Bronchial responsiveness (histamine PC2o) and peripheral blood eosinophil counts were measured in 23 asthmatic subjects, of whom 14 were atopic and nine non-atopic. In the group as a whole there was an inverse correlation between baseline eosinophil count and histamine PC20 (r = -0O71; p < 0001). For atopic subjects a relationship between eosinophil count and histamine PC 20 was observed (r = -0 74; p < 0 01), but there was no correlation between eosinophil count and baseline FEV1 or baseline FEV1 and histamine PC20. For the non-atopic subjects a similar relationship between eosinophil count and histamine PC20 was seen (r = -0-68; p < 0-05) and a less significant inverse correlation between baseline eosinophil count and baseline FEV, (r = 0-65; p < 0-05). These results show a relationship between eosinophil count and non-specific bronchial responsiveness in both atopic and non-atopic asthma.Eosinophilia in association with reversible airways obstruction has been recognised since the early 1900s but the precise role of the eosinophil has not been fully established. It appears to have the potential for a dual role, on the one hand releasing enzymes capable of degrading mast cell mediators and modulating their effects' but on the other contributing to tissue damage by deposition of major basic protein in the bronchi.2 In patients with stable asthma the peripheral blood eosinophil count shows wide variation3 and eosinophilia does not differentiate atopic from non-atopic asthma. In non-atopic asthma a relationship between the peripheral blood eosinophil count and the FEV1 has been observed and the eosinophil count shown to be useful in monitoring disease activity.4 In addition, a relationship between eosinophil count and methacholine PC20 has been observed in subjects with allergen induced late phase asthmatic reactions.5We have investigated the relationship between the peripheral blood eosinophil count and bronchial responsiveness determined by histamine challenge in subjects with atopic and non-atopic asthma.

The procedure produced a rise in effective static compliance from a mean of 17 (SD 6) ml/cm H20 to 24 (9) ml/cm H20 at four hours. Bronchial lavage was associated with a significant excess of respiratory infections. A feature common to most patients was undertreatment before admission to hospital.Although the hospital mortality from acute severe asthma is less than 1% 1 mechanical ventilation (intermittent positive pressure ventilation: IPPV) is life saving in a few patients. We have reviewed the efficacy and safety of IPPV and therapeutic bronchial lavage in the management of acute severe asthma in a district general hospital. Furthermore, we have analysed the pattern of asthma before IPPV in an attempt to identify preventable factors.

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Venous whole-blood eosinophil counts were performed on 50 occasions in 42 patients with varying patterns of asthma. None of the patients studied had received systemic corticosteroids during the previous year.

Sixty patients with acute severe asthma were treated by conventional methods in all respects except for the use of steroids. Patients who were not currently taking systemic steroids (30) received none during the severe attack, and those who were currently taking systemic steroids (30) were given 400 mg hydrocortisone daily. The results were compared to a further group of 30 patients with acute severe asthma of similar severity who were treated in the same hospital by the same methods but with much larger doses of hydrocortisone (1200 mg daily). All 60 patients recovered and the time course, changes in heart rate and peak expiratory flow (PEFR) were similar in all groups. These results suggest that steroids are of doubtful value in the treatment of acute severe asthma and further randomized and controlled trials are required.