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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…