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1C. A. Bobb, 2T. Ritz, 3G. Rowlands, 4C. Griffiths. 1Starnet Community Health Sciences St Georges Hospital Medical School, London, UK, 2Southern Methodist University, Department of Psychology, Dallas, USA, 3Institute of Primary Care and Public Health, London South Bank University, London, UK, 4MRC Asthma UK Centre in Allergic Mechanisms of Asthma, Centre for Health Sciences, Barts and the London School of Medicine and Dentistry, London, UK

Background Allergy contributes significantly to asthma exacerbation, yet avoidance of allergic triggers is rarely addressed in detail in regular asthma review in primary care.

Objective To determine whether structured, individually tailored allergen and trigger avoidance advice, given as part of a primary care asthma review, improves lung function and asthma control.

Methods In a randomised controlled trial 214 adults with asthma in six general practices were offered either usual care during a primary care asthma review or usual care with additional allergen and trigger identification (by skin prick testing and structured allergy assessment) and avoidance advice according to a standardised protocol by trained practice nurses. Main outcome measures were lung function, asthma control and asthma self-efficacy.

Results Both intervention groups were equivalent in demographic and asthma-related variables at baseline. At 3-month follow-up, patients receiving the allergen and trigger avoidance review showed significant improvements in lung function (assessed by blinded research nurses) compared with those receiving usual care. Adjusted post-treatment means: forced expiratory volume in 1 s (FEV1) intervention 2.58 litres (2.52–2.63) vs control 2.44 (2.38–2.50) p<0.01; lung age 58.8 years (56.6–60.6) vs 62.0 (59.8–64.3) p<0.05, respectively. No significant differences were found in self-report measures of asthma control. Asthma-specific self-efficacy improved in both groups but did not differ between groups.

Conclusion Allergen and trigger identification and avoidance advice, given as part of a structured asthma review delivered in primary care by nurses results in clinically important improvements in lung function but not self-report of asthma control.

Trial registration number ISRCTN45684820.


K. L. Clearie, P. A. Williamson, S. Vaidyanathan, P. Short, A. Goudie, B. J. Lipworth. Asthma and Allergy Research Group, University of Dundee, Ninewells Hospital and Medical School, Dundee, UK

Introduction and Objectives Elite swimmers have high rates of rhinoconjunctivitis and exercise-induced bronchospasm (EIB). Moreover, exposure to chlorine and chlorine metabolites is known to induce hyper-reactivity. In track and winter sports athletes, prolonged high-volume gas exchange is thought to generate an osmolar bronchial challenge through drying and cooling of the airways. Mannitol challenge is an osmolar challenge and thought to be a reliable surrogate of EIB in athletes. Elite swimmers also generate high levels of gas exchange, but, unlike other athletes, their environment is warm, humidified and chlorinated. We sought to assess the effects of chlorine and exercise on the unified airway of national level elite swimmers.

Methods The Scottish National Youth Squad underwent exhaled tidal (FENO) and nasal (NNO) nitric oxide measurement, peak nasal inspiratory flow (PNIF) and forced expiratory volume in 1 s (FEV1) before, immediately after and 4–6 h postswimming. A standardised sport-specific exercise test was carried out during an intensive lactate set. Swimmers also performed mannitol challenge and a health questionnaire.

Results 61 swimmers were assessed: 8/59 (14%) of swimmers had a positive mannitol challenge; 9/57 (16%) of swimmers had a positive exercise test. Only one swimmer was positive to both. Swimmers with a positive mannitol had a significantly higher baseline FENO than those with a positive exercise challenge. A significant decrease in FENO was observed prechlorine exposure vs immediate-postchlorine and delayed-postchlorine exposure: mean (95% CI) 18.7 ppb (15.9 to 22.0) vs 15.9 ppb (13.3 to 19.1, p<0.01) and 13.9 ppb (11.5–16.7, p<0.01), respectively. There were no significant differences in NNO. Mean (SEM) PNIF increased from 142 (6) l/min at baseline to 163 (6) l/min immediately postexposure (p<0.01). Delayed postexposure PNIF was not significantly different from pre-exposure.

Conclusions No association was found between mannitol and standardised sport-specific exercise challenge in elite swimmers. Mannitol but not excercise was associated with a high baseline FENO. Thus mannitol may identify swimmers with a “traditional” inflammatory asthmatic phenotype, while field-based exercise challenge may identify a swimmer’s specific bronchoconstrictor response to hyperventilation in a chlorine-rich environment. A sustained fall in FENO following chlorine exposure suggests that a non-cellular, perhaps neurogenic, response may be involved in this group of athletes.


B. K. Butland, H. R. Anderson, C. J. Cates. St George’s, University of London, London, UK

Introduction The SMART trial (Chest 2006) reported evidence of an increased risk of asthma-related death in patients treated with regular salmeterol, a long-acting β2-agonist (LABA). This association may be tempered by concomitant prescribing of inhaled corticosteroids (ICS). We examined the relationship between asthma death and recent asthma medication, including effect modification by ICS, age and deprivation.

Methods The asthma death case–control study consisted of 532 asthma deaths (cases) and 532 hospital admissions for asthma (controls), matched for index date (date of death or date of hospital admission), age and hospital (BMJ 2005). For the current analysis (funding: GlaxoSmithKline), a more detailed “blind” extraction of recent medications (within 2 and >2–6 months of the index date) and disease recorded in anonymised primary care records was conducted. Conditional logistic regression analyses were adjusted for sex, age of asthma onset, obesity, chronic obstructive pulmonary disease (COPD), other chronic lung diseases, previous asthma admissions, other asthma drugs and deprivation.

Results There was no evidence of an overall association between asthma death and mention of LABA in the primary care record in the 2 or >2–6 months prior to the index date (fig 1). Among controls with mention of LABA, most (92%) had a concomitant mention (within 1 month) of ICS. For the >2–6 months prior to the index date, a significant interaction was observed between age and LABA, with odds ratios of 0.63 (95% CI 0.34 to 1.15) and 1.35 (0.90 to 2.03) for the <45 and 45–64 year age groups, respectively. Any association between asthma death and short-acting β2-agonists (SABAs) in the previous >2–6 months differed significantly between English, Scottish and Welsh regions. Oral corticosteroids, ICS and antibiotics mentioned in the previous 2 months were each significantly associated with a lower risk of asthma death.

Conclusions In this British case–control study there was no evidence of an overall association between asthma death and the recent mention of LABA in the primary care record. The lower risk of asthma death associated with oral corticosteroids, ICS and antibiotics may reflect appropriate health-seeking behaviour and/or medical treatment. Evidence of possible effect modification merits consideration in the context of other studies.

Abstract S48 Figure 1

Association between asthma medication mentioned in the primary care record prior to the index date* and asthma death (adjusted OR† and 95% CI).



1J. B. Morjaria, 2P. Haldar, 2A. J. Wardlaw, 1I. D. Pavord. 1Department of Respiratory Medicine, Addenbrookes Hospital, Cambridge University Hospitals NHS Trust, Cambridge, UK, 2Institute of Lung Health, Glenfield Hospital, University Hospitals of Leicester NHS Trust, Leicester, UK

Background We have previously shown that sputum evidence of eosinophilic airway inflammation is associated with a good response to corticosteroids in patients with asthma, cough and chronic obstructive pulmonary disease (COPD). A subset of patients with sputum eosinophilia also have a raised sputum neutrophil count. It has been suggested that this inflammatory phenotype may be associated with a poor response to corticosteroids.

Aim To test the hypothesis that patients with a mixed sputum granulocyte phenotype have a reduced response to corticosteroids.

Methods 61 subjects, who met the criteria for ATS refractory asthma, had postbronchodilator forced expiratory volume in 1 s (FEV1) and visual analogue score (VAS) for symptoms of cough, breathlessness and wheeze each on a score of 100 mm scale, before and after 2 weeks of prednisolone (0.5 mg/kg up to a maximum of 40 mg).

Results Twenty subjects with eosinophilia (>3% eosinophils and <61% neutrophils) and 12 subjects with a mixed pattern (>3% eosinophils and >61% neutrophils) were identified. The mean change in postbronchodilator FEV1 and VAS in the sputum eosinophilia group was 0.24 litre (95% CI 0.04 to 0.45; p = 0.038) and −21.4 mm (95% CI –29.4 to −13.4; p<0.001), whilst that in the mixed sputum granulocyte group was 0.01 litre (95% CI −0.12 to 0.14; p = 0.901) and −11.3 mm (95% CI −24.4 to 1.8; p = 0.113). There were no between-group differences in postbronchodilator FEV1 (0.23 litres, 95% CI −0.06 to 0.5; p = 0.113) and VAS (−10.1 mm, 95% CI −24.9 to 4.7; p = 0.174) after correcting for the baseline sputum eosinophil count.

Conclusion Our data suggest that there is not a large difference in response to oral prednisolone in patients with asthma with sputum eosinophilia and mixed granulocytic phenotypes. Larger studies may highlight small, albeit clinically important, differences.