The document summarizes a seminar on alopecia that was held on April 5, 2005. It was organized by the Department of Dermatology at MMCH and Renata Limited. The seminar featured speakers who discussed the structure of hair and hair follicles, the hair cycle, types of alopecia including alopecia areata, its clinical features, histology, differential diagnosis, and treatment options. Alopecia areata is an autoimmune condition characterized by patchy non-scarring hair loss that typically affects the scalp but can also involve other hairy areas of the body.

2. SEMINAR ON ALOPECIASEMINAR ON ALOPECIA
Chairperson : 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

3. HAIR AND HAIR FOLLICLE

4. INTRODUCTIO
N
Hairs are keratinized elongated
structures derived from invaginations of
epidermis and project out from most of
the body surface.

5. AREAS WITHOUT HAIR:AREAS WITHOUT HAIR:
 PalmsPalms
 SolesSoles
 LipsLips
 NipplesNipples
 Glans penisGlans penis
 ClitorisClitoris
 PrepucePrepuce
 Labia minoraLabia minora
 Inner surface ofInner surface of
labia majoralabia majora

6. RACIAL PREVALENCE :RACIAL PREVALENCE :
• Whites are hairiest.Whites are hairiest.
• Asians are least hairy andAsians are least hairy and
• blacks fall in between.blacks fall in between.

7. TYPES OF HAIR
Morphologically :
• Straight : Asians , whites.
• Spiral : Blacks, whites.
• Helical : Whites.
• Wavy : Whites.

8. 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 bodyfine hairs cover most of the body
of youngsters and adults.of youngsters and adults.
Terminal hair:Terminal hair: long, coarse, pigmented hairs withlong, coarse, pigmented hairs with
larger diameters.larger diameters.

9. NUMBER OF HAIRS
Scalp : about 1,00,000 hairs.
Face : about 600 hairs /cm2
.
Rest of the body : about 60 hairs/cm2
.

10. 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).

11. 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.

12. STRUCTURE OF HAIR AND HAIR FOLLICLE:STRUCTURE OF HAIR AND HAIR FOLLICLE:

13. 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.

14. 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 come is lanugo hair at eyebrow andFirst hair come is lanugo hair at eyebrow and
upper lip at twelveupper lip at twelve
weeksweeks of gestation.of gestation.
DEVELOPMENT OF HAIR (Contd.)DEVELOPMENT OF HAIR (Contd.)

15. 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 eyebrowFirst hair to come is lanugo hair at eyebrow
and upper lip at 12and upper lip at 12
weeks of gestation.weeks of gestation.
DEVELOPMENT OF HAIR (Contd.)DEVELOPMENT OF HAIR (Contd.)

16. HAIR EMBRYOLOGYHAIR EMBRYOLOGY

17. 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.

18. 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.

19. 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.

20. TELOGENTELOGEN (RESTING PHASE)(RESTING PHASE)
 Lasts for about 100 days.Lasts for about 100 days.
 Club-shaped proximal end shed from theClub-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 toGrowth 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 fromBut new hair does not “push out” the hair from
the previous cycle.the previous cycle.

21. 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.

22. 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 toMelanocytes 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)

23.  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.)

25. 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 toFailure 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.

26. CLASSIFICATION OF ALOPECIACLASSIFICATION 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.

27. 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.

28. 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.

29. 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.

30. 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.

31. 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.

32. ALOPECIA AREATAALOPECIA AREATA
• Definition:Definition:
Rapid and complete loss of hair in one orRapid 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 oneyebrows, eye lashes and less commonly on
other hairy areas of the body.other hairy areas of the body.

33. ALOPECIA AREATA

34. ALOPECIA
AREATA

35. ALOPECIA AREATA(Contd.)ALOPECIA AREATA(Contd.)
• Epidemiology:Epidemiology:
Approximately 1.7% of the population willApproximately 1.7% of the population will
experience an episode of alopecia aerataexperience an episode of alopecia aerata
during their life time.during their life time.

36. 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)

37. ALOPECIA AREATA (Contd.)
-Triggered by environmental factors-
 Trauma.
 Neurogenic inflammation.
 Infections agents.

38. TraumaTrauma NeurogenicNeurogenic
InflammationInflammation
InfectionsInfections
agentsagents
Aberrant expression of MHC (due toAberrant expression of MHC (due to
failure of repression)failure of repression)
Release of cytokinesRelease of cytokines
Aberrant expression of adhesionAberrant expression of adhesion
moleculesmolecules
ETIOPATHOGENESISETIOPATHOGENESIS

39. Attack onAttack on
melanogically active anagen falliclemelanogically active anagen fallicle
Production of follicular auto- antigenProduction of follicular auto- antigen
(Kerationcyte and melanocyte origin)(Kerationcyte and melanocyte origin)
Follicular damage in anagen and rapidFollicular damage in anagen and rapid
premature transformation to telogen.premature transformation to telogen.
Haematopoietic cell migration (T-cell)Haematopoietic cell migration (T-cell)

40. 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.

41. 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.

42. 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.
!

44. 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.

45. EXTENSIVE PATCHY ALOPECIA AREATA.

46. DIFFUSE PATTERN OF HAIR LOSS IN ALOPECIA AREATA

47. 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 bodyAlopecia universalis” – Loss of entire body
hair including scalp hair.hair including scalp hair.
““Ophiasis” – Loss of hair confluent along theOphiasis” – Loss of hair confluent along the
temporal and occipital scalp.temporal and occipital scalp.
““Sisaipho”- Loss of hair of entire scalp exceptSisaipho”- Loss of hair of entire scalp except
temporal and occipital area.temporal and occipital area.

48. ALOPECIA UNIVERSALIS

49. ALOPECIA TOTALIS

50. OPHIASIS PATERN OF ALOPECIA AREATA

51. ASSOCIATED DISEASE
Higher incidence of alopecia areata in
patients of-
1. Atopic dermatitis.
2. Autoimmune disease –
* SLE
* Thyroiditis.
* Myasthenia
gravis.
* Vitiligo.
3. Lichen planus.
4. Down syndrome.

52. HISTOLOGY
• Peribulbar, Perivascular and outer-
root sheath infiltration with T-cells and
macrophages.
• The follicular size are diminished and
identified in more superficial dermis.

53. DIFFERENTIAL DIAGNOSIS
1. Tinea capitis.
2. Trichotilomania.
3. Secondary syphilis
4. Congenital triangular alopecia.
5. Alopecia neoplastica.
6. Early lupus erythematosus.

54. 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).

55. 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.

56. 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.

57. TREATMENT (CONTD.)
• Contact sensitizer –
- Squaric acid dibutyle ester,
- Diphencyprone,
- Dinitrochlorobenzene.
⇒Psychological support.
⇒In extensive scalp hair loss- cosmetically
expectable alternatives.

58. HEALED ALOPICIA UNIVERSALIS
AFTER PUVA THERAPY

59. 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.

60. ANDROGENETIC ALOPICIA

61. ANDROGENETIC ALOPICIA

62. 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.

63. 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)

64. ETIOPATHOGENESISETIOPATHOGENESIS (Contd.)(Contd.)
TestesteroneTestesterone 55ααRR Dihydrotesterone.Dihydrotesterone.
• 55ααR has two Isozyme, 5R has two Isozyme, 5ααR1 and 5R1 and 5ααR2R2
• 55ααR1 ubiquitously distributed in skinR1 ubiquitously distributed in skin
particularly in sebaceous gland.particularly in sebaceous gland.
• 55ααR2 is found in outer root sheath andR2 is found in outer root sheath and
dermal papillae.dermal papillae.

65. ANDROGENANDROGEN
Androgen - androgen receptor complex in cytoplasmAndrogen - androgen receptor complex in cytoplasm
transformation of receptor to expose DNA binding domaintransformation 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,

66. ETIOPATHOGENESISETIOPATHOGENESIS (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 reductiondermis and miniaturization or reduction
of hair presentof hair present..

67. 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.

68. PATTERN OF HAIR LOSS

69. Androgenetic alopecia in womenAndrogenetic alopecia in women
Etiology :
i. Genetic Predisposition,
ii. Androgen excess,
Ovarian cause-
- Polycystic ovarian syndrome,
- Other ovarian tumor,
. Unilateral benign
microadenoma.
. Leydig cell tumor
. Hilar cell tumor.

70. 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.

71. CLINICAL FEATURECLINICAL FEATURE
Pattern of hair loss :Pattern of hair loss :
““Christmas tree pattern”-Christmas tree pattern”- diffuse anddiffuse and
progressive reduction of density andprogressive 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.

72. ANDROGENETIC ALOPECIA IN WOMEN

74. 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 lossMajority of women with pattern hair loss
havehave
• No increased serum androgen,No increased serum androgen,
• No other sign symptom ofNo other sign symptom of
androgen hypersensitivity.androgen hypersensitivity.

75. 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).

76. TREATMENT (CONTD.)TREATMENT (CONTD.)
3.3. In women – spironolactone ( >100In 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-androgenminigraft from non-androgen
dependent site (occiput).dependent site (occiput).

77. 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.

78. 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.

79. 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

80. - 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.)

81. 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.

82. Pathology
1. > 12% to 15% of terminal follicles are in
telogen.
2. Follicle itself is not diseased.
3. No inflammation or dystrophic changes.

83. 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.

84. 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).

85. 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.

86. TRICHTILLOMANIATRICHTILLOMANIA
• A neurotic practice of plucking or breakingA neurotic practice of plucking or breaking
hair from scalp or eyelash resulting usuallyhair from scalp or eyelash resulting usually
localized or widespread areas of alopecialocalized 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.

87. TRICHOTILOMANIA

88. TRICHOTILOMANIA IN A WOMEN

89. 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.

90. ALOPICIA OF SECONDARY SYPHILIS