Solar Urticaria

SU is a rare UVR- or visible radiation-induced wealing of exposed skin. The more common primary SU occurs spontaneously, and the very rare secondary form follows photosensitization to drugs or chemicals . Primary SU is slightly more common in women, with onset at any age but mostly between 10 and 50 years. The eruption develops on exposed skin within 5 to 10 minutes and fades within an hour or two. Regularly uncovered sites such as the face and backs of hands are occasionally spared. A tingling sensation and patchy erythema generally precede separate or confluent wealing, the latter sometimes generalized and in severe instances occasionally associated with headache, nausea, bronchospasm, faintness, or systemic collapse. Secondary SU generally follows exposure to substances such as tar, pitch, dyes, drugs such as the discontinued benoxaprofen, or very rarely endogenous porphyrin in the porphyrias. Avoidance of the inducing radiation, the use of appropriate sunscreens, or in particular adequate doses of nonsedating antihistamines helps approximately half of patients. Resistant cases sometimes respond to low-dose narrowband UVB phototherapy, low-dose PUVA or particularly plasmapheresis, or failing that, very rarely to intravenous immunoglobulin or cyclosporine. However, a proportion of SU patients do poorly with all therapy.

Histopathology.

The epidermis appears unremarkable. In the dermis, there is edema as evidenced by mild collagen bundle separation, along with slight, rarely moderate, perivascular and interstitial inflammatory cell infiltration with eosinophils and occasionally also neutrophils and lymphocytes .

Pathogenesis. Any UVR or visible radiation waveband, specific for a given patient, may induce primary SU . Wealing is probably mediated through allergic type I hypersensitivity to cutaneous or circulating, irradiation­induced allergen. Presumed circulating antibodies have also been identified, very likely of the IgE type. In secondary SU, the eruption apparently follows direct nonimmunologic injury after UVR absorption by the responsible chemical or drug and its secondary transfer to adjacent susceptible tissue. Histamine is probably the major chemical mediator in both forms.