title: Cord blood IgE: its determinants and prediction of development of asthma and other allergic disorders at 12 months.
abstract: BACKGROUND
  The value of cord blood IgE in predicting the development of asthma and other IgE-mediated allergic diseases is unclear.
  
  
  OBJECTIVE
  The purpose of this study is twofold: (1) to determine factors affecting cord blood IgE level and (2) to determine whether cord blood IgE predicts the development of asthma and other IgE-mediated allergic diseases in high risk (defined as those with at least one first degree relative with asthma or 2 first degree relatives with other IgE-mediated allergic diseases) infants at 12 months.
  
  
  METHODS
  The study utilized cord blood obtained from a group of high risk infants who took part in a randomized controlled trial to assess the effectiveness of an intervention program in the primary prevention of asthma and other IgE-mediated allergic diseases. Total IgE and cotinine in the cord blood were measured. Assessment of the infants was done at 12 months for these diseases.
  
  
  RESULTS
  Sixty-four (17.8%) infants had detectable total IgE in cord blood >0.5 kU/L. The proportion of infants with elevated cord blood IgE was significantly higher among nonwhites, birth during winter months, and those with a maternal history of asthma. There was no correlation between cord blood IgE and cord blood cotinine level. Cord blood IgE was found to be a significant predictor for the development of urticaria due to food allergy but not for other outcomes.
  
  
  CONCLUSIONS
  Both genetic and environmental risk factors play a role in determining the level of IgE in cord blood. Cord blood IgE was a significant risk factor for the development of urticaria due to food allergy at 12 months of life. As urticaria due to food allergy is a prodrome for anaphylaxis, measurement of IgE in cord blood may be indicated in infants at high risk for developing allergic diseases so that preventive measures can be applied.
authors.affiliation: University of British Columbia, Vancouver, Canada.
authors.forename: A
authors.initials: A
authors.lastname: Kaan
authors.forename: H
authors.initials: H
authors.lastname: Dimich-Ward
authors.forename: J
authors.initials: J
authors.lastname: Manfreda
authors.forename: A
authors.initials: A
authors.lastname: Becker
authors.forename: W
authors.initials: W
authors.lastname: Watson
authors.forename: A
authors.initials: A
authors.lastname: Ferguson
authors.forename: H
authors.initials: H
authors.lastname: Chan
authors.forename: M
authors.initials: M
authors.lastname: Chan-Yeung
mesh_terms: D000328:Adult; D001249:Asthma / Q000209:etiology*; D001724:Birth Weight; D005260:Female; D005312:Fetal Blood / Q000276:immunology*; D006801:Humans; D006967:Hypersensitivity / Q000209:etiology*; D007073:Immunoglobulin E / Q000097:blood*; D007223:Infant; D007231:Infant, Newborn; D008297:Male; D012044:Regression Analysis; D012621:Seasons; D012907:Smoking / Q000009:adverse effects
chemical_list: D007073:Immunoglobulin E