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dermal fibrosis

Pathophysiology:

■ Contact Dermatitis: Cell-mediated, delayed type IV immunologic reaction

■ Atopic Dermatitis: Results from a complex interaction between immunologic, genetic, environmental, and pharmacologic factors.

References:

1. Beltrani VS, Beltrani VP. Contact dermatitis. Ann Allergy Asthma Immunol 1997; 78:160-173.

2. Machado-Pinto J, McCalmont TH, Golitz LE. Eosinophilic and neutrophilic spongiosis: clues to the diagnosis of immunobul-

lous diseases and other inflammatory disorders. Semin Cutan Med Surg 1996; 15:308 -316.

3. Cooper KD. Atopic dermatitis: recent trends in pathogenesis and therapy. J Invest Dermatol 1994; 102:128-137.

4. Hurwitz RM, DeTrana C. The cutaneous pathology of atopic dermatitis. Am J Dermatopathol 1990; 12:544-551.

Synonym: Bloch-Sulzberger's disease. Clinical Presentation (Fig. 8):

■ Appears in female neonates during the first weeks

■ Distinctive vesicular eruption that follows the lines of Blaschko

■ Vesicular phase replaced by verrucous lesions after several weeks to months

■ Spongiosis with numerous intraepidermal eosinophils

■ Intraepidermal microvesicles containing eosinophils

■ Dyskeratotic keratinocytes (may be extensive)

■ Superficial perivascular infiltrate of eosinophils

Differential Diagnosis of Eosinophilic Spongiosis:

Pathophysiology:

■ Genodermatoses caused by a mutation on the X chromosome, that is, localized to Xq28; lethal in males.

References:

1. Phan TA, Wargon O, Turner AM. Incontinentia pigmenti case series: clinical spectrum of incontinentia pigmenti in 53 female patients and their relatives. Clin Exp Dermatol 2005; 30:474-480. Erratum in: Clin Exp Dermatol 2005; 30:618.

2. Hadi-Rabia S, Froievaux S, Bodak N, et al. Clinical study of 40 cases of incontinentia pigmenti. Arch Dermatol 2003; 139:1163-1170.

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