**7. Solar urticaria (SU)**

Solar urticaria (SU) is characterized by wheals and sometimes angioedema after visible or ultraviolet (UV) light exposure [44]. Young adults are more commonly affected with a female predominance. The lesions which develop within 10 min of solar exposure are limited to the exposed areas. There are some variants of SU. Monfrecola et al. reported a case of solar urti‐ caria with delayed onset [45]. Torinuki reported two cases with solar urticaria manifesting pruritic erythema but no whealing [46].

It is thought that some unknown photo‐allergens that are produced in the skin after sun expo‐ sure cross‐react with IgE on mast cells, and as a result, histamine and other inflammatory mediators are released. Norris et al. and Esdaile et al. claimed that bruised skin is more prone to the formation of SU. They tried to explain this by the migration of photo‐allergens into the skin through damaged vessels [47, 48].

In a chronic urticaria patient, after history taking, if there is a suspicion of SU, we should per‐ form provocation test. For this purpose, solar simulators can be used. Provocation should be performed on body areas which are usually not exposed to sunlight, such as the buttocks, and UVA, UVB, and visible light should be used separately. In a positive test result which means flare and whealing within 10 min of the exposure, threshold testing should also be done using increasing radiation doses [8].

It is difficult to manage SU. Avoidance of the sunlight exposure is almost impossible. According to the guidelines, H1 antihistamines are the first‐line treatment options. But only one‐third of the patients respond well to the antihistamines. Repeated sunlight exposure can induce tolerance [45]. For this purpose, PUVA and narrow‐band UVB can be used. Güzelbey et al. reported successful treatment of SU with anti‐immunoglobulin E therapy [49]. There are few other studies in the literature showing the efficacy or inefficacy of omalizumab [50, 51].

Hughes et al. and Correia et al. reported that SU can be successfully treated with intravenous immunoglobulin [52, 53]. On the contrary, Llamas‐Velasco et al. claimed that intravenous immunoglobulin was ineffective in the treatment of SU [54]. In 2011, Haylett et al. revealed that systemic photoprotection was possible with alpha‐melanocyte‐stimulating hormone (afamelanotide). Its mechanism of action is to increase melanization of the skin. With this effect, it protects the skin from the penetration of UV and visible wavelengths [55].
