Hirsutism

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Last modified 22/04/2025

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166 Hirsutism

Instruction

Examine this patient.

Salient features

History

• Age of onset

• Rate of progression of hirsutism

• History of thinning of scalp hair, or deepening of voice

• History of obesity

• Drug history: corticosteroids, androgen, phenytoin, minoxidil, diazoxide, ciclosporin

• Take a menstrual history: oligomenorrhoea, infertility, acne, seborrhoea or voice change suggest polycystic ovaries

• Family history (familial).

Examination

• Excessive hair growth, particularly over the face (Fig. 166.1) and upper and lower limbs.

Note: The amount and distribution of hair is an index of androgen effect. Terminal hairs on the face, around the areolae or on the lower abdomen or lower back may be normal, but hair on the upper back, shoulders and upper abdomen suggests a more marked increase in androgen production.
image

Fig. 166.1 Hirusutism.

Proceed as follows:

• Tell the examiner that you would like to:

• check the BP and urine for sugar
• look for signs of virilization (receding hairline, muscular development, breast atrophy, clitoromegaly).

• Comment on cushingoid features, if any.

Diagnosis

This patient has hirsutism (lesion) caused by polycystic ovarian disease (etiology) that is cosmetically unacceptable (functional status).

Questions

What do you understand by the term hirsutism?

Hirsutism is the male pattern of hair growth in women and consists of excessive terminal hair (androgen-sensitive hair). It is abnormal, particularly on the chin, sternum, upper abdomen and upper back in women. Terminal hair may normally occur on the arms, legs, upper lips, linea alba and periareolar area in women. To be active in hair follicles, testosterone has to be converted locally to dihydrotestosterone by 5α-reductase. The sensitivity of the hair follicle to androgens is governed largely by cutaneous 5α-reductase activity. Consequently, similar androgen production profiles may produce different hair growth patterns in different women. Even in hirsute women, hair growth may have greatly variable patterns.

The degree of hirsutism can be assessed by the Ferriman–Gallwey Score, which records distribution and severity of excess body hair on a scale of 1–4 for nine regions (J Clin Endocrinol Metab 1961;21:1440–7).

Why do you want to take a menstrual history?

If menstruation is normal, it indicates that there is no increase in testosterone production. However, if menstruation is abnormal, the commonest cause is polycystic ovary disease (POCD or Stein–Leventhal syndrome), which is the underlying cause in 92% of the women with hirsutism (the popular belief that most cases of hirsutism are idiopathic is untrue).

Advanced-level questions

What other causes of hirsutism are there?

• Cushing syndrome

• Adrenal or ovarian tumours

• Acromegaly

• Drugs:

• those that increase vellus growth: phenytoin, minoxidil, diazoxide, ciclosporin
• those that increase terminal hair growth: androgens.

• Familial

• Ethnic: a ‘male-pattern’ of hirsutism is common in women whose ancestors hail from southern Europe.

What is the relationship between body weight and hirsutism?

Hirsute women are more likely to be obese than non-hirsute women. Therefore, weight loss must be a priority in treating overweight women with hirsutism.

What is the role of testosterone in hirsutism?

Testosterone is the most potent androgen and is derived directly from ovarian secretion (60%) and from peripheral conversion of androstenedione (40%). About 65% of testosterone is strongly bound to sex hormone-binding globulin (SHBG) and 33% is weakly bound to albumin. The remaining 2% is free testosterone and can enter target cells to exert its androgenic effect. Other androgens include androstenedione (secreted in equal amounts by adrenals and ovaries) and dehydroepiandrosterone (derived exclusively from the adrenals).

What is the pathophysiology of polycystic ovary disease?

It is caused by an abnormality of pulsatile secretion of gonadotrophin-releasing hormone (GnRH), which causes increased secretion of luteinizing hormone (LH) and follicle-stimulating hormone (FSH). This results in hyperplasia of the ovarian thecal cell leading to multiple follicular cysts and excessive androgen synthesis and anovulation.

Remember: POCD is the association of hyperandrogenism with chronic anovulation in women without specific underlying diseases of adrenals or pituitary glands.

How would you investigate suspected polycystic ovary disease?

• Ovarian ultrasonography is the most accurate investigation; typically it shows thickened capsules, multiple cysts of 3–5 mm diameter and a hyperechogenic stroma (Fig. 166.2).

• Biochemistry:

• Total testosterone levels may be normal, but free androgens are raised
• SHBG is low
• LH : FSH ratio is raised, usually greater than 2 : 1, but FSH level is low or normal
• Mild hyperprolactinaemia is common and rarely exceeds 1500 mU/l.
image

Fig. 166.2 Transvaginal ultrasonography during the follicular phase of a menstrual cycle, showing the fluid-filled antrum of a developing follicle (dark circle); the polycystic ovary is typically enlarged and contains an abnormally increased number of developing follicles.

(With permission from Mitani et al. 2007.)

Is glucose metabolism affected in polycystic ovary disease?

POCD is associated with hyperinsulinaemia and insulin resistance, and consequently patients may have impaired glucose tolerance. The site of insulin resistance is skeletal muscle and fatty tissue, not the liver (as in non-insulin-dependent diabetes mellitus). It is believed that full expression of POCD requires both the insulin abnormality and the disorder of androgen biosynthesis.

How would you treat hirsutism?

• Treatment is directed towards the underlying cause of hyperandrogenism

• Mild hyperandrogenism that is idiopathic or mild POCD: oral contraceptives

• Severe hirsutism: anti-androgens (spironolactone, cyproterone acetate, flutamide) and finasteride (5α-reductase inhibitor) prevent the cutaneous conversion of testosterone to active dihydrotestosterone; GnRH analogues (leuprolide, nafarelin)

• Local treatment: shaving, epilation, laser-assisted epilation (phototricholysis), waxing, electrolysis or bleaching.

IF Stein (1887–1976), a US gynaecologist, and ML Leventhal (1901–1971), a US obstetrician (Stein IF, Leventhal ML. Amenorrhea associated with bilateral polycystic ovaries. Am J Obstet Gynecol 1935;29:181–191).

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