polycystic ovarian syndrome
Last edited 04/2023 and last reviewed 10/2023
In the UK, up to 33% of women have polycystic ovaries (i.e. 10 or more follicles per ovary detected on ultrasound).
Of these, an estimated 33% have polycystic ovarian syndrome (PCOS), generally defined in the UK as polycystic ovaries together with one or more characteristic features (hirsutism, acne, male-pattern baldness, amenorrhoea or oligomenorrhoea, or raised serum concentrations of testosterone and/or luteinising hormone) .
In polycystic ovarian syndrome the associated metabolic abnormalities (abnormal serum lipid concentrations and insulin resistance) also put some women at an increased risk of developing diabetes mellitus (1)
| NICHD (1990) Diagnostic Criteria for PCOS is: |
| Clinical Hyperandrogenism (Ferriman-Gallwey Score >8) or Biochemical Hyperandrogenism (Elevated Total/Free Testosterone) AND |
| Oligomenorrhea (Less Than 6-9 Menses per Year) or Oligo-Ovulation AND |
| Polycystic Ovaries on Ultrasound (>= 12 Antral Follicles in One Ovary or Ovarian Volume >= 10 cm3) |
| Rotterdam (2003) Diagnostic criteria for PCOS - two out of three of: |
| Clinical Hyperandrogenism (Ferriman-Gallwey Score >8) or Biochemical Hyperandrogenism (Elevated Total/Free Testosterone) OR |
| Oligomenorrhea (Less Than 6-9 Menses per Year) or Oligo-Ovulation OR |
| Polycystic Ovaries on Ultrasound (>= 12 Antral Follicles in One Ovary or Ovarian Volume >= 10 cm3) |
| AE-PCOS Society (2009) Diagnostic Criteria for PCOS is: |
| Clinical Hyperandrogenism (Ferriman-Gallwey Score >8) or Biochemical Hyperandrogenism (Elevated Total/Free Testosterone) PLUS Either of: |
| Oligomenorrhea (Less Than 6-9 Menses per Year) or Oligo-Ovulation OR |
| Polycystic Ovaries on Ultrasound (>= 12 Antral Follicles in One Ovary or Ovarian Volume >= 10 cm3) |
Thyroid dysfunction, congenital adrenal hyperplasia, hyperprolactinaemia, androgen-secreting tumours and Cushing’s syndrome must to be excluded before making a diagnosis of PCOS (1).
Although the primary aetiology of PCOS is unknown
- insulin resistance with compensatory hyperinsulinaemia is a prominent feature of the syndrome and seems to play an important physiopathological role in hyperandrogenism, in both lean and obese women with PCOS (5,6)
- hyperinsulinaemia increases ovarian androgen biosynthesis, both in vivo and in vitro (7,8)
- decreases the hepatic production of sex hormone-binding globulin (SHBG)(9)
- leading to increased bioavailability of free androgens
- PCOS task force recommends to utilize either follicle number per ovary (>=25) when a sophisticated US transducer >= 8MHz is available or, otherwise, an ovarian volume of >=10 ml to define PCOS morphology (10)
Suggested differential diagnoses and screening tests (11)
- pregnancy - pregnancy test
- hypothyroidism - TSH
- hyperprolactinemia - PRL
- Cushing's syndrome - 24-hour urine free cortisol
- late-onset CAH (congenital adrenal hyperplasia) - 17-hydroxyprogesterone
- ovarian tumor - total testosterone
- hyperthecosis - total testosterone
- adrenal tumor - dehydroepiandrosterone sulfate (DHEAS)
Ovulatory dysfunction can still occur with regular cycles and if anovulation needs to be confirmed serum progesterone levels can be measured (12).
If irregular menstrual cycles are present a diagnosis of PCOS should be considered (12)
Reference:
- RCOG (2007) Long-term consequences of polycystic ovary syndrome.
- Zawadski JK, Dunaif A. Diagnostic criteria for polycystic ovary syndrome: towards a rational approach. In: Dunaif A, Givens JR, Haseltine FP, Merriam GR, editors. Polycystic Ovary Syndrome. Boston: Blackwell Scientific Publications; 1992. pp. 377-384.
- Rotterdam ESHRE/ASRM-Sponsored PCOS Consensus Workshop Group, authors. Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome. Fertil Steril. 2004;81:19-25.
- Azziz R, Carmina E, Dewailly D, et al. Task Force on the Phenotype of the Polycystic Ovary Syndrome of The Androgen Excess and PCOS Society. The Androgen Excess and PCOS Society criteria for the polycystic ovary syndrome: the complete task force report. Fertil Steril. 2009;91:456-488.
- Dunaif A et al. Profound peripheral insulin resistance, independent of obesity, in polycystic ovary syndrome. Diabetes 1989;38:1165-74.
- Tsilchorozidou T, Overton C, Conway GS. The pathophysiology of polycystic ovary syndrome. Clinical Endocrinology2004;60(1):1-17.
- Barbieri RL, Makris A, Randall RW, Daniels G, Kistner RW,Ryan KJ. Insulin stimulates androgen accumulation inincubations of ovarian stroma obtained from women with hyperandrogenism. Journal of Clinical Endocrinology and Metabolism 1986;62:904-10.
- Adashi EY, Resnick CE, D'Ercole AJ, Svoboda ME, Van Wyk JJ.Insulin-like growth factors as intraovarian regulators of granulosa cell growth and function. Endocrine Review1985;6:400-20.
- Nestler JE, Powers LP, Matt DW, Steingold KA, Plymate SR,Rittmaster RS, et al. A direct effect of hyperinsulinemia onserum sex hormone-binding globulin levels in obese women with the polycystic ovary syndrome. Journal of ClinicalEndocrinology and Metabolism 1991;72:83-9.
- Dewailly D., Lujan M.E., Carmina E., Cedars M.I., Laven J., Norman R.J. Definition and significance of polycystic ovarian morphology: a task force report from the androgen excess and polycystic ovary syndrome society. Hum Reprod Update. 2014;20(3):334-352
- Sheehan MT. Polycystic ovarian syndrome: diagnosis and management. Clin Med Res. 2004 Feb;2(1):13-27.
- Teede HJ, Misso ML, Costello MF, Dokras A, Laven J, Moran L, Piltonen T, Norman RJ; International PCOS Network. Recommendations from the international evidence-based guideline for the assessment and management of polycystic ovary syndrome. Fertil Steril. 2018 Aug;110(3):364-379.