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Chronic photosensitivity dermatitis (CPD) (also named actinic reticuloid) is an unusual disease classically referred often in elderly men. Affected patients have severely itchy, thickened dry skin in areas exposed to the sun throughout the years.
A Caucasian female patient who worked most of her life outside who had \"chronic dermatitis\" in her neck started planting chrysanthemum in her garden on a sunny day. Later, she presented edema, erythema, papules, and a few vesicles in her neck with severe pruritus.
A skin biopsy revealed the diagnosis of CPD, along with positive testing for ultraviolet B (UVB), minimal erythema doses (MED) for UVB (MEDB) UVA (MEDA) and PhotoPath.
Direct immunofluorescence (DIF) stains using anti-human antibodies against fibrinogen, albumin, IgG, IgM, lambda, kappa, and C3c and C1q were positive at the base membrane area of the dermal epidermal junction, in the papillary dermis, as well as the neurovascular bundles in all the dermis and the extracellular matrix, especially those under the blisters.
With this case, we suggest not forgetting the importance of using DIF in reactivated CPD cases in addition to the photo patch testing.

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Photosensitivity represents an increased inflammatory reaction to sunlight, which can be observed particularly in the autoimmune disease lupus erythematosus. Cutaneous lupus erythematosus (CLE) can be provoked by ultraviolet (UV) radiation and can cause both acute, nonscarring and chronic, scarring skin changes. In systemic lupus erythematosus, on the other hand, provocation by UV radiation can lead to flare or progression of systemic involvement. The etiology of lupus erythematosus is multifactorial and includes genetic, epigenetic and immunologic mechanisms. In this review, we address the effect of UV radiation on healthy skin and photosensitive skin using the example of lupus erythematosus. We describe possible mechanisms of UV-triggered immune responses that could offer therapeutic approaches. Currently, photosensitivity can only be prevented by avoiding UV exposure itself. Therefore, it is important to better understand the underlying mechanisms in order to develop strategies to counteract the deleterious effects of photosensitivity.
UNASSIGNED: Photosensitivität stellt eine verstärkte entzündliche Reaktion auf Sonnenlicht dar, die üblicherweise bei der Autoimmunerkrankung Lupus erythematodes beobachtet werden kann. Der kutane Lupus erythematodes (CLE) kann sowohl akute, nicht vernarbende als auch chronische, vernarbende Hautveränderungen hervorrufen. Beim systemischen Lupus erythematodes kann es zudem durch Provokation mittels UV-Strahlung zu einem Aufflammen oder Progress der systemischen Beteiligung kommen. Die Ätiologie des Lupus erythematodes ist multifaktoriell und umfasst genetische, epigenetische und immunologische Mechanismen. In dieser Übersichtsarbeit gehen wir auf die Wirkung von UV-Strahlung auf gesunde Haut und photosensitive Haut am Beispiel des Lupus erythematodes ein. Wir beschreiben mögliche Mechanismen der UV-getriggerten Immunreaktionen, die therapeutische Ansätze bieten könnten. Gegenwärtig kann eine Photosensitivität nur dadurch verhindert werden, dass man die UV-Exposition selbst vermeidet. Daher ist es wichtig, die zugrunde liegenden Mechanismen besser zu verstehen, um Strategien zu entwickeln, die den schädlichen Auswirkungen der Photosensitivität entgegenwirken.

UNASSIGNED: Amidst the emergence of new therapeutic options, traditional therapeutic plasmapheresis (TPE) used in diseases involving a toxic substance in the plasma, remains a viable alternative for cases of recalcitrant solar urticaria (SU). We emphasize the importance of documenting successful experience with repeated plasmapheresis to increase awareness amongst physicians and dermatologists regarding this effective treatment option.
UNASSIGNED: We reported a case of recalcitrant SU that had not responded to a combination of H1-antihistamines, immunosuppressants, omalizumab and intravenous immunoglobulin. We introduced serial TPE, which involved two consecutive days of procedures for each course was introduced. We detailed the regimen and highlighted the clinical and objective benefits observed with multiple treatments. Additionally, we compared this to other plasmapheresis regimens and their treatment responses previously reported for solar urticaria.
UNASSIGNED: Our patient underwent serial TPE, totaling 42 procedures over five years. Following the last TPE session, phototesting showed a sustained prolongation of minimal urticating doses (MUDS), which exceeded the maximum tested doses across nearly all ultraviolet (UV) and visible light ranges, with the exception of the two short ultraviolet B (UVB) wavelengths. MUDs increased to 25 from 6 mj/cm2 at 307.5± 5nm, and to 500 from 15 mj/cm2 at 320 ± 10nm, before the initial TPE. In our review, we included five articles covering eight SU patients who received TPE. Of these, the five patients with positive intradermal tests responded particularly well immediately after treatment. However, the condition relapsed within two weeks in one patient and within two months in another. In contrast, the other three patients with negative intradermal tests, showed no significant benefits from the treatment. No serious side effects from TPE were reported amongst the patients.
UNASSIGNED: This review underscores the efficacy of serial plasmapheresis procedures in treating refractory cases of SU, high3lighting the robust results observed.

Solar urticaria is a rare idiopathic photodermatosis. According to the current knowledge its pathogenesis is most likely based on an allergic type I reaction to an autoantigen activated by ultraviolet (UV) radiation or visible light. As many of the patients suffer from severe forms of the disease, it may therefore severely impair the quality of life of those affected. In contrast, polymorphous light eruption is a very common disease, which, according to the current data, can be interpreted as a type IV allergic reaction to a photoallergen induced by UV radiation. As the skin lesions heal despite continued sun exposure, the patients\' quality of life is generally not significantly impaired. These two clinically and pathogenetically very different light dermatoses have shared diagnostics by means of light provocation and an important therapeutic option (light hardening). Herein, we present an overview of the clinical picture, pathogenesis, diagnosis and available treatment options for the above-mentioned diseases.
UNASSIGNED: Lichturtikaria ist eine seltene idiopathische Lichtdermatose, deren Pathogenese nach aktuellem Wissensstand am ehesten auf einer allergischen Typ-I-Reaktion gegenüber einem durch ultraviolette (UV) Strahlung oder sichtbares Licht aktivierten Autoantigen beruht. Schwere Verlaufsformen sind möglich, die Erkrankung kann daher die Lebensqualität der Betroffenen stark beeinträchtigen. Im Gegensatz hierzu handelt es sich bei der polymorphen Lichtdermatose um eine sehr häufige Erkrankung, die gemäß der aktuellen Datenlage als eine allergische Typ-IV-Reaktion gegenüber einem durch UV-Strahlung induzierten Photoallergen interpretiert werden kann. Da die juckenden Papeln, Bläschen oder Plaques bei fortgesetzter Sonnenexposition mit hieraus resultierender Ausbildung einer Lichtschwiele abheilen, ist die Lebensqualität der Patienten in der Regel geringfügiger und eher kurzfristig beeinträchtigt. Gemeinsam ist diesen beiden klinisch und pathogenetisch sehr unterschiedlichen Photodermatosen, dass die jeweilige Diagnose mittels Lichtprovokation bestätigt werden kann und dass das sogenannte Licht-Hardening eine wichtige Therapieoption darstellt. Die vorliegende Arbeit präsentiert eine Übersicht über das klinische Bild, die Pathogenese, Diagnostik und die verfügbaren Therapieoptionen beider Erkrankungen.

The autoimmune disease lupus erythematosus (lupus) is characterized by photosensitivity, where even ambient ultraviolet radiation (UVR) exposure can lead to development of inflammatory skin lesions. We have previously shown that Langerhans cells (LCs) limit keratinocyte apoptosis and photosensitivity via a disintegrin and metalloprotease 17 (ADAM17)-mediated release of epidermal growth factor receptor (EGFR) ligands and that LC ADAM17 sheddase activity is reduced in lupus. Here, we sought to understand how the lupus skin environment contributes to LC ADAM17 dysfunction and, in the process, differentiate between effects on LC ADAM17 sheddase function, LC ADAM17 expression, and LC numbers. We show through transcriptomic analysis a shared IFN-rich environment in non-lesional skin across human lupus and three murine models: MRL/lpr, B6.Sle1yaa, and imiquimod (IMQ) mice. IFN-I inhibits LC ADAM17 sheddase activity in murine and human LCs, and IFNAR blockade in lupus model mice restores LC ADAM17 sheddase activity, all without consistent effects on LC ADAM17 protein expression or LC numbers. Anti-IFNAR-mediated LC ADAM17 sheddase function restoration is associated with reduced photosensitive responses that are dependent on EGFR signaling and LC ADAM17. Reactive oxygen species (ROS) is a known mediator of ADAM17 activity; we show that UVR-induced LC ROS production is reduced in lupus model mice, restored by anti-IFNAR, and is cytoplasmic in origin. Our findings suggest that IFN-I promotes photosensitivity at least in part by inhibiting UVR-induced LC ADAM17 sheddase function and raise the possibility that anifrolumab ameliorates lupus skin disease in part by restoring this function. This work provides insight into IFN-I-mediated disease mechanisms, LC regulation, and a potential mechanism of action for anifrolumab in lupus.

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Patients presenting with a linear, erythematous, blistering eruption may experience a sudden painful sunburn that seems to get worse rather than better with time. In warm climates, exposure to the common fig tree (Ficus carica) may be the culprit. Dermatologists should recognize fig phytophotodermatitis as a possible cause and help the patient connect their symptoms with the inciting agent as well as administer proper treatment.