Forty patients with solar urticaria, 16 male and 24 female, were examined personally during the past 25 years. The median age at onset of symptoms was 32 years, ranging from 13 to 76 years. Most commonly (45%) solar urticaria first appeared during the third decade. The mean duration of the disease was 3.6 years at presentation. The action spectrum was found in the visible light range in 24 patients (60%), in the ultraviolet (UV) A range in four, in the UVB in four, from the UVA to UVB in three, from the UVA to visible light in one and in a broad range from UVB to visible light in four patients. An inhibition spectrum was detected in 13 of 19 patients (68%), occurring at longer wavelengths than the action spectrum in 12 of these cases. The augmentation spectrum was found in only four of 14 patients (29%) examined. Twenty-four of 31 patients (77%) developed an urticarial reaction to autologous serum, which had been previously irradiated in vitro at the action spectrum for that patient. In a single patient, solar urticaria was caused by a drug, namely chlorpromazine. In two patients, polymorphic light eruption occurred in association with solar urticaria. No single modality of treatment was satisfactory, but combined use of antihistamines, sunbathing, psoralen UVA photochemotherapy and/or sunscreening agents partially suppressed the symptoms.

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Oral administration of psoralen and whole body exposure to UVA (oral PUVA) has been used for the treatment of 113 patients with severe atopic dermatitis (AD). 8-Methoxypsoralen (8-MOP) was given at a dose of 0.5-0.6 mg/kg two hours prior to UVA (3-8 J/cm2) irradiation. Patients were treated three times a week while hospitalized. Other medications which had been given before PUVA therapy were permitted. At four and eight weeks after PUVA therapy, the severity score of AD had decreased by 51% and 80%, and the cumulative doses of UVA were 51.2 J/cm2 and 115.3 J/cm2, respectively. The amounts and strength of topical cortico-steroids were decreased during PUVA therapy. No adverse effects that required discontinuation of the PUVA therapy were observed. After discharge, maintenance therapy with UVB phototherapy and/or conventional treatment of AD kept the patients in remission in the outpatient clinic. The QOL of patients was greatly improved. Photochemotherapy with oral 8-MOP can be indicated in patients with severe, widespread AD, especially if standard therapy fails. This is the first report of oral PUVA therapy in a large series of Japanese patients with AD.

A patient with psoriasis vulgaris had been successfully treated with PUVA and UVB therapy. During maintenance phototherapy, he suddenly became photosensitive and developed eczematous eruption. Minimal response doses to UVB and UVA were extremely low -1.09 mJ/cm 2 and 0.3 J/cm 2 , respectively. No chemical substances were identified as the responsible photosensitizer. The condition was diagnosed as chronic actinic dermatitis (CAD). PUVA therapy was unsatisfactory C hronic actinic dermatitis (CAD) is a disabling eczematous eruption induced by extremely low doses of ultraviolet (UVB and UVA) and occasionally also visible light radiation. The mechanism underlying the disorder remains unknown. Allergic or photoallergic dermatitis is often associated with CAD, although the relevance is not clearly understood. An auto-immune process may be involved, at least in some cases of CAD. The present patient developed CAD during the treatment of psoriasis vulgaris with PUVA and UVB photo(-chemo)therapy. He became highly sensitive to UVB and UVA radiation. Case reportIn 1994, a 55-year-old Japanese man was referred to our clinic because of psoriasis vulgaris, which affected almost all parts of the body except the face (Fig. 1). PUVA photochemotherapy was carried out three times a week with oral 8-methoxypsoralen (8-MOP) at 30 mg (0.5 mg/ kg), and subsequent exposure to UVA at 5 J/cm 2 . The eruption disappeared almost completely after 21 treatments at a cumulative dose of 105 J/cm 2 . Thereafter, the patient received UVB phototherapy (29 treatments of 300 ∂ 900 mJ/cm 2 /treatment) as a maintenance treatment, and occasionally topical PUVA therapy (22 treatments with 0.3% 8-MOP lotion plus 200 ∂ 800 mJ/cm 2 UVA/ treatment) to recurred lesions at a dermatology practitioner until 1999. In the summer of 1999, the cutaneous changes suddenly expanded and became erythrodermic 157 because it was not possible to administer an adequate dose of UVA. Oral cyclosporine, topical corticosteroid and sunscreen were used with beneficial therapeutic effects on psoriasis and CAD. As far as we know, the development of CAD during phototherapy has not been previously reported. Key words: chronic actinic dermatitis; photo-(chemo)therapy; psoriasisduring the course of phototherapy. The patient was referred again to our clinic.Physical examination in October 1999 showed scaling erythema on almost all parts of the body., Scales were thick and silvery, especially on the scalp. Light-exposed areas including the face, earlobes, neck, V-zone of the upper chest, extensor aspect of forearms and dorsum of hands were more severely affected, revealing infiltrated or lichenified plaques associated with pruritus.A skin biopsy from the lichenified plaque on the dorsum of the hand showed hyperkeratosis, focal parakeratosis, elongated rete ridges, epidermal and papillary dermal infiltration of lymphocytes.Since the distribution of the skin changes suggested a photosensitivity condition, PUVA therapy was attempted only to the left forearm, using 30 mg of oral 8-MOP and 2...

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