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Effectors of inflammation in actinic prurigo
J E Arrese1, L Dominguez-Soto, M T Hojyo-Tomoka
1Department of Dermatopathology, University Medical Center of Liège, Belgium.
Background:
Actinic prurigo is a specific familial photodermatosis of uncertain pathogenesis.
Objective:
Our purpose was to investigate the immunohistologic presentation of actinic prurigo to explore the involved pathomechanisms.
Methods:
The present immunohistochemical study was performed on biopsy specimens from 20 Mexican patients presenting with a severe and perennial form of the disease.
Results:
The dense inflammatory infiltrate was composed predominantly of helper T type 1 lymphocytes admixed with scattered B-cell lymphoid follicles and numerous dermal dendrocytes. Keratinocytes contained abundant tumor necrosis factor-alpha and calprotectin.
Conclusion:
In subjects genetically predisposed to actinic prurigo, ultraviolet light may trigger excessive tumor necrosis factor-alpha production by keratinocytes whose sustained release in turn exerts its proinflammatory activity and deleterious epidermal effects. Such a cascade of events is in line with the therapeutic benefit already reported when thalidomide is used to treat actinic prurigo.