2007 [http://www.rcog.org.uk/womens-health/clinical-guidance/long-term-consequences-polycystic-ovary-syndrome-green-top-33].