Alopecia Areata

Ibn e Sina Emergency Hospital

Dermatology and Venerology Department
Prepared by: Dr.Ellaha “Sahak”
Under Supervision of: Pro. Dr. Abdul Wakeel “Parwany”
Hair emberyogenesis
• Morphologically hair follicle development has been divided into 8
stages
• Follicle formation begins on the head and then moves downward to
the remainder of body in utero
• The hairs first formed are lanugo hairs which are nonpigmented ,soft
and fine they typically shed between the 32nd and 36th weeks of
gestation
Hair follicle
• Hair follicles grow at a slant with major part of the hair developing from
epithelial cells and only papilla developing from mesenchymal cells and
fibroblasts
• The upper follicle is permanent but the lower follicle regenerates with
each hair cycle.
• Hair follicle can be divided in 2 parts ( in relation to insertion of arrector
pili M)
• The upper part
• A. infundibulum: from ostium to the opning of sebaceous duct.
• B. isthmus : from sebaceous duct to the attachment site of arrector pili M
Cont…
• The lower part-
• A. stem: from attachment to arrector pili M to adamsons fring
• B. from adamsons fring to base of follicle.
• Hair bulb
• Consist of 5 major structures( in to out):
• 1. dermal hair papilla
• 2. hair matrix cells
• 3. hair shaft- consisting of medulla( soft keratin)
• Cortex and hair cuticle( hard keratin)
• 4. inner root sheath
• 5. outer root sheath
Outer root sheath
• The cells of outer root sheath change considerably throughout the follicle
• Infundibulum: it resembles epidermis and forma granular layer during
keratinization.
• Isthmus: cells keratinize in a trichilemmal fashion, lacking a granular
layer.
• Keratinocytes in the ORS form the bulge at the base of the isthmus.
• Moving downward cells become larger and are abundant in glycogen in
the suprabulbar region.
• Bulb: single,flattened cell layer.
Inner root sheath
• Extends from the base of bulb to isthmus.
• It has 4 parts:
• companion layer provides a slippage plane between the IRS and the ORS.
Cells of this layer are flat compare to the cuboidal ORS cells.
• henle’s layer- one cell layer tick, frist to develop keratohyaline granules
and keratinize.
• Huxley’s layer- 2-4 cell layer thick and keratimize above henle layer at a
region known as adamson’s fringe.some cells from here protrude and
directly attach to the companion layer
• Inner root sheath cuticle.
Definition
• AA is a common autoimmune hair disorder
• This condition of hair loss can affect any hair bearing area at any given
time
• Approximately 0.2 % of the world population is suffering from AA
• Both genders are equally affected
• It’s the most common form of alopecia in children
• The familial occurrence is approximately 15%
• 5% of AA can develop to AA totalis
• 1% of AA can develop to AA universalis
Etiology and pathogenesis
• The main drivers of the disease pathogenesis are autoactive cytotoxic CD8 T
cells, which affect hair follicles and sometimes nails , interferon gama
driven immune response, interferon gama induced chemokines
• The cytotoxic subset of CD8 + NKCG2D+ T cells within the inflammatory
infiltrate in alopecia areata and an upregulation in the hair follicle
• NK cells play a regulatory role in AA
• Patients with AA have a genetic predisposition
• Experience of major emotional stress
• T cells that recognize antigen in association with MHC class 1
• MCH class 1 may lead to attack by NKC
• Antioxidant—Oxidant imbalance
Clinical features

• AA is characterized by an acute onset

• Typically presents with Oval or round shaped , well circumscribed, bald
patches with a smooth surface in diffuse distribution
• Characteristic hallmarks of AA black dots
• Patches are usually without further symptoms but my cause mild Itching
and erythema
Cont..
• Involvement of nails can occur with pitting or sandpaper like
appearance
• It has been describe in association with a variety of other disorders
like cataract, thyroid disease, vitiligo, AD, psoriasis, Cronkhite- Canada
diabetes ,lupus erythematouse and Dawn syndrome
Diagnosis
• Clinical features
• Exclamation points
• Nail changes
• Dermatoscopic examination ( presence of follicular ostia)
• Hair pulling test
• Canities subita ( sudden whiting of the hair )
• Scalp biopsy ( 4mm punch processed for horizontal section)
• Additionally laboratory tests to rule out thyroid dys, and iron or
vitamins deficiencies
Exclamation Mark

Nail Pitting in AA
Characteristic dermoscopic features of AA
• Black dots ( cadaverous hairs)
• Yellow dots
• Tapering hairs (exclamation mark)
• Broken hairs
• Vellus hairs
DDx trichotillomania and AA
• Shaving of 2 to 3cm of scalp hairs then put bandage on the area
• After one week we evaluate the area if there are growing hairs it
clarifies that patient have trichotillomania otherwise the area without
growing hairs confirms AA
Pathology
• Scalp biopsy reveals a generalized miniaturization and marked
increase in catagen and telogen hair follicle
• In acute phase is characterized by a peribulbar immune infiltrate
centered around the hair bulb which has been described as swarm of
bees
• Infiltrate is made up of CD4, CD8 and NK cells
• Oftenly mast cells, plasma cells and eosinophils also can seen
• Sometimes an immune infiltrate can seen around the hair bulb of
miniaturized hairs in the upper dermis
Complications
• Increase incidence of sunburns and skin cancers
• Nasopharyngeal and ophthalmologic inflammations
• Changes in appearance frequently cause a diminished sense of
personal well being and self esteem
Prognosis and clinical course
• The course of the disease is variable and characterized by an irregular
relapsing course
• 5% of cases develop to AA totalis and 1% of cases are develop to AA
univarsalis
• Spontaneouse regrowth of hair is common
• 60% 0f patients have at least a partial regrowth by one year
• 40% of patients have relapses within the first year
• Poor prognosis is linked to involvement of the Occiput or hairline
• Presence of nail changes and early onset
SALT SCORING
Management
Topical corticosteroid
• super potent ( class 1 and class 2)
• efficacy has been proven for class 1 corticosteroid when use in combination
with minoxidil

Intralesional corticosteroids
• IL corticosteroids ( triamcinolone acetonide or triamcinolone hexacetonide)
injection concentration 2.5 -10mg\ml every 4 to 6 weeks
• Total amount 15-40mg
• Response is often seen after 4 to 8 weeks
 Side effects
• Nonpermanent skin atrophy
• indentation of the scalp skin

PRP ( platelet Rich Plasma)

• its beneficial in monotherapy or in combination with other therapies

Systemic corticosteroids
• the use of systemic corticosteroids are controversial
• They should not be used as routine treatments
• Dosage vary from an initial 20-40mg of prednisone daily, with tapering 5mg daily in
a few weeks
• Different pulse therapies regimens with short term high doses
• Oral prednisolone 100-300mg or IV methylprednisolone 250mg

Topical minoxidil
• minoxidil solution 2% or 5% but its more effective when it combine with
class 1 and class 2 topical corticosteroids

Prostaglandin analogs
• like latanoprost and bimatoprost have been effective in the treatment
of AA of eyebrows and eyelashes
Anthralin
• Is an irritant that may have a nonspecific immunomodulating effect ( anti –
Langerhans cell)
• Its usually used in the treatment of psoriasis
• Anthralin is used as a 0.2% to 1% cream or ointment its usually applied daily to
affected scalp areas and left on for 20 to 30 min
• For first 2 weeks and then for 45 min daily for 2 weeks up to a maximum of 1hr
daily
• In effective treatment new hair growth can usually be seen after 2 to 3 month
• Side effects: irritation, scaling, folliculitis, and regional lymphadenopathy
• Its not suitable for eyebrow and beard area
• Patients who treat with anthralin should protect eyes from ultraviolet
• Brown discoloration of the treated skin can occured
 Topical immunotherapy
• Its not approved by FDA
• But seems to be a vary effective therapeutic option with a good safety
profile
• The exact mechanism of action is not fully understood
• A decreased in peribulbar CD4+ /CD8+ lymphocyte ratio and shift of T
lymphocytes away from the perifollicular area to the interfollicular
area and dermis
• Diphenylcyclopropenone is the most commonly used contact
sensitizer
• Its compounded in an acetone base and stored in opaque bottles to
protect the solution from photodegradation
Cont…
• Applying a small amount of a 2% solution to a small scalp area 1 week
prior to treatment start sensitizes the patient
• The solution is then applied weekly to the scalp starting at a
concentration of 0.0001% the scalp should not be washed for 48hrs
• After treatment and should be protected from ultraviolet
• Carefully increase the concentration every week until the patient
develops a mild erythema and mild itching
• The highest concentration used is 2%
• Side effects: lymphadenopathy in 100%, severe contact eczema,
discoloration
Photo( CHEMO) therapy
• Ultraviolet B light has been reported to be useful in some patients
with AA
• Further therapeutic options include both oral and topical
administration of psoralen followed by ultraviolet A irradiation
• Psoralen and ultraviolet A therapy may affect T cell function and
antigen presentation
Cyclosporine
• Systemic cyclosporine at doses of 4 to 6mg/ kg/ day
• Cyclosporine can be combined with low dose oral prednisone
• Side effects: elevated serum transaminase, cholesterol levels,
headaches, dysesthesia, fatigue, diarrhea, gingival hyperplasia.
• Janus kinase inhibitors
• Interferon gama, interleukin-2, and interleukin-15 play a significant
role in maintaining the autoreactive CD8+ T cell
• Oral baricitinib and tofacitinib citrate
References
1. Robert Chalmers, Jonathan Barker, Christopher Griffiths, Tanya Bleiker, Daniel Creamer – Specific
Cutanause Structure Acquried Disorder of the Hair: Part 8 /Chapter 89 - 198, Rook’s Textbook of
dermatology, 9th ed United Kingdom 2016.
2. Sewon Kang MD MPH, Masayuki Amagai MD PhD, Anna L. Bruckner MD MSCS, Alexander H. ENK MD,
David J. Margolis MD PhD, Amy J. McMichael MD, Jeffrey S. Orringer MD – Disorder of the Hair and Nails:
Part 16 /Chapter 87 – 1517 Fitzpatrick’s Dermatology, 9th ed United State.