SEMINAR ON ALOPECIA Chairperson: Dr. Shahab Uddin Ahmed Chowdhury. Associate Professor & Head of...

SEMINAR ON ALOPECIASEMINAR ON ALOPECIAChairperson : Dr. Shahab Uddin Ahmed Chowdhury.

Associate Professor & Head of the dept. Department of Dermatology, MMC.

Speakers : Dr. Mohammad Shoeb Khan, MD (Part-II)

& Dr. Mohammed Saiful Islam Bhuiyan,

MD (Part-II), FCPS (Part-II) Medical Officers,

Department of Dermatology, MMCH.

Date & Time : 5th April, 2005 at 2.00 pm.

Organized by : Department of Dermatology, MMCH. &

Renata Limited

HAIR AND HAIR FOLLICLE

INTRODUCTION

Hairs are keratinized elongated

structures derived from invaginations of

epidermis and project out from most of

the body surface.

AREAS WITHOUT HAIR:AREAS WITHOUT HAIR:

Palms Palms SolesSoles Lips Lips Nipples Nipples Glans penisGlans penis

Clitoris Clitoris PrepucePrepuce Labia minoraLabia minora Inner surface ofInner surface of

labia majoralabia majora

RACIAL PREVALENCE :RACIAL PREVALENCE :

• Whites are hairiest.Whites are hairiest.• Asians are least hairy and Asians are least hairy and • blacks fall in between.blacks fall in between.

TYPES OF HAIR

Morphologically :

• Straight : Asians , whites.

• Spiral : Blacks, whites.

• Helical : Whites.

• Wavy : Whites.

HAIR TYPES (Contd.)HAIR TYPES (Contd.)

Fetal hair -Fetal hair -Lanugo hairLanugo hair :: soft, fine, lightly pigmented hairs. soft, fine, lightly pigmented hairs.

Adult hair -Adult hair -Vellus hair :Vellus hair : fine hairs cover most of the body fine hairs cover most of the body

of youngsters and adults.of youngsters and adults.

Terminal hair:Terminal hair: long, coarse, pigmented hairs with long, coarse, pigmented hairs with

larger diameters.larger diameters.

NUMBER OF HAIRS

Scalp : about 1,00,000 hairs.

Face : about 600 hairs /cm2.

Rest of the body : about 60 hairs/cm2.

LENGTH, WIDTH AND GROWTH RATE

Length : range from <1mm to > 1 meter.

Average uncut scalp hair : 25 – 100 cm.

(exceptionally 170 cm)

Width : from 0.005 to 0.06mm.

Growth rate: about 1 cm/ month (terminal hair).

FUNCTIONS

1. Protects body surface from external injury.2. Helps in sensory function.3. Psycho – social importance.4. Forensic importance.

i. Identification of race, sex, age and religion. ii. Cause of death- can be determined. iii. Time of death- can be determined.

5. Assist thermo- regulation: mainly in lower animals.

STRUCTURE OF HAIR AND HAIR FOLLICLE:STRUCTURE OF HAIR AND HAIR FOLLICLE:

DEVELOPMENT OF HAIR

Ectodermal origin-

1. Hair bud – develops from epidermis and

penetrates the dermis.

2. Hair shaft – grows from cells in the

centre of hair bud.

3.3. Inner root sheath – develops from cells in Inner root sheath – develops from cells in thethe

periphery of hair bud.periphery of hair bud.

Mesodermal origin:Mesodermal origin: Outer root sheath.Outer root sheath.

First hair come is lanugo hair at eyebrow First hair come is lanugo hair at eyebrow

and and upper lip at twelve upper lip at twelve

weeksweeks of gestation.of gestation.

DEVELOPMENT OF HAIR (Contd.)DEVELOPMENT OF HAIR (Contd.)

3.3. Inner root sheath – develops from cells in theInner root sheath – develops from cells in the

periphery of hair bud.periphery of hair bud.

Mesodermal origin :Mesodermal origin : Outer root sheath.Outer root sheath.

First hair to come is lanugo hair at eyebrow First hair to come is lanugo hair at eyebrow

and upper lip at 12 and upper lip at 12

weeks of gestation.weeks of gestation.

DEVELOPMENT OF HAIR (Contd.)DEVELOPMENT OF HAIR (Contd.)

HAIR EMBRYOLOGYHAIR EMBRYOLOGY

HAIR CYCLEHAIR CYCLE

It is believed that each hair follicle goesIt is believed that each hair follicle goes

through 10-20 hair cycle in a life time. through 10-20 hair cycle in a life time.

There are four phases-There are four phases-

1.1. Anagen :Anagen : growing phase.growing phase.

2.2. Catagen:Catagen: involuting phase. involuting phase.

3.3. Telogen :Telogen : resting phase.resting phase.

4.4. Exogen :Exogen : hair shedding phase.hair shedding phase.

ANAGEN (GROWING PHASE)

Last for about 1000 days.

Follicular cells grow, divide and become

keratinized to form growing phase.

A darkly pigmented portion is evident just

above the hair bulb.

CATAGEN (INVOLUTING PHASE)

Lasts for about 10 days.

Scalp hairs show a gradual thinning and

decrease of the pigment.

Melanocytes cease producing melanin.

Matrix keratinocytes abruptly cease

proliferating so that lower follicle involutes

and regresses.

TELOGENTELOGEN (RESTING PHASE) (RESTING PHASE)

Lasts for about 100 days.Lasts for about 100 days. Club-shaped proximal end shed from the Club-shaped proximal end shed from the

follicle during telogen or subsequent anagen.follicle during telogen or subsequent anagen. Growth of a new anagen hair leads to Growth of a new anagen hair leads to

shedding of any remaining telogen hair.shedding of any remaining telogen hair. But new hair does not “push out” the hair from But new hair does not “push out” the hair from

the previous cycle.the previous cycle.

EXOGENEXOGEN (HAIR SHEDDING PHASE)(HAIR SHEDDING PHASE)

Recently added phase.The term describes relationship between hair

shaft and base of telogen follicle. Hairs can be retained for more than one

cycle.Shedding phase is most likely independent of

anagen and telogen.

PIGMENTATION OF HAIRPIGMENTATION OF HAIR

Hair color is determined by melanocytes.Hair color is determined by melanocytes.

Melanocytes are present in the bulb.Melanocytes are present in the bulb.

Melanocytes feed melanosomes mainly to Melanocytes feed melanosomes mainly to

the medulla and cortex.the medulla and cortex.

Melanocytic follicles produce melanin- Melanocytic follicles produce melanin-

. eumelanin (dominant in brown-black hairs). eumelanin (dominant in brown-black hairs)

. phaeomelanin (dominant in red-blond hairs) . phaeomelanin (dominant in red-blond hairs)

Greying of hair – due to decreased

number and activities of melanocytes.

Vitiligo – due to destruction of

melanocytes.

Albinism – due to inactivity of

melanocytes.

PIGMENTATION OF HAIR (Contd.)PIGMENTATION OF HAIR (Contd.)

ALOPECIAALOPECIA•

• Absence or loss of hair especially of the scalp.Absence or loss of hair especially of the scalp.

• Pathophysiology of hair loss : Pathophysiology of hair loss :

1. Production failure –1. Production failure – Failure to produce or continue to Failure to produce or continue to produce a normal hair follicle.produce a normal hair follicle.

2.2. Aberration of – Aberration of – Normal hair cycle.Normal hair cycle. Production of a normal hair shaft.Production of a normal hair shaft.

3. Destruction of –3. Destruction of – Hair follicle.Hair follicle.

CLASSIFICATION OF ALOPECIA CLASSIFICATION OF ALOPECIA

1. FOCAL HAIR LOSS • Non-Scarring:

A. Abnormality of cycling-

i. Alopecia areata.

ii. Syphilitic alopecia.

B. Production decline-

i. Androgenetic alopecia.

ii. Triangular alopecia.

FOCAL HAIR LOSSFOCAL HAIR LOSS (Contd.)(Contd.)

C.C. Hair breakage-Hair breakage-

i.i. Trichotillomania. Trichotillomania.

ii. Tinea capitis.ii. Tinea capitis.

iii. Traction alopecia.iii. Traction alopecia.

iv. Primary or acquired hair shaft abnormality.iv. Primary or acquired hair shaft abnormality.

SCARRING ALOPECIA

A. Lymphocytic-

i. Chronic Cutaneous LE (DLE).

ii. Lichen planopilaris.

iii. Classic pseudopellade of Brocq.

iv. Alopecia mucinosa.

v. Central centrifugal cicatricial alopecia.

vi. Keratosis follicularis spinulosa decalvans.

SCARRING ALOPECIASCARRING ALOPECIA (CONTD.)(CONTD.)

B. NeutrophilicB. Neutrophilic – –

i. Folliculitis decalvans.i. Folliculitis decalvans.

ii.ii. Dissecting folliculitis/cellulitis.Dissecting folliculitis/cellulitis.

C. Mixed-C. Mixed-

i. Folliculitis (acne) keloidalis.i. Folliculitis (acne) keloidalis.

ii. Folliculitis (acne) necrotica.ii. Folliculitis (acne) necrotica.

iii. Erosive pustular dermatitis. iii. Erosive pustular dermatitis.

Diffuse Hair LossDiffuse Hair Loss

A.A. Abnormality of cycling –Abnormality of cycling –i. Alopecia areata.i. Alopecia areata.

ii. Telogen effluvium.ii. Telogen effluvium.

iii. Anagen effluvium.iii. Anagen effluvium.

iv. Loose anagen syndrome.iv. Loose anagen syndrome.

B.B. Hair shaft abnormality-Hair shaft abnormality-i. Hair breakage.i. Hair breakage.

ii. Unruly hair.ii. Unruly hair.

Diffuse Hair LossDiffuse Hair Loss (Contd.)(Contd.)

C.C. Failure of follicle production-Failure of follicle production-

i. Congenital universal atrichia.i. Congenital universal atrichia.

ii. Alrichia with papular lesions.ii. Alrichia with papular lesions.

iii. Hereditary vitamin-D- resistantiii. Hereditary vitamin-D- resistant

rickets.rickets.

ALOPECIA AREATAALOPECIA AREATA

• Definition:Definition:

Rapid and complete loss of hair in one or Rapid and complete loss of hair in one or

most often several round or oval patches, most often several round or oval patches,

usually on the scalp, bearded area, usually on the scalp, bearded area,

eyebrows, eye lashes and less commonly on eyebrows, eye lashes and less commonly on

other hairy areas of the body.other hairy areas of the body.

ALOPECIA AREATA

ALOPECIA AREATA

ALOPECIA AREATA(Contd.)ALOPECIA AREATA(Contd.)

• Epidemiology:Epidemiology:

Approximately 1.7% of the population will Approximately 1.7% of the population will

experience an episode of alopecia aerata experience an episode of alopecia aerata

during their life time.during their life time.

ALOPECIA AREATA (Contd.)ALOPECIA AREATA (Contd.)

EtiologyEtiology Exact cause is still unknown.Exact cause is still unknown. It is an autoimmune disease-It is an autoimmune disease-

- Mediated by the cellular arm - Mediated by the cellular arm (T- cell, macrophages ).(T- cell, macrophages ).

- Modified by genetic factors - Modified by genetic factors

(HLA-R4,DR11,DQ7)(HLA-R4,DR11,DQ7)

ALOPECIA AREATA (Contd.)

-Triggered by environmental factors-

Trauma.

Neurogenic inflammation.

Infections agents.

TraumaTrauma Neurogenic Neurogenic InflammationInflammation

Infections Infections agentsagents

Aberrant expression of MHC (due to Aberrant expression of MHC (due to failure of repression)failure of repression)

Release of cytokinesRelease of cytokines

Aberrant expression of adhesion Aberrant expression of adhesion moleculesmolecules

ETIOPATHOGENESISETIOPATHOGENESIS

Attack on Attack on

melanogically active anagen falliclemelanogically active anagen fallicle

Production of follicular auto- antigen Production of follicular auto- antigen (Kerationcyte and melanocyte origin)(Kerationcyte and melanocyte origin)

Follicular damage in anagen and rapid Follicular damage in anagen and rapid premature transformation to telogen.premature transformation to telogen.

Haematopoietic cell migration (T-cell)Haematopoietic cell migration (T-cell)

FOUR DISTINCT STAGES OF ALOPECIA AREATA

i. Acute hair loss.

ii. Persistant (Chronic) baldness.

iii. Partial telogen to anagen conversion

(incomplete revcovery).

iv. Normal recovery.

CLINICAL FEATURECLINICAL FEATURE

• Rapid and complete loss of hair in one

or several patches.

• Site – Scalp, bearded area, eyebrows,

eye lashes and less commonly other

areas of body.

• Size – Patches of 1-5 cm in diameter.

CLINICAL FEATURE (CONTD.)

• “Exclamation point” hair- at the periphery of

hair loss, there are broken hairs, whose distal

ends are broader than the proximal end.

!

EXCLAMATION MARK HAIRS

CLINICAL FEATURE (CONTD.)

• Few resting hairs may be found within the patches.

• “Going gray overnight”- a mysterious phenomenon

is observed in fulminant alopecia areata.

• In about 10% cases of long standing extensive

alopecia areata, some nail changes develop.

EXTENSIVE PATCHY ALOPECIA AREATA.

DIFFUSE PATTERN OF HAIR LOSS IN ALOPECIA AREATA

CLINICAL FEATURE (CONTD.)CLINICAL FEATURE (CONTD.)

““Alopecia totalis” – Total loss of scalp hair.Alopecia totalis” – Total loss of scalp hair.

““Alopecia universalis” – Loss of entire body Alopecia universalis” – Loss of entire body hair including scalp hair.hair including scalp hair.

““Ophiasis” – Loss of hair confluent along the Ophiasis” – Loss of hair confluent along the temporal and occipital scalp.temporal and occipital scalp.

““Sisaipho”- Loss of hair of entire scalp except Sisaipho”- Loss of hair of entire scalp except temporal and occipital area.temporal and occipital area.

ALOPECIA UNIVERSALIS

ALOPECIA TOTALIS

OPHIASIS PATERN OF ALOPECIA AREATA

ASSOCIATED DISEASEHigher incidence of alopecia areata inpatients of-

1. Atopic dermatitis.2. Autoimmune disease –

* SLE * Thyroiditis. * Myasthenia

gravis. * Vitiligo.

3. Lichen planus.4. Down syndrome.

HISTOLOGY

• Peribulbar, Perivascular and outer-

root sheath infiltration with T-cells and

macrophages.

• The follicular size are diminished and

identified in more superficial dermis.

DIFFERENTIAL DIAGNOSIS

1. Tinea capitis.

2. Trichotilomania.

3. Secondary syphilis

4. Congenital triangular alopecia.

5. Alopecia neoplastica.

6. Early lupus erythematosus.

TREATMENT

Spontaneous recovery is extremely common

for patchy alopecia areata.

For localized patchy alopecia areata-

• Steroid- both local (intralesional and

topical) and systemic (in short course).

TREATMENT (CONTD.)

- High potent topical steroid used as first

line therapy.

- Intralesional steroid given at 4-6 weeks

interval.

- Systemic steroid (Short course, <8 weeks)

alone or in conjunction with topical steroid.

TREATMENT (CONTD.)

If lack of response after several months therapy-

• Topical 1% Anthralin cream - applied for 15-20

minutes and then shampooed off the treated side.

• 5% topical minoxidil – as a single agent or as an

adjuvant with topical Anthralin.

• PUVA.

TREATMENT (CONTD.)

• Contact sensitizer –

- Squaric acid dibutyle ester,

- Diphencyprone,

- Dinitrochlorobenzene.

Psychological support.

In extensive scalp hair loss- cosmetically

expectable alternatives.

HEALED ALOPICIA UNIVERSALIS AFTER PUVA THERAPY

PROGNOSISPROGNOSIS

Poor prognostic marker-Poor prognostic marker-

-- Early onset (Prepubertal)Early onset (Prepubertal)

-- Extensive involvement.Extensive involvement.

-- Prolong duration (>5years)Prolong duration (>5years)

-- Ophiasis.Ophiasis.

ANDROGENETIC ALOPICIA

ANDROGENETIC ALOPICIA

ANDROGENETIC ALOPECIAANDROGENETIC ALOPECIA

Synonyms :Synonyms : Male Pattern alopecia,Male Pattern alopecia,

Male pattern baldness,Male pattern baldness,

Common baldnessCommon baldness

Secretarial alopecia.Secretarial alopecia.

Definition :Definition : It is a very common, potentiallyIt is a very common, potentially

reversible scalp hair loss that generally sparesreversible scalp hair loss that generally spares

parietal and occipital areas (Hippocraticparietal and occipital areas (Hippocratic

wreath) of the scalp.wreath) of the scalp.

ANDROGENETIC ALOPECIA (Contd.)ANDROGENETIC ALOPECIA (Contd.)

Age :Age : Twenties or early thirties.Twenties or early thirties.

sites :sites : Chiefly vertex and frontotemporalChiefly vertex and frontotemporal

regions.regions.

Etiopathogenesis:Etiopathogenesis:

• Exact mechanism is still unknown.Exact mechanism is still unknown.

• Hereditary (Probably autosomal dominant) &Hereditary (Probably autosomal dominant) &• Androgen (specifically dihydrotestesterone)Androgen (specifically dihydrotestesterone)

ETIOPATHOGENESIS ETIOPATHOGENESIS (Contd.)(Contd.)

Testesterone Testesterone 55RR Dihydrotesterone. Dihydrotesterone.

• 55R has two Isozyme, 5R has two Isozyme, 5R1 and 5R1 and 5R2R2

• 55R1 ubiquitously distributed in skin R1 ubiquitously distributed in skin

particularly in sebaceous gland.particularly in sebaceous gland.

• 55R2 is found in outer root sheath and R2 is found in outer root sheath and

dermal papillae.dermal papillae.

ANDROGENANDROGEN

Androgen - androgen receptor complex in cytoplasmAndrogen - androgen receptor complex in cytoplasm

transformation of receptor to expose DNA binding domain transformation of receptor to expose DNA binding domain

binds to androgen response element of DNAbinds to androgen response element of DNA

Transcription and translationTranscription and translation

certain effector protein,certain effector protein,

ETIOPATHOGENESIS ETIOPATHOGENESIS (Contd.)(Contd.)

EFFECTSEFFECTS

- Shortening of anagen and - Shortening of anagen and

lengthening of telogenlengthening of telogen

- Follicle become short and sclerosis of - Follicle become short and sclerosis of

dermis and miniaturization or reduction dermis and miniaturization or reduction

of hair presentof hair present..

CLINICAL FEATURE

• Hair loss starts any time after puberty

“Whisker hairs” – first sign of impending

male pattern alopecia, appear at the

temple.

• “Professor’s angle” – anterior hair line

recedes backward on each side.

• Eventually entire top of the scalp become

devoid of hair.

PATTERN OF HAIR LOSS

Androgenetic alopecia in womenAndrogenetic alopecia in womenEtiology :i. Genetic Predisposition,

ii. Androgen excess,

Ovarian cause-

- Polycystic ovarian syndrome,

- Other ovarian tumor,

. Unilateral benign

microadenoma.

. Leydig cell tumor

. Hilar cell tumor.

ETIOLOGY (CONTD.)ETIOLOGY (CONTD.)• Adrenal cause

- Congenital adrenal hyperplasia (androgenital

syndrome) due to deficiency of –

21 hydroxylase (most common)

11-β hygroxylase.

3-β hydroxysteroid dehydrogenase.

- Tumor

Adrenal adenoma

Carcinoma.

CLINICAL FEATURECLINICAL FEATURE

Pattern of hair loss :Pattern of hair loss :

““Christmas tree pattern”-Christmas tree pattern”- diffuse and diffuse and

progressive reduction of density and progressive reduction of density and

diameter of hairs in the mid scalp.diameter of hairs in the mid scalp.

• Maintenance of frontal hair lines with onlyMaintenance of frontal hair lines with only

slight recession. slight recession.

ANDROGENETIC ALOPECIA IN WOMEN

CLINICAL FEATURE (CONTD.)CLINICAL FEATURE (CONTD.)

Other evidence of androgen excess:Other evidence of androgen excess:• Acne.Acne.• Hirsutism.Hirsutism.• Menstrual irregularities.Menstrual irregularities.

Majority of women with pattern hair loss Majority of women with pattern hair loss havehave

• No increased serum androgen,No increased serum androgen,• No other sign symptom of No other sign symptom of

androgen hypersensitivity.androgen hypersensitivity.

TREATMENTTREATMENT

1.1. Topical Minoxidil (2% & 5%)Topical Minoxidil (2% & 5%)

-non specific hair growth promoter -non specific hair growth promoter

affecting anagen induction.affecting anagen induction.

- M/A is not clear, its ca channel - M/A is not clear, its ca channel

opener activity is important. opener activity is important.

2.2. Systemic Finesteride (1mg daily).Systemic Finesteride (1mg daily).

TREATMENT (CONTD.)TREATMENT (CONTD.)

3.3. In women – spironolactone ( >100 In women – spironolactone ( >100

mg daily). mg daily).

- Flutamide (250-500 - Flutamide (250-500

mg bid or tid). mg bid or tid).

- Cyproterone actate.- Cyproterone actate.

4. Surgical treatment- Micrograft & 4. Surgical treatment- Micrograft & minigraft from non-androgen minigraft from non-androgen dependent site (occiput).dependent site (occiput).

TELOGEN EFFLUVIUMTELOGEN EFFLUVIUM

It is a reaction pattern to a variety ofIt is a reaction pattern to a variety of

physical and mental stressors representsphysical and mental stressors represents

a precipitous shift of a percentage ofa precipitous shift of a percentage of

anagen hairs to telogen. anagen hairs to telogen.

Causes of Telogen EffluviumCauses of Telogen Effluvium EndocrineEndocrine

-- Hypo- or hyperthyroidism.Hypo- or hyperthyroidism.-- Postpartum.Postpartum.-- Peri- or postmenopausal state.Peri- or postmenopausal state.

NutritionalNutritional-- Biotin deficiency.Biotin deficiency.-- Caloric deprivation.Caloric deprivation.-- Essential fatty acid deficiency.Essential fatty acid deficiency.-- Iron deficiency.Iron deficiency.-- Protein deprivation.Protein deprivation.-- Zinc deficiency.Zinc deficiency.

Causes of Telogen EffluviumCauses of Telogen Effluvium (Contd.)(Contd.)

DrugsDrugs- Angiotensin-converting enzyme inhibitors.Angiotensin-converting enzyme inhibitors.- Anticoagulants.Anticoagulants.- Antimitotic agents.Antimitotic agents.- Benzimidazoles.Benzimidazoles.- Beta blockers.Beta blockers.- InterferonInterferon- LithiumLithium

- Oral contraceptives.Oral contraceptives.- Retinoids.Retinoids.- Vitamin A excess.Vitamin A excess.

Physical stressPhysical stress- AnemiaAnemia- Surgery.Surgery.- Systemic illness.Systemic illness.

Psychological stressPsychological stress

Causes of Telogen EffluviumCauses of Telogen Effluvium (Contd.) (Contd.)

Events related to pathogenesis of telogen effluvium

I. Short anagen- by drugs, fever, physiological

stress.

II. Prolonged anagen- Pregnancy.

III. Conversion of telogen follicle to anagen

follicle.

Pathology

1. > 12% to 15% of terminal follicles are in

telogen.

2. Follicle itself is not diseased.

3. No inflammation or dystrophic changes.

CLINICAL PRESENTATION

• “Lots of hairs coming out by the roots” complained by patient.

• Diffuse hair loss with clinically perceptible thinning of hairs usually 3-5 weeks of inciting signal and shedding continue for about 3-4 month after removal of inciting cause.

• 150 to > 400 hair loss daily. • Hair density may take 6-12 months to

return to base line. • Pull test.• Clip test.

TREATMENT

• No specific therapy.• In majority cases hair will grow spontaneously

within few month after removing inciting cause.• In some patients with chronic telogen effluvium-

- 5% minoxidil solution, 70% success in man .- For Premenopausal women, 5% minoxidil

solution + cyproterone acitate 50 mg from day 5 to 15 of menstrual cycle taken

together with ethynnyl estradiol (0.035

mg/day).

TREATMENT (CONTD.)

For post menopausal women,

- Cyproterone acetate 50 mg/day.

- Spironolactone (50- 100 mg/day) or flutamide

125- 250 mg/ day alternative to cyproterone

acetate.

TRICHTILLOMANIATRICHTILLOMANIA

• A neurotic practice of plucking or breaking A neurotic practice of plucking or breaking

hair from scalp or eyelash resulting usually hair from scalp or eyelash resulting usually

localized or widespread areas of alopecia localized or widespread areas of alopecia

contains hairs of varying length.contains hairs of varying length.

• Mostly girls under age of 10 years.Mostly girls under age of 10 years.

• Disturbed mother- child relationship. Disturbed mother- child relationship.

TRICHOTILOMANIA

TRICHOTILOMANIA IN A WOMEN

ALALOOPECIA SYPHILITICAPECIA SYPHILITICA

• Typical motheaten appeorance on the occipital

scalp or generalized thinning of hairs or both.

• Eyebrows, eyelash and body hairs also

involved.

• It may be one or sole cutaneus manifestation of

secondary syphilis.

• Treatment of syphilis may reverse the hair loss.

ALOPICIA OF SECONDARY SYPHILIS