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Cow's milk allergy as a predictor of bronchial hyperresponsiveness and airway inflammation at school age
L P Malmberg1, K M Saarinen, A S Pelkonen
1Department of Allergy, Skin and Allergy Hospital, Helsinki University Central Hospital, Helsinki, Finland. pekka.malmberg@hus.fi
Insights
Children with a history of IgE-positive cow's milk allergy (CMA) show increased airway inflammation and bronchial hyperresponsiveness (BHR) at school age. IgE-negative CMA did not show these associations, but early cow's milk exposure was linked to less BHR.
Area of Science:
- Pediatric Allergy and Immunology
- Respiratory Medicine
- Immunology
Background:
- Cow's milk allergy (CMA) is linked to childhood asthma, but prospective data on airway inflammation and bronchial hyperresponsiveness (BHR) are limited.
- Understanding the long-term respiratory effects of CMA is crucial for early intervention.
Purpose of the Study:
- To investigate cow's milk allergy (CMA) as a risk factor for childhood airway inflammation and bronchial hyperresponsiveness (BHR).
Main Methods:
- Prospective follow-up of 118 children with CMA, with clinical visits at a mean age of 8.6 years.
- Measurements included exhaled nitric oxide (FeNO) and histamine bronchial challenge.
- Comparison with 80 control subjects from the same cohort.
Main Results:
- Children with a history of CMA exhibited higher FeNO levels and increased bronchial responsiveness to histamine compared to controls.
- IgE-positive CMA was significantly associated with increased FeNO and BHR, independent of early wheeze and parental smoking.
- IgE-negative CMA showed no association with FeNO or BHR; early cow's milk exposure correlated with reduced BHR.
Conclusions:
- IgE-positive cow's milk allergy (CMA) is a significant predictor of airway inflammation and bronchial hyperresponsiveness (BHR) in school-aged children.
- IgE-negative CMA does not appear to confer the same respiratory risks.
- Early cow's milk exposure may have a protective effect against BHR.
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 (FE(NO) ) 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 FE(NO) 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 FE(NO) , 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 FE(NO) 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 FE(NO) , 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 FE(NO) and BHR at school age. Very early exposure to CM was associated with less BHR.
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