Allergy must also be a factor

BMJ 1995; 311 doi: https://doi.org/10.1136/bmj.311.7005.629d (Published 02 September 1995) Cite this as: BMJ 1995;311:629
  1. Thomas A E Platts-Mills,
  2. Gary P Rakes,
  3. Peter W Heymann
  1. Head, division of allergy and clinical immunology Assistant professor of paediatrics Associate professor of paediatrics University of Virginia Health Sciences Center, Department of Medicine, Charlottesville, VA 22908, USA

    EDITOR,--Sebastian L Johnston and colleagues from Southampton report impressive data supporting an association between viral infections (predominantly rhinoviruses) and exacerbations of asthma among children of school age.1 The association they observed was so strong that it is not surprising that they imply that there could be a causal relation between viral infection and exacerbations of asthma. They recognise that the argument that rhinoviruses could cause exacerbations of asthma is not new. They do not, however, mention that there have been multiple unsuccessful attempts in the past to show experimentally that these viruses can induce attacks of asthma (D A Tyrrel, W Busse, C Reed, J Gwaltney; separate personal communications). Indeed, the only model in which rhinovirus has been consistently shown to produce features of asthma in the lung is one combining viral infection with allergen challenge.2 3

    Johnston and colleagues do not state which of the children were allergic at the time of the study. Studies at Poole General Hospital (64 km from Southampton), however, showed that being allergic to dust mites was the strongest risk factor for developing asthma4 and for being admitted to hospital.5 Indeed, it has been reported that atopy in the cohort studied was associated with “lower FEV 1 [forced expiratory volume in one second], greater within day and between day variation in PEF [peak expiratory flow] and greater severity of respiratory symptoms.”6

    For at least two reasons it seems inevitable that allergy to common inhalant allergens and rhinovirus infection are cofactors for attacks of asthma in childhood--because of the results of the experimental studies and because these two risk factors are too common to be distinct. In our study of children presenting to the University of Virginia's paediatric emergency room with acute episodes of wheezing we found that the combination of rhinovirus culture and IgE antibody to common allergens was the strongest risk factor of wheezing.7 More recently, we have confirmed this association by using the polymerase chain reaction to detect rhinovirus.8 Thus, although the reported association between exacerbations of asthma and viral infections is striking, the group from Southampton should recognise that the children almost certainly have to be primed to respond in this way. The commonest well recognised cause of priming is exposure to a foreign protein to which the children have made an immediate hypersensitivity response, and this is the only model for which there is convincing experimental evidence.


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