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Diagnosis and treatment of actinic prurigo
Author(s) -
HojyoTomoka MaríaTeresa,
VegaMemije MaríaElisa,
CortesFranco Roberto,
DomínguezSoto Luciano
Publication year - 2003
Publication title -
dermatologic therapy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.595
H-Index - 68
eISSN - 1529-8019
pISSN - 1396-0296
DOI - 10.1046/j.1529-8019.2003.01606.x
Subject(s) - medicine , photodermatosis , dermatology , prurigo , pathogenesis , thalidomide , ultraviolet light , human leukocyte antigen , population , ultraviolet therapy , immunology , ultraviolet b , antigen , xeroderma pigmentosum , psoriasis , dna , chemistry , genetics , environmental health , photochemistry , dna damage , multiple myeloma , biology
Actinic prurigo (AP) is an idiopathic photodermatosis that affects mainly the mestizo population in Latin America. It has an early onset, a slight predominance in women, and affects the sun‐exposed areas of the skin, causing erythematous papules and lichenified plaques secondary to intense and chronic pruritus. Lesions can be induced by both ultraviolet A (UVA) and ultraviolet B (UVB). An association with several human leukocyte antigen (HLA) alleles has been reported. AP is unique among all photodermatoses in its remarkable response to thalidomide. In the past the microscopic features of AP have been considered as nonspecific; however, the constant finding of dense lymphocytic inflammatory infiltrates and the immunogenetic features of AP support the existence of an immunologic mechanism in its pathogenesis.