Alopecia Areata Abdullatif Sami Al RashedDermatology block 5.5 College of medicine, King Fiasal University Al Ahsa, Saudi Arabia

Introduction A localized loss of hair in round or oval areas with no

apparent inflammation of the skin.

Nonscarring; hair follicle intact; hair can regrow.

Clinical findings: Hair loss ranging from solitary patch to complete loss of all terminal hair.

Prognosis: good for limited involvement. Poor for extensive hair loss.

Management: intralesional triamcinolone effective for limited number of lesions.

Etiology Unknown.

Association with other autoimmune diseases and immunophenotyping of lymphocytic infiltrate around hair bulbs suggests an anti–hair bulb autoimmune process

Age of Onset Young adults (<25 years);

children are affected more frequently.

Clinical Manifestations Duration of Hair Loss: Gradual over weeks to

months.

AW: Autoimmune thyroiditis. Down syndrome. Autoimmune poly-endocrinopathy-candidiasis–ectodermal dysplasia syndrome.

Hair Round patched of hair loss. Single or multiple. May

coalesce.

Alopecia often sharply defined with normal-appearing skin with follicular openings present.

Exclamation mark hairs.

Diagnostic: broken-off stubby hairs (distal ends are broader than proximal ends)

Sites of Predilection Scalp most commonly.

Any hair-bearing area. Beard, eyebrows, eyelashes, pubic hair.

Types Alopecia Areta: Solitary or multiple areas of hair

loss

Alopecia Universalis: Total loss of all terminal body and scalp hair

Alopecia Totalis: Total loss of terminal scalp hair.

Ophiasis: Bandlike pattern of hair loss over periphery of scalp.

Nails Fine pitting “Hammered brass” of dorsal nail plate.

Also: mottled lunula, trachyonychia (rough nails), onychomadesis (separation of nail from matrix)

Differential Diagnosis Tenia Capits

Early scarring alopecia

Secondary syphilis (Alopecia areolaris mouth eaten appearance of the beard)

Trichotillomania

Pattern hair loss

Lab tests Serology.

ANA (to rule out SLE) rapid plasma reagin (RPR) test (to rule out secondary syphilis).

KOH Preparation. To rule out tinea capitis.

Histopathology: Acute lesions show peribulbar, perivascular, and outer root

sheath mononuclear cell infiltrate of T cells and macrophages; follicular dystrophy with abnormal pigmentation and matrix degeneration. May show increased number of catagen/telogen follicles.

Course Spontaneous remission more with patchy AA, not

with AAT or AAU

Poor prognosis if: Late onset Fx of AA Atopy Nail involvement and body hair loss

High recurrence

Management No curative TTT

Psychological support

Steroids (interlesional or systemic)

Cyclosporin

Oral PUVA (Photochemotherapy).

Induction of Allergic Contact Dermatitis: Dinitrochlorobenzene, squaric acid dibutylester, or

diphencyprone Causes local discomfort due to allergic contact dermatitis and

swelling of regional lymph nodesposes a problem.

Reference

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