1. HIRSUTISM Dr. Maysa’khadra MBBS, MMed(RHHG)
A/P Reproductive Endocrinology and Infertility
Jordan University Hospital

2. Introduction
Def: the presence of terminal ( coarse) hairs in females in a male-like pattern.
It affects 5-15% of women
Usually associated with an underlying endocrine disoder : in 70-80% of women with hirsutism this is PCOS
Idioaapthic Hirsutim: isloated condition

3. Normal Hair Growth
50 million hair follicle on the human body, 100, ,000 are found on the scalp
Palms, soles and lips are the only body parts lacking hair follicles
Few hair follicles form after birth
After the age of 40 years hair follicles decrease in number

4. Normal Hair Growth Three types of hairs:
Lanugo: a soft hair densely covering the fetus, usually shed in the 1st 4 months postpartum
Vellous: soft longer than lanugo hair (< 2cm), non pigmented which covers the body
Terminal longer, pigmented , makes up the yebrows, scalp and axillary and pubic areas

5. Normal Hair Growth Three phases of hair growth:
anagen: active growing phase
catagen: involuting phase : when the hair stops growing
telogen resting phase , when the hair is shed
There is disharmony in the phases of hair growth ; thus while some hairs are in the anagen , others are resting
The overall length of the hair is determined by the duration of the anagen phase

6. Regulation of Hair Growth
Multifactorial; local and systemic factors and sex hormones act on dermal papillae to promote hair growth
Deficiences in thyroid and growth hormone alter anage; telogen ratio in scalp and body hair
testosterone 5-α reductase Dihydrotesterone in the hair follicle
Andostenedione and Dehydroepiandrosterone are metabolized in the skin to Testosterone and DHT

7. Regulation of Hair Growth
Sensitivity of hair follicles to androgens varies over the body.
Hair growth in the eyelashes, eyebrows and the occipital and lateral aspects of the scalp is mostly independent of androgenic effects
axillae and pubic areas are sensitive to low levels of androgens
Chest, lower abdomen, face, upper thighs and lower back need high levels of androgens to increase hair growth. Thus when hairs are found in these areas they are described as ‘male pattern’ and considered pathological in women

8. Aetiology Androgen Excess: PCOS Androgen secreting tumors
Non classical congenital adrenal Hyperplasia
Other causes
Non androgenic factors
Idiopathic factors

9. Polycystic Ovary Syndrome
Most common cause of hirsutism, 70-80% of cases
Diagnosis based on the revised criteria adopted in Rotterdam 2004: 2 out of 3 are enough for the diagnosis after the exclusion of other causes:
oligo- or anovulation
clinical or biochemical hyperandrogenism
Morphological features of polycystic ovaries on Ultrasound scan

10. Polycystic ovaries on Ultrasound scan

11. PCOS and IR Insulin resistance is important in the etiology
Insulin increases androgen levels by increasing androgen production by the ovarian theca cells and indirectly by reducing hepatic synthesis of SHBG.
30-75% of women with PCOS are overweight, which increases insulin resistance and exacerbates hyperandrogenaemia.

12. Androgen secreting tumors
Ovarian or adrenal
they are rare , between 1 in 300 and 1000
suspect if onset is rapid, or if they lead to virilisation or they are associated with cushingoid features.
Diagnosis is best by clinical presentation
ovarian tumours associated with androgen excess : arrenoblastomas; Leydig, hilar and thecal cell tumours; and luteomas of pregnancy
>50% of adrenal tumors associated with hirsutism are malignant

13. Non classical congenital adrenal HyperplasiaAR
% of hisute women
21- hydroxylase ceficiency resulting in high 17-OH progesterone, which is androgenic

14. Other causes Thyroid dysfunction Acromegaly Cushing syndrome
Hyperprolactinemia
women with these conditions present with symptoms other than hirsutism

15. HAIRAN
Hyperandrogenic insulin-resistant acanthosis nigricans syndrome is an inherited condition that occurs in 3% of women with hirsutism
Extremely high levels of insulin due to severe insulin resitance
Women are severly hyperandrogenic
Very difficult to treat
they can cause virilization

16. Androgenic drugs
Testosterone, Danazol and anabolic steroids all induce hirsutism via their inherent androgenic prosperities

17. Non-androgenic factors
unknown mechanism on hair follicle independent of androgens
Drugs:
Phenytoin
Minoxidil
Diazoxide
Psoralen
Pencillamine

18. Idiopathic Hirsutism all other causes are excluded normal menses
normal ovarian appearance
No detectable hormonal abnormalities
No evidence of adrenal or ovarian tumors
prevalence is less now with more diagnostic techniques (6-7%)

19. Evaluation In depth History
Drugs, changes in weight or facial contour, presence of acne, hair loss/balding, menstrual and reproductive history and relevant family history , such as premature male balding and diabetes in the context of PCOS
Physical Exam: extent, type and pattern of hair growth, signs of virilisation , thyroid enlargement, galactorrhea, pelvic / abdominal masses, cushingoid features, obesity and signs of systemic illness

20. Ferriman and Gallwey (1961) scoring system
They scored the density of hair at 11 different body sites; namely the upper lip, chin, chest, upper back, lower back, upper abdomen, lower abdomen, arm, forearm, thigh, and lower leg
0: absence of terminal hair,4: extensive terminal hair growth,Scores > 6 were deemed significant
Hatch et al 1981 modified scheme (9 sites) excluding lower legs and forearms as these are less sensitive to androgens
These schemes are typically used for research rather than clinical setting

21. Ferriman and Gallwey scoring system

22. Evaluation
Mild hirsutism ( FG 8-15) without any other features such as menstrual irregularities can be treated cosmetically and investigated further if treatment fails or hirsutism worsens
Moderate- severe hirsutism ( FG > 15), it is likely that androgen excess is present , the possible causes should be investigated. History and examination would dictate which investigations are appropriate

23. Investigations
Free testosterone levels are the most sensitive measure of hyperandrogenism
A very high ( > ng/ml) testosterone level increases the likelihood of neoplasm
Increased DHEA-S indicates an adrenal source
Non- classical congenital adrenal hyperplasia; increased testosterone and 17-OH progesterone > 200ng/dl ( can be slightly elevated in PCOS).
Pelvic US can help in the diagnosis of PCOS or ovarian tumors though can be normal in both of these conditions.

24. Management
Lifestyle changes, cosmetic , physical and hormonal therapies
Cosmetic and hormonal therapies are effective as long as they are in place, more permanent reductions cab be achieved using physical methods

25. Life style changes and weight reduction
Weight loss reduce hyperandrogenism and insulin resistance , esp. in overweight women with PCOS
Weight reduction of 5-10% can improve hirsutism by 40-55% within 6 months of weight loss
In obese women with PCOS, weight loss programmes should be first line of intervention, to include low calorie diet and exercise over 6 months

26. Cosmetic methods
Plucking, waxing, bleaching, the use of depilatory creams.
shaving should be avoided as it leads to blunt hairs that may feel like stubble- although no increase in hair growth which is a misconception.
Depilatory and creams decrease local hair but chronic use can cause skin irritation
plucking and waxing can cause folliculitis and ingrown hairs in androgenic areas

27. Physical
Electrolysis: expensive, time consuming (18 months to 4 years), painful and really practical for a limited area. It may cause depigmentation and scarring.
Laser photothermolysis: used to destroy hair follicles without damaging nearby tissue. It can cover a wider area than electrolysis. It is best for fair skin women. It reduces hair density by 30% after 3-4 sessions

28. Hormonal therapy
The basis of action is either the suppression of androgen production or blocking of the action of androgens on the skin.
This results in the hairs reverting back to vellus-type hair.
it takes 9-12 months for the maximum effects to be noticed. Can be combined with cosmetic measures.

29. Hormonal therapy Combined oral contraceptive pill Cyproterone acetate
Spironolactone
Finesteride
Flutamide
Insulin sensitizers: metformin
Cell cycle inhibitors: Eflornithine
Gonadotrophin-releasing hormone agonists