J. Gass, M. Johns, N. Burrows
Mar 1, 2007
Clinical and Experimental Dermatology
mas were hardly evident in the skin biopsy, the patient was diagnosed as having CSS because of a history of asthma, eosinophilia, and paraesthesia. She was treated with prednisolone 40 mg daily. After 1 month of treatment, phototesting with visible light was again performed, but no urticarial lesion was provoked, and the serum IgE (76 U ⁄ mL), eosinophilia (1.1 · 10 ⁄ L), and RF (35.3 IU ⁄ L) was reduced. Although this is the first association between CSS and solar urticaria, a swollen swimmer , who developed both CSS and angio-oedema involving the face, neck, and limbs, has been reported, and also a patient with hypereosinophilic syndrome, who presented with solar urticaria. In our case, the weals usually disappeared within 24 h, but occasionally lasted 2 days. The patient definitely had solar urticaria, but the sites where weals occurred were not strictly restricted to sun-exposed areas. In addition, urticarial weals were strongly evoked by injection of the autologous serum preirradiated with visible light. As has been suggested in ordinary solar urticaria, the weal-provoking factor(s) seems to be a light-sensitive substance circulating in the patient’s serum. Solar urticaria should be considered as one of the cutaneous manifestations of conditions in which eosinophils are disordered, such as CSS.