Getting to the Root of Hair Loss Disorders/Alopecia...
Transcript of Getting to the Root of Hair Loss Disorders/Alopecia...
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Getting to the Root of Hair Loss
Disorders/Alopecia Treatment
Matt L. Leavitt, D.O., FAOCDDiplomate ABHRS
Founder, Chairman, CEO
Advanced Dermatology & Cosmetic Surgery
Founder, Medical Hair Restoration
Executive Medical Advisor, Bosley
Associate Clinical Professor, NOVA, KCUM
President, Hair Foundation
Chairman, KCU-ADCS Orlando Dermatology Residency
_____
New Wave Dermatology
April 12, 2018
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Matt L. Leavitt, D.O., FAOCD
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Matt L. Leavitt, D.O., FAOCD
Golden
Follicle
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Getting to the Root of Hair Loss
Disorders/Alopecia Treatment
Matt L. Leavitt, D.O., FAOCDDiplomate ABHRS
Founder, Chairman, CEO
Advanced Dermatology & Cosmetic Surgery
Founder, Medical Hair Restoration
Executive Medical Advisor, Bosley
Associate Clinical Professor, NOVA, KCUM
President, Hair Foundation
Chairman, KCU-ADCS Orlando Dermatology Residency
_____
New Wave Dermatology
April 12, 2018
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Disclosures
No relevant disclosures
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Objectives
• Discuss the hair cycle
• Describe an evaluation for hair loss
• Distinguish between scarring and non-scarring
alopecia
• Compare and contract treatments for pattern vs.
disease-related hair loss
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Hair Physiology: Two Major Types of Hair
•Terminal–Large in size
–Pigmented
–Frequently medullated
–Can grow to
considerable length
–Bulb in subcutaneous
fat
–Typical hair of scalp
•Vellous– Small in size
– Lightly pigmented
– Non-medullated
– Do not grow more
than 2 cm in length
– Hair bulb in
reticular dermis
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Hair Growth Cycle
• Hair growth generally non-synchronized
• Anagen or Growth Period - 90% of follicles
• 2-8 year period of activity cellular proliferation
• Catagen – 1-2% of follicles
– Transition Stage
- bulbar portion of follicle is almost totally
degraded 2-4 weeks
• Telogen or Resting Stage-10% or less
(usually 6-8%)
– 2-4 months
– “Club” hair
– Period of almost complete inactivity
is stable
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Hair Facts
• Numbers
– Average number of hairs on the scalp is
estimated to be 100,000
– Up to 100-150 hairs are postulated to be shed
every day
– Approximately 50% loss is usually necessary
to detect visible hair loss
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Scarring/Cicatricial Non Scarring
Primary Secondary
MalignancyInfection Trauma
Alopecia
Focal Diffuse
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Non-Scarring Alopecia
• Diffuse
– Even distribution of hair loss in area of loss
• Focal
– Unifocal or multifocal and limited or
widespread
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Cicatricial Alopecia
• Visible loss of follicular ostia
• Destruction follicle on H&E exam
• Inflammatory infiltrate targets hair follicle
• Replacement with fibrous tissue
• Progressive permanent hair loss
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Scarring Alopecia
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1° Scarring Alopecia Classification
1. Lymphocytic
2. Neutrophilic
3. Mixed
Chronic Cutaneous Discoid Lupus Erythematosis
Lichen Planopilaris
Classic Pseudopelade (Brocq)
Central Centrifugal Cicatricial Alopecia
Alopecia Mucinosa
Keratosis Follicularis Spinulosa Decalvans
Folliculitis Decalvans
Dissecting Cellulitis / Folliculitis
Folliculitis Keloidalis
Folliculitis (acne) Necrotica
Erosive Pustular Dermatosis4. Non-Specific
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Lymphocytic Scarring Alopecias
Discoid Lupus Erythematosus (DLE)
Females 20-40 years of age
50% of cases have scalp involvement
5-10% of patients with DLE will develop systemic
lupus
Extra cranial lesions can help w/ Dx
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Scarring Alopecia 2/2 Lupus
~11 mos s/p
1st
transplant
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Lichen Planopilaris (LPP)
● Females 40-60 years of age
● Extra cranial lichen planus is present 25%-50%
patients
● Etiology is unknown- possible anitgenic stimulus
● Three types of lesions are present:
1) Perifollicular erythematous/violaceous papules
& spinous/follicular keratotic papules
2) Atrophic, smooth shiny patches
3) Typical lesions of LP- generally not seen
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Lichen Planopilaris
● Multifocal/scattered areas throughout the scalp is a
typical distribution
● Disease activity is limited to the
hair bearing periphery of
scarred patches
● Slowly progressive disease that can
lead to extensive area of hair loss
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Frontal Fibrosing Alopecia
▫ Specific patterned clinical variant of LPP
affecting the frontal hairline
▫ Postmenopausal women >40 years of age,
rarely men
▫ Progressive alopecia
▫ Creates a band like area of alopecia
3-8cm wide contrasts with photodamaged skin
▫ Lesions of LPP can be seen at hairline
Source: “Scarring and Non-Scarring Alopecias” presentation, Waldman, M. MD, 3/2011
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Frontal Fibrosing Alopecia
● Eyebrows thinned/absent
● Axillary hair loss has also been reported
● Lesions of extra-cranial lichen planus are not
seen
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Photo Courtesy Francisco Jimenez MD
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Psuedopelade of Brocq
● Multiple meanings depending on which
study or which person referencing
● Primary Pseudopelade of Brocq- Idiopathic
● Secondary Pseudopelade of Brocq- Final
stage of several scarring disorders (LPP,
DLE)
Pseudopelade of Brocq = LPP?
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Pseudopelade of Brocq
● Adult females
● 1-2cm atrophic, oval-round, ivory plaques:
“Footprints in the Snow”
● May see isolated and grouped kinked hairs
● Minimal to no inflammation with few symptoms
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Lichen Planopilaris Treatment
Steroids:
• Topical – ex. Clobetasol 0.05% soln, oint, foam
pulsed: 2 week on, 1 week off
• Intralesional – Triamcinolone 4-10 mg/cc
• Intramuscular - Triamcinolone) 40-80 mg
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Lichen Planopilaris Treatment
Other Treatments:
• Hydroxychloroquine
• Doxycycline
• Finasteride 1-2.5 mg
• Minoxidil 5%
• Pioglitazone
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Lichen Planopilaris
• Evaluate for drug-related (gold) and
Hepatitis C
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Before
After
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Lichen Planopilaris /Frontal
Fibrosing Alopecia
s/p 2 eyebrow
transplants
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Lichen Planopilaris /Frontal Fibrosing Alopecia
s/p 2 hair
transplants
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Female Pattern Hair Loss
~10 mos s/p 1st
hair transplant
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Central Centrifugal Cicatricial Alopecia
(CCCA)
● Follicular Degeneration Syndrome (FDS), “Hot
Comb Alopecia”
● African American women in 30’s-40’s
● Originally thought to be secondary to liquified
hot petrolatum and other hair care practices
● Trauma due to long-standing traction
● Etiology is still unknown
● Also associated with pattern CCCA:
- FDS - Folliculitis decalvans
– - Pseudopelade - Tufted hair folliculitis
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Central Centrifugal Cicatricial Alopecia
● Progressive symmetric centrifugal
scarring that starts at the midline/vertex
scalp
● “Pins & Needles”, pruritus, tenderness
● Minimal erythema
● Scalp can be smooth and shiny
● Perifollicular hyperpigmentation may be
seen
● Incomplete alopecia
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Central Centrifugal Cicatricial Alopecia
• Treatment
– Topical and Intralesional Steroids
– Calcineurin Inhibitors (i.e. Tacrolimus oint)
– Tetracyclines (i.e. Doxycycline)
– Cyclosporine
– Hydroxychloroquine
– Hair Transplantation (counsel about realistic
expectations)
– Wigs and Hair Pieces
– Topical Camouflage Agents (i.e. powders and sprays)
– Transition to natural hairstyles that limit tension, heat,
and chemicals
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Treatment
Primary Cicatricial Alopecia
– Lymphocytic• Steroid
▪ High potency topical steroid – Clobetasol, Betamethasone, Ultravate
▪ Oral steroid – Prednisone
▪ Intralesional or Intramuscular steroid - Triamcinolone
• Topical non-steroidal anti-inflammatory - Tacrolimus oint
• Low dose antibiotic - Doxycycline, Minocycline
• Oral retinoids - Acitretin
• Immunosuppressants – Cyclosporine, Mycophenolatemofetil, Hydroxychloroquine
• Excision of burned out small localized lesions (koebnerization is possible)
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Neutrophilic Cicatricial Alopecias
Folliculitis Decalvans
● Pustular eruption of the scalp that leads to
patchy scarring alopecia
● M=F, younger
● Staph. aureus is commonly cultured
● Abnormal host response to Staph aureus??
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Peripheral disease activity
Am. Fam. Physician
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Dissecting Cellulitis
● 80% patients are African-American age18-40
● Initially develop a follicular pustule
occipital/vertex scalp that
transforms into a painful nodule
● Multifocal disease with interconnecting tracts
● A cerebriform appearance develops
● Depressed, hypertrophic, keloidal scarring
● Tx: Isotretinoin 1mg/kg
Oral steroids
Dapsone
Antibiotics- keflex, bactrim
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Treatment
Primary Cicatricial Alopecia
- Neutrophilic• Antibiotics
▪ Clindamycin/Rifampin for staph
▪ Alternative antistaphylococcal antibiotics (top and po)
• Oral retinoids – Isotretinoin
• Incision and Drainage
• Laser Ablation
• Intralesional steroids
• Antitumor necrosis factor biologic agents
• Excision of burned out small localized lesions (koebnerization is possible)
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Mixed Cell Scarring Alopecias
Acne (Folliculitis) Keloidalis
• Occipital scalp and nape of neck
• Flesh colored discrete papules
• May be pustules, nodules or plaques
• May form abscesses or sinuses
▪ Treatment:
▪ IL steroids
▪ Oral Antibiotics: tetracycline
▪ Topical antibiotics (clindamycin) and steroids
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Folliculitis Keloidalis
Mixed Cell Scarring Alopecias
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2° Cicatricial Alopecia
Infections
Dermatoses
Bullous Disorders
Physical & Chemical causes
Radiation
Drugs
Autoimmune Disorders
Neoplasia
Granulomatous
Developmental / Hereditary
Miscellaneous
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Non-Scarring Hair Loss
Differential Diagnosis of Hair Loss
• Diffuse
– Breakage
• Anagen effluvium
• Hair shaft disorder
• Physical or chemical processing
– Telogen effluvium
– Androgenetic alopecia (women)
– Alopecia areata, totalis or universalis
– Loose anagen syndrome
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Differential Diagnosis: Non-Scarring Cont’d.
• Focal
– Infection
– Traumatic
– Alopecia Areata
– Hair breakage
– Androgenetic alopecia (men and women)
– Developmental
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Anagen Effluvium
• Direct toxic insult to rapidly dividing kerotinocytes
• Dystrophic hairs from abrupt interruption of hair growth
• Copious hair loss
• Common causes
– Radiation - Chemotherapy - Colchicine
– Plants - Heavy metals
. Lecythis Ollaria . Thallium
. Loucaena glauca . Mercury
. Arsenic
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Telogen Effluvium
• History and Exam
– Visible and rapid progression of hair loss
– Increase from 10% to 30-50% telogen hairs
• 150-700 hairs / day
– Hairs easy to comb out
– Lags inciting event by approximately 3
months
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Causes of Telogen Effluvium
Acute Stress (hemorrhage) Drugs
Childbirth (postpartum) Allopurinol (Zyloprim)
Chronic Systemic Illness Clofibrate (Atromid-S)
Cancer Cocaine
Leukemia Warafin (Coumadin)
Hodgkin’s Disease Heparin
Tuberculosis Oral Contraceptives
Cirrhosis Propylthiouracil
Crash Dieting Febrile IllnessInfluenza
Chronic Iron Deficiency Lobar pneumonia
Psychogenic Stress Pertussis
Thyroid Disease Scarlet Fever
Source: Women and Hair Loss, Dr. Matt Leavitt, p. 44, 2005
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Hair Loss Questionnaire: Hair History
• How long ago did you first notice hair loss?
• Since this started, have you been losing hair at the same rate or at a faster rate
• How many hairs are you losing daily?
– Do you feel you have been shedding excessively? Do you feel your scalp is slowly thinning out without losing excessive numbers of hair?
– Which did you notice first, shedding or thinning?
• Has your hairline or temporal areas receded?
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Hair History Continued
• Are you losing hair from the entire scalp, or over the top
of the scalp? Does your hair seem dull, brittle or
uncombable?
• Is your hair lost from the roots, breakage or both?
– Do you have symptoms, i.e. itching, scaling, etc.
• Are you losing hair from any other parts of your body?
• Do you have a habit of twirling, scratching or pulling your
hair?
• List any family members who have hair thinning,
receding or loss?
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Hair History Continued
• List all health problems, current or in the past, including any surgeries
• List all allergies
• Do you have a history of :– Pregnancy - Diabetes - Anemia
– Infertility - Severe Acne - Ovarian Cysts
– Thyroid Disease - Menstrual Irregularity - Excessive Tiredness
– Iron Deficiency - Prolonged Fever - Increased facial hair
– Discharge from
nipples
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Hair History Continued
• Have you ever been pregnant?– Number of pregnancies? Number of children?
– Any complications during pregnancy?
– Did you lose any hair during/after pregnancy?
– Did you lose any hair after any pregnancy or surgery?
• Do you take birth control pills?
• Have you donated blood in past 3 years
• Do you have a vegetarian diet
• Are you too hot ? Too cold?
• had chemotherapy or radiation?
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Hair History Continued
• In the past year have you had
– Surgery - Marriage
– General Anesthesia - Divorce
– Serious Injury - Death in family
– Childbirth - New Job
– Prolonged high fever – New residence
– Weight loss/gain
– Other
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Hair History/Medications
• Cholestorol
• Parkinsons
• Ulcer
• Anti-coagulants
• Gout
• Anti-arthritics
• Drugs from Vitamin A
• Anti-seizure
• Miscellaneous
• Tricyclic Anti-depressants
• Beta Blockers
• Calcium Channel blockers
• Non-steroid Anti-inflammatory
• Aspirin products
• Anabolic steroids
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Telogen Effluvium
• Visible telogen shedded hairs• Root of hair appears bulbous or
onion-shaped
• Hair dull and limp
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Telogen Effluvium
• Most frequent cause postpartum (telogen gravidurum)
• 1/3 – ½ postpartum mothers report mild-to-moderate hair loss
• Corrects self 6-18 months
• 90% cases correct without
intervention
• Greater than 6 months – chronic
telogen effluvium
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Telogen Effluvium
● Bi-temporal thinning may be present
● Positive Pull Test for telogen (club) hairs
● Shorter, regrowing frontal hairs may be seen
in resolving state
● Chronic:
- Subtle onset in women 40-60’s
- Continuous shedding with fluctuations
- Normal appearing densities
- Shortened anagen phase
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Work Up
● CBC,CMP
● TSH
● FSH/LH, Free and Total Testosterone, DHEA-S
● Iron, Iron Binding Capacity, Transferrin
● Ferritin: best test for Iron deficiency
▪ Best between 50-70µg/L
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Treatment of Telogen Effluvium
• Reassurance -- tendency towards resolution
• Minoxidil 5%
• Clobetasol pulsed, 2 weeks on, 1 week off
• IL triamcinolone 5 mg/cc
• Correct any reversible causes of hair loss
– Anemia, thyroid abnormality, dietary deficiencies
(inadequate protein, low iron, B12, folic acid),
medications
• Alternative styling to mask defects
• Gentle hair care
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Male Pattern AGA Female Pattern AGA
Non-Scarring Androgenetic Alopecia
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Androgens- Women
• Role in women is not completely understood
• Women can have baldness in the presence of normal
and high androgen levels
• Pattern is different in women
• No complete areas of baldness
• Don’t respond equally as men do to anti-androgen
therapies
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Androgens- Women
• Aromatase enzyme converts testosterone to estrone,
estradiol and estrase (E’s)
• The E’s increase SHBG which bind androgens
• Women treated with Aromatase inhibitors experience
FPHL
• Aromatase levels are decreased in balding scalp vs
non-balding areas
• Women have significantly higher levels of scalp
aromatase compared to men
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Female Pattern
• History
– Family History (may be difficult to pinpoint)
– Slow onset, slow progression
– Rate of loss is generally stable
– Hair loss is from root
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Hair Loss: Physical Examination and Tests
• Ludwig Scale : Stage I, II, III
Savin Scale : D 1, 2, 3, 4, 5, 6
• Scalp – Normal - Scaling
– Erythema - Focal hair loss
– Papules/pustules - Scarring
– Excoriations - Follicular plugging
• Density– Normal - Mild thinning-crown
– Sparse-Crown - Mild thinning-diffuse
– Sparse-Diffuse
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Hair Loss: Physical Examination and Tests
• Hair Pull Test : Positive / Negative
• Broken Hairs : Absent / Present
• Laboratory : KOH Exam
Microscopic Trichogram
Hair Shaft Exam
• Diagnosis
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Hair Loss: Physical Examination and Tests
• Plan
– 3 day hair count requested
– 5 mm punch biopsy
– Blood tests:
- CBC with Diff - HIV
- Protime with INR - DHEAS
- Free testosterone - Ferritin
- TSH, T4 Free
- Hep Panel
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Female Pattern: Examination
• Hairline and temporal mostly maintained
– 90% maintain temple
– 85% maintain hairline
• Most follow Ludwig Pattern
with widening part
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Female Pattern: Examination
• Miniaturization
– Finer, smaller, slower-growing, less
pigmented hairs
– Thinning more common early than noticeable
areas of hair loss
– Ratio of less than 4 terminal hairs to 1
miniaturized hair
– Telogen may increase to
30% of hair
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Female Pattern – Ludwig Scale
Type I - Mild Type II -Moderate Type III - Severe
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Male Pattern Androgenetic Alopecia
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Male Pattern Androgenetic Alopecia
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Common MPHL Patterns: Norwood Classification
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•Hormones : Dihydrotestosterone (DHT) is a
key factor in the development of male
pattern hair loss (MPHL) among genetically
predisposed men
•Genetics : Autosomal dominant and/or
polygenic. Inherited from either or both
parents
•Hence the term: Androgenetic Alopecia
Etiology of Male Pattern Hair Loss
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•T is converted to DHT by the enzyme 5a- Reductase
-Two isozymes of 5a-R, Type l and Type ll
-Type ll 5a-R localizes to hair and prostate
•DHT levels are elevated in balding scalp tissue
•Over time, increased DHT causes normal “terminal” hairs
to become “miniaturized” hairs, the hallmark of MPHL.
Role of DHT in Male Pattern Hair Loss
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Androgens: 5 α Reductase
• Two Isoforms 1 and 2
• Type 1: Sebaceous Gland
Pilosebaceous Apparatus
• Type 2: Prostate Gland
Outer Root Sheath
Dermal Papilla
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Progression of MPHL
• Hair cycles are shortened in MPHL
– Cycles may shorten to as little as 6-8 months
– Anagen (growing) phase reduced to 6-8 weeks
• Hairs “miniaturize” over time to become progressively
thinner, finer, shorter, and less pigmented
• Men may have already lost 50% of hair count before
it is noticed1
1. Habif TP. Clinical Dermatology: A Color Guide to Diagnosis and Therapy. 3rd ed. St. Louis, Mo.: Mosby-Year Book, Inc.;1996:44.
77
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Progression of MPHL
DHT DHTDHT
78
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Minoxidil
• Medical - Minoxidil
– Mechanism of Action
• Non-specific biological response modifier
• Acts directly on viable sub-optimally
functional follicles: potassium channel
agonist
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Mechanism
Of Action
Hair cycle stimulation
Opening of potassium channels
Vascularization(VEGF)
Cell proliferation
Boyera et al. Skin Pharmacol. 1997;10:206.
Buhl. J Invest Dermatol. 1991;73S.
Kiesewetter et al. J Invest Dermatol. 1991;96:295.
Lachgar et al. Br J Dermatol. 1998;138:407.
Michelet et al. J Invest Dermatol. 1997;108(2):205-209
VEGF= Vascular Endothelial Growth Factor.
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Patient Treatment
• Medical - Minoxidil
– Benefits
• Enlargement of miniaturized follicles --
increase diameter
• Conversion of telogen hair to anagen
• Prolongs anagen -- slows progression of
hair loss
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Using Minoxidil: Practical Suggestions
• Apply Minoxidil topical solutions once daily
• Towel dry or blow dry hair before application
• Apply Minoxidil directly on the scalp
• Wash hands after application
• Apply 5 minutes before using styling aids
• Do not shampoo or swim for 4 hours after
application
• Let solution dry before going to bed
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5a-Reductase
Propecia
Why Propecia Works
Effects of Androgens on Scalp Hair in Men
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Propecia® 5 Year Safety Profile
Any sexual AE
Libido decreased
Erectile dysfunction
Ejaculation disorder
Sexually-related AE
Resulting in discontinuation
Propecia placebo
(N=323) (n=23)
2 (0.6) 0
1 (0.3) 0
1 (0.3) 0
0 0
0 0
Kaufman, KD. Eur. J. Dermatology, 2002
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Post-Finasteride Syndrome
• Sexual SEs – decreased labido, erectile
dysfuntion, decrease in semen volume…
• Physical SEs – gynecomastia, fatigue, muscle
atrophy, tinnitus
• Mental SEs – memory impairment, depression,
suicidal ideation
http://www.pfsfoundation.org
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Uncertainties in Adverse Event Reporting
• Significant amounts of data regarding SEs stems from meta-
analyses which tend to be weak in assessing clinical harm in
several clinical trials
• Men may be unlikely to spontaneously report sexual issues
especially if asked by a female provider, nurse, or assistant
• Available finasteride toxicity data from clinical trials is often
biased, of poor quality, and limited
• Clinical trials have provided insufficient information to
establish safety
• The extent of persistence of sexual side effects is not clear
due to the length of time patients are followed in a study
▪ Adverse Event Reporting in Clinical Trials of Finasteride for Androgenic Alopecia A Meta-analysis, Steven M, et al, JAMA
Dermatol. 2015;151(6):600-606.
▪ Finasteride and the Uncertainties of Establishing Harms. Moore TJ.JAMA Dermatol. 2015 Jun;151(6):585-6. doi:
10.1001/jamadermatol.2015.37.
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FDA-Mandated Label Changes for
Finasteride
“A revision to the (Finasteride) label to include libido disorders, ejaculation disorders, and orgasm disorders that continued after discontinuation of the drug…
A revision to include a description of reports of male infertility and/or poor semen quality that normalized or improved after drug discontinuation.”
http://www.pfsfoundation.org
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Low Level Laser Therapy (LLLT)
• Low-power lasers or light-emitting diodes (LEDs)
are applied to the surface of the skin to stimulate
cell function for improved hair growth (this is
known as Photobiomodulation (PBM))
• The wavelength is typically between 630-670nm
in the red visible light spectrum
https://www.bosley.com
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LLLT:
Hypothesized Mechanism of Action
The following theories of the mechanisms of action
of LLLT have been published.
• Anagen Induction
• Increased Vascularization
• Reduction of Inflammation
• Increase ATP Synthesis
• Regulation of Oxidative Stress
• Delay of Follicular Apoptosis
• Reverses Miniaturization
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Clinical Studies on Efficacy and Safety
• The efficacy and safety of the HairMax LaserComb® in
the treatment of androgenetic alopecia (AGA) in males
and females has been demonstrated in 7 clinical trials
involving 460 subjects.
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Macro Images from Clinical Study
After approximately six months of treatment these clinical images
provide evidence of (1) reverse miniaturization of vellus hair, (2)
increased number of hairs per follicular unit and (3) revival of
dormant hairs. These results are both medically and scientifically
significant.
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• Premium on maintenance of hair and
preservation of donor hair
• Irregular pattern in hairline
Hair Transplantation
The Procedure : Design
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DR. LEAVITT
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DR. LEAVITT
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• Old
– wide spaces between
grafts● Grafts very close together
The Procedure: Design
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● No scarring
● Natural at every stage
● No evidence of transplants
The Procedure: Design
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• Ellipse
• Advantage -- less
transsection of hair
• Efficient utilization of
donor and greater
availability of donor
The Procedure
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Sutured donor area
Hair combed
over suture at
time of surgery
The Procedure
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Follicular Unit Extraction (FUE)
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Follicular Unit Extraction (FUE)
Immediate Post-Op
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FUE Immediately After Donor Extraction
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FUE
Before
4 days Post-Op
After
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Manual FUE InstrumentsFUE
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FUE Drill
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Robotic-assisted FUE
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FUE Complication
• Overharvesting/Donor Depletion
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• Dissection
• Follicular Units
• Microscopes/magnification
The Procedure: Graft by Section
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• Follicular Bundle (1-3 hairs)
-grafts cut so naturally
occurring bundles are
maintained
The Procedure: Graft by Section
Dissecting a strip into Follicular Bundles
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• Insertion
• Minde
• SP 90
• Sharp Point
• 18 gauge
The Procedure: Site Creation/Recipient
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Alopecia Areata
● 1-2% of population
● Non scarring alopecia with a lifetime risk of 1.7%
M=F
● 60% of patients develop the first patch before 20
years of age
● Abrupt onset and asymptomatic
● Round-oval smooth bald patches
● “Exclamation point hairs”- broken hairs tapered
proximally
● Majority of patients will regrow within 1 year
● 50-80% sporadic
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Alopecia Areata (AA): Exclamation Point Hair
• Onset of alopecia areata
– Growth stops, anagen arrests
– Follicle breaks at skin level
– Trichorrhexis nodosa type fracture
– Hair pull is positive with dystrophic
and telogen hairs
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Alopecia Areata
● Autoimmune etiology
● Combination of environmental and genetic factors
may initiate hairloss, but an exact cause is
unknown
● High frequency positive family hx (10-42%), esp. in
early onset patients
● Class II antigens have been associated with early
and more extensive disease
● Filaggrin gene mutation – alopecia
totalis or universalis
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Alopecia Areata:
Etiology / Autoimmune
• Peribulbar infiltrates
– Composed mainly of T-cells• T-cells are oligocional / autoreactive
• Follicular components / autoantibodies
• AA linked with autoimmune thyroiditis
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Alopecia Areata
• Treatment
– Corticosteroids
• Beneficial effect
– Contact sensitizers
• Also have a positive effect
– Jak inhibitors
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JAK Inhibitors
Janus Kinases: An Ideal Target for the Treatment of Autoimmune Diseases
Author links open overlay panel, MassimoGadina, Journal of Investigative Dermatology Symposium Proceedings
Volume 16, Issue 1, December 2013 , Pages S70-S72
JAK-STAT Inhibitors inhibit janus-
associated kinases (JAK) 1, 2, 3, leading
to disruption of cytokine and growth factor
signaling, thus interfering with the
inflammatory cascade
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Alopecia Areata
● Patterns:
1) Oval/round- most common
2) Reticular
3) Ophiasis- parietal
temporo-occipital
4) Diffuse- entire scalp
● Alopecia totalis- 100% scalp
● Alopecia universalis-
100% scalp and body
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Alopecia Areata
● Nail dystrophy may be present
- 10-66%
- nail pitting most common
- other nail findings
. Longitudinal ridging
. Brittle
. Onycholysis
. Periungual erythema
. Onychomadesis
● 7-10% patients develop
severe chronic form
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Alopecia Areata : Treatments
• Corticosteroids
– Beneficial effect
• Contact sensitizers
– Also have a positive effect
• JAK inhibitors
• Topical, IL, and Systemic Steroids
Topical tacrolimus
Topical synsitizers- DNCB, Squaric Acid
PUVA
Cyclosporine
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Disease Associations
• Atopy
• Autoimmune diseases
• Downs and Turner Syndrome
• Thyroid disease
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Alopecia AreataExclamation Point Hairs
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Chemical Alopecia
• Tints, bleaches, straighteners, permanents used
too frequently or improperly
• Long-term chemical damage can cause scarring
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Hair Care Questions
• How often do you shampoo
• List the products you use on your hair
• Do you bleach or color your hair
• Do you use strengtheners, pomades, relaxers,
perms?
• Have you changed your hairstyle in last 6
months
• Do you wear extensions, fall or wig
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Hair Care Questions
• Do you braid, plait, tease, wear a bun / ponytail
• Do you use rubber bands, hair pins, barrettes or
other ornaments
• Do you use hot or sponge rollers?
• Do you use curling iron?
• Do you blow dry your hair
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Traction Alopecia
• Hair styles that put excess tension or pull hair
– Most common among African Americans
– Hair breakage and/or patches of baldness
– May see erythema, scaling, pustules
– Most common in frontal or temporal areas
– Persistence of short hairs along anterior margins
– Long-term traction can cause scarring
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Trichotillomania
● Obsessive-compulsive
● Irregular patches of alopecia with broken
off hairs of irregular length
● Treatment:
- counseling
- behavior change
- SSRI’s
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• Additional slides for education
• Will not be presented
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Hair Shaft Abnormalities
• Increased Fragility
– Monilethrix
• Shaft has regular and internodes
(resembles pearl necklace) with internodal
fragility, leading to breakage and alopecia
• Autosomal dominant, variable pinstruc
• Mutation in hair keratin (hHb6) in cortex
• Hair breaks almost flush with skin
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Hair Shaft Abnormalities
• Pseudomonilethrix
• Trichorrhexis congenita
– Most common
– Congenital or acquired
– May have normal hair at birth but within few months
breaks, variable lengths, and alopecia
– Associated with mental retardation and
argininosuccinic aciduria
– Due to in-born error in urea synthesis
– Brush-like aspect at the extreme frontage of nodule
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Hair Shaft Abnormalities
• Increased fragility
– Pili torti• Flattened hair shaft twisted through
180 degrees on its own longitudinal arms
• Two types– Early onset Ronchese type
– Late type Beare type
• Associations– Menkes
– Crandall or Björnsteds syndrome
– Bazeks
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Miscellaneous Hair Shaft
• Peripilar cast – pseudonits
– Tubular masses of amorphous material of varied
length and diameter
– Seen with psoriasis, seborrhea
– Distingushed from true nit by lack of mobility and
because they uniformly surround hair
• Deposits lacquer, paint, glue
– Extraneous material throughout scalp hair but
localized to areas of contact
– Unlike peripilar cast deposits cannot easily be moved
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Tinea Capitis
• Fungal infection which predominantly affects children
– Most common fungal infection in children 4 and 7 yrs
• Caused by 2 types of organisms:
– Trichophyton, Microsporum
• More than 95% of tinea capitis cases are caused by T. tonsurans (anthropophilic dermatophyte) in the US
– The remaining 5% are usually caused by M. canis (zoophilic organism).
• Favus
– Usually caused by T. schoenleinii
– Distinguished by hyphae in parallel
arrangements to the hair
– Air spaces can be seen within the shaft
– Patches develop into scutula-cup shaped crust
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Infections: Ecotothrix
• Caused by hyphae on the hair shaft that produce arthroconida
– Transmitted most often by infected animals
• Most common is microsporum canis
– Broken hairs with fine powdery dandruff
– Results in destruction of cuticle
– Using Woods lamp may show
• Fluorescent – microsporum spp
• Non-fluorescent – trichophyton
rubron and some
microsporum spp
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Infections: Endothrix
●Spread person-to-person
●Arthroconidia found in hair shaft
●Does not fluoresce under Woods lamp
●Presents form black dot to patchy alopecia to kerion
●Black dot result of invasion in shaft which breaks off at
surface
●Usually caused by T. tonsurans in USA and T.
violaceum subtropical
●Small, chronic with only few
hairs infected