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 1  (autosomal recessive) 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/

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