Cord blood-IgE as risk factor and predictor for atopic diseases
- PMID: 9677130
- DOI: 10.1046/j.1365-2222.1998.00241.x
Cord blood-IgE as risk factor and predictor for atopic diseases
Abstract
Background: Cord blood-IgE as risk factor or predictor for atopic diseases in infants has been discussed in a large number of papers with contradictory results. Our aim was to evaluate cord blood-IgE as risk factor and predictor for atopic dermatitis, recurrent wheezing and sensitization with emphasis on a clear-cut distinction between risk factor and predictor.
Methods: A cohort of 1314 newborns was recruited in six German obstetric departments and followed-up for 5 years. Four hundred and ninety-nine infants (38%) were considered to be at high risk with at least two atopic family members and/or a cord blood-IgE value above the threshold of 0.9 kU/L. At follow-up visits, parents filled in a questionnaire, the infants were clinically examined, and blood samples were taken.
Results: With regard to early onset atopic dermatitis up to 12 months we found that the odds ratios at the cord blood-IgE cut-off points of 0.70 kU/L and 1.25 kU/L with values of 0.53 and 0.32, respectively, were smaller than one (i.e. protective factors) and highly statistically significant. No significant association was found between elevated cord blood-IgE and recurrent wheezing. There was a strong positive association between elevated cord blood-IgE levels and sensitization at 12 months, but even in this case the predictive performance was rather poor: a maximum positive predictive value of 42% was attained with a cut-off point of 3.0 kU/L, but the sensitivity was only 10%.
Conclusion: We conclude that even when elevated cord blood-IgE levels are identified as a strong risk factor for sensitization, their poor predictive performance may make them useless as a basis for preventive measures.
Comment in
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Intrauterine environment and fetal allergic sensitization.Clin Exp Allergy. 1998 Jun;28(6):655-9. doi: 10.1046/j.1365-2222.1998.00321.x. Clin Exp Allergy. 1998. PMID: 9677126 No abstract available.
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