Polycystic ovary syndrome (PCOS) is a common endocrine disorder, characterised by excess androgen production and the presence of multiple immature follicles (“cysts”) within the ovaries.
You can however have one of these in the absence of the other
The pathophysiology of PCOS relates to excess androgen production, and this is usually due to one or both of:
Excess LH (luteinising hormone) production: the anterior pituitary releases gonadotropin in response to gonadotropin-releasing hormone. This leads to excess androgen production by the ovaries.
Hyperinsulinemia and insulin resistance: Hyperinsulinemia may stimulate the ovary to over-produce testosterone and prevent the follicles from growing normally to release eggs. This causes the ovaries to become polycystic.
Most women with PCOS have “cysts” found on their ovaries. These are immature follicles which have had their ovulation phase arrested. This occurs due to an elevated baseline of LH and lack of LH surge (as in a normal menstrual cycle)
Despite the high levels of LH, the increased circulating androgens suppress the LH surge (which is required for ovulation to occur). Follicles develop within the ovary, but are arrested at an early stage (due to the disturbed ovarian function) – and they remain visible as “cysts” within the ovary.
Risk factors:
Obesity
Diabetes
Family history
Premature adrenarche (pubic hair)
The genetic inheritance of PCOS is complex but appears to be inherited in an autosomal dominant fashion
Symptoms:
Usually presents in a woman around puberty - mid 20s
Hirsutism - especially face, chest and back (most common symptom)
Chronic pelvic pain
Infertility
Acne
Oligomenorrhoea (<9 a year) or amenorrhoea
Obesity and weight gain
Alopecia
Clinical exam:
Hirsutism
Hyperandrogenism - acne, hair loss and male pattern baldness
PCOS can present similarly to other endocrine disorders, including:
Thyroid dysfunction: particularly hypothyroidism can lead to hair loss and menstrual cycle irregularities. However, hirsutism is rare.
Congenital adrenal hyperplasia (21-hydroxylase deficiency): this causes cortisol deficiency and may also lead to androgen excess, leading to a clinical picture indistinguishable from that of PCOS.
Cushing’s syndrome: excess cortisol production -weight gain, acne, hypertension, insulin resistance).
Hyperprolactinaemia: . Galactorrhoea is usually present.
Bedside investigations:
Urine hCG
Blood glucose - insulin resistance and T2DM
Lab tests:
Baseline - FBC, U&Es, CRP
Testosterone (total and free) - raised
Sex hormone-binding globulin (SHBG) - normal to low
Testosterone to SHBG ratio - may be raised
LH and FSH - often raised, and a LH:FSH ratio >3 suggests PCOS
Lipid screen
Oral glucose tolerance test to assess insulin resistance
Other tests to exclude other causes e.g. TFTs, prolactin
Imaging:
Most important imaging for PCOS is a pelvic ultrasound scan (usually transvaginal)
20 or more follicles (cysts) on at least one ovary and/or
Increased ovarian volume
The syndrome can exist without polycystic ovaries
Diagnosis of PCOS is based on the Rotterdam criteria.
Two of the following three criteria must be met to make a diagnosis of PCOS: