Dr Khaldoun Khamaiseh FRCOG MRCP

Consultant in O& G & reproductive endocrinology

Telogen: resting phase: 3 months

Anagen: Active growing phase: 2-7 years

Catagen: shedding phase: 2-3 weeks

The length of each phase is different in various parts of the body affecting hair lenth : scalp has long anagen and short telogen resulting in long hair

Excess hair, male pattern Incidence 15% Includes : Chin, upper lip, chest, upper and lower back, upper

and lower abdomen, upper arm, thigh and buttocks The Ferriman Gallwey scoring system is used to evaluate the

degree of hirsutism before and after treatment

Virilization: severe form, with male hair and habitus, increased muscle mass, increased libido, clitoromegaly, deepening of the voice

Androgens causes hair growth (free active form)

8-15 mild

Above 15 significant

Testosterone

Dihydrotestosterone

Androstenodione

Dehydroepiandrosterone(DHEA)

Dehydroepiandrosterone sulphate(DHEAS)

Acne

Oily skin

Frontal balding

Acanthosis nigricans(Insulin resistance)

Strongest androgen is DHT

It is 10 times stronger than T

The enzyme responsible for conversion of T to DHT is alpha reductase

Other androgens are weaker

There is poor correlation between the presence or severity of hirsutism and serum levels of T and DHT

Spectrophotometry better than radio immunoassay in measuring T level due to reduced interference from non‐testosterone androgens but are not widely available

T is mostly protein bound

Only 1% is free and active

80% bound to Sex hormone binding globulin (SHBG)

19% bound to albumin

Estrogen increases the level of SHBG

PCOS

Adrenal tumours

Ovarian tumours

Ovarian hyperthecosis

Cushing’s syndrome

Hyperprolactinaemia

Congenital adrenal hyperplasia

Iatrogenic: Drugs

The chronology of symptom commencement and progression is important and can be indicative of specific disease processes.

Rapid excessive hair growth, deepened voice and breast atrophy would be more indicative of an adrenal tumour

Slow development of hirsutism and menstrual irregularities occurring soon after puberty, classically due to PCOS.

Disruption of the timing of puberty can be associated with congenital adrenal hyperplasia (CAH) and Cushing's syndrome. A family history is also important as both PCOS and CAH can occur in other family members.

PCOS defined as the presence of 2 out of 3 of the

following

Oligo or anovulation

Hyperandrogenism (clinical or biochemical)

Polycystic ovaries

after exclusion of other causes(Late onset CAH, Cushing

syndrome,hyperprolactinaemia,ovarian and adrenal

tumours )

1. Hyperandrogenism,anovulation and PCO(50%)

2. Hyperandrogenism+anovulation, normal ovaries (14.6%)

3. Hyperandrogenism and PCO, regular ovulatory cycles (28.9%)

4. Anovulation and PCO ,no hyperandrogenism

(5.7%)

Insulin resistance causes high level of Insulin. This stimulates androgen secretion from the ovary (Burghen)

Acts on the liver decreases SHBG and IGFBP-2 (Leo et al 2003) thus increase the free active fraction of Testosterone

Autosomal recessive

21 hydroxylase deficiency in 95% of cases results in low cortisol, then ACTH increased and drives androgen production

Accounts for 5% of women with hirsutism

Autosomal recessive

Strong family history

T level above 5 nmol/l

Classic 21‐hydroxylase deficiency commonly presents in infancy. Severely virilised females with ambiguous genitalia. Salt wasting and adrenal crises can occur in some patients and are important causes of neonatal death.

Non‐classic 21‐hydroxylase deficiency tends to present in puberty (late onset) oresents with hyperandrogenism but have preserved cortisol and aldosterone production, so salt wasting and adrenal crises are not common features of this condition.

Many female patients can present in early adulthood with menstrual disturbance or hirsutism.

Hirsutism is present in 80% of patients.

Cushing's syndrome results from increased circulating concentrations of cortisol and can present insidiously with centripetal weight gain, facial plethora, supraclavicular fat pads, abdominal striae and signs of hyperandrogenism, such as hirsutism, acne and male pattern baldness.

Secondary to an ACTH secreting pituitary tumour (Cushing's disease)

Autonomous cortisol secretion by the adrenal glands due to adrenocortical neoplasms or hyperplasia

Exogenous administration of glucocorticoids

Ectopic ACTH secretion in neoplasia including small cell lung carcinomas and carcinoid tumours.

Sertoli Leydig cell tumours: most common virilising ovarian tumours account for 0.5% of all ovarian neoplasms.

Hilar cell tumour Brenner tumour. These tumours are characterised by striking

elevations in serum testosterone but normal DHEA‐S

Computerised tomography, magnetic resonance imaging and ultrasound are used to make the diagnosis

Accounts for most of the cases of hyperandrogenaemia in postmenopausal women

Describes the presence of luteinised theca cell nests in the ovarian stroma.

When compared with PCOS, hyperthecosis is typically associated with more severe hyperandrogenism and virilisation.

Testosterone concentrations are much higher than in PCOS and may exceed 7 nmol/l.15

Short Synacthen test: 17 OH progesterone and cortisol measured before and 1 hr after 250 ug of synthetic ACTH given IV or IM

Cosmetic treatments: Waxing, Laser, electrolysis & depilatory creams: effective while waiting for medical RX to work

Medical treatment takes 3-6 months

Electrolysis is the only permanent RX but expensive and needs expertise

Removing the hair does not increase the rate of growth

Weight loss , insulin sensitizers

COC, containing cyproterone acetate and drospirenone: Diane 35, Yasmin, Yaz

Cyproterone actetae is a progesterone,25-50 mg D3-D 13 cycle

Spiranolactone,weak diuretic 25 mg-200 mg daily

Flutamide:

blocks androgen receptors S/E hepatotoxicity

Finasteride: of 5 alpha reductase inhibitor given 5 mg daily less S/E’s

Hyperandrogenism in women is a common and distressing condition

The most common cause is PCOS

2–5 nmol/l are associated with PCOS while concentrations above 5 nmol/l should prompt investigation for another cause.

Prior to making a diagnosis of PCOS, other possible causes of hyperandrogenism should be excluded.

Thank you