This document summarizes key aspects of hair growth and disorders of excessive hair growth or hirsutism. It discusses the typical hair follicle cycle and differences between vellus and terminal hair. Common causes of hirsutism include polycystic ovary syndrome (PCOS), congenital adrenal hyperplasia, and androgen-secreting tumors. Evaluation involves assessing degree of hair growth and signs of virilization, with lab tests to identify underlying etiology. Treatment aims to suppress androgens and may include weight loss, oral contraceptives, antiandrogens like spironolactone, and sometimes surgery or medication targeting the specific hormone excess.

1. Dr Mandeep Bhandal

2.  Each hair follicle develops at about 8-10wks of
gestation as a derivative of epidermis.
 Number of hair follicles is set from birth
 Main difference between sexes is the degree of
differentiation of the hair
 Hair grows in a mosaic pattern(in a given area ,hair
are in different stages of development)
2

3. Adults have two types of hair: Vellus and Terminal.
 Vellus hair : Soft, fine, colorless, and usually short.
Grow on the face, chest, and back and
give the impression of "hairless" skin.
 Terminal hair : longer, coarser, darker hair that grows
on the scalp, pubic, and armpit areas in
both adult men and women.

4.  Anagen : Growth phase,85- 90 % of the life cycle
 Catagen : The transitional period from growing to
resting lasting 2 to 4 weeks
 Telogen : Quiescent phase ,lasting 2-4 months
The growth phase or the anagen phase is primarily
influenced by disorders that stimulate hair growth
as well as therapeutic modalities.

5.  Androgen sensitive hair :
Depend upon androgen input for hair growth.
Face , neck, chest ,abdomen ,axillary, upper arms
,inner thighs and pubic hair, part of the scalp hair.
 Less Androgen dependent :
Forearms ,hands , lower legs

6. ADRENAL
PITUITARY
OVARY
DHEAS
DHEA
AND,STEN,ONE
PERIPHERAL
CONVERSION
TESTOSTERONE
HAIR FOLLICLE
DIHYDROTESTERONE
ACTH LH

7.  Ovary
 Adrenal gland
Androgens are metabolised in:
 Skin
 Adipose tissue
 Liver
 Placenta

8. Testosterone Androstendione DHA DHAS
25%
25%
99%
90%
50%
50%
50% 10%
OVARY
ADRENAL
CORTEX

9. The production rate of testosterone
in the normal female is 0.2 to 0.3 mg/day
Normal total testosterone concentration
in serum is below 0.8ng/ml

10. Normal women Hirsute women
80% SHBG 79% SHBG
19% Albumin 19% Albumin
1% Free 2% Free

11. IT MAY BE EITHER
 HYPERTRICHOSIS
 HIRSUTISM
 VIRILIZATION
11

12. HYPERTRICHOSIS : REFERS TO HAIR DENSITY
OR LENGTH BEYOND THE ACCEPTED LIMITS
OF THE NORMAL FOR THE PARTICUALR
AGE,RACE OR SEX.
• May be generalised or localised and may consist of
lanugo, vellus or terminal hair.
• Frequently associated with the use of medication
such as antiepileptics
12

13. HIRSUTISM : APPEARANCE OF EXCESSIVE COARSE
(TERMINAL)HAIR IN A PATTERN NOT NORMAL IN
THE FEMALE
 The abnormal distribution of excess hair growth ,such
as face ,chest or upper abdominal hair
 Affects 5-10% of women
 May also signal the presence
of a hormone imbalance or a
hormone-producing tumor.
13
dpankar

14. VIRILIZATION : REFERS TO CONCURRENT
PRESENTATION OF HIRSUTISM WITH A
BROAD RANGE OF SIGNS SUGGESTIVE OF
ANDROGEN EXCESS,SUCH AS
 Acne,
 Frontotemporal balding,
 Deepening of the voice ,
 Decrease in breast size
 Clitoral hypertrophy
 Increased muscle mass
 Amenorrea / oligomenorrhea
14

15.  Increased serum androgens
 Decreased levels of SHBG-> increased free testosterone
 Increased responsiveness of target organ to normal
circulating androgens
 Increased activity of 5 alpha reductase
Normal women Hirsute women
80% SHBG 79% SHBG
19% Albumin 19% Albumin
1% Free 2% Free

16.  Main stimulus- Testosterone
 Testosterone – binds – androgen receptors
DHT
Androstenediol
Activation of
5 alpha reductase
Terminal hair

17. Androgens Lengthen Anagen phase
Increase hair follicle size
Increase hair follicle diameter
Increase sebum secretion

18.  HIRSUTISM ALONE
 HIRSUTISM AND ACNE
 HIRSUTISM AND OVULATORY DISORDERS
 HIRSUTISM AND SIGNS OF VIRILIZATION

19.  Androgenic ( 75-85% )
 Non Androgenic
 Idiopathic

20.  PCOD(70-80%)
 Hyperandrogenism - 6.8%
 The hyperandrogenic insulin-resistant acanthosis nigricans
syndrome (HAIR-AN) - 3 %
 21-hydroxylase non-classicaI adrenal hyperplasia (late-
onset CAH) - 1.6%
 Hypothyroidism - 0.7%
 21-hydroxylase-deficient congenital adrenal hyperplasia -
0.7%
 Hyperprolactinemia - 0.3%
 Androgenic tumors - 0.2%
 Cushing’s syndrome - 0-1%

21.  Acromegalics.
 chronic skin problems,
 Non-androgenic anabolic drugs.
Danazol (Danocrine)
Norplant
Metoclopramide (Reglan)
Anabolic steroids
Methyldopa (Aldomet)
Phenothiazines
Progestins
Reserpine (Serpasil)
Testosterone

22. Tumors of the ovaries and the adrenal glands secrete excess
hormones including androgen.
Ovarian tumors Adrenal tumors
Granulosa -theca cell tumors Adrenal adenoma
Arrhenoblastoma Adrenal carcinoma
Gonadoblastomas
Lipoid cell tumors ACTH secreting tumors
Dysgerminoma
Brenner's tumor

23.  Functional adrenal hyperandrogenism
 Hypereactio luteinalis of pregnancy - transient increase
in androgen levels during pregnancy
 Thecoma of pregnancy - Transient androgen secreting
tumor during pregnancy
 True hermaphroditism - condition where both male and
female internal sex organs are present

24. Genetics
 There are very obvious family and racial differences in
hirsutism patients. In some women, the skin is very
sensitive to even low levels of androgens and their
follicles produce primarily terminal (coarse and dark)
hair.

25. In 70-80 % cases of hirsutism
5-10% of women in reproductive age
Fulfills the Rotterdam criteria
Hyperandrogenism
Amenorrhoea /oligomenorrhoea
USG features of PCOD
Anovulation
Infertility
Obesity

27. IGFBP-1
IGF1
Hyperinsulinemia
Ovarian stimulation
Hyperandrogenism
Insulin resistance
Genetic defects
of insulin receptor
Autoantibodies to
insulin receptor
Ovarian insulin
receptors LH/FSH
Ovarian IGF-I
receptors
PCOS Hyperthecosis
SHBG
Free
Testosterone
Defects of tyrosine
kinase

28.  It is a familial disorder of adrenal steroid
biosynthesis
 Autosomal recessive mode of inheritance.
 The defect is expressed as adrenal enzyme
deficiency.
 5 major Enzymes deficiencies are clinically
important
 21-Hydroxylase
 11-b-Hydroxylase
 17-a-Hydroxylase
 3-b-Hsteroid hydrogenase
 20,22 Desmolase deficiency

29. The enzyme deficiency causes
reduction in end-products,
accumulation of hormone precursors
& increased ACTH production.
The clinical picture reflects the
effects of inadequate production of
cortisol & aldosterone and the
increased production of androgens &
steroid metabolites.

30. Result of a 21-Hydroxylase Deficiency

31. In less severe forms (late onset CAH)
 Genitalia is normal at birth.
 Precocious pubic hair &
 Clitoromegaly
 Excess facial or body hair appear later in
childhood, often accompanied by tall stature
 Varying virilizing symptoms ranging from
oligomenorrhea to hirsutism and infertility

32. 17-OHP
17-OHP
< 200ng/dl
Rules out
adrenal
hyperplasia
21-hydroxylase
deficiency
17-OHP
> ng/dl
ACTH
stimulation test
Normal
Abnormal
Adrenal
hyperplasia

33.  Diagnosis
History- rapid onset
Imaging- USG/CT scan
Hormone profile – Testosterone levels

34. Testosterone
assay
Testosterone
<200ng/dl
Anovulatory
hirsutism
Testosterone
> 200ng/dl
Palpable
adnexal mass
laparotomy
Normal pelvic
scan
imaging
laparotomy

35.  A very rare disease
 The clinical state of increased free circulating
glucocorticoid

36. Hypercotisolism
Lipid mobilization 
Lipid Catabolism 
Moon-face
buffalo hump
truncal obesity
Violaceous striae
Hepatic glucose
production ↑
Insulin resistance
Glucose intolerance
Hirsutism(65%)
Protein metabolism
Negative nitrogen balance
Disruption of water and
electrocytes metabolism
Proximal muscle
weakness
Dependent edema
Hypertension
Hypokalemic
Metabolic alkalosis
Lipid redistribution

37.  History- Onset and progression
 Physical examination
 Assess the severity of hirsutism (+/- virilisation)
 Acertain the underlying cause
 Investigations
 Treatment

38.  Onset and progression
Most of the causes begins in early adolescence
Presentation may be late depending upon the cause
Rapid progression – androgen secreting tumors

39.  Degree and extent
Ferriman gallwey scale
Quantifies the extent of hair growth in 9 most
androgenic sensitive sites
Hair growth is graded 0-4 at each site
Score of 8 or more (max 36) indicates hirsutism

41.  Associated signs of virilisation
(May occur in CAH, HAIR-AN syndrome, Androgen secreting
tumor, Acanthosis nigricans)
Clitoral hypertrophy
Deepening of voice
Acne
Male pattern baldness
Breast atrophy
Android habitus

42.  History of drug intake producing androgenicity
 Family history- correlated
 Mild hirsutes- during puberty, pregnancy, postmenopause
 Hirsutism with rapid onset- Evaluation for adrenal /ovarian
tumor
 High testosterone levels (>200ng/100ml)- Androgen
producing tumor
 Patients with primary amenorrhoea with virilism-
karyotyping for y carrying dysgenetic gonads

44.  Late onset CAH-
D/t partial deficiency of 21- hydroxylase enzyme
17- OHP is elevated
 Cushing disease-
24 hr urinary free cortisol excretion- (10-90µg)
Late evening plasma cortisol level – (< 15 µg/dl )
Overnight Dexa suppression test

45. Adrenal tumors
 Any age
 Rapid onset
 Hirsutes++
 Virilism+
 Amenorrhoea
 DHEAS ↑↑(>700µg/100ml)
 T- normal or ↑
 Dexa suppression test- negative
 IVP
 CT-scan
 MRI
 Any age
 Rapid onset
 Hirsutes++
 Virilism+
 Amenorrhoea
 T- ↑( >200 ng/100ml)
 DHEAS- normal
 Sonography
 Laparoscopy
 biopsy
Ovarian tumors

46. Diagnosis Menstrual Total DHAS LH 17OHP Sourse of
Pattern Testoste- Androgens
rone
PCOS Irregular Elevated mildly Elevated Normal OVARY
elevated
CAH Irregular Elevated Often Usually Markedly Adrenals
Normal Normal elevated
Idiopatic Regular Normal Normal Normal Normal Skin
hirsutism

47. Principles of management
 To remove excess hair
 To suppress or neutralise the action of androgen
 To remove the source of excess androgen

48.  Best results are achieved by combination treatment
including antiandrogens, suppression and topical
treatments
 Goal should be to reduce the time spent mechanically
removing unwanted hair.
 The choice of drug depends mainly on its tolerability by
each individual patient.

49.  Weight Reduction
Associated with reduction of
hyperinsulinemia and androgen excess
BMI should not be > 25

50. Drugs- ( depending upon the site of production of
excess androgens)
 OCPS
 Progestrogens
 Antiandrogens
 Spironolactone
 Dexamethasone
 GnRH Analogues
 Combined approach

51. OCP’s in PCOS
OCP’s
 SHBG
 Androgen
binding
capacity
 Free Androgens
Adrenal
steroids
Folliculogenesis
Ovary
Pituitary
Gn






52. CLINICAL BENEFITS
Helpful in treatment of Hirsutism
Excellent cycle control
Decreases acne
No weight gain.
METABOLIC BENEFITS
No effect on carbohydrate metabolism
No deterioration in the glycemic and insulinemic
response to glucose load.
No effect on serum lipid concentration.
Safe for long term use

53. Cyperoterone acetate:
 A progestin that also has strong antiandrogenic
action.
 Inhibits gonadotrophin secretion and interferes with
androgen action on target organs by competing for
androgen receptors
 Dosage- 100mg from D5-D14 with ethinyloestradiol
30µg, from D 5 to D25
 Side effects: Nausea, fatique, weight gain, loss of
libido, mastalgia

54.  Spironolactone:
(Antialdosterone antiandrogenic compound)
 Inhibits ovarian and adrenal androgen biosynthesis
 Competes for androgen receptors in hair follicle
 Inhibits 5 alpha reductase activity
 Dosage -100-200mg daily, maintenance dose is 25-50
mg daily
 Side effects- fatigue,menstrual irregularities,
hyperkalaemia

55. Finasteride:
 5 alpha reductase inhibitor that inhibits conversion of
testosterone to more active 5 alpha hydroxy
testosterone
 Dosage- 5 mg daily

56. Flutamide:
 Androgen receptor antagonist
 Dosage – 100-200mg daily
 Side effects - hepatotoxic , Dry skin
 Should be combined with a contraceptive
 Marked beneficial effect in 6 months

57.  Mode of action
Suppress pituitary adrenal axis - suppression of
endogenous ACTH secretion
 Use –
In adrenal or mixed adrenal and ovarian
hyperandrogenism

58. Glucocorticoid Dosage Frequency
Hydrocortisone 10-20 mg Twice daily
Prednisone 2.5-5 mg Nightly or
alternate days
Dexamethasone 0.25-0.50 mg Nightly

59.  Metformin: Antihyperglycemic drug ,in treatment of
hirsutism associated with insulin resistance (e.g. PCOD)
 Eflornithine: (13.9% cream)
US FDA approved
 It irreversibly inhibits ornithine decarboxylase (ODC), an
enzyme that catalyzes the rate-limiting step for follicular
polyamine synthesis, which is necessary for hair growth.
 Improvement occurs gradually over a period of 4-8 weeks
or longer.
 Most reported adverse reactions consisted of minor skin
irritation.

60.  After 1 – 2years, medication can be stopped to
observe the return of ovulatory cycles.
 Even in anovulatory pts, testosterone suppression
continues for 6months to 2 years after
discontinuing treatment
 If anovulation persists, return of hirsutism
expected.
How long should treatment be continued?

61.  Bleaching - can cause irritation, purities, skin
discoloration
 Shaving - Shaving does not lead to worsening of
hirsutism and is a good short-term solution for
facial hair.
- Does not affect the rate or duration of
anagen phase, or diameter of hair
- But yields a blunt tip – illusion of thicker hair
 Plucking, Waxing - scarring, folliculitis,
hyperpigmentation
 Depilatory creams - Irritant dermatitis
 Electrolysis - painful, erythema, inflammation,
scarring
 Laser

62.  Removal of the source
Adrenal or ovarian tumour – surgically treated
Cushing disease – Adrenalectomy
Radiation to pituitary
Removal of ACTH producing tumor
Iatrogenic cases – Offending drug to be stopped

63.  Hirsutism is a symptom of underlying cause
 Commonest cause is PCO
 Progression may hint to diagnosing tumor
 Treatment – Medicines/ Cosmetic