Calcipotriol and Polymorphic Light Eruption

Polymorphic light eruption (PLE) is a photodermatosis with an extremely high prevalence, particularly among young women (up to 20%). The disease is characterized through itchy skin lesions on sun-exposed body sites occurring after sun exposure mostly in spring and early summer. Its etiopathogenesis is unknown but resistance to ultraviolet radiation (UVR)-induced immunosuppression with subsequent immune reactions against skin photoneoantigens has been suggested. The phenomenon of UVR-induced immunosuppression (suppression of CHS) has been well known for many years. Recent findings showed that regulatory T cells (CD4+CD25+FoxP3+) (Tregs), a subset of T helper cells, are crucial in UVR-induced immunosuppression. However, the requirements for the maintenance of peripheral CD4+CD25+ T cells, important in suppression of immune responses, are still incompletely understood. Recent work suggests that cutaneous RANKL might be the physiologic missing link that couples UVR to immunosuppression. Epidermal RANKL, expressed in keratinocytes of inflamed skin due to e.g. UVR exposure was shown to control the number of Tregs via activation of dendritic cells, hereby mediating UVR-induced immunosuppression (e.g. suppression of allergic contact hypersensitivity responses). In addition to the suppression of local cutaneous hyperallergic responses, the development of systemic autoimmunity is suppressed. A strong inducer of RANKL expression and of Tregs is vitamin D3 that has been reported to have immunosuppressive effects. Interestingly, patients with autoimmune disorders (e.g. lupus erythematosus) may exhibit reduced vitamin D3 blood levels. This randomized, double blinded left-right body side experimental comparison study was designed to assess the preventive effect of the vitamin D3 analogue calcipotriol in patients with PLE. The hypothesis is tested that treatment with a calcipotriol-containing cream can prevent the UVR-induced development of PLE skin lesions. Better insight into t