Effecters of inflammation in actinic prurigo

Background: Actinic prurigo is a specific familiar photodermatosis of uncer tain 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 spec imens from 20 Mexican patients presenting with a severe and perennial form of the disease. Results: The dense inflammatory infiltrate was composed predominantly of he lper T type 1 lymphocytes admixed with scattered B-cell lymphoid follicles and numerous dermal dendrocytes. Keratinocytes contained abundant tumor nec rosis factor-alpha and calprotectin. Conclusion: In subjects genatically predisposed to actinic prurigo, ultravi olet light may trigger excessive tumor necrosis factor-alpha production by keratinocytes whose sustained release in turn exerts its proinflammatory ac tivity and deleterious epidermal effects. Such a cascade of events is in li ne with the therapeutic benefit already reported when thalidomide is used t o treat actinic prurigo.