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The first half of the meeting was devoted to the early life origins of asthma and opened with an address from Michael Silverman (Paediatric Respiratory Medicine at the Royal Postgraduate Medical School, London, U.K.). There are problems with the proper definition of early asthma in childhood, and the concepts of asthma which have been derived from clinical and epidemiological work on school children and young adults cannot be applied to pre-school children. If one sticks to a definition of asthma as a. chronic inflammatory condition in which heightened bronchial responsiveness is associated with recurrent, reversible airway obstruction, then the syndrome of asthma cannot be shown to exist in this age group. There is no evidence concerning the nature or persistence of an inflammatory process in the airways of wheezy young children. There is also no evidence to support a greater degree of bronchial responsiveness in wheezy infants (or in any wheezy children up to the age of 7 years) compared with their non-wheezy counterparts. Finally, there are few, if any, data on the variability of airway obstruction with time in children with wheezing conditions under 5 years of age.

A total of 104 asthmatic patients with symptoms of asthma and/or a ‘morning dip’ in the peak expiratory flow rate (PEFR) who were receiving multiple therapies, including inhaled or oral steroids, were treated in addition once nightly with controlled-release theophylline in an 8-week double-blind, placebo-controlled crossover study. Theophylline produced an improvement in symptoms of cough, wheeze, sleep disturbance and PEFR in the 73 completing patients compared to run-in and placebo treatment. Theophylline also produced an improvement in the forced expiratory volume in 1 s and forced vital capacity relative to baseline, and in the difference between actual and predicted PEFR values. Nausea was the most frequent side-effect but both patients' and investigators' global impressions of the effect of study medication were in favour of theophylline.

Loratadine is a highly selective, long-acting, H1-receptor antagonist. In a randomized, double-blind, crossover study, we evaluated the effects of loratadine, 10 and 20 mg, and placebo administered once daily for 3 days on the skin-wheal responses to histamine, the airway responses to inhaled histamine and methacholine, and the skin-wheal and airway responses to allergen in 12 subjects with asthma. There was no evidence of a bronchodilator action 3 hours after a third oral dose. In the airways, the geometric mean of the provocative concentration of histamine causing a 20% fall in FEV1 after placebo or loratadine, 10 and 20 mg, was 0.68 mg/ml, 2.71 mg/ml (p, not significant), and 5.96 mg/ml (p less than 0.05), respectively. The concentration ratios (value after active treatment/value after placebo) for loratadine, 10 and 20 mg, were 5.1 (p less than 0.05) and 13.4 (p less than 0.05). Neither dose of loratadine had any significant effect on the methacholine dose-response relationship. In the skin, loratadine also displaced the histamine log-concentration response curves to the right with concentration ratios of 4.7 and 6.7, respectively. Loratadine, 10 and 20 mg, had no protective effect on the early or late-phase bronchoconstrictor responses to inhaled allergen. In the skin, loratadine, 20 mg, significantly inhibited the mean wheal area to allergen. Thus, in the dose regimens studied, although loratadine is a moderately potent and selective H1 antagonist in the skin and airways, it failed to attenuate the early and late airway responses to inhaled allergen.