ABSTRACT
Although the pathogenesis of JSE is currently unknown, few would question the etiologic role of ultraviolet light. However, monochromatic phototesting is typically normal and the action spectrum for JSE remains elusive. Some authors consider JSE to simply be a localized variant of polymorphic light eruption (PLE),4 but we believe it has sufficiently characteristic clinical features to merit its distinction from other photodermatoses. Some patients appear to have a genetic predisposition and in one JSE case series a positive family history of the condition was demonstrated in 13 of 18 patients. Another curious feature of JSE is the occurrence of outbreaks, although to date no infectious cause has been identified. The first reported outbreak in the UK was in 1953 when a children’s camp in Surrey had to be closed prematurely as a contagious infectious disease was suspected when 121 of 150 children there developed pruritic lesions on their ears. No infectious agent was isolated during this outbreak and it was concluded that environmental factors – the combination of bright sunlight and cold air on exposed sites – were responsible for the eruption. A similar incident was reported in 18 patients in Switzerland in 1942,5 and a further outbreak occurred amongst a company of Spanish soldiers. Some cases of JSE have resembled erythema multiforme both clinically and
JSE may represent a photo-induced variant of erythema multiforme,5 although others have found no link.4
