Hirsutism Aboubakr Elnashar

Benha University Hospital, Egypt

Aboubakr Elnashar

Outline

• Introduction

• Definition

• Causes

• Clinical evaluation

• Investigations

• Treatment

• Guidelines

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Introduction

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Gynecological,

Endocrinological,

Cosmetic &

Psychogenic: {great anxiety, nature of the

disease, social acceptance}

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Incidence

Not known

Mediterranean> Asian

American females: 10%

European: 5%

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Cycle growth of hair

Several months 2 weeks 3

months Aboubakr Elnashar

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

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

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Androgen production Androstenedione

Testosterone

Adrenal DHEA Ovary

DHEAS

50% 50% 50%

25% 25%

90% 10%

100%

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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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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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Definitions

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Virilization:

Defiminization: Atrophy of the breast & vagina

Musculinization: Hirsutism,

deepening of voice

temporal balding.

Increase: size of the clitoris,

muscular mass &

libido

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Main Causes of Virilization

1-CAH

2- Iatrogenic

3- Ovarian tumour

4- Cushing's syndrome.

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Hirsutism: Latin hirsutus = shaggy, hairy

Excessive growth of

terminal hair in

male sexual sites. Excessive: Socially unacceptable to the patient F& G score >8

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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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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

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.

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Causes

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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 syndrome Aboubakr Elnashar

A. Ovarian: 1. PCOS: 90%

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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.

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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

Hirsutism

Hirsutism Aboubakr Elnashar

Hirsutism Aboubakr Elnashar

Acne Hirsutism

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PCOS with hirsutism

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Ovarian orgin. Lateral mammary hirsutism, score 1 Aboubakr Elnashar

Grading scale for female pattern hair loss

mild but obvious female

pattern hair loss

Female androgenic alopecia

Frontal and temporal hair loss

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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.

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Hirsutism in a young woman with PCOS. Note the

acne lesions and excessive hair on her face and

neck.

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PCOS with hirsutism (Ferriman and Gallwey

score 4) on the abdomen Aboubakr Elnashar

Examples of hirsutism

affecting

the back,

chest, and

abdomen

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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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Uterus and adnexa during

caesarian section—both

ovaries were enlarged

(mean diameter 8 cm).

Luteoma

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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

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Adrenal SAHA.

Central hirsutism,

score 2

Adrenal SAHA. Severe

papulo-pustular acne and

central hirsutism

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Cushing's Syndrome

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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 %

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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

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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

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C. PERIPHERAL

1. Idiopathic: Regular ovulation &

normal androgen levels

2. Insulin resistance

– HAIRAN syndrome:

HyperAndrogenic

Insulin-Resistant Acanthosis Nigricans

– 5H syndrome acanthosis nigricans.

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3. Aromatase deficiency

4. Glucocorticoid resistance

5. Hyperprolactinema can cause an

increase in DHEAS. TT with

bromocriptin: dec PRL & DHEAS

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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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Clinical evaluation

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Primary objective:

1. Confirm diagnosis

2. Determine degree

3. Exclude life threatening diseases

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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

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Examination .General:

Thyroid disease,

Cushing syndrome,

Signs of virilization,

Signs of insulin resistance e.g.

acanthosis nigricans.

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.Breast:

Galactorrhea {Hyperprolactinaemia can be

accompanied by increase in adrenal

androgen}

.Pelvic:

mass

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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

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Degree of hair growth (Ferriman & Gallwey,1961)

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b. Macnight (1964):

divided the body into 7 areas:

Face

Neck

Shoulders

Chest

Abdomen

back

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Investigations

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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.

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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

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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

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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.

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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%

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Endocrine Society, 2008

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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

Ovarian tumors should be suspected

1. Rapid onset of virilization

2. Unilateral adenxal mass

3. Testosterone >200 ng/dl.

•TVS, CT or MRI.

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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

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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

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Screening for Cushing syndrome •Rare

•Indications: Centripetal obesity, buffalo hump

Moon face, Virilization

Pigmented stria, Hypertension

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Dexamethazone suppression test

( 1 mg orally at bed time)

Free cortisol (ug/dl

> 6 < 6

long term dexamethazone test Normal

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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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Treatment

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Androgen

Excess

Society,2012 Aboubakr Elnashar

Lines of treatment

I. General

II. Specific

III. Local

IV. Surgery

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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

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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: Metformin Aboubakr Elnashar

I. Ovarian suppression 1. Oral contraceptive pills

The first line of therapy

Mechanism:

P: suppress ov steroidogenesis

E: inc SHBG: dec FT

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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 benefits Aboubakr Elnashar

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

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.

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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

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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.

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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

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II. Adrenal suppression Glucocorticoids

Indication:

1.High not moderate elevation of DHEAS (Sperof,2005)

2. CAH

Mechanism:

inhibit ACTH dependant androgen

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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

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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

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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

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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

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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

3. Flutamide (Eulexin)

Indication: under tertiary center supervision

Severe cases

Failure of spironolactone & OCPs

Dose:

250 - 500 mg/d

Mechanism:

antiandrogen.

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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.

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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

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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)

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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).

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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

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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

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

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2. Bleaching (remove hair pigment)

•Hydrogen peroxide, often combined with amonia.

•Face, arms

Hair lightens & softens, inexpensive

Hair discoloration, skin irritation, Lack of effectiveness

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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 stubble

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b. Chemical depilators:

•Break down & dissolve hair by hydrolysing

disulhide bonds.

•Extremities, groin, face

Quick, inexpensive, effective

Regrowth in days, skin irritation

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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

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b. Waxing: group plucking

•Face, eyebrows, groin, trunk, extremities

Regrowth can take 6 weeks

Pain, postinflam pigmentation, scarring, slow,

expense, irritation, folliculitis

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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

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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

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IV. Surgery

•Tumor

•LOD

Discrepant & variable response.

Modest & sustained improvement in 25% (Amer et al, 2002).

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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).

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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

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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.

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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.

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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).

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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).

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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

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

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

Benha University Hospital, Egypt

Email: elnashar53@hotmail.com

Aboubakr Elnashar