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.

A man in his 50s was diagnosed with solar urticaria following monochromated light testing that demonstrated exquisite photosensivity to ultraviolet (UV) A, UV B (UVB) and visible light.Treatment options for this photodermatosis are limited; UVB phototherapy is one modality that can be appropriate in some patients. This is administered at very low doses in a controlled environment to induce skin hardening.1 To self-treat his condition, the patient used a commercial sunbed on two occasions several days apart. He noted an immediate flare of solar urticaria after first use with associated dizziness. Following the second use, he felt generally unwell and was witnessed to lose consciousness and displayed jerky movements of his limbs while a passenger in a car. Investigations including a head MRI and an EEG were normal; an anoxic seizure caused by a flare of solar urticaria was later confirmed.Solar urticaria is a rare photodermatosis that is poorly understood and difficult to treat. The condition has a significant impact on the quality of life of patients. Severe cases can be associated with systemic symptoms that could be life-threatening.

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Solar urticaria is a rare photodermatosis with several unknown pathogenic, clinical and therapeutic aspects. This study analysed the clinical and therapeutic features of a long-term follow-up solar urticaria cohort, with a focus on omalizumab management and outcomes, and characterized omalizumab response with the use of the high-affinity immunoglobulin E (IgE) receptor (FcεRI) and the Urticaria Control Test. An observational, unicentric, ambispective study was conducted from 2007 to 2023. Solar urticaria was diagnosed in 41 patients with a median follow-up of 60 months. Thirteen patients were prescribed omalizumab, with a median treatment time of 48 months. A significant decrease in FcεRI baseline levels and subsequent median increase in Urticaria Control Test was evidenced after omalizumab prescription in all patients. Drug survival at 48 months was at 88.9%. Omalizumab stepping-down protocol led to sustained omalizumab discontinuation in only 1 patient. Median basal Urticaria Control Test was lower (p < 0.01) in patients who were prescribed omalizumab and in patients without remission. This study contributes to our knowledge of omalizumab outcomes in real-life clinical practice and highlights the pathogenic importance of IgE-mediated pathways in solar urticaria, where FcεRI emerges as a possible biomarker of omalizumab response.

BACKGROUND: Solar urticaria is a rare photodermatosis characterized by rapid-onset sunlight-induced urticaria, but its pathophysiology is not well understood.
OBJECTIVE: We sought to define cutaneous cellular and molecular events in the evolution of solar urticaria following its initiation by solar-simulated UV radiation (SSR) and compare with healthy controls (HC).
METHODS: Cutaneous biopsy specimens were taken from unexposed skin and skin exposed to a single low (physiologic) dose of SSR at 30 minutes, 3 hours, and 24 hours after exposure in 6 patients with solar urticaria and 6 HC. Biopsy specimens were assessed by immunohistochemistry and bulk RNA-sequencing analysis.
RESULTS: In solar urticaria specimens, there was enrichment of several innate immune pathways, with striking early involvement of neutrophils, which was not observed in HC. Multiple proinflammatory cytokine and chemokine genes were upregulated (including IL20, IL6, and CXCL8) or identified as upstream regulators (including TNF, IL-1β, and IFN-γ). IgE and FcεRI were identified as upstream regulators, and phosphorylated signal transducer and activator of transcription 3 expression in mast cells was increased in solar urticaria at 30 minutes and 3 hours after SSR exposure, suggesting a mechanism of mast cell activation. Clinical resolution of solar urticaria by 24 hours mirrored resolution of inflammatory gene signature profiles. Comparison with available datasets of chronic spontaneous urticaria showed transcriptomic similarities relating to immune activation, but several transcripts were identified solely in solar urticaria, including CXCL8 and CSF2/3.
CONCLUSIONS: Solar urticaria is characterized by rapid signal transducer and activator of transcription 3 activation in mast cells and involvement of multiple chemotactic and innate inflammatory pathways, with FcεRI engagement indicated as an early event.

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