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Authors’ reply
  1. J Henderson,
  2. R Granell,
  3. J Sterne
  1. Avon Longitudinal Study of Parents and Children (ALSPAC), University of Bristol, Bristol, UK
  1. Dr J Henderson, ALSPAC, University of Bristol, Bristol BS8 2BN, UK; a.j.henderson{at}bris.ac.uk

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We thank Dr Ventura and colleagues for their interest in our paper and for drawing attention to the phenomenon of non-atopic persistent asthma (NAPA). We agree that non-atopic airway inflammation is a potential mechanism for modification of early life influences on airway development. In our paper we highlighted the strong positive association of persistent wheeze with atopy1 but, as shown in table 2, the prevalence of atopy in this group was 42%. As persistent wheeze comprised 7% of the total population, non-atopic persistent wheeze would be expected to occur in around 4% of this unselected population-based sample. This contrasts with the prevalence of NAPA of 1% reported by Ventura and colleagues from their specialist clinic population in Italy and raises important questions about comparing results from different population samples. It is not clear from their letter how Ventura and colleagues defined persistent asthma but, without frequent early life measures, it would be difficult to disentangle intermediate onset (62% atopic) from persistent wheeze in our model. As both these phenotypes were very strongly associated with persistent wheezing and with physician-diagnosed asthma in later childhood, such misclassification could alter the inferences of their respective associations with objective markers of atopy and airway function. Ventura et al make some interesting observations about the early life course of NAPA which are highly relevant to our attempts to disentangle the course of early childhood wheezing trajectories. Clearly, there are more complexities to emerge from approaches to defining the various sub-phenotypes of asthma, and detection of rare phenotypes—even in relatively large population samples—remains a challenge. The trade-off between population size and the intensity of detailed phenotyping with relevant biomarkers that is feasible in very large epidemiological surveys exemplifies some of these difficulties, although the application of non-invasive markers of inflammation in this setting shows some promise.2 There is a need to understand the variation of phenotypes within asthma and how these relate to clinical and pathological end points. A greater understanding of genetic determinants of components of the asthma phenotype,3 harmonisation of outcomes between studies and exploration of environmental interactions with genetic variants will hopefully reveal modifiable targets for disease treatment and prevention.

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  • Competing interests: None.

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  • Letters
    G Longo E Panontin G Ventura
  • Correction
    BMJ Publishing Group Ltd and British Thoracic Society