Summary Few studies have been made of the prevalence of onychomycosis among ordinary people. We therefore investigated 800 people aged between 6 and 80 years, in different age groups. We found 162 persons in whom onychomycosis was clinically suspected. However, only the 91, in whom the fungal culture was positive for dermatophytic fungi, were included in the final prevalence numbers. We found a prevalence of 13‐0% in men, 4‐3% in women, and 8–4% in the entire population including children. Onychomycosis was not found in any of the 200 people aged less than 20 years. The prevalences found in this study are much higher than those reported in the earlier studies made elsewhere in Europe.

To determine whether topical provocation could be used for the diagnosis of fixed drug eruption (FDE) instead of systemic provocation, we applied the suspected drug at various concentrations (1-10%) in either petrolatum, 94% ethanol or dimethyl sulphoxide (DMSO) as an open test on both clinically normal skin and on previous FDE lesions in 24 patients with established FDE due to phenazone salicylate, a sulphonamide, doxycycline, trimethoprim, chlormezanone, a barbiturate, or carbamazepine. In 18 of the 24 patients, local provocation of FDE was seen at sites or previous eruption but never on clinically normal skin. With some drugs, e.g. phenazone salicylate, positive provocation of FDE was seen with all the vehicles used; with sulphamethoxazole and trimethoprim, a positive result was seen only in DMSO. To study cross-reactions to other phenazone derivatives in patients with an FDE caused by phenazone salicylate, we applied topical phenazone, aminophenazone and propyphenazone to sites of previous FDE lesions in three patients. In all three, a positive reaction was seen with phenazone, but only one patient showed positive results with aminophenazone and propyphenazone. The present study suggests that topical provocation is useful with several drugs causing FDE. Testing should always be performed on sites of previous FDE, and the sensitivity of the open topical testing can be increased in certain cases by using a vehicle which increases penetration of the drug.

To determine whether inhalant allergens could induce eczematous lesions we studied 17 patients with atopic eczema (with or without allergic rhinitis), 13 patients with allergic rhinitis without atopic eczema and 10 healthy control subjects. The allergens, birch pollen (Betula verrucosa) and house dust mite (Dermatophagoides pteronyssinus), were applied in aluminium chambers for 48 h on clinically normal skin. In 17 patients with atopic eczema, six epicutaneous test reactions of the delayed type to birch pollen and three to house dust mite were seen at 48 or 72 h. In 13 patients with allergic rhinitis without eczema there was one delayed reaction to birch pollen and none to house dust mite. No delayed type test reactions to either allergen were seen in the controls. Biopsies of the positive test sites revealed an eczematous reaction with epidermal spongiosis and microvesiculation. Immunostaining of cryostat sections showed dermal cell infiltrates consisting of mainly T lymphocytes (ratio of T4:T8, 2-6:I) and to a lesser degree Langerhans and indeterminate T6+ cells. 50-90% of the cells were Ia+. The numbers of basophils and mast cells did not exceed 10-15%.

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

In this multicentre, double-blind, parallel group study, we evaluated the efficacy and safety of continuous treatment with itraconazole, 200 mg daily for 3 months, in comparison with itraconazole pulse therapy, 400 mg daily 1 week per month for 3 months, in the treatment of toe-nail onychomycosis. The study included 129 patients with distal subungual onychomycosis of the toe-nails, confirmed by microscopy and positive for dermatophyte culture; 65 received continuous treatment and 64 received pulse therapy. Patients were followed up for 9 months after treatment. After 12 months, there were 62 evaluable patients in the continuous group and 59 evaluable patients in the pulse group. The clinical response (i.e. the size of the affected area and the progress of the infection) and mycological cure (i.e. negative results on microscopy and culture) were the main outcome measures. A clinical response was defined as a cure or a marked improvement. Clinical response rates were 69%, in the continuous group, and 81% in the pulse group at month 12; the corresponding mycological cure rates were 66 and 69%. A better improvement in signs and symptoms was noted in the pulse group. Six patients were withdrawn from treatment because of adverse events, not all of which were thought to be drug-related. There were no clinically relevant laboratory abnormalities. We conclude that both regimens are effective, safe and well tolerated. The superiority of one treatment over the other was not established, but the results tended to favour pulse therapy. Equivalence testing confirmed that pulse therapy was at least equivalent to continuous treatment.