Solar urticaria: Clinic, diagnostic, course and therapy management in 27 patients

Abstract

Background and objectives: Solar urticaria is a rare photodermatosis, the diagnosis and therapy of which have not yet been standardized. The aim of this research was to use innovative radiation sources for diagnostics with defined and reproducible emission spectra and doses. A uniform therapy step scheme was to be created. Patients and methods: In a longitudinal study, 27 patients with solar urticaria were examined over 13 years. With a characteristic anamnesis, the diagnosis was confirmed with phototesting (photoprovocation) from various radiation sources (UVB, UVB-311nm, UVA, UVA-1, green light, red light) and a therapy step scheme was designed consisting of light protection, antihistamines, rush hardening with UVA-1, and administration of omalizumab. Results: Action spectrum: UVB 44 %, UVA 70 %, UVA-1 89 %, green light 37 % and red light 22 %. Rush hardening with subsequent maintenance therapy was performed on 20 patients, 17 of whom were hereby adequately protected. In three further patients, omalizumab was additionally administered. Conclusions: Phototesting with UVB, UVB311nm, UVA, UVA-1, and visible light with innovative radiation sources is uniformly possible in every major skin clinic. With the help of the therapy step scheme the patients can be adjusted well. Rush hardening with UVA-1 is a safe method to help the patients during the sunny season. Omalizumab as the last therapy option is effective, but currently only possible in off-label use.

Pathogenesis of solar urticaria: Classic perspectives and emerging concepts

“…The SU action spectrum is relatively distinct amongst photodermatoses, as it can vary radically between patients and extend across the entire UV spectrum, although a majority of patients are sensitive to either the UVA or visible light wavebands. 3,6,9,[23][24][25] From a photobiologic perspective, this accords with in vitro activation experiments, where autologous injection of serum fractions containing proteins of vastly divergent molecular weights successfully elicited SU symptoms in several patients. 20 Unfortunately, analysis of action spectra has not resulted in the identification of putative chromophores that produce mast cell activation in SU.…”

“…Since the development of phototesting in 1953, 22 it has become possible to define more precisely the action spectrum for SU patients and to gain insights into its causal chromophores. The SU action spectrum is relatively distinct amongst photodermatoses, as it can vary radically between patients and extend across the entire UV spectrum, although a majority of patients are sensitive to either the UVA or visible light wavebands 3,6,9,23‐25 . From a photobiologic perspective, this accords with in vitro activation experiments, where autologous injection of serum fractions containing proteins of vastly divergent molecular weights successfully elicited SU symptoms in several patients 20 .…”

“…4 There is also limited evidence supporting geographic restriction of cases as sizable hospital-based SU cohorts have been described in several countries, including the U.K., France, Germany, Belgium, Spain, Italy, Australia, Japan and Si ngapore. 3,[6][7][8][9]23,[25][26][27]46 Although a lack of population-level data precludes comparison of SU prevalence between these countries, this observed geographic dispersion does suggest that shared environmental factors, particularly variation in incidental exposure to solar electromagnetic radiation due to latitude and climate, 47 are insufficient to produce disease in most individuals. Similarly, a lack of temporal variation in SU incidence, evidenced by reports of static annual incidence of SU over a 16-year period in two large Spanish photodermatology centres, suggests that changing environmental factors in local communities do not singularly drive large fluctuations in SU incidence, i.e., epidemics.…”