This document provides an overview of hirsutism. It begins with definitions of terms like hirsutism, virilization, and hypertrichosis. It then discusses the causes of hirsutism, which can include polycystic ovary syndrome (PCOS), ovarian tumors, adrenal tumors, and other conditions. The document reviews approaches to clinical evaluation and investigations for hirsutism, including the Ferriman-Gallwey scoring system. It provides guidelines on tests to measure androgens and rule out conditions like congenital adrenal hyperplasia. Overall, the document provides a comprehensive review of hirsutism, including its definition, causes, evaluation, and treatment guidelines.

1. Hirsutism
Aboubakr Elnashar
Benha University Hospital, Egypt
Aboubakr Elnashar

2. Outline
• Introduction
• Definition
• Causes
• Clinical evaluation
• Investigations
• Treatment
• Guidelines
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3. Introduction
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4. Gynecological,
Endocrinological,
Cosmetic &
Psychogenic: {great anxiety, nature of the
disease, social acceptance}
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5. Incidence
Not known
Mediterranean> Asian
American females: 10%
European: 5%
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6. Cycle growth of hair
Several months 2 weeks 3
months Aboubakr Elnashar

7. Types of hair
Lanugo
Fetal hair
Vellus
Short,
fine,
Unpigmented
Before puberty
Terminal
Long,
coarse,
pigmented
arises from
vellus hair
Clinically, terminal hairs can be distinguished from vellus
hairs primarily by their length (i.e.`0.5 cm) and the fact
that they are usually pigmented.Aboubakr Elnashar

8. Non sexual Ambi-sexual Male sexual
Sites Lower parts of
the scalp, eye
brow, lashes,
fore-arms, lower
legs
Temporal &
vertical parts of the
scalp,
axilla,
lower pubic hair.
Ears,
nasal tip,
chin,
sternum,
upper pubic triangle,
back.
Depend on Growth hormone
from pituitary
Androgen in low
concentration from
the adrenals &
ovaries in females &
adrenals in male
Androgen in
high
concentration
Sites of hair
Aboubakr Elnashar

9. Androgen production
Androstenedione
Testosterone
Adrenal DHEA Ovary
DHEAS
50% 50%
50%
25% 25%
90% 10%
100%
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10. Androgen in the blood
Male Normal female Hirsute female
Free 3% 1% 2%
Albumin 19% 19% 19%
SHBG 78% 80% 79%
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11. Androgen at target cell (hair follicle)
Testosterone (T)
5œ-reductase.
Dihydrtestosterone (DHT)
Androstanediol
Glucuronide
3 alpha androstanediol glucuronide(3 alpha AG)
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12. Definitions
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13. Virilization:
Defiminization:
Atrophy of the breast & vagina
Musculinization:
Hirsutism,
deepening of voice
temporal balding.
Increase: size of the clitoris,
muscular mass &
libido
Aboubakr Elnashar

14. Aboubakr Elnashar

15. Main Causes of Virilization
1-CAH
2- Iatrogenic
3- Ovarian tumour
4- Cushing's syndrome.
Aboubakr Elnashar

16. Hirsutism: Latin hirsutus = shaggy, hairy
Excessive growth of
terminal hair in
male sexual sites.
Excessive: Socially unacceptable to the patient
F& G score >8
Aboubakr Elnashar

17. Hypertrichosis
Excessive growth of
(Lanugo, vellus or terminal) hair in
non-sexual sites (James et al,
2005)
•Cong
Acquired
•Localized
Generalized
Congenital hypertrichosis
lanuginosa
Drug-induced hypertrichosis
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18. Aboubakr Elnashar

19. Hirsutism:
•Not an increase in the number of
hair follicles but an alteration in their
character.
•An increase in the transformation
of the vellus to terminal hair.
{Androgens will convert lanugo &
vellus hair to terminal hair}.Aboubakr Elnashar

20. Hirsutism is a consequence of several factors.
An increase in:
1. Androgen production
2. The sensitivity of the androgen receptors at
the level of the hair follicle.
3. The activity of 5œ-reductase.
Aboubakr Elnashar

21. Causes
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22. A. Ovarian:
1. PCOS: 90%
2. Tumors: 0.5%
Virilizing ovarian tumors
Luteoma of pregnancy
3. Dysgenesis
B. Adrenal:5%
1. Cong adrenal
hyperplasia
2. Tumors
3. Cushing syndrome
C. Peripheral
1. Idiopathic: Regular
ovulation & normal
androgen levels
2. Insulin resistance
– HAIRAN syndrome:
HyperAndrogenic
Insulin-Resistant
Acanthosis Nigricans
– 5H syndromeAboubakr Elnashar

23. A. Ovarian:
1. PCOS: 90%
Aboubakr Elnashar

24. Rotterdam Criteria Of PCOS, 2003
2 out of 3 features are present:
1. Oligomenorrhoea and or Anovulation
2. Clinical Hyperandrogenism and/or
hyperandrogenemia.
3. Polycystic ovaries (U/S).
After exclusion of other etiologies.
Aboubakr Elnashar

25.  Clinical Hyperandrogenism
1. Hirsutism: The primary
clinical indicator of androgen
excess .
2. Acne : Potential marker
3. Androgenic alopecia: Poor
marker unless with
Oligomenorrhoea.
 Hyperandrogenemia
• FT) or FTI) are the more
sensitive methods
• Routine measurement of
Androstenedione: are not
recommended.
• DHEAS is raised in small
fraction of patient with
PCOS .Aboubakr Elnashar

26. Hirsutism
Hirsutism Aboubakr Elnashar

27. Hirsutism
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28. AcneHirsutism
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29. PCOS with hirsutism
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30. Ovarian orgin. Lateral mammary hirsutism, score 1
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31. Grading scale for female pattern hair loss
mild but obvious female
pattern hair loss
Female androgenic alopecia
Frontal and temporal hair loss
Aboubakr Elnashar

32. Rotterdam U/S Criteria of PCOS
At least one of the following:
• 12 or more follicles measuring 2–9 mm in diameter
• increased ovarian volume (>10 cm3).
 The distribution of follicles and a description of the
stroma are not required for diagnosis.
 The presence of a single PCO is sufficient to
provide the diagnosis.
Aboubakr Elnashar

33. Hirsutism in a young woman with PCOS. Note the
acne lesions and excessive hair on her face and
neck.
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34. Aboubakr Elnashar

35. Aboubakr Elnashar

36. PCOS with hirsutism (Ferriman and Gallwey
score 4) on the abdomen
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37. Examples of hirsutism
affecting
the back,
chest, and
abdomen
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38. 2. Ovarian Tumors:0.5%
Virilizing ovarian tumors
arrhenoblastoma,
hilus cell tumor,
lipod cell tumor,
granulosa cell tumor
Luteoma of pregnancy
{ Not true tumor but an
exaggerated reaction of ovarian
stroma to chorionic gonadotropins.
It is solid, usually unilateral &
regress after labour}
3. Ovarian dysgenesis
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39. Uterus and adnexa during
caesarian section—both
ovaries were enlarged
(mean diameter 8 cm).
Luteoma
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40. B. Adrenal:5%
1. Cong adrenal hyperplasia
2. Tumors
3. Cushing syndrome
Congenital adrenal
hyperplasia
Androgen secreting tumor
Centipetal obesity in Cushing's
syndrome Aboubakr Elnashar

41. Aboubakr Elnashar

42. Aboubakr Elnashar

43. Adrenal SAHA.
Central hirsutism,
score 2
Adrenal SAHA. Severe
papulo-pustular acne and
central hirsutism
Aboubakr Elnashar

44. Cushing's Syndrome
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45. Aboubakr Elnashar

46. Centripetal obesity 79-97
Facial plethora 50-94
Glucose intolerance 39-90
Weakness, proximal myopathy 29-90
Hypertension 74-87
Psychological changes 31-86
Easy bruisability 23-84
Hirsutism 64-81
Oligomenorrhea or amenorrhea 55-80
Acne, oily skin 26-80
Abdominal striae 51-71
Ankle edema 28-60
Backache, vertebral collapse,
fracture rare
Clinical manifestations %
Aboubakr Elnashar

47. Cushing’s Syndrome
One should be aware of the possibility of
Cushing’s syndrome in women with stigmata of
the :
PCOS &
Obesity
as it is a disease of insidious onset and dire
consequences
Aboubakr Elnashar

48. Forearm of a women man with
Cushing's disease showing multiple
ecchymoses due to minimal trauma.
30-year-old woman with Cushing's
disease showing round, plethoric
"moon" face, facial hirsutism, and
increased supraclavicular fat pads
Aboubakr Elnashar

49. C. PERIPHERAL
1. Idiopathic: Regular ovulation &
normal androgen levels
2. Insulin resistance
– HAIRAN syndrome:
HyperAndrogenic
Insulin-Resistant Acanthosis Nigricans
– 5H syndrome acanthosis nigricans.
Aboubakr Elnashar

50. Aboubakr Elnashar

51. 3. Aromatase deficiency
4. Glucocorticoid resistance
5. Hyperprolactinema can cause an
increase in DHEAS. TT with
bromocriptin: dec PRL & DHEAS
Aboubakr Elnashar

52. Hirsutism
Anabolic
steroids
Danazol
Metoclopramide
Methyldopa
Phenothiazines
Progestins
Reserpine
Testosterone
Hypertrichosis
Cyclosporine
Diazoxide
Hydrocortisone
Minoxidil
Penicillamine
Phenytoin
Psoralens
Streptomycin Hunter, 2003
D. Drugs
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53. Clinical evaluation
Aboubakr Elnashar

54. Primary objective:
1. Confirm diagnosis
2. Determine degree
3. Exclude life threatening diseases
Aboubakr Elnashar

55. History
.Virilization, psychological
.Onset & duration:
Rapidly progressive virilization: androgen secreting tumors
.Menstrual history:
PCOS, Pregnancy
.Family history:
Hair patterns are similar in families
.Drug intake
Aboubakr Elnashar

56. Examination
.General:
Thyroid disease,
Cushing syndrome,
Signs of virilization,
Signs of insulin resistance e.g.
acanthosis nigricans.
Aboubakr Elnashar

57. .Breast:
Galactorrhea {Hyperprolactinaemia can be
accompanied by increase in adrenal
androgen}
.Pelvic:
mass
Aboubakr Elnashar

58. Degree of hirsutism
Photography or scoring systems
a. Ferriman & Gallwey(1961): 9 areas
upper lip,
chin,
chest
upper abdomen,
lower abdomen,
upper arm,
thighs,
upper back,
lower back/buttocks
minimal=1, mild=2, moderate=3, severe=4
>8 = hirsutism
15 = organic cause
Aboubakr Elnashar

59. Degree of hair growth
(Ferriman & Gallwey,1961)
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60. Aboubakr Elnashar

61. b. Macnight (1964):
divided the body into 7 areas:
Face
Neck
Shoulders
Chest
Abdomen
back
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62. Investigations
Aboubakr Elnashar

63. Total testosterone:
measures the ovarian & adrenal activity.
When testing for elevated androgen levels: measure
an early morning plasma total testosterone level as the
initial test.
Aboubakr Elnashar

64. Free testosterone
Good correlation with total production rate
(= secretion rate + peripheral conversion rate)
Good correlation with degree of virilization
If the plasma total testosterone is normal in the
presence of risk factors for hyperandrogenism or the
presence of hirsutism that progresses despite therapy:
measuring an early morning plasma total and free
testosterone
Free androgen index(FAI)=
TX 100 / SHBG if > 4.5: PCOS
•Not done routinely in presence of hirsutism
Aboubakr Elnashar

65. 17 OHP:
an intermediate metabolite in steroidogensis in the adrenals.
In patients with a high likelihood of congenital
adrenal hyperplasia [positive family history, member of
a high-risk ethnic group such as Ashkenazi Jews
(prevalence 1 in 27), Hispanics
(1 in 40), and Slavics (1 in 50)], we recommend
measurement of an early morning follicular phase level
of 17-hydroxyprogesterone.
 DHEAS:
Good marker of Adrenal A production
Not essential
Aboubakr Elnashar

66. DHES is not essential (Speroff,2005)
1. If 17 OHP is normal: adrenal enzyme defect can be
excluded .
2. Moderate elevations of DHES can be suppressed by
suppression of ovulation.
3. DHES > 700 ug/dl is rare & is associated with high levels
of T
4. Imaging of the adrenals is more cost-effective than
measuring DHES.
Aboubakr Elnashar

67. 3 alpha androstanediol glucuronide
•Metabolite of DHT
•Good marker of peripheral androgen action
•Inc {increased activity of 5 alpha reductase} {end organ
hypersensitivity}
•Not done routinely:
1. No change in diagnosis & treatment,
2. Values overlap in 20%
Aboubakr Elnashar

68. Endocrine Society, 2008
Aboubakr Elnashar

69. Testosterone (ng/dl)
>200 <200
U/S of the ovary Anovulation
(PRL, endom biopsy)
Adenxal mass Nothing
Laparotomy CT of the adrenala & ovaries
Laparotomy
Aboubakr Elnashar

70. Ovarian tumors should be suspected
1. Rapid onset of virilization
2. Unilateral adenxal mass
3. Testosterone >200 ng/dl.
•TVS, CT or MRI.
Aboubakr Elnashar

71. Screening for late onset adrenal hyperplasia
•Incidence: 1-5%
•Clinical indication of ACTH stimulation test:
Strong family history
Severe hirsutism from puberty
Flatness of the breast
Hypertension
Short stature
Aboubakr Elnashar

72. 17 oh P(ng/dl) morning
< 200 > 200
Rules out adrenal hyperplasia ACTH stimulation test (0.25
21-hydroxylase deficiency mg ACTH I.V.& 17 oh P at time
zero & after 1 hour)
Normal Abnormal
Rules out adrenal hyperplasia Adrenal hyperplasia
Aboubakr Elnashar

73. Screening for Cushing syndrome
•Rare
•Indications:
Centripetal obesity, buffalo hump
Moon face, Virilization
Pigmented stria, Hypertension
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74. Dexamethazone suppression test
( 1 mg orally at bed time)
Free cortisol (ug/dl
> 6 < 6
long term dexamethazone test Normal
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75. PCOS T
LH/FSH
usually inc
2/1
Late-onset CAH 17-OH-P >200 ng/dL
Androgen-secreting ov tumor Total T >200 ng/dL
Androgen-secreting ad tumor DHEAS >700 g/dL
Cushing syndrome Cortisol Increased
Exogenous androgen use Toxicology
screen
Increased
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76. Treatment
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77. Androgen
Excess
Society,2012
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78. Lines of treatment
I. General
II. Specific
III. Local
IV. Surgery
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79. I. General
•Reassurance:
•explain the condition, treatment regimen & the time required
•Stop smoking
•Weight reduction:
{Inc SHBG: Dec FT}
Keep BMI around 21 kg / m2
Dec the risk of DM & CVD
Aboubakr Elnashar

80. II. Specific
I. Ovarian suppression:
1. OCPs 2. Progestagen 3. GnRha
II. Adrenal suppression: Corticosteroids
III. Antiandrogens:
1. Spironolactone 2. Cyproterone acetate
3. Flutamide 4. Ketoconazole
IV. 5 alpha reductase inhibitors: Finasteride
V. Insulin sensitizer: MetforminAboubakr Elnashar

81. I. Ovarian suppression
1. Oral contraceptive pills
The first line of therapy
Mechanism:
P: suppress ov steroidogenesis
E: inc SHBG: dec FT
Aboubakr Elnashar

82. Best type:
Avoid OCs containing norethisterone or levonorgestrel
less androgenic or antiandrogenic
high estrogen
Diane (cyproterone acetate),
Yasmin (Drospirenone)
Clordion, Gestafortin, Lormin, NonOvlon, Normenon,
Verton (Chlormadinone acetate)
Gynera (gestodene),
Marvelon (desogestrel),
Cilest (norgestimate).
Effect:
1. Dec T after 1-3 mo.
2. Additional benefitsAboubakr Elnashar

83. We do not suggest one particular OCP over another for
treating hirsutism (Endocrine Society, 20108)
most androgenic progestin:
Levonorgestrel, norethisterone
low androgenicity:
norgestimate and desogestrel
progestins with antiandrogenic activity
drospirenone and CPA
One small trial did not demonstrate a difference
in hirsutism efficacy between an OCP containing
levonorgestrel and one containing desogestrel
Levonorgestrel may adversely affect metabolic biomarkers
when compared with other less androgenic progestins, but
there are no data to suggest that these effects are associated
with adverse clinical outcomes.Aboubakr Elnashar

84. OCPs containing either 30–35 g ethinyl estradiol or the
lower-dose 20-g preparations may be used for suppression of
ovarian androgens. There are no clinical trials of 20-g
OCPs for hirsutism, but these lower-dose preparations
appear to be as effective as the 30- to 35-g preparations for
acne.
Aboubakr Elnashar

85. 2. Progestins
Indication: If pills is contraindicated or unwanted
Mechanism:
inhibit ov steroidogenesis,
inc clearance of androgen,
inhibit 5 alpha reductase
dec SHBG:inc FT
Dose: DMPA: 150 mg IM / 3 mo.
MPA: 30 mg PO / d
Effect: comparable to OCPs
Aboubakr Elnashar

86. 3. Gn Rh analogue
Indications:
Failure of usual management
Overweight with severe hirsutism
Dose:
leuprolide acetate depot: IM / mo.
The initial stimulatory effect can be avoided by starting
therapy in the luteal phase when Gnt are already
suppressed by elevated progesterone levels.
Once maximal response has been obtained OCP or
antiandrogen for long term suppression of hair growth.
Treatment should be limited to 6 mo.
Aboubakr Elnashar

87. Mechanism of action:
Side effects:
of estrogen deficiency
Use with OCPs:
{avoid problems associated with E deficiency & add
benefits}
Effects:
highly effective & better than OCP alone
Aboubakr Elnashar

88. II. Adrenal suppression
Glucocorticoids
Indication:
1.High not moderate elevation of DHEAS (Sperof,2005)
2. CAH
Mechanism:
inhibit ACTH dependant androgen
Aboubakr Elnashar

89. Dose:
Nocturnal {maximal suppression of the CNS
adrenal axis that peaks during sleep}
Dexamethazone: 0.3 mg or 0.25 mg/ other evening
Prednisone: 3 mg
Adrenal hyperplasia: higher doses
Effects:
1. No cortisol suppression
2. No Cushingoid side effects
Aboubakr Elnashar

90. Aboubakr Elnashar

91. III. Antiandrogens
1. Spironolactone (Aldactone)
Dose:
100-200 mg/d
remission: dec dose to 25-50 mg
100-200 mg/d from D1-D21
Mechanism :
on receptor
ovary & adrenals
Liver
kidney
Aboubakr Elnashar

92. Side effects: minimal.
Mens irregularities, mastalgia, feminization of
male fetus, transient diuresis, hyperkalemia,
?carcinogenic
Use with OCP:
1. Dramatic effect, but not impressively better
2. Prevent feminization of male fetus
3. Regular menstruation
Effects: maximal by 6mo
Cessation : relapse
Aboubakr Elnashar

93. 2. Cyproterone acetate (androcure)
Dose:
50-100 mg from D5 to D15 &
EE2: 30-50 ug from D5 to D25.
Dec dose after remission
Mechanism:
on receptors
Progestational effect
Weak corticosteroid effect
Aboubakr Elnashar

94. Side effects:
mens irregularities, mastalgia, feminization of
male fetus, loss of libido, fatigue, edema, weight
gain, decrease HDLP & cholesterol, glucose
intolerance.
Use with EE2 or OCPs
Effects:
maximal by 3mo
improvement in 60-90%
Cessation: relapse
Aboubakr Elnashar

95. 3. Flutamide (Eulexin)
Indication: under tertiary center supervision
Severe cases
Failure of spironolactone & OCPs
Dose:
250 - 500 mg/d
Mechanism:
antiandrogen.
Aboubakr Elnashar

96. Side effects:
dryness of the skin, increase appetite
hepatotoxicity, expensive.
It is unsuitable for treatment of hirsuitism (Speroff, 2005)
Use with OCPs:
1. Add benefit 2. Avoid block androgen receptors in male fetus.
Effects:
Similar or better than Spironolactone
We do not recommend one antiandrogen over another, except that
we recommend against the use of flutamide.
Aboubakr Elnashar

97. Aboubakr Elnashar

98. IV. 5 alpha reductase inhibitors
Finasteride (Proscar)
Indication: under tertiary center supervision.
Severe cases
Mode of action:
Inhibit 5 alpha reductase activity: blocking conversion of T to DHT.
Dose:
2.5 - 5 mg /d
Aboubakr Elnashar

99. Side effects:
very minimal. Teratogenic
Use with OCPs:
To avoid risk on male fetus & added benefits.
Effects:
Flutamide or Spironolactone is more effective
Drugs in this class:
Finasteride 5 mg (Proscar}
Finasteride 1 mg (Propecia)
Dutasteride (Avodart)
Aboubakr Elnashar

100. V. Insulin sensitizer
Metformin
•PCOS
IH: {insulin resistance} (Unluhizarci et al, 2004).
•1500 mg/d
•Dec serum insulin & T.
Dec F&G score (Kazerooni et al, 2003 ; Kelly & Gordon, 2003)
•Metformin Vs Dianette (EE2: 35 ug + cyproterone acetate: 2 mg)
Dianette was more effective (Harborne et al, 2003).
Aboubakr Elnashar

101. Cochrane library (2003)
•Cyprotrone acetate was compared to (spironolactone, flutamide,
finastride, GnRHa, Ketconazole):
No differences in clinical outcomes
Spironolactone 100 mg/d is superior to finastride 5 mg/d & low
dose cypr acetate 12.5 mg/d (first 10 days of the cycle) up to 12
months after the end of the treatment
Aboubakr Elnashar

102. III. Local
Suppress hair growth:
Eflornithine Hydochloride (Vaniqa)
Remove hair pigment: Bleaching
Temporary depilation:
shaving, chemical depilators
Temporary epilation: plucking, waxing
Permanent removal:
Electrolysis, Laser & intense pulsed light
Aboubakr Elnashar

103. 1. Suppress hair growth
Eflornithine 13.9% (Vaniqa) cream
•Inhibits ornithine decarboxylase (an enzyme in hair
dermal papilla that is essential for hair growth).
•Face, neck
Can be used with other tt e.g. lasers, intense
pulsed light
Regrowth can take 2 ms: Must be continued
indefinitely to prevent regrowth
S effects: stinging, burning, tingling
Aboubakr Elnashar

104. 2. Bleaching (remove hair pigment)
•Hydrogen peroxide, often combined with amonia.
•Face, arms
Hair lightens & softens, inexpensive
Hair discoloration, skin irritation, Lack of effectiveness
Aboubakr Elnashar

105. 3. Temporary depilation
(remove part of hair)
a. Shaving:
•All areas
Inexpensive, effective & does not cause
change in hair quality, quantity or texture.
Daily need, skin irritation, quick regrowth
folliculitis, time consuming, beard stubbleAboubakr Elnashar

106. b. Chemical depilators:
•Break down & dissolve hair by hydrolysing
disulhide bonds.
•Extremities, groin, face
Quick, inexpensive, effective
Regrowth in days, skin irritation
Aboubakr Elnashar

107. 4. Temporary epilation
(remove the entire hair)
a. Plucking:
•Face, eyebrows, nipples, bikini area
Effective for small amount, inexpensive, regrowth
can take weeks
Pain, skin irritation, postinflam pigmentation,
folliculitis, slow, ingrown hairs, scarring
Aboubakr Elnashar

108. b. Waxing: group plucking
•Face, eyebrows, groin, trunk, extremities
Regrowth can take 6 weeks
Pain, postinflam pigmentation, scarring, slow,
expense, irritation, folliculitis
Aboubakr Elnashar

109. 5. Permanent removal
(destruction of the dermal papilla)
a. Electrolysis:
•Needle is inserted into the hair follicle & a current
is used to destroy the dermal papilla.
•All areas, usually the face
May give permanent removal
Pain, scarring, painful,
repeat treatments needed
time consuming, expensive, pigmentation
Aboubakr Elnashar

110. b. Laser & intense pulsed light
•Selective phototricholysis. A light source sufficient to penetrate to
the follicular bulge & the papillae is directed at the hair by probe.
•All areas
May give permanent hair reduction, efficient, painless
Dark hair required, expensive, scarring, skin pigmentation,
repeated treatments usually necessary
Aboubakr Elnashar

111. Aboubakr Elnashar

112. IV. Surgery
•Tumor
•LOD
Discrepant & variable response.
Modest & sustained improvement in 25%
(Amer et al, 2002).
Aboubakr Elnashar

113. Guidelines
Endocrine Society 2008
Diagnosis of hirsutism
1. We suggest against testing for elevated
androgen levels in women with isolated mild
hirsutism because the likelihood of identifying a
medical disorder that would change management
or outcome is low (2).
Aboubakr Elnashar

114. 2. We suggest testing for elevated androgen levels
in women with (2)
• Moderate or severe hirsutism
• Hirsutism of any degree when it is sudden in
onset, rapidly progressive, or when associated with
any of the following:
– menstrual irregularity or infertility
– central obesity
– acanthosis nigricans
– rapid progression
– clitoromegaly
Aboubakr Elnashar

115. Treatment of hirsutism
1. For women with patient-important hirsutism
despite cosmetic measures, we suggest either
pharmacological therapy or direct hair removal
methods (2).
The choice between these options depends on
(a) patient preferences,
(b) The extent to which the area of hirsutism that
affects wellbeing is amenable to direct hair
removal, and
(c) access to and affordability of these alternatives.
Aboubakr Elnashar

116. 2.Pharmacological treatments
a. Monotherapy
For the majority of women, we suggest oral
contraceptives to treat patient-important hirsutism
(2)
because of its teratogenic potential, we
recommend against antiandrogen monotherapy
unless adequate contraception is used (1| ).
For women who cannot or choose not to
conceive, we suggest the use of either oral
contraceptive preparations (OCPs) or
antiandrogens
The choice between these options
depends on patient preferences regarding efficacy,
side effects, and costs.Aboubakr Elnashar

117. We suggest against the use of flutamide
therapy (2).
We suggest against the use of topical
antiandrogen therapy for hirsutism (2).
We suggest against using insulin-lowering
drugs as therapy for hirsutism (2).
Aboubakr Elnashar

118. For women with hirsutism who do not have
classic or nonclassic congenital adrenal
hyperplasia due to 21-hydroxylase deficiency
(CYP21A2), we suggest against glucocorticoid
therapy (2).
We suggest glucocorticoids for women with
hirsutism due to non classic congenital adrenal
hyperplasia (NCCAH) who have a suboptimal
response to OCPs and/or antiandrogens, cannot
tolerate them, or are seeking ovulation induction
(2).
Aboubakr Elnashar

119. We suggest against using GnRH agonists
except in women with severe forms of
hyperandrogenemia, such as ovarian
hyperthecosis, who have a suboptimal response
to OCPs and antiandrogens (2).
For all pharmacologic therapies for hirsutism,
we suggest a trial of at least 6 months before
making changes in dose, changing medication, or
adding medication (2).
Aboubakr Elnashar

120. b. Combination therapy
If patient-important hirsutism remains
despite 6 or more months of monotherapy with an
oral contraceptive, we suggest adding an
antiandrogen (2).
Aboubakr Elnashar

121. 3. Direct hair removal methods
For women who choose hair removal therapy,
we suggest laser/photoepilation (2).
For women undergoing photoepilation therapy
who desire a more rapid initial response, we
suggest adding eflornithine cream during
treatment (2).
For women with known hyperandrogenemia
who choose hair removal therapy, we suggest
pharmacologic therapy to minimize hair regrowth
(2).
Aboubakr Elnashar

122. Benha University Hospital, Egypt
Email: elnashar53@hotmail.com
Aboubakr Elnashar