1. 1
HIRSUTISM
Prof, M.C.Bansal.
Founder Principal & Controller;
Jhalwar Medical college And hospital, Jhalawar.
Ex . Principal & controller;
Mahatmagandhi Medical College And Hospital,

2. EXCESSIVE HAIR
GROWTH
IT MAY BE EITHER
HYPERTRICHOSIS—Excess of hair
growth all over the body.
HIRSUTISM—Male type sex hair
growth in females.
VIRILIZATION—Excess sex hair growth
and other hyper androgenic effects on
female genitalia and body.

3. 3
DEFINITION
HYPERTRICHOSIS : REFERS TO HAIR
DENSITY OR LENGTH BEYOND THE
ACCEPTED LIMITS OF THE NORMAL
FOR THE PARTICUALR AGE,RACE
OR SEX.
• The excess hair may be generalised or
localised and may consist of lanugo,
vellus or terminal hair.
• It is frequently associated with the use
of medication such as antiepileptics

4. Inherited types
CONGENITAL HYPERTRICHOSIS
LANUGINOSA – confluent generalised over
growth of silvery blonde to grey lanugo hair
at birth or early infancy, autosomal dominant,
associated dental anomalies.
AMBRAS syndrome- longer thicker hair more
over the face,ears and shoulders, facial
dysmorphism and dental anomalies.
CONGENITAL GENERALISED
HYPERTRCHOSIS – X linked dominant
4

5. Acquired types
ACQUIRED HYPERTRICHOSIS
LANUGINOSA – seen in underlying
malignancy
DRUG INDUCED – following minoxidil
therapy, diazoxide, phenytoin sodium,
cyclosporine, topical tacrolimus.
POEMS syndrome
PORPHYRIA CUTANIA TARDA –
hexachlorobenzene, underlying hepatic
tumour.
5

6. Localised hypertrichosis
Congenital
 Hairy elbow
 Spina bifida
 Trichomegaly
Acquired
 Interferon
 Repeated trauma
 Congenital AV fistula
6

7. 7
DEFINITION
HIRSUTISM : APPEARANCE OF
EXCESSIVE COARSE
(TERMINAL)HAIR IN A PATTERN NOT
NORMAL IN THE FEMALE
Definition highlights the abnormal
distribution of excess hair growth ,such
as facial ,chest or upper abdomen.

8. Hirsutism in
an young girl
with PCOD

9. Abdominal Hair Growth
___PCOD

10. HIRSUTISM

11. 11
DEFINITION
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 ,
A DECREASE IN BREAT SIZE
CLITORAL HYPERTROPHY

12. 12
INCREASED MUSCLE MASS
AMENORREA / OLIGOMENORRHEA
Virilization is seen less frequently than
hirsutism and may reflect a severe underlying
pathologic condition ,such as Male sex
hormone producing Ovarian / adrenal tumors
Hirsutism and virilization are closely
interlinked and hirsutism may actually be the
first manifestation of a condition that
ultimately will lead to virilization if left
untreated

13. Acne &
Hirsutism

14. Clitoral Enlargement In female hrmophodyte secondary to cogenital
adrenal hyperplasia

15. 15
BASIC FACTS ABOUT
HAIR
Each hair follicle develops at about 8-10wks of
gestation as a derivative of epidermis.
Number of hair follicles is set from birth
Hair grows from a individual hair follicle that are
part of a pilosebaceous gland unit
Main difference between sexes is the degree of
differentiation of the hair
Human hair growth is continuous
Hair grows in a mosaic pattern(in a given area ,hair
are in different stages of development)

16. 16
BASIC FACTS ABOUT
HAIR
Some condition may cause a high level
of synchrony between the growth cycles
of hair ,leading to the appearance of
either massive hair loss (alopecia)or
excess hair for a limited period of time

17. 17
BASIC FACTS ABOUT
HAIR
Growth cycle of the Hair: ACT
Anagen : Growth phase,85- 90 % of the life
cycle
Catagen : rapid involution Phase
Telogen : Quiescent phase
The growth phase or the anagen phase is
primarily influenced by disorders that
stimulate hair growth as well as therapeutic
modalities.

18. 18
BASIC FACTS ABOUT
HAIR
Three types of Hair :
Lanugo : Body hair seen in the fetus and
newborn
Vellus : Fine adult hair covering the body
Terminal hair : Thick pigmented hair of scalp
and pubic area
Thickness of the terminal hair varies form one
individual to other depending upon genetic,
and possibly nutritional

19. 19
BASIC FACTS ABOUT
HAIR
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 independent :
Forearms ,hands .lower legs

20. ANDROGEN INDUCED
HAIR GROWTH
20
adrenal
pitutary
ovary
ACTH LH
TESTOSTERONE
HAIR FOLLICLE

21. Androgens are C-19 steroids produced in:
• Adrenal gland
• Ovary
• Androgens are metabolised in:
 Skin
 Adipose tissue
 Liver
 Placenta
21

22. 22
Testosterone Androstendione DHA
DHAS
ADRENAL
CORTEX
OVARY
50
50
90
10
99
50
25
25
Origin of circulating
androgens

23. 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
23

24. Hair & sebaceous Follicle Response to
Hyperandrogenism

25. 25
PRESENTATION OF
HIRSUTISM
HIRSUTISM ALONE
HIRSUTISM AND ASSOCIATED
PILOSEBACEOUS UNIT
OVERACTIVITY (ACNE)
HIRSUTISM AND OVULATORY
DISORDERS
HIRSUTISM AND SIGNS OF
VIRILIZATION

26. 26
PRESENTATION OF
HIRSUTISM
Hirsutism alone is the greatest
challenge,patients usually go to dermatologist
Hirsutism wIth acne is frequently develop in
teenage girls
Hirsutism with ovulatory disorders comes
mostly to gynecologist
Hirsutism with virilization requires immediate
work-up

27. 27
CAUSES OF HIRSUTISM
Excess androgen production
Relative circulating androgen excess
and low binding globulins
Excess end organ response
Patient perception

28. 28
DISORDERS OF EXCESS
ANDROGEN PRODUCTION
Source of androgen :
Exogenous
Endogenous (most common)
Two primary endogenous sources :
Adrenal glands
Ovaries

29. Mechanism of excessive
hair growth
Main stimulus- Testosterone
Testosterone – binds – androgen
receptors
29
Activation of
5 alpha reductase
DHT
TERMINAL HAIR
ANDROSTENEDION

30. ANDROGEN
Lengthen Anagen phase
Increase hair follicle size
Increase hair follicle diameter
Increase sebum secretion
30

31. 31
Normal women Hirsute women
80% SHBG 79% SHBG
19% Albumin 19% Albumin
1% Free 2% Free

32. Causes of hirsutism
Androgenic ( 75-85% )
Non Androgenic
Idiopathic
32

33. ANDROGENIC
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%
33

34. NON ANDROGENIC
Acromegalics.
chronic skin problems,
Non-androgenic anabolic drugs.
Danazol (Danocrine)
Norplant
Metoclopramide (Reglan)
Anabolic steroids
Methyldopa (Aldomet)
Phenothiazines
Progestins
Reserpine (Serpasil)
Testosterone 34

35. Tumor related causes of
hirsutism
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
35

36. 36
COMMON CAUSES OF ECTOPIC ACTH SECRETION
Small cell carcinoma of the lung 50%
Endocrine tumors of foregut origin 35%
Thymic carcinoid
Islet cell tumor
Medullary carcinoma thyroid
Bronchial carcinoid
Pheochromocytoma 5%
Ovarian tumors 2%

37. Miscellaneous causes of
hirsutism
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
37

38. 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.
38

39. 39
DISORDERS OF EXCESS
ANDROGEN PRODUCTION
ADRENAL ANDROGEN EXCESS
May be linked to genetically determined
steroid synthesis enzyme deficiency
Malignant adrenal neoplastic process
Other conditions like Cushing’s syndrome

40. 40
DISORDERS OF EXCESS
ANDROGEN PRODUCTION
ADRENAL ANDROGEN EXCESS
Three recognised adrenal enzyme deficiencies :
21 alpha Hydroxylase defieiency
11-beta-Hydroxylase deficiency
3-beta-ol-dehydrogenase deficiency
Classical forms are usually presented in
prenatal or neonatal period as ambiguous
genitalia in female
Nonclassic forms are linked with hirsutism

41. 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.
41

42. 42

43. 43
 ACTH ↑
 Cortisol ↓
 Aldosterone ↓
 17-OH-progesterone↑
 Testosterone ↑
 Urinary 17-ketosteroids↑
ESSENTIALS OF
DIAGNOSIS

44. 44
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
GIRLS WITH CAH
Varying virilizing symptoms
ranging from oligomenorrhea
to hirsutism and infertility

45. 45
DISORDERS OF EXCESS
ANDROGEN PRODUCTION
21-alpha-Hydroxylase deficiency:
Most common ,<1% to >10%
Prevalence depends on ethnic
origin(common in slavs,1/50 Hispanics 1/40,
ashkenazi jews 1/27
Cushing’s syndrome :Hirsutism with weight gain
and growth retardation as the primary
manifestation,with acne and other cutaneous
problems

46. causes
46
ACTH-dependent States
ACTH-secreting pituitary tumor ( Cushing’ s disease ) 90-95%
Pituitary CRH-secreting neoplasm ( ectopic CRP syndrome )
Nonpituitary ACTH-secreting neoplasm ( ectopic ACTH syndrome )
ACTH-independent States
Adrenal adenoma/carcinoma
Micronodular /macronodular adrenal disease
Exogenous Sources
Glucocorticoid intake
Psychiatric Conditions (Pseudo-Cushing Disorders)
Depression
Alcoholism

47. 47
CLINICAL FEATURES OF GLUCOCORTICOID
EXCESS
Weight gain
90%
“ Moon facies” 75
Hypertension 75
Violaceous striae 65
Hirsutism 65%
Glucose intolerance 65
Proximal muscle weakness 60
Plethora 60
Menstrual dysfunction 60
Acne 40
Easy bruising 40
Osteopenia 40
Dependent edema 40
Hyperpigmentation 20
Hypokalemic metabolic alkalosis
15

48. 48
DISORDERS OF EXCESS
ANDROGEN PRODUCTION
OVARIAN ORIGIN
Most common cause is
POLYCYSTIC OVARIAN SYNDROME
Other
Neoplastic ovarian disease

49. PCOS
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
49

50. Pathogenesis
dpankar 50

51. Increased ovarian androgen biosynthesis in the
polycystic ovary syndrome results from abnormalities
at all levels of the hypothalamic–pituitary–ovarian
axis. The increased frequency of luteinizing hormone
(LH) pulses in the polycystic ovary syndrome appears
to result from an increased frequency of
hypothalamic gonadotropin-releasing hormone
(GnRH) pulses.
The latter can result from an intrinsic abnormality in
the hypothalamic GnRH pulse generator, favoring the
production of luteinizing hormone over follicle-
stimulating hormone (FSH) in patients with the
polycystic ovary syndrome, in whom the
administration of progesterone can restrain the rapid
pulse frequency
51

52. . By whatever mechanism, the relative increase in
pituitary secretion of luteinizing hormone leads to an
increase in androgen production by ovarian theca
cells.
Increased efficiency in the conversion of androgenic
precursors in theca cells leads to enhanced
production of androstenedione, which is then
converted by 17 -hydroxysteroid dehydrogenase (17 )
to form testosterone or aromatized by the aromatase
enzyme to form estrone. Within the granulosa cell,
estrone is then converted into estradiol by 17.
52

53. . Numerous autocrine, paracrine, and endocrine factors
modulate the effects of both luteinizing hormone and
insulin on the androgen production of theca cells; insulin
acts synergistically with luteinizing hormone to enhance
androgen production. Insulin also inhibits hepatic synthesis
of sex hormone–binding globulin, the key circulating
protein that binds to testosterone and thus increases the
proportion of testosterone that circulates in the unbound,
biologically available, or "free," state. Testosterone inhibits
and estrogen stimulates hepatic synthesis of sex
hormone–binding globulin. The abbreviation scc denotes
side-chain cleavage enzyme, StAR steroidogenic acute
regulatory protein, and 3 -HSD 3 -hydroxysteroid
dehydrogenase. Solid arrows denote a higher degree of
stimulation than dashed arrows.
53

54. 54
Lab.Evaluation of
Hirsutism
Three basic hormonal evaluation
1. Total testosterone
2. DHEAS
3. 17-hydroxyprogesterone

55. Normal ranges
Total testosterone 20-80 ng/dl
Free testosterone 0.3-1.9 ng/dl
Bioavailable testosterone 0.8- 10 ng/dl
Free androgen index ( T/SHBG x 100)
Androgen producing tumor > 200 ng/dl
55
The Testosterone
level

56. 56
RELATIVE ANDROGEN
EXCESS AND SHBG
<3 % TESTOSTERONE IS FREE
Mostly bound to Sex hormone binding
globuline(SHBG)
Dcrease in SHBG leads to Excess free
Testosterone
Causes of Reduced SHBG :
PCOS(Chronic anovulation) and
Obesity

57. 57
EXCESS REPONSIVITY
TO ANDROGEN
TESTOSTERONE
5-ALPHA –
REDUCTASE
DIHIDROTESTOSTERONE
Excessive response of the receptor to DHT(may be
due to mutation of the highly polymorphic region in
gene of the receptor located on X Chromosome
Over activity of the 5-alpha-reductase (Type –1 and
Type 2,type –1 is involved in hirsutism )
TARGET CELLS
RECEPTOR

58. 58
Flowchart for investigation
of hirsutism

59. 59
BASIC APPROACH TO
THE DIAGNOSIS OF
HIRSUTISM AND
VIRILIZATION
SYMPTOMS AND HISTORY
SIGNS
PHYSICAL EXAMINATION
INVESTIGATION

60. 60
APPROACH TO
DIAGNOSIS
Patient may present with ovulatory problems
and hirsutism may not be reported
There may be normal hair pattern but patient
complains about hirsutism
Evident virilization should investigated at
once

61. 61
APPROACH TO
DIAGNOSIS
Careful history regarding the timing of
onset and chronological progression
Precocious puberty with androgen
excess suggests adrenal enzyme
defect
Family history : androgen excess
disorders

62. 62
APPROACH TO
DIAGNOSIS
Physical examination
Establish presence of hirsutism and
quantifying it
Presence of acne and virilization and
rule out hypertrichosis
Skin hyperpigmentation,acanthosis
nigricans suggests insulin
resistance.Often associated with PCOD

63. 63
APPROACH TO
DIAGNOSIS
Measurement of weight and height and
blood pressure: defects relates to
adrenal enzyme defects
Galactorrhoea
Tanner staging : Hirsutism before
Tanner stage 3 to 4 is alarming and
suggests a serious pathology
Visual genital examination for virilization

64. 64
APPROACH TO
DIAGNOSIS
Degree and extent
FERRIMAN GELLWAY SCORE
score
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

65. 65

66. 66
APPROACH TO
DIAGNOSIS
INVESTIGATION:
FOR VIRILIZATION :
Work-up focuses of the identification on the
source of androgen excess
Rule out exogenous androgen
Evidence of endogenous androgen excess:
Serum total testosterone
Serum dehydroepiandrosterone sulfate
(DHEAS)

67. 67
APPROACH TO
DIAGNOSIS
INVESTIGATION:
FOR VIRILIZATION
Imaging studies:Pelvic sonography
Adrenal imaging(USG,CT)
Specialized studies :
Selective venous catherization(adrenal or
ovarian)
Radioisotope studies

68. 68
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
ADRENAL TUMOR OVARIAN TUMOR

69. 69
APPROACH TO
DIAGNOSIS
INVESTIGATION :
HIRSUTISM: Goal is to rule out serious
potential life threatening conditions and gain
information that helps in treatment
Evaluation of Androgen excess:
Testosterone ,total preferred
DHEAS
In selected cases : 17-OHP(fasting morning
sample)

70. 70
APPROACH TO
DIAGNOSIS
Evaluation of accompanying medical disorder
Ovulation disorder :FSH,LH
Thyroid dysfunction:TSH
Hyperprolactinemia :PRL
Other investigations ( inselected cases)
Androgen production :Androstenedione,
3-alpha Androstenediol glucuronide
Provocative tests : Corticotropin stimulation
tests,Insulin resistance determination

71. Differentation of
hyperandrogenism
71
Diagnosis Menstrual Total DHAS LH 17OHP Sourse of
Pattern Testoste- Androgen
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

72. 72
THERAPEUTIC OPTIONS
VIRILIZATION
GOAL: Identify the underlying cause
and correcting it
Usually related to malignant process
and requires surgical approach

73. 73
THERAPEUTIC OPTIONS
HIRSUTISM
GOAL:
The prevention of further stimulation of
hair growth
Cosmetic correction of the
problem

74. 74
THERAPEUTIC OPTIONS
BASIC STEPS OF MANAGEMENT OF
HIRSUTISM ARE:
DEFINE THE PROBLEM
QUANTIFY THE DEGREE OF HIRSUTISM
INDENTIFY THE PATHOPHYSIOLOGY
CORRECT THE PROBLEM,WHETHER
ACUTE OR CHRONIC
DEFINE SUCESSWITH THE PATIENT
FOLLOW UP

75. 75
THERAPEUTIC OPTIONS
Regular follow up is indicated at
appropriate intervals,usually every 3- 6
months

76. 76
THERAPEUTIC OPTIONS
GENERAL MEASURES :
Eliminating causative factors
Optimizing weight Weight Reduction
Associated with reduction of hyperinsulinemia
and androgen excess.BMI should not be > 25
Manage hair
Bleaching Cutting or shaving
Electrolysis Laser epilation

77. 77

78. Removal of the
source
78
Adrenal or ovarian tumour – surgically
treated
Cushing disease –
Adrenalectomy
Radiation to pituitary
Removal of ACTH producing tumor
Iatrogenic cases – Offending drug to
be stopped

79. 79
THERAPEUTIC OPTIONS
Management of excess ovarian androgen
production :
Standard therapy is :combined E+P,most
commonly OCs
It reduces ovarian androgen production
It increases SHBG
It induces competition at the cellular level for
binding to the androgen receptor

80. 80
THERAPEUTIC OPTIONS
Choice of OC
EE + Norgestimate approved in USA
Cyproteroneacetate used as progesterone
component in Ocs
Cyproterone 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

81. OVARIAN SUPPRESSION BY LONG
ACTING GnRH ANALOGUE
Can be used for functional ovarian
androgen overproduction and even for
malignant condition
But to be used for long with back-up
Treatment is expensive and results are
inconsistent
Use is reserved for patients resisting to
initial therapy.
81

82. 82
THERAPEUTIC OPTIONS
Long acting GnRH analogues used
But there is doubt that this therapy will
be beneficial over Ocs
INSULIN SENSITIZING AGENTS:
For PCO with acanthosis nigicans
Commonly used agent is : Metformin and
Troglitazone,Pioglitazone,Rosiglitazone

83. 83
Drosperinone in PCOS
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

84. 84
THERAPEUTIC OPTIONS
MANAGEMENT OF EXCESS
ADRENAL ANDROGEN PRODUCTION
Metabolic correction of the
disorder,usually with exogenous
steroids
Dexamethasone,mostly used,But
LIMITED ROLE

85. Glucocorticoids
85
Mode of action
Suppress pituitary adrenal axis -
suppression of
endogenous ACTH secretion
Use –
In adrenal or mixed adrenal and
ovarian hyperandrogenism

86. Glucocorticoid Dosage Frequency
Hydrocortisone 10-20 mg Twice daily
Prednisone 2.5-5 mg Nightly or
a
alternate days
Dexamethasone 0.25-0.50 mg Nightly
86
Glucocorticoid preparations used in
monotherapy & combined with antiandrogens

87. 87
THERAPEUTIC OPTIONS
Management directed to the target organ
and cells
Competition with Androgen
receptors:Spironolactone,Flutamide,
Ketoconazole,Cyproterone acetate
5-alpha reductase Inhibitors
:Finasteride

88. 88
CPA
50-100 mg/day on menstrual cycle days
5-15 with ethinyl estradiol 20-35 mg on days 5-25
Spironolactone
100-200 mg/day (given in divided doses twice daily)
Finasteride
2.5-5 mg/day
Flutamide
250-500 mg/day (high dose)
62.5 to - <250 mg (low dose)
DOSES

89. 89
THERAPEUTIC OPTIONS
androgen receptors
competitors
SPIRONOLACTONE:
Best studied and as Gold standard
Mechanism :Androgen receptors blockade
Suppression of Androgen biosynthesis
Increased metabolic clearance of teststerone
( Testosterone  Estrogen )
50-200 mg/day in two divided doses
Spironolactone + OC is well established
regimen

90. 90
THERAPEUTIC OPTIONS
androgen receptors
competitors
FLUTAMIDE :
Blocks the androgen receptors
Decreases androgen production
May have therapeutic value in cases of
PCOS
Usually used with Ocs
KETOCONAZOLE:
Equally effective but danger of liver toxicity
Last resort of treatment.

91. CIMETIDINE= 300mg BD
LEAST POTENT ANDROGEN
RECEPTOR BLOCKER
Clinical reports disappointing.
CLINICALLY NOT EFFECTIVE.
91

92. Recent
Eflornithien: vaniqua (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. 92

93. 93
THERAPEUTIC OPTIONS
SELECTING BEST THERAPY:
Correct underlying medical problem
Correct thyroid/hyperprolactinemia
PCO :oral contraceptives
Ocs + spironolactone is usually the choice
75 –80% patients shows response
Atleast 6 months is needed for evidence of
response

94. Cosmetic treatments for
Hirsutism
94
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

95. 95
THERAPEUTIC OPTIONS
If response is seen in 6 months then
treatment should be continued for
further 6 months and in most cases for
number of years

96. 96
Hirsutism is a symptom of underlying
cause
Commonest cause is PCO
Progression may hint to diagnosing
tumor
Treatment – Medicines/ Cosmetic
To summarise