View clinical trials related to Polymorphic Light Eruption.
Filter by:The primary objective of this Clinical Investigation was to assess the protective efficacy of a medical device (FOTO ULTRA ISDIN® SOLAR ALLERGY FUSION FLUID) against the polymorphic light eruption induced by the UVA. The secondary objective of this Clinical Investigation was to assess the local safety and the overall tolerability of the test MD on the basis of AE/SAE reporting.
Polymorphic light eruption (PLE) is the most common form among UV-inducible disorders with a prevalence of approximately 11-21% worldwide and a clear predisposition of women. Usually, within several hours after an intense UV exposure, most likely in spring or early summer, the formation of itchy skin lesions particularly at the upper arms and V-neck and neck is distinctive for PLE. It has been suggested that the development of a potential photo-induced antigen may initiate a delayed-type hypersensitivity reaction in PLE (causing the skin rash) and the microbiota of the skin may be involved. We thus hypothesized that eliminating the microbiota of the skin by disinfection may affect the formation of PLE. The concept of this study covers a combined interindividual and intraindividual half-body comparison of the skin reactions of disinfected and contralateral non-disinfected areas upon UV exposure in PLE patients and healthy subjects.
This study was to evaluate the safety and efficacy of afamelanotide in patients suffering from polymorphic light eruption (PLE).
The molecular mechanisms of action of photo(chemo)therapy in skin diseases are investigated in this study. The phototherapeutic modalities employed include UVB (ultraviolet B), UVA (ultraviolet A), PUVA (psoralen+UVA) and/or extracorporeal photochemotherapy (photopheresis). The study will address whether and how photo(chemo)therapy affects specific biologic pathways in different skin disorders and search for predictive biomarkers.
Polymorphic light eruption (PLE) is a common photodermatosis with a high prevalence of approximately 11 to 21% in the population. Similar to lupus erythematosus (LE), an UV-inducible systemic autoimmune disease, PLE has a female preponderance with a mean onset in the second to third decade of life. PLE lesions are very itchy and typically appear on sun-exposed body sites in spring or early summer. The quality of life in patients with PLE is often severely disturbed, as evidenced by high levels of anxiety and depression. For prophylaxis besides conventional sunscreens, photo(chemo)therapy is effective in many cases, when administered over several weeks for hardening in early spring before the first natural sun exposure takes place. However, because prolonged treatment with UVB and/or photochemotherapy is potentially carcinogenic, the search for pathogenic mechanisms and new treatment options in PLE is ongoing. The exact pathogenesis of PLE is currently unknown but findings suggest an autoimmune-type background with resistance to UV-induced immune suppression and simultaneous immune reactions against skin photo-neoantigens. The investigators have recently found that PLE patients had significantly reduced 1,25-(OH)2-vitamin D3 serum levels (13-14ng/ml) compared to the normal population (>30ng/ml). In addition, the investigators were able to demonstrate in an intra-individual half-body trial that topical administration of an immunostimulatory 1,25-(OH)2-vitamin-D3 analogue calcipotriol reduced PLE symptoms in an experimental study. In the proposed randomized double-blinded placebo-controlled trial the investigators attempt to study the effect of oral vitamin D3 supplementation (2 x 40.000 IE, given orally two weeks apart) on PLE symptoms.
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 the pathogenesis of PLE may give clues to develop new therapeutic strategies.
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 UV-induced immunosuppression with subsequent immune reactions against skin photoneoantigens has been suggested. Regulatory T cells (CD4+CD25+FoxP3+) (Tregs), a subset of T helper cells, are crucial for the induction of immunosuppression. We will test the hypothesis that PLE patients show pathogenic fluctuating Treg levels and function and related parameters over the seasons of the year, possibly being responsible for lack of immune modulation and autoimmunity in PLE. Natural or medical photohardening may normalize Treg deficiency in PLE and lead to clinical adaption in summer. Better insight into the pathogenesis of PLE may give clues to develop new therapeutic strategies.
Polymorphic light eruption (PLE) is a common photodermatosis characterized by the appearance of itching, erythema, papules or vesicles on sun-exposed skin. Though etiology is unclear it is hypothesized that it is an abnormal immune response to autologous antigens generated by ultraviolet radiation (UVR). This randomized, double blinded left-right body side experimental comparison study was designed to assess the preventive effect of a sunscreen and topical DNA repair enzyme-containing after-sun lotion in PLE.