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Predicting risk of asthma in wheezing infants
  1. A Raza,
  2. R J Kurukulaaratchy,
  3. S H Arshad
  1. The David Hide Asthma and Allergy Research Centre, St Mary's Hospital, Newport, Isle of Wight, UK
  1. Dr S H Arshad, IIR Research Division, MP: 810, Level F, South Academic Block, Southampton General Hospital, Tremona Road, Southampton SO16 6YD, UK; sha{at}soton.ac.uk

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Devulapalli et al’s paper1 attempts to answer the commonly encountered clinical question, “what is the risk of asthma in this wheezy infant?” While welcoming this attempt, we wish to put this into perspective and draw comparison with our similar work on the Isle of Wight Birth Cohort published 5 years ago.2

Findings that children with asthma at 10 years often had recurrent bronchial obstruction (RBO+ve) at 2 years are not new. We previously reported that recurrent chest infections at 2 years (causing airway obstruction and wheeze) increases the risk of asthma development at 10 years by more than fourfold.3 A simple risk score such as that of Devulapalli et al, not reliant on invasive testing, is an attractive concept. However, there are significant shortcomings in this work. For wide acceptability, the factors contributing to the risk scores should be unambiguous. The proposed risk score relies on “severity”, which is difficult to define and measure in this context. Hospitalisations for wheezing in infancy do not necessarily reflect a set degree of severity. Secondly, the outcome variable of diagnosed asthma is potentially contentious given the subjective nature of that label. The reasons for not including an objective measure such as bronchial hyperresponsiveness to consolidate asthma diagnosis is not clear. Alternatively, a phenotypic analysis using “wheeze” rather than “asthma” may be less prone to subjective bias. We have demonstrated4 that most childhood asthma originated in infancy as “early onset persistent wheeze”. We feel that a phenotypic understanding is vital in asthma where analysis of isolated events in time could convey a misleading snapshot of a complex disease. Finally, any case control study is prone to misclassification based on response evaluation and investigator bias. Reliance on such methodology to create a risk score could draw into question the potential validity of that tool.

The authors fail to compare their “risk score” with our published risk scores to show that theirs is indeed an improvement on what has already been known. We proposed a simple and practical risk scoring system for outcome of early life wheeze2 comprising four factors (family history of asthma, recurrent chest infections at 2 years, absence of nasal symptoms in infancy and atopic sensitisation at 4 years), showing independent significance for persistence of early wheeze to age 10 years in our cohort. The presence of all four was associated with a positive predictive value of 83.3 and a negative predictive value of 63.9 for persistent disease, compared with corresponding values of 54.3 and 86.8 with the score outlined by Devulapalli and colleagues.1

The ability to accurately predict outcome of early life wheeze is clearly desirable. However, any new proposal should be considered in the context of existing work. Comparisons should be made in terms of sensitivity and specificity, and common ground should be sought to eventually develop a predictive scoring system, which is practical, valid and clinically useful. We are certainly not there, yet!

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  • Competing interests: None.

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