Alopecia areata

Question 1

Alocalized 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 rom solitary patch to complete loss of all terminal hair

Answer 1

Alopecia areata

Question 2

Prognosis and mgt

Answer 2

good or limited involvement. Poor or extensive hair loss.

■ Management: intralesional triamcinolone effective for limited number of lesions.

Question 3

How many percent has been assoc w family history?

Answer 3

10-20%

Question 4

Age of onset and prevalence

Answer 4

Youngadults(<25years); children are a ected more requently. Can occur at any age.
PREVALENCE 1.7% o the US population experi- encesatleastoneepisodeo AAinalietime

Question 5

Pathogenesis

Answer 5

Follicular damage occurs in anagen
by rapid trans ormation to catagen and telogen; then to dystrophic anagen status. Whilethediseaseisactive, olliclesare unable to progress beyond early anagen.
■ Follicular stem cell is spared; hair ollicles are not destroyed (there is no scarring

Question 6

manif

Answer 6

Hair : Alopecia often sharply defined with normal- appearingskinwith follicularopenings present

“Exclamation mark” hairs. Diagnostic broken-o stubby hairs (distal ends are broader than proximal ends

Scattered, discrete areas o alopecia (Fig.31-9)orcon uentwithtotallosso scalp hair

Diffuse AA of scalp (noncircumscribed) givestheappearanceo thinnedhair

Question 7

Ophiasis, Aa, AAT, AAU. differentiate

Answer 7

Alopecia areata (AA): Solitary or multiple areaso hairloss(Figs.31-8and31-9).
■ AA totalis (AAT): otal loss o terminal scalp hair.
■ AA universalis (AAU): otal loss o all terminal body and scalp hair (Fig. 31-10).
■ Ophiasis: Bandlike pattern o hair loss over peripheryo scalp

Question 8

nail appearance

Answer 8

Finepitting(“hammeredbrass”)o dorsal nail plate

Question 9

lab exam

what is ruled out in ANA and RPR?

Answer 9

SEROLOGY ANA (to rule out SLE); rapid plasma reagin (RPR) test (to rule out secondary syphilis). KOHPREPARATION Ruleouttineacapitis. DERMATOPATHOLOGY Acute lesions show peribulbar, perivascular, and outer root sheath mononuclearcellin ltrateo cellsandmacro- phages; ollicular dystrophy with abnormal pig- mentation and matrix degeneration. May show increased number o catagen/telogen ollicles

Question 10

Tx

Answer 10

GLUCOCORTICOIDS Topical. Superpotent agents notusuallye ective.
IntralesionalInjection. Fewandsmalllesions o AAcanbetreatedwithintralesionaltriam- cinolone acetonide, 3 to 7 mg/mL. SystemicGlucocorticoids. Mayinduce regrowth, but AA recurs on discontinuation. SYSTEMICCYCLOSPORINE Induces regrowth, but AA recurs when drug is discontinued

INDUCTION OF ALLERGIC CONTACT DERMATITIS
Dinitrochlorobenzene, squaric acid dibutyles- ter, or diphencyprone reported to be success ul, but local discom ort resulting rom allergic contactdermatitisandswellingo regional lymph nodes poses a problem. ORALPUVA(PHOTOCHEMOTHERAPY) Variably
e ective,ashighas30%,andworthatrialin patients who are highly distressed about the problem. Entire body must be exposed. JANUSKINASEINHIBITORS (“JAKinhibitors:”rux- olitinibandtoacitinib)areFDAapproved or moderate to severe (greater than 30% loss) dis- easeandaree ective.Ithasyettobedetermined how long such agents have to be administered