Nosing out the future asthmatic?

``Is it asthma, doctor? '' must be among the commonest questions asked by anxious parents of a wheezy child, and the paediatrician dealing with this problem must sigh for a simple answer to a super®cially simple question. According to the simple (and excellent) de®nition of the Paediatric Consensus Group (1), asthma is ``wheeze and/or cough in a setting where asthma is likely, and other, rarer, conditions have been excluded''. Therefore, if the child truly is wheezing (and this may be dif®cult to determine even in English, but much more so in languages with no word for ``wheeze'' [2]), then, by de®nition, the child has asthma ± of a sort. However, it is abundantly clear that the word ``asthma'' covers a number of phenotypes (Crimi et al. [3], Table 1), and that re®ning my opening question would lead to the supplementary question, ``Does my child have the sort of asthma that means his airways are in ̄amed, and that if he is not treated aggressively, his airways will undergo structural remodelling and later develop ®xed air ̄ow obstruction? '' The dif®culty is that we simply do not know how to answer that question. At one end of the spectrum of the wheezing phenotypes (4) are the virus-associated wheezers; they have neither a personal nor a signi®cant family history of atopic disease, and wheeze only with viral colds. There is compelling evidence that the basis of their symptoms lies in prenatal events affecting baseline airway calibre. This evidence includes the detection of airway obstruction soon after birth in infants of mothers who smoked in pregnancy, or were atopic, or, interestingly but inexplicably, had hypertension of pregnancy (5±7); the detection of air ̄ow obstruction prior to the ®rst wheezy episode (8±10); the absence of an association between bronchial hyperreactivity and wheeze (11, 12); the poor response of viral associated symptoms to inhaled corticosteroids (13); the lack of airway eosinophilia on blind lavage studies (14); and the excellent prognosis for long-term lung function, whatever treatment is given (15). At the other extreme is the infant who has atopic dermatitis and perhaps multiple food allergies, with wheezing with viral colds, but also wheezing triggered by dust, furry pets, and other triggers. Even in this group, half will remit by the early school years (16). The vast majority of wheezers fall neatly between these extremes, and this makes advising parents and planning treatment sensibly very dif®cult. De®ning the wheezing phenotype is of great practical therapeutic importance. Up to 50% of children wheeze before the age of 6 years. Evidence from a randomized controlled trial in adults (17) and observational data in children (18) suggest that delay in initiating inhaled corticosteroids may prejudice ultimate lung function. On the other hand, overtreatment with even low-dose inhaled steroids may cause growth failure (19), and, according to animal studies, possible reduction in alveolarization in the developing lung (20). The obvious way to resolve these dif®culties is to ®nd a way of measuring airway in ̄ammation in these small infants. Studies using serum levels of markers such as eosinophil cationic protein have either been unpromising or lacked follow-up for a suf®cient length of time to allow a balanced judgement of their importance (21, 22). Unfortunately, sputum induction is not feasible in Allergy 2000: 55: 685±687 Printed in UK. All rights reserved Copyright # Munksgaard 2000