Cow's milk allergy as a predictor of bronchial hyperresponsiveness and airway inflammation at school age
Article first published online: 4 JUL 2010
© 2010 Blackwell Publishing Ltd
Clinical & Experimental Allergy
Volume 40, Issue 10, pages 1491–1497, October 2010
How to Cite
Malmberg, L. P., Saarinen, K. M., Pelkonen, A. S., Savilahti, E. and Mäkelä, M. J. (2010), Cow's milk allergy as a predictor of bronchial hyperresponsiveness and airway inflammation at school age. Clinical & Experimental Allergy, 40: 1491–1497. doi: 10.1111/j.1365-2222.2010.03567.x
- Issue published online: 8 SEP 2010
- Article first published online: 4 JUL 2010
- Submitted 11 January 2010; revised 4 May 2010; accepted 28 May 2010.
- airway inflammation;
- bronchial hyperresponsiveness;
- follow-up studies;
- food allergy
Background Cow's milk allergy (CMA) has been found to be associated with an increased incidence of asthma at school age. However, prospective population-based studies of CMA and the development of airway inflammation and bronchial hyperresponsivess (BHR) are lacking.
Objective The aims of this study was to evaluate CMA as a risk factor for BHR and airway inflammation presented later in childhood.
Methods We followed prospectively 118 children with CMA and invited them to a clinical visit at a mean age of 8.6 years including the measurement of exhaled nitric oxide (FENO) and bronchial challenge with histamine. Ninety-four patients and 80 control subjects from the same cohort participated.
Results At school age, children with a history of CMA had higher FENO levels (P=0.0009) and more pronounced responsiveness to histamine (P=0.027) than their controls. Stratified analysis showed a significant difference only in IgE-positive CMA. Multinomial logistic regression analysis showed that IgE-positive CMA [odds ratio (OR) 3.51; 95% confidence intervals (CI) 1.56–7.90; P=0.002] and a history of wheeze during the first year of life (OR 2.81; 95% CI 1.16–6.84; P=0.023) were independent explanatory factors for increased FENO, and IgE-positive CMA (OR 3.37; 95% CI 1.03–10.97; P=0.044) and parental smoking (OR 3.41; 95% CI 1.14–10.22; P=0.028) for increased BHR, whereas for IgE-negative CMA, no associations with FENO or BHR were found. In the CMA group, those exposed to CM very early at the maternity hospital, had less BHR (P=0.002).
Conclusions Compared with their controls, children with a history of IgE-positive CMA show signs of airway inflammation, expressed as higher FENO, and more pronounced bronchial responsiveness to histamine at school age. In contrast to IgE-negative CMA, IgE-positive CMA is a significant predictor of increased FENO and BHR at school age. Very early exposure to CM was associated with less BHR.
Cite this as: L. P. Malmberg, K. M. Saarinen, A. S. Pelkonen, E. Savilahti and M. J. Mäkelä, Clinical & Experimental Allergy, 2010 (40) 1491–1497.