The association of maternal prenatal IgE and eczema in offspring is restricted to non-atopic mothers
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作者:
Hicks, William B.
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Henry Ford Hosp, Dept Internal Med, Div Allergy & Clin Immunol, Detroit, MI 48202 USAHenry Ford Hosp, Dept Internal Med, Div Allergy & Clin Immunol, Detroit, MI 48202 USA
Hicks, William B.
[1
]
Nageotte, Christian G.
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Henry Ford Hosp, Dept Internal Med, Div Allergy & Clin Immunol, Detroit, MI 48202 USAHenry Ford Hosp, Dept Internal Med, Div Allergy & Clin Immunol, Detroit, MI 48202 USA
Nageotte, Christian G.
[1
]
Wegienka, Ganesa
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Henry Ford Hosp, Dept Biostat & Res Epidemiol, Detroit, MI 48202 USAHenry Ford Hosp, Dept Internal Med, Div Allergy & Clin Immunol, Detroit, MI 48202 USA
Wegienka, Ganesa
[2
]
Havstad, Suzanne
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Henry Ford Hosp, Dept Biostat & Res Epidemiol, Detroit, MI 48202 USAHenry Ford Hosp, Dept Internal Med, Div Allergy & Clin Immunol, Detroit, MI 48202 USA
Havstad, Suzanne
[2
]
Johnson, Christine C.
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Henry Ford Hosp, Dept Biostat & Res Epidemiol, Detroit, MI 48202 USAHenry Ford Hosp, Dept Internal Med, Div Allergy & Clin Immunol, Detroit, MI 48202 USA
Johnson, Christine C.
[2
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Ownby, Dennis R.
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Med Coll Georgia, Dept Pediat, Div Allergy & Clin Immunol, Augusta, GA 30912 USAHenry Ford Hosp, Dept Internal Med, Div Allergy & Clin Immunol, Detroit, MI 48202 USA
Ownby, Dennis R.
[3
]
Zoratti, Edward M.
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Henry Ford Hosp, Dept Internal Med, Div Allergy & Clin Immunol, Detroit, MI 48202 USAHenry Ford Hosp, Dept Internal Med, Div Allergy & Clin Immunol, Detroit, MI 48202 USA
Zoratti, Edward M.
[1
]
机构:
[1] Henry Ford Hosp, Dept Internal Med, Div Allergy & Clin Immunol, Detroit, MI 48202 USA
[2] Henry Ford Hosp, Dept Biostat & Res Epidemiol, Detroit, MI 48202 USA
[3] Med Coll Georgia, Dept Pediat, Div Allergy & Clin Immunol, Augusta, GA 30912 USA
The risk of developing eczema is thought to be influenced by both genetic and environmental factors. Prenatal factors including the intrauterine environment may influence risk. We examined the relationship of maternal total IgE obtained during pregnancy to the incidence of atopic dermatitis in their 2-yr-old offspring. Subjects were participants in an unselected Detroit area birth cohort. Serum IgE was measured from 458 mothers in the third trimester of pregnancy along with prenatal family and environmental histories. Children were evaluated at approximately 2 yr of age for current or past eczema by maternal questionnaire and physician examination. Among the 458 children, 20.3% (n = 93) had a doctor confirmed diagnosis of eczema. Prenatal IgE was higher among women whose children developed AD vs. women whose children did not [ Geometric means and 95% confidence intervals 52.7 IU/ml (40.9-68.0) vs. 32.9 IU/ml (28.0-38.7), p = 0.010]. The association was only seen in a subgroup of 181 women without allergic sensitization (specific IgE > 0.35 IU/ml) to a panel of eight common allergens. Of the women without allergic sensitization, the mean serum IgE was 24.1 IU/ml (15.5-37.6) among those whose children had a diagnosis of eczema. The mean serum IgE was 11.2 IU/ml (9.2-13.6) among those whose children did not have a diagnosis of eczema (p-value 0.002). Maternal prenatal IgE level among women who are not sensitized to common allergens is associated with increased risk of eczema in offspring.