No abstract

No abstract

RATIONALE: Higher food IgE has been associated with asthma morbidity, but it is not known whether this is (a) independent of highlevel aeroallergen sensitization and (b) related to allergen consumption among sensitized individuals. METHODS: 1170 individuals with asthma from NHANES 2005-6 were included. IgE to cow's milk, peanut, egg, shrimp, and 15 aeroallergens was measured. Allergen consumption was captured by questionnaires. Food sensitization was categorized as non-sensitized (IgE<0.35 kU/L), low (>50.35-2kU/L), moderate (2kU/L-''95% PPVs'') or high (>''95% PPVs''). Aeroallergen sensitization was defined as: (1) any aeroallergen IgE > _0.35, (2) level of aeroallergen-specific IgE [non-sensitized, low (<2kU/L) or high (> _2kU/L)], and (3) number of different aeroallergen sensitizations. Logistic regression models of Emergency Department (ED) visits included food-IgE level, age, sex, race, income, and (a) magnitude of aeroallergen sensitization or (b) interaction of food-IgE level and relevant allergen consumption. RESULTS: Adjusted odds of an ED visit for asthma were higher in those with high food-IgE (OR: 8.4; 95%CI: 2.8-25). Adjusting for any aeroallergen IgE > _0.35 , level of aeroallergen-specific IgE , and number of different aeroallergen sensitizations attenuated but did not eliminate the relationship between food-IgE and ED visits (OR: 6.6 [95% CI 1.2-4.3], 6.5 [2.1-20.4], and 4.4 [1.1-1.7], respectively). There was no increase in asthma ED visits among those with elevated food-IgE who reported consuming that food (p>0.2). CONCLUSIONS: Although high food-specific IgE predicts asthma exacerbation independent of aeroallergen sensitization, allergen consumption does not appear to modify this risk, suggesting that unrecognized food allergy is not the likely cause of this relationship.

No abstract

No abstract