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ALOPECIA AREATA
Bahar PEZÜKLİ
CONTENTS
Introduction
Epidemiology
Patogenesis
Clinical features
Associated diseases
Diagnosis
Differential diagnosis
Treatment
Prognasis
Alopekia (in Greek); hair loss
Alopecia areata is a non-cicatricial (non-scarring)
alopecia that is postulated to be a hair-specific
autoimmune disease, with genetic factors involved in
disease susceptibility and severity
Involvement sites:
Scalp - 66.8-95%
Beard - 28% of males
Eyebrows - 3.8%
Extremities - 1.3%
EPIDEMIOLOGY
< 25 years
Sixty percent of patients present with their first patch
before 20 years of age
F/ M :1/1
All races effected equally.
PATOGENESIS
T-lymphocyte interaction with follicular antigens
(autoantigens) has been implicated in alopecia
areata.
In immunofluorescence, antibodies to anagen-phase
hair follicles were found.
CLINICAL FEATURES
It commonly seen as oval or round patches and
sharply defined.
There is nonscarring hair loss.
“Exclamation point” hair
can be seen.
Hair
Presentations;
Alopecia totalis; loss of all scalp hair.
Alopecia universalis; loss of all scalp
and body hair.
Some patients
complain of itching, tenderness, or a burning sensation
before the patches appear.
Ophiasis pattern; band- like pattern
of hair loss over periphery of
temporal and occipital scalp.
Nails
Most common sign is pitting.
trachyonychia (sandpapered nails)(longitudinal
striations)
Mottled lunula, brittle nails, onycholysis.
ASSOCIATED DISEASES
-Associated diseases:
Atopy (allergic rhinitis, atopic dermatitis, asthma)
Autoimmune thyroid disease(e .g . Hashimoto’s
thyroiditis), vitiligo,
Inflammatory bowel disease
Autoimmune polyendocrinopathy syndrome type
(autosomal recessive)
1
Type 1 diabetes increased in relatives of patients with
alopecia areata
-HLA associations
DIAGNOSIS
History and physical examination
ANA, RPR
DIFFERENTIAL DIAGNOSIS
Tinea capitis
Secondary syphillis
Trichotillomania (short and broken hairs)
Traction alopecia
Telogen effluvium (Hair loss occurs over the entire
scalp with telogen effluvium)
TREATMENT
Because of unpredictable course, treatment is difficult.
Treatments control but do not cure and do not prevent
the spread of AA. Treatments according to age and
severity
Glucocorticoids; topical, intralesional, systemic.
Minoxidil ( Minoksil, Rogain)
Anthralin
Prognosis
The course is unpredictable; recovery may be
complete or partial. Several episodes of loss and
regrowth are typical. The prognosis for total
permanent regrowth in cases with limited involvement
is excellent.
Most patients entirely regrow hair within 1 year without
treatment; 10% develop chronic disease and may
never regrow hair.
Patients with a family history of AA, young age at
onset, immune diseases, nail dystrophy, atopy, and
extensive hair loss have a poor prognosis.
REFERENCES
Dermatology, Jean L Bolognia, Chapter 69
Clinical Dermatology,Thomas P. Habif, Chapter 24
http://emedicine.medscape.com/
THANK YOU…