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Epidemiology and Pathogenetic Mechanisms of Polymorphic Light Eruption Janssens, A.S

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Epidemiology and Pathogenetic Mechanisms of Polymorphic Light Eruption Janssens, A.S Epidemiology and pathogenetic mechanisms of polymorphic light eruption Janssens, A.S. Citation Janssens, A. S. (2008, January 17). Epidemiology and pathogenetic mechanisms of polymorphic light eruption. Retrieved from https://hdl.handle.net/1887/12576 Version: Corrected Publisher’s Version Licence agreement concerning inclusion of doctoral thesis in the License: Institutional Repository of the University of Leiden Downloaded from: https://hdl.handle.net/1887/12576 Note: To cite this publication please use the final published version (if applicable). 1 Introduction Introduction The research described in this thesis was initiated in 2002, when our group became member of the so-called SUNALL consortium. This was a multidisciplinary group of scientists from six different European countries interested in the pathogenesis of polymorphic light eruption (PLE). The scientific collaboration was funded by the European Commission. The main goal of the joint projects was to shed more light on pathogenetic mechanisms of PLE, but also to provide epidemiologic data, clues on mechanisms of (photo-) therapies and tools to improve diagnosis. A prerequisite was that all parties agreed on a definition of the studied subject. The clinical members of the SUNALL consortium reached consensus that polymorphic light eruption (PLE) is primarily a recurrent pruritic eruption comprising papules and/or vesicles and/or plaques, which occur on sun exposed skin sites, and which heal without scarring. We agreed to include patients with a classical history of PLE who also had positive ANA antibodies. However, the presence of antibodies against SSA and SSB was accepted as an exclusion criterion. Eczematous sun-induced lesions were not regarded as PLE. In this introduction, recent insight into epidemiology, pathogenetic mechanisms, Ch ap t er 1 photo provocation procedures, differential diagnostic aspects and treatment of PLE are discussed, and questions addressed in this thesis are formulated. 10 Epidemiology The term polymorphous light eruption was first used by the Dane Rasch in 1900. 1 Before that time, several names were used to describe this idiopathic photodermatosis, such as eczema solare, summer prurigo, summer itch, solar dermatitis and benign summer eruption. PLE is the most common idiopathic photodermatosis. Epidemiological data on PLE are sparse, but the prevalence is estimated to be around 10-20% in the USA, England and Ireland. 2 The male/female ratio varies between 1:2 and 1:4 and the disease occurs preferentially in young women. Underlying genetic and/or hormonal differences together with the difference between women and men in seeking medical attention for dermatological problems seem to be likely causes of this gender difference. 3 A contributing role of the female sex hormone 17-oestradiol has been investigated to explain the gender differences of PLE. The role of 17-oestradiol on immunosuppression and contact hypersensitivity (CHS) caused by ultraviolet B (UVB) irradiation, was investigated in male mice intraperitoneally injected with the hormone and in female mice treated with anti-estradiol. 4 The results suggested that 17-oestradiol prevented UVB-induced suppression of the CHS response caused by lower concentrations of immunosuppressive cytokines (IL-10) produced by keratinocytes. Hormonal contraceptives can induce photosensitivity and are very widely used by women. These hormones could, as an exogenous factor, contribute to this female dominated prevalence of PLE. 5;6 Two studies based on interviews, conducted in the USA by Morison and Stern and in Sweden by Ros and Wennersten, have made clear that only 3-15 % of the responders with a history consistent of PLE, sought medical attention. 7;8 These surveys indicate that the prevalence of PLE is probably much higher than normally reported. PLE has a wide geographical distribution and it is believed to be more frequent in temperate than tropical climates. 9 In another epidemiological study, the prevalence and clinical characteristics of polymorphic light eruption were assessed by a questionnaire survey among 172, 196 and 182 subjects in Perth, Ballarat and London, respectively. The prevalence was 5.2% in Perth (latitude 32 degrees), 3.6% in Ballarat (37.5 degrees) and 14.8% in London (51.5 degrees). The age of onset (mostly diagnosed in the first three decades) and male/female ratio (1:3) were similar in all three areas. Development of tolerance during the summer was more common in Perth (66.7%) and Ballarat (71.4%) than in London (40.7%). 9 PLE is mainly a disease affecting the fair-skinned population. It is also believed that PLE occurs mainly in UV-unadapted skin. A study conducted among tourists visiting Hawaii illustrated that the cutaneous disorders of the Caucasian island visitors differed significantly from those observed in the local population. In the visitor group, over one-third of the diagnoses were light-induced conditions. The most common disease observed was the papulovesicular variant of polymorphous light eruption. 10 In another 10-year study conducted in Nigeria, light-sensitive dermatoses appeared not to be common among the black people. Only 64 cases (about 0.4% of all dermatological patients) had light-sensitive dermatoses. Two patients with polymorphic light eruption were visiting Caucasians. 11 Outline 1 To improve on the available epidemiological data, the SUNALL consortium has conducted a questionnaire survey among 6,895 individuals in 6 different European countries. We investigated the prevalence of PLE and its dependence on geographical latitude, gender, occurrence during springtime or sunny holidays and skin type. This survey is described in chapter 2. Verwijderd: Chapter Aetiology and pathogenetic mechanisms of PLE The rash of PLE is induced by exposure to ultraviolet radiation (UVR). The evoking wavelengths apparently vary between patients, but typical lesions occurred following irradiation with broadband UV-B lamps (290-320 nm), UV-A (320-400 nm) or solar simulated radiation.12-16 Normal UV-induced immune reactivity Our knowledge and understanding of the effects of UV radiation on human health and topical effects on the skin comes from studies that combine elements of photobiology, immunology and dermato-oncology. From photoimmunological investigations it is recognized that UV irradiation suppresses cutaneous T-cell- mediated immunity in humans. 17 Most studies used the contact hypersensitivity (CHS) and delayed type hypersensitivity (DTH) responses to Introductiona variety of | 11 sensitising agents (such as di-nitrofluorbenzene (DNFB)) as a model to study the effects of UV radiation on immune responses. 18;19 In the CHS reaction, a hapten is applied onto the skin, and antigen-presenting cells (APC), mainly epidermal Langerhans cells (LC) take up the antigens and migrate to regional lymph nodes, where they interact with naïve T-helper cells to initiate the response. After expansion and differentiation, the T cells enter the circulation and upon a next contact with the same antigen on the skin, they cause local CHS response with symptoms of redness, itching and swelling. The DTH response is similar, except that the antigen is introduced by the intradermal or subcutaneous route. The initiation of UVR-induced immune suppression of the skin is accompanied by depletion of epidermal LCs, dermal and epidermal influx of CD11b+ neutrophils 18;20 and macrophages and release of cytokines, in particular interleukin 10 (IL-10). UVR-induced immune suppression of CHS and DTH responses is achieved by a single or repeated low-dose UVB irradiation before the application of the antigen, leading to an absence of a visible response and possibly to tolerance to this antigen. These immune suppressive responses take place in every healthy person. UV-induced suppression of cellular immunity can be thought of as a sound Ch ap t er 1 physiological reaction. What if the above mechanisms become disturbed or diminished? It is hypothesized that an imbalance of UV-induced pro-inflammatory 12 reactions and immunosuppression could lead to a pathological skin reaction to a UVR-induced antigen (photoantigen), and that a UV-induced allergy e.g. PLE could develop. Prior histological examination of PLE lesions revealed some features that were also found in DTH responses, such as the expression of intercellular adhesion molecule-1 (ICAM-1) and upregulation of major histo-compatibilty complex class II (MHC class II) on keratinocytes. 16 Also, the switch from a predominance of CD4+ lymphocytes in infiltrates of new PLE lesions to a predominance of CD8+ lymphocytes in older PLE lesions 13 resembled the change observed in a DTH response. To unravel early pathogenetic mechanisms, other investigators focused on the pre-lesional UV-triggered skin responses in PLE patients. In 1999, Kölgen and co-workers reported that epidermal LCs of PLE patients persisted in the epidermis upon a high dose of UVB irradiation. 21 That contrasted with the depletion in healthy subjects. Other investigators reported that CD11b+ macrophage-like cells infiltrate the epidermis 48 and 72 h after UV exposure in skin of healthy individuals. 19 The authors suggested that the ability to induce locally a state of in vivo tolerance is closely associated with the expansion of class II MHC+/CD11b+ monocytes/macrophages in the dermis and epidermis. 19 Kölgen et al. showed that these CD11b+ cells infiltrated the epidermis in PLE patients in lower numbers than in healthy control subjects upon a single high UVB exposure and that these
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