Polymorphic light eruption.

Abstract

Polymorphic light eruption (PLE) describes a broad clinical spectrum including a number of different yet overlapping clinical subgroups. In the absence of an understanding of pathogenic mechanisms it remains unclear whether these subdivisions are appropriate. The action spectrum for PLE usually includes the ultraviolet A (UVA) spectrum, but a proportion of patients respond principally to UVB. This diversity in action spectra remains unexplained, as does the difficulty in artificial induction of lesions, particularly when physiologically relevant doses of UV radiation are employed. Models for the pathogenesis of PLE must explain several characteristic features of the condition, including nonuniform susceptibility of exposed skin areas, higher incidence in temperature climates, particularly in spring, and progressive tolerance during the summer months in some patients. Although unproven, an immunological mechanism is consistent with such features and is supported by immunohistological changes and keratinocyte ICAM-1 expression, similar to known type IV hypersensitivity reactions, and clinical response of severe cases to immunosuppression with azathioprine. Other recently proposed mechanisms include an abnormality in cutaneous arachidonic acid metabolism in response to UV irradiation, and excessive leukotriene B4 release by circulating leukocytes following UVA irradiation.