Hirsutism is excessive growth of terminal hair in women in an androgen-dependent distribution. This involves the upper lip, chin, chest, lower abdomen, back, forearm and thighs.
The hair is pigmented and thick and should be differentiated from hypertrichosis, which is the generalized growth of thin, non-pigmented hair that is typically found all over the body from childhood onwards( vellus hair)
Pathophysiology;
- There are three phases of hair growth- anagen, catagen, telogen
- Androgens increase the size of the hair follicle, the hair fibre diameter, and the duration that terminal hairs spend in the anagen phase
- Male pattern hair growth occurs in areas where relatively high levels of androgen are required for pilosebaceous unit differentiation
- However, the androgens will cause hair loss in the scalp region, in part by reducing the duration the scalp hairs remain in the anagen phase
- Nearly all hirsute women have an increased rate of production of androgens, which may be adrenal or ovarian in origin
Causes of hirsutism
- Idiopathic
- Congenital adrenal hyperplasia
- Polycystic ovarian syndrome
- Exogenous androgen administration
- Androgen secreting tumours
- Cushing’s syndrome
Clinical features;
- The severity is subjective to different women
Important aspects in the history and physical examination;
- Age of onset
- Stable vs progressive hair growth
- Drug and menstrual history
- BMI
- Blood pressure
- Emotional distress/ depression
- Examine for virilization- deep voice, clitoromegaly, male pattern balding and breast atrophy
- Look for associated features such as acne vulgaris or Cushing’s syndrome
-Hirsutism of recent onset suggests an androgen-secreting tumour
-Ferriman Gallwey Score can be conducted, although it has limitations since ethnic/ racial groups influence e hair growth
Investigations
1. Blood sample for testosterone, LH, prolactin and FSH
- Further investigation if there are signs of Cushing’s syndrome
- If testosterone is more than two times the upper limit of normal for females, idiopathic hirsutism and PCOS are less likely, especially if the LH and FSH are low
2. Short ACTH stimulation test- measurement of 17-OH-progesterone.
- To diagnose congenital adrenal hyperplasia due to 21-hydroxylase deficiency.
3. Lack of suppression of testosterone following a 48-hour low dose dexamethasone suppression test is confirmatory
- The tumour is then sought through a CT scan or MRI
4. Serum IGF-1 in those with features of excess growth hormone
5. Pelvic ultrasound- to aid in the identification of ovarian or adrenal tumours
Management
It depends on the cause.
1. PCOS-
- Weight loss
- Combined oral contraceptives
- Anti-androgens
- Cosmetic measures
- Metformin, glitazones
2. Congenital adrenal hyperplasia;
- Glucocorticoid replacement
3. Exogenous androgen administration- stop steroid misuse
4. Androgen secreting tumour- surgical excision
5. Cushing’s syndrome- treat the underlying cause
6. Idiopathic-
- Cosmetic measures
- Anti-androgens
Other measures;
- Direct hair removal through electrolysis and photo epilation. However, women with underlying hyperandrogenemia may experience regrowth, and this can be prevented by giving anti-androgens
*Combined oral contraceptives are the first line in the management of hyperandrogenemia. An anti-androgen is added if there is a suboptimal response after six months of therapy
- COCs have the additional benefit of contraception and cycle management. They also have the benefit of preventing endometrial hyperplasia in PCOS
- In women with a reliable form of contraception, anti-androgens or COCs can be used as monotherapy from the initial stage since the COCs and anti-androgens have similar efficacy. This is because anti-androgens can have harmful effects on a male fetus
