HIRSUTISM

Definition  Hirsutism Excessive growth of hair in abnormal position on the body  Virilism Masculinization of female i.e. deepening of voice, male type baldness, clitoral hypertrophy, breast atrophy, increased musculature and oligo or amenorrhoea

Pathogenesis Increased circulating androgens ovarian or adrenal in origin Increased free testosterone due to decreased SHBG Increased peripheral conversion of testosterone to DHT due to increased 5 alpha reductase activity Genetic ir racial predisposition

Causes 1.Ovarian PCOS Tumours 2.Adrenal CAH Tumours 3.Pituitary Tumours ACTH secreting (Cushing’s disease) Prolactin secreting Growth hormone secreting (acromegaly)

Causes 4. Ectopic ACTH producing tumours (bronchus, pancreas, thyroid, thymus) 5. Iatrogenic Androgenic drugs(testosterone, danazol,glucocorticoids,progestogens, phenytoin) 6. Idiopathic

Polycystic Ovarian Syndrome LH:FSH ratio of 3:1 Baseline estrogen level increased Hyperprolactinaemia (15%) Testosterone slightly raised (< 5 nmol/L) Ultrasound criteria Peripheral distribution of 10 or more follicles 2 to 8 mm in diameter increased ovarian stroma Increased ovarian volume

Idiopathic Hirsutism Absence of an identifiable pathology Increased end organ sensitivity to normal androgens level due to increased 5 alpha reductase activity Regular menstrual cycle Normal ovaries on ultrasound Serum testosterone <5 nmol/l (After excluding all possible organic causes) Normal LH,FSH, prolactin and estrogen

Congenital Adrenal Hyperplasia Excessive production of androgens due to deficiency of enzymes required for biosynthesis of glucocorticoids Raised testosterrone level > 5 nmol/l Raised serum 17 alpha hydroxy progesterone Raised urinary ketosteroids

Cushing Syndrome Over production of cortisol by adrenals due to excessive production of ACTH 24 hrs urinary free cortisol plasma cortisol ACTH levels

Androgen Producing Ovarian tumours Mostly benign in young females < 30 yrs Androblastoma, luteoma Hirsutism is rapid in onset Signs of virilism Serum testosterone grossly elevated Diagnosed by USG, CT or MRI

Adrenal Tumours Marked hirsutism associated with virilism Common in premenopausal women Serum testosterone & DHEAS are markedly raised Final diagnoses is made by CT scan or MRI

Acromegaly Excessive production of growth hormones by pituitary adenoma Raised growth hormone levels during GTT. In normal subjects growth hormone levels are suppressed during GTT X – ray skull, CT scan and MRI may be useful

Iatrogenic Hirsutism Androgenic drugs Hair growth returns to normal once the drug intake is stopped

Management  History Duration of complaint Hair distribution on body & rate of growth Weight gain, oligomenorrhoea, infertility with hirsutism suggestive of PCOS Deepening of voice, reduction in breast size, secondary amenorrhoea, changes in external genitalia to rule out adrenal or ovarian tumours

H/o primary amenorrhoea with hirsutism suggests CAH Changes in facial appearance, striae on skin, polyuria & polydypsia indicates Cushing syndrome Drug history H/o galactorrhoea & enlargement of extremities suggests acromegaly Family history

Examination Weight & BP Whole body inspection Examination of breasts, extremities, facial changes Ophthalmic exam Abdominal exam for any mass Pelvic exam for clitoromegaly, labial thickening, uterus and adnexa

Investigations a.Hormonal levels  First line in every patient FSH, LH, testosterone, prolactin, and DHEAS  Second line 17 alpha hydroxyprogesterone, cortisol & growth hormone

Investigations Ultrasonography Ct & MRI of pituitary & adrenals

Treatment Aims of treatment Counselling Weight control Cosmetic treatment Suppression of excessive androgen production Prevent new hair growth by antiandrogens

Cosmetic treatment Useful in mild hirsuitism Must be used alongwith medical therapy Methods are: shaving, bleaching, waxing, plucking,electrolysis & laser. Laser & electrolysis are most satisfactory

Antiandrogens Cyproterone acetate –Can be used alone or with COC –Preferred is Diane-35 Spironolactone Flutamide Ketoconazole

Suppression of excessive androgen production  Ovarian suppression COC GnRH analogues Surgical –Ovarian wedge resection –Laproscopic drilling –Bilateral oophorectomy

 Adrenal suppression Small nocturnal dose of dexamethasone( mg) to lower elevated levels of DHEAS Combination of COC & dexa can be used  5 alpha reductase inhibitors Finasteride to suppress active form of testosterone

Efficacy of treatment Take 03 to 06 months to show its effects 60 – 70 % improvement by the end of 12 months Maintenance therapy is needed to prevent recurrence

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