The drugs responsible for eighty-six cases of fixed drug eruption have been identified, and in all but two were confirmed by challenge. The series included sixteen cases of generalized buUous fixed eruption, which resembles Lyell's syndrome. The main causative drugs were phenazones and barbiturates, both in the series as a whole and in the group of the most severe cases. The same drugs were the most frequent causative agents in a report from Finland 10 years ago.A fixed drug eruption is characterized by one or more erythematous plaques or blisters. The lesions recur in the same places after challenge. After frequent challenges additional macular or blistering lesions may arise and in this way a severe, generalized bullous type of fixed eruption can be induced. The responsible agents vary from country to country, and from time to time, depending on local usage.We have studied the causes of fixed drug eruptions retrospectively in hospital patients' records from the past decade, paying particular attention to the generalized bullous type and to the challenge tests performed. METHODSThe study was based on 92 patients with fixed eruptions treated in the Department of Dermatology, University Central Hospital, Helsinki, from 1971 to 1980. There were 76 cases of localized and 16 of generalized bullous type. The agent responsible for the reaction was traced in -86 cases and confirmed with a positive challenge test in all but two.An oral challenge test was performed as described by Kauppinen (1983). The test dose was determined individually for each patient, paying attention to the severity of the initial reaction, the nature of the drug suspected and the interval from the reaction to the challenge. The onset of the reaction and the rise of temperature were followed for 24 h. If the result was negative, a

A case of localized heat urticaria is reported in a 51-year-old woman who within a few minutes of contact with warm water developed erythema and swelling sharply localized to the heated area. After a hot bath urticarial lesions appeared over large areas of her body, accompanied by a feeling of weakness, but no other systemic symptoms. After challenge with heat by immersing her left arm in water heated to 42 degrees C, a rapid decrease of her serum complement level of factor B was demonstrated, suggesting that activation of an alternative complement pathway plays a role in this form of urticaria. Biopsies for immunofluorescent study of complement and immunoglobulins were negative at 30 and 180 min after heat challenge. The dermal fibres and endothelial cells of dermal vessels were capable, in vitro, of complement binding before and after exposure to heat.

A retrospective study supplemented with follow-up was carried out in 163 children, aged 6 months to 16 years, who were hospitalized because of acute, recurrent or chronic urticaria in 1976-1980. Etiologic agents were identified in 55% of cases. Physical factors were the commonest causes, especially in cases of chronic urticaria, while infections predominated in acute urticaria. 81% of the children participated in the follow-up study. Follow-up for a year or more revealed that 53% of the children had become symptom-free, 36% still had symptoms but less frequently and in 11% urticaria was unresolved. The results indicate that the etiologic factors in childhood urticaria are similar to those found in adults and that prognosis is favorable, particularly when the etiology is established.

Celery and parsley were confirmed as etiological agents in 14 patients with severe attacks of angio-edema and urticaria. All of the patients proved to be atopic. Without exception they all had positive prick test reactions to mugwort. The patients were examined using the scratch - chamber test method and all of them showed positive reactions to celery and 12 patients to parsley. No peroral provocation tests were performed because of the severity of the reactions in the past. Passive transfer by the prausnitz-Küster technique was positive in two patients.

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