By Gary M. White, MD
Solar urticaria (SU) is characterized by erythema and wheals that appear immediately after exposure to ultraviolet radiation and/or visible light.
Pruritus, erythema, and wheals appear within minutes of exposure to ultraviolet (UV) and visible light and generally resolve in a few hours. Significant changes in action spectrum and degree of photosensitivity may occur over years in solar urticaria. However, changes over shorter periods of time are likely to be minor. In one study [Am J Contact Dermat 2000;11:89-94] solar urticaria affected both sexes. Nearly half of patients are free of disease within 5 years. In about one fourth of cases, solar urticaria is associated with dermatographic urticaria or atopic dermatitis.
In one review, urticaria occurred before the 15th minute of sun-exposure in 95% of the patients and resolved spontaneously after its interruption within 1h in 76.4%. Determination of the action spectra revealed UVA sensitization in 91.8% of the patients, alone (49.2%) or with UVB (24.6%) or visible light (14.75%) [Eur J Dermatol. 2013 Apr 1;23(2):202-7].
Workup can include a drug history, porphyrins, ANA, Ro, La, and phototesting. The action spectrum may include UVB, UVA, and/or visible light.
Prevention of the disease by sun and visible light protection is the best approach. A sunscreen applied immediately upon wakening and reapplied several times a day is recommended. Because visible light may aggravate solar urticaria, physical-block sunscreens (containing iron oxide, titanium dioxide, and/or zinc oxide) should be used. Antihistamines can decrease the symptoms somewhat.
Alternatively, sunbathing or ultraviolet therapy to harden the skin has been used. There are some complexities to this approach. The following article summarizes them well: [Clin Exp Deramatol 2013;38;446-7]. Briefly, action-spectrum hardening is done by first determining the causative action spectrum and then exposing the patient to increasing levels of that wavelength. Unfortunately, this is time-consuming, risks SU exacerbation, and induces only short-term tolerance requiring treatment at close intervals, e.g., 1-2/week. In addition, some patients have a broad-activating spectrum so knowing the exact wavelength to use may be difficult.
A better approach may be treating with an inhibitory UV spectrum. In this case, the therapeutic spectrum differs from the causative spectrum. For example, UVB therapy may be used for patients who develop lesions to visible light or UVA. Or, UVA1 may be used for patients triggered by UVB or UVA2. See JAAD 2012;67;e5-9 for a cohort of patients treated with NB-UVB in this manner.
Photopheresis might be of some benefit in selected patients with otherwise intractable solar urticaria. Cyclosporin therapy was very successful in one case and is a possible treatment in severe cases of solar urticaria where other treatments have failed, especially in countries where treatment is necessary only for a few months during summer [Photodermatol Photoimmunol Photomed 1997;13:61-3].
For resistant cases, intravenous immunoglobulin (IVIG), cyclosporin, azathioprine, and omalizumab have been reported beneficial in small series and case reports.
Afamelanotide has been used with success in solar urticaria. In one study, melanization following afamelanotide administration was accompanied by reduction in solar urticaria response across a broad spectrum of wavelengths [Br J Dermatol. 2011 Feb;164(2):407-14].
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