Polycystic ovarian syndrome

Published on 09/03/2015 by admin

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Last modified 09/03/2015

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Chapter 5 Polycystic ovarian syndrome

Definition. The definition of polycystic ovarian syndrome (PCOS) was revised in 2003 (Rotterdam Consensus criteria). The diagnosis is based on two out of three of the following criteria:

• oligo or anovulation

• clinical and/or biochemical signs of hyperandrogenism

• polycystic ovaries, defined as at least one of the following:

• 12 or more follicles measuring 2–9 mm in diameter

• increased ovarian volume (>10 cm³)

If there is evidence of a dominant follicle (>10 mm) or a corpus luteum, the scan should be repeated during the next cycle. Only one ovary fitting this definition or a single occurrence of one of the above criteria is sufficient to define the PCOS. It does not apply to women taking the oral contraceptive pill. Regularly menstruating women should be scanned in the early follicular phase (days 3–5). Oligomenorrhoeic and amenorrhoeic women should be scanned either at random or between days 3 and 5 after a progestogen-induced bleed and the exclusion of other aetiologies (congenital adrenal hyperplasia, androgen-secreting tumours, Cushing’s syndrome).

Prevalence. Prevalence is 5%–7% overall, 85% of oligomenorrhoeic females, 90% of women with hirsutism and 30% of infertile women.

Clinical presentation

• menstrual irregularities

• amenorrhoea or oligomenorrhoea

• variable menstrual loss

• infertility

• androgen excess, such as hirsutism or acne

Aetiology

• Aetiology is multifactorial.

• About 50% of women with PCOS have affected sisters.

• Multiple candidate genes have been identified, but it is likely that a number of different pathways, both genetic and environmental, contribute to the same phenotype.

Pathophysiology

PCOS is characterised by ovarian, hypothalamic–pituitary, peripheral and adrenal dysfunction. The phenotype develops through chronic anovulation of any aetiology and a clear sequence of events is therefore not identifiable.

Ovaries

• High luteinising hormone (LH) levels drive ovarian androgen production.

• High intraovarian androgen concentrations inhibit follicular maturation and lead to inactive granulosa cells with minimal aromatase activity.

• The large number of ovarian follicles produces a high inhibin B, which inhibits follicle-stimulating hormone (FSH).

Hypothalamus–pituitary

• Hypothalamic dysfunction is associated with increased gonadotropin-releasing hormone agonist (GnRH) frequency and tonic (i.e. non-cyclic) LH release, elevating the LH/FSH ratio. The increase in LH is more pronounced in lean patients.

• The large number of ovarian follicles produces a high inhibin B, which inhibits FSH, but as FSH is not fully suppressed, continuous follicular recruitment and stimulation proceeds, but not to the level of full maturation and ovulation.

• Increased oestrogen production stimulates an increase in prolactin.

Peripheral compartment

• Reduced sex hormone-binding globulin (SHBG) concentrations perpetuate hyperandrogenaemia:

• hyperinsulinaemia

• hepatic dysfunction

• Peripheral alteration in insulin-like growth factor (IGF-1), androgen and oestrogen levels perpetuate hypothalamic dysfunction.

• Obesity reduces SHBG and increases peripheral aromatisation of androgens (androstenedione), which produces a chronic hyperoestrogenic state with reversal of the oestrone:oestradiol ratio.

Adrenal compartment

• dysregulation of cytochrome p-450c17 (as in the ovaries), but dehydroepiandrosterone sulfate (DHEAS) (of adrenal origin) is only increased in 50% of PCOS

• exaggerated adrenarchal response

Consequences of PCOS

Related

Examination Obstetrics _ Gynaecology