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A member on Docplexus had a query on hirsuitism.

I have uploaded simple under graduate level lecture on Hirsuitism and Cong Adr Hyperplasia, which should give a simple and lucid overview of the distressing condition.

Several treatment options are available. Never forget to tell the patient that benefits will begin in 3 months time or so, otherwise they will run from clinic to clinic without relief.

Published in: Health & Medicine
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  1. 1. Virilization
  2. 2. Virilization Clinical features associated with a high level of male hormones in women. • Hirsuitism • Acne • Deepening of voice • Increased muscle mass • Breast atrophy
  3. 3. Hirsutism • Excessive growth of thick terminal hair in a male distribution in women (upper lip, chin, chest, back, lower abdomen, thigh, forearm) • Most common presentation of endocrine disease. • DD: Hypertrichosis, which is generalised excessive growth of vellus hair. • The aetiology is androgen excess
  4. 4. Androgens and Hirsuitism • Hirsutism can be caused by either an increased level of androgens or an oversensitivity of hair follicles to androgens. • Testosterone stimulates hair growth, (size, intensity of growth and pigmentation).
  5. 5. obesity/insulin and Hirsuitism • High circulating levels of insulin are implicated in women for the development of hirsutism. • Obese (insulin resistant hyperinsulinemic) women are at high risk of becoming hirsute. • Treatments that lower insulin levels lead to a reduction in hirsutism. • High concentration of insulin (directly and through IGF I) is thought to stimulate theca cells in ovaries to produce androgens.
  6. 6. Hirsuitism: Causes • Idiopathic • Polycystic ovarian syndrome • Congenital adrenal hyperplasia • Exogenous androgen administration • Androgen-secreting tumour of ovary or adrenal cortex
  7. 7. Hirsuitism: Idiopathic • Often familial Mediterranean or Asian background • Investigations: normal • Treatment: –Cosmetic measures –Anti-androgens
  8. 8. Hirsuitism: PCOS • Aetiology -poorly understood • Constellation of clinical and biochemical features of varying severity –Obesity –Oligomenorrhoea/ Secondary amenorrhoea –Infertility –multiple cysts in the ovaries
  9. 9. Hirsuitism: PCOS Mechanisms* Manifestations Pituitary dysfunction High serum LH High serum prolactin Anovulatory menstrual cycles Oligomenorrhoea Secondary amenorrhoea Cystic ovaries Infertility Androgen excess Hirsutism Acne Obesity Hyperglycaemia Elevated oestrogens Insulin resistance Dyslipidaemia Hypertension
  10. 10. Hirsuitism: PCOS • Investigations: LH:FSH ratio > 2.5:1 Minor elevation of androgens Mild hyperprolactinaemia • Treatment Weight loss Cosmetic measures Anti-androgens Insulin-sensitising drugs
  11. 11. Hirsuitism: Congenital adrenal hyperplasia • 95% 21-hydroxylase deficiency • Clinical Features: –Pigmentation –History of salt-wasting in childhood –Ambiguous genitalia –Adrenal crisis when stressed
  12. 12. Hirsuitism: Congenital adrenal hyperplasia • Investigations – Elevated androgens, suppressible with dexamethasone –Abnormal rise in 17OH-progesterone with ACTH • Treatment –Glucocorticoid replacement administered in reverse rhythm to suppress early morning ACTH
  13. 13. Hirsuitism: Exogenous androgens • Athletes Virilised • Investigations: –Low LH and FSH –Analysis of urinary androgens may detect drug of misuse • Treatment: –Stop steroid misuse
  14. 14. Hirsuitism: Androgen-secreting tumour ovary or adrenal cortex • Rapid onset virilisation: –clitoromegaly –deep voice –balding –breast atrophy
  15. 15. Hirsuitism: Androgen-secreting tumour ovary or adrenal cortex • Investigations: – High androgens which do not suppress with dexamethasone or oestrogen – Low LH and FSH – CT or MRI usually demonstrates a tumour • Treatment: – Surgical excision
  16. 16. Hirsuitism : Clinical approach • The severity of hirsutism is subjective • Important observations are – – Drug and menstrual history – Calculation of BMI – Measurement of BP – Examination for virilisation (clitoromegaly, deep voice, male-pattern balding, breast atrophy) – Acne vulgaris – Cushing's syndrome • When recent & with virilisation, suggestive of a rare androgen-secreting tumour
  17. 17. Hirsuitism:Investigations Random blood sampling for testosterone, prolactin, LH and FSH
  18. 18. Hirsuitism:Investigations • Random blood – testosterone, Prl, LH and FSH. • If Cushingoid features +: Overnight 1 mg Dexa suppression test
  19. 19. Hirsuitism:Investigations • Random blood – testosterone, Prl , LH and FSH. • If Cushingoid : Overnight 1 mg DST • If testosterone levels are high (with low LH & FSH): look for source of excess androgen
  20. 20. Hirsuitism:Investigations • Random blood – testosterone, Prl , LH and FSH. • If Cushingoid : Overnight 1 mg DST • If testosterone high (with low LH & FSH): ? source • Suspected CAH (21-hydroxylase deficiency): short ACTH stimulation test, with measurement of 17OH-progesterone
  21. 21. Hirsuitism: Investigations • Androgen-secreting tumours: Testosterone is not suppressible by –Dexamethasone • Overnight or • 48-hour low-dose suppression test –Oestrogen (30 μg / day X 7 days) • CT or MRI of the adrenals and ovaries
  22. 22. Hirsuitism: Treatment • Cosmetic measures - shaving, bleaching and waxing • Electrolysis and laser treatment : for small areas • Eflornithine cream : Inhibits ornithine decarboxylase in hair follicles & may reduce hair growth
  23. 23. Hirsuitism: Treatment • Weight reduction for obese patients with PCOS –enhances insulin sensitivity –reduces the peripheral conversion of androgens by adipose tissue –reduces metabolic clearance of cortisol, thereby reducing ACTH-dependent adrenal androgen secretion
  24. 24. Hirsuitism: Treatment If these conservative measures have failed- • Anti-androgen therapy The life cycle of hair follicles is at least 3 months, so no improvement is likely before this. Only replacement hair growth is suppressed. • Insulin-sensitising drugs (thiazolidinediones and biguanides) Have a role but unless the patient has lost weight, the hirsutism will return once discontinued.
  25. 25. ANTI-ANDROGEN THERAPY • Androgen receptor antagonists –Cyproterone acetate –Spironolactone • 5 α-reductase inhibitors (prevents conversion of testosterone to active form)- –Finasteride • Suppress ovarian steroid production and elevate SHBG (sex hormone-binding globulin ) – Oestrogen (+ Cyproterone acetate) • Suppress adrenal androgen production- –Glucocorticoids