Successful treatment of solar urticaria with anti-immunoglobulin E therapy

Authors

  • O. Güzelbey,

  • E. Ardelean,

  • M. Magerl,

  • T. Zuberbier,

  • M. Maurer,

  • M. Metz

    Corresponding author
      *Department of Dermatology and Allergy
      Charité– Universitätsmedizin Berlin
      Charitéplatz 1
      D-10117 Berlin
      Germany
      Tel.: +49 30 450 518159
      Fax: +49 30 450 518972
      E-mail: martin.metz@charite.de
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  • A possible new treatment alternative and new insight into the pathogenesis of solar urticaria.

*Department of Dermatology and Allergy
Charité– Universitätsmedizin Berlin
Charitéplatz 1
D-10117 Berlin
Germany
Tel.: +49 30 450 518159
Fax: +49 30 450 518972
E-mail: martin.metz@charite.de

Solar urticaria is characterized by intense pruritus and wheal and flare-type skin reactions at the sites exposed to sunlight. The eliciting factor is UVA, UVB and/or visible light with individual action spectra for each patient (1). Nonsedating H1-antihistamines are the first line therapy for solar urticaria, but in severe cases conventional antihistaminic treatment is often unsuccessful. High-grade sun blockers are usually not sufficient, and light-hardening therapy, although sometimes quite effective, is not appropriate for long-term treatment because of the risk of skin tumour development.

We present the case of a 52-year-old caucasian female patient with severe solar urticaria who experienced wheals and pruritus induced by sun- and interior light. Minimal sun exposure, e.g. during the short walk to her car in the mornings, sufficed to induce cutaneous symptoms, and prolonged light exposure resulted on occasion in systemic symptoms including dizziness, headaches and respiratory problems. Consequently, this patient experienced a major reduction in her quality of life because of her urticaria, which significantly interfered with her private and professional life.

The patient was diagnosed with solar urticaria in February 2007 by light provocation, revealing a threshold for UVA light of 1.4 J/cm2. Since then, the patient has been treated with various nonsedating and sedating antihistamines (up to eightfold the recommended daily dose), histaglobin injections, various diets and Helicobacter pylori eradication therapy, none of which resulted in a significant reduction of her symptoms. Initially, we treated the patient with a UVA rush hardening regimen (2), which lowered the UVA threshold considerably. However, the patient still had light-induced symptoms and was unable to continue the twice weekly UVA exposures needed for maintaining the reduced UVA threshold.

The pathogenesis of solar urticaria is still poorly understood. One of the favoured hypotheses is that irradiation with light produces a photoallergen within the skin, which crosslinks specific immunoglobulin E (IgE) bound to the FcɛRI-receptor on cutaneous mast cells. The ensuing mast-cell degranulation then leads to the release of a wide range of mediators, including histamine, which cause pruritus and the typical wheal and flare reaction. This hypothesis offers the possibility that anti-IgE treatment can be effective in the treatment of solar urticaria.

Omalizumab is a recombinant humanized monoclonal antibody against IgE. It acts by binding free IgE at the same site that IgE would bind to its high-affinity receptor (FcεRI) on mast cells, thereby reducing free IgE in the serum (3). Recently, successful treatment of cholinergic urticaria (4), cold urticaria (5) and chronic urticaria (6) with omalizumab has been reported. Because of these positive reports, and because none of the previous treatment strategies had been successful in our patient, we began to treat our patient with 150 mg omalizumab every 4 weeks. The patient does not suffer from allergic rhinitis or other allergies, had total IgE levels of 22.0 kU/l, and is otherwise healthy.

Within 4 weeks after the first injection of omalizumab the patient reported back to us with a dramatic improvement of light-induced symptoms. Standardized light-provocation test with UVA and UVB 4 weeks after the first injection was completely negative, even at high doses of UV light (Fig. 1). The patient reported that she did not have a single wheal since the first injection of omalizumab, although she was frequently exposed to sun light. Furthermore, her respiratory problems improved and she was able to stop antihistamine medication completely.

Figure 1.

 Omalizumab treatment effectively prevents light-induced symptoms in a patient with solar urticaria. The patient presented herself in our department before treatment with omalizumab (A) and on a sunny day 4 weeks after treatment (B). Before and 4 weeks after treatment, standardized light-provocation test (Saalmann-Multitester SBC LT 400) with UVA (lower row) and UVB (upper row) was performed (C, D). The numbers indicate the UV-doses applied in each field in J/cm2 or mJ/cm2, respectively. UVB irradiation shows only a mild erythema (C), irradiation with UVA shows characteristic wheals with a threshold of 1.4 J/cm2 before treatment (C), and no detectable erythemas, wheals or pruritus 4 weeks after the start of the omalizumab therapy (D).

This is to our knowledge the first report of a successful treatment of solar urticaria with omalizumab. The observed rapid improvement of the symptoms during anti-IgE therapy supports the hypothesis that solar urticaria might be mediated by IgE. The entity of the photoallergen remains unclear. Further clinical trials should investigate whether anti-IgE treatment is in general beneficial for patients with solar urticaria; these future investigations might also help to understand the pathogenic mechanism of the disease.

This case shows that solar urticaria can be rapidly and successfully treated with omalizumab at the recommended dosage, even in the context of relatively low total IgE levels.

We thank Jodie Urcioli for proofreading the manuscript.

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