Food, drug, insect sting allergy, and anaphylaxis
Maternal consumption of peanut during pregnancy is associated with peanut sensitization in atopic infants

https://doi.org/10.1016/j.jaci.2010.08.036Get rights and content

Background

Peanut allergy is typically severe, lifelong, and prevalent.

Objective

To identify factors associated with peanut sensitization.

Methods

We evaluated 503 infants 3 to 15 months of age (mean, 9.4 months) with likely milk or egg allergy but no previous diagnosis of peanut allergy. A total of 308 had experienced an immediate allergic reaction to cow's milk and/or egg, and 204 had moderate to severe atopic dermatitis and a positive allergy test to milk and/or egg. A peanut IgE level ≥5 kUA/L was considered likely indicative of peanut allergy.

Results

A total of 140 (27.8%) infants had peanut IgE levels ≥5 kUA/L. Multivariate analysis including clinical, laboratory, and demographic variables showed frequent peanut consumption during pregnancy (odds ratio, 2.9; 95% CI, 1.7-4.9; P < .001), IgE levels to milk (P = .001) and egg (P < .001), male sex (P = .02), and nonwhite race (P = .02) to be the primary factors associated with peanut IgE ≥5 kUA/L. Frequency of peanut consumption during pregnancy and breast-feeding showed a dose-response association with peanut IgE ≥5 kUA/L, but only consumption during pregnancy was a significant predictor. Among 71 infants never breast-fed, frequent consumption of peanut during pregnancy was strongly associated with peanut IgE ≥5 kUA/L (odds ratio, 4.99, 95% CI, 1.69-14.74; P < .004).

Conclusion

In this cohort of infants with likely milk or egg allergy, maternal ingestion of peanut during pregnancy was strongly associated with a high level of peanut sensitization.

Section snippets

Subjects

The cohort includes 512 infants enrolled at 3 to 15 months of age (mean age, 9.4 months; median age, 9 months) at 5 sites: Mount Sinai School of Medicine, New York, NY; Duke University Medical Center, Durham, NC; Johns Hopkins University School of Medicine, Baltimore, Md; National Jewish Health, Denver, Colo; and the Arkansas Children's Hospital, Little Rock, Ark. Enrollment criteria included atopic children at risk to develop peanut allergy as previously described.12 Briefly, enrollment

Relationship of peanut sensitization to clinical, demographic, and dietary characteristics

Of the 512 subjects enrolled, blood samples were obtained in 503 and analyzed further. Overall, 270 of 503 children (53.7%) had a positive SPT to peanut, 305 (60.6%) had detectable (≥0.35 kUA/L) IgE to peanut, and 346 (68.8%) had sensitization detected by at least 1 of the test methods at enrollment. There were 140 (27.8%) children with peanut IgE levels ≥5 kUA/L. The association of key categorical clinical and demographic factors with elevated peanut IgE levels ≥5 kUA/L are shown in Table I

Discussion

We found that maternal ingestion of peanut during pregnancy had a dose-dependent association with peanut sensitization and likely peanut allergy in infants with likely egg or milk allergy. Our result is in accordance with a previous small study.21 In that study, 25 children with IgE to peanut were compared with 18 who had positive tests to milk or egg but not peanut. Ingestion of peanut more than once per week during pregnancy trended toward being a risk for peanut sensitization (OR, 3.97; P =

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    Supported by NIH-NIAID U19AI066738 and U01AI066560. The project was also supported by grant nos. UL1 RR025780 (National Jewish), UL1 RR 029887 (Mount Sinai), UL 1 RR029884 (Arkansas), UL 1 RR024128 (Duke), and UL1 RR 025005 (Johns Hopkins) from the National Center for Research Resources, a component of the National Institutes of Health. Its contents are solely the responsibility of the authors and do not necessarily represent the official view of the National Center for Research Resources or National Institutes of Health.

    Disclosure of potential conflict of interest: S. H. Sicherer is a consultant for the Food Allergy Initiative and an advisor for the Food Allergy & Anaphylaxis Network and receives research support from the NIH-NIAID and the Food Allergy Initiative. D. Stablein receives grant support from the NIH. R. A. Wood receives grant support from the NIH. A. W. Burks is a consultant for ActoGeniX NV, Intelliject, McNeil Nutritionals, Novartis, and Schering-Plough; is a minority stockholder in Allertein and MastCell, Inc; is on the advisory board for Dannon Co Probiotics; is on the expert panel for Nutricia; receives grant support from the National Institutes of Health, the Food Allergy & Anaphylaxis Network, and the Wallace Research Foundation; has provided legal consultation services/expert witness testimony in cases related to food allergy; is on the Medical Board of Directors for the Food Allergy & Anaphylaxis Network; is a Dermatological Allergy Committee member for ACAAI; is a Study Section member for the NIH-HAI; serves on the reviewer board for the Journal of Allergy and Clinical Immunology; and is a member of the FDA. S. M. Jones receives research support from the National Peanut Board, the NIH-NIAID, and Dyax Corp; serves on the Medical Advisory Board for the Food Allergy & Anaphylaxis Network; and is a steering committee member for Sanofi-Aventis. Donald Y. M. Leung is the medical director for the Food Allergy Initiative. H. A. Sampson is a consultant for Allertein, LLC; receives research support from the Food Allergy Initiative and the NIH-NIAID; is a consultant/scientific advisor for the Food Allergy Initiative; and is 45% owner of Herbal Springs, LLC. The rest of the authors have declared that they have no conflict of interest.

    Clinical Trials.gov identifier: NCT00356174

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