Clinical Characteristics of Patients with Peanut Allergy

Clinical Characteristics of Patients with Peanut Allergy

137 Clinical Characteristics of Patients with Peanut Allergy T. D. Green1, G. S. Labelle1, P. H. Steele1, L. A. Lee1, V. S. Mankad1, L. W. Williams1...

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Clinical Characteristics of Patients with Peanut Allergy

T. D. Green1, G. S. Labelle1, P. H. Steele1, L. A. Lee1, V. S. Mankad1, L. W. Williams1, K. J. Anstrom2, A. W. Burks1; 1Pediatric Allergy and Immunology, Duke University Medical Center, Durham, NC, 2Duke Clinical Research Institute, Duke University Medical Center, Durham, NC. RATIONALE: Studies of pediatric patients with peanut allergy suggest that the age of onset is decreasing. Our objective was to look for recent changes and evaluate clinical characteristics among a group of referred patients. METHODS: We reviewed characteristics of patients diagnosed with peanut allergy and evaluated in the Duke Pediatric Allergy and Immunology clinic over the past 5 years. RESULTS: Of 50 patients, 60% were male and 40% were female. Median ages of first known exposures and reactions were 22.5 months (range 1-51) and 24 months (1-79), respectively. Median ages of first reactions were 32.5 months for girls, and 23.5 months for boys. Thirty percent of patients were diagnosed based on suggestive laboratory evaluation (CAPFEIA, skin prick test), without a history of peanut ingestion. Egg allergy was the most common additional food allergy, present in 52%; tree nut allergy was present in 10%. Thirty-eight percent were born in October, November, or December, while 18% were born in April, May, or June. CONCLUSIONS: Median ages of first known exposures and reactions in this population of referred patients are similar to those in a referred group studied ten years ago. A significant percentage of referred patients will be diagnosed based on laboratory evaluation alone. Egg allergy appears to be more common than tree nut allergy in these patients. Consistent with other studies, boys seem to react at younger ages, and patients with peanut allergy may be more likely to be born during the months of October through November than April through June. Funding: Duke University Medical Center Early Exposures to Peanut and Sensitization at a Children’s Hospital Clinic A. P. Stallings, A. D. Hogan; Pediatrics, Children’s Hospital of the King’s Daughters, Eastern Virginia Medical School, Norfolk, VA. RATIONALE: Identify risk factors in peanut-allergic children that would explain the increasing prevalence of peanut allergy. METHODS: One hundred eleven children were enrolled between March and August 2005 with a history of peanut allergy and either a positive prick skin test (PST) or a serum peanut-specific IgE (PN-IgE). RESULTS: Of those enrolled, 48 % were female, 54% were Caucasian, and 83% had atopic dermatitis. The mean age was 4.5 years (0.6-17 years). Allergies were reported in the immediate family in 82%. During pregnancy, 79 % of mothers ate peanuts. Seventy percent breastfed, and of these, 97% ate peanut products. The mean breastfeeding duration was 6.7 mo (2wks-2.5 years). Fifty nine percent remembered when peanut butter was introduced. The average age was 15.8 months (2-60 months), but 58% (n=38) got peanut butter under 12 months, and 76% (n=50) under two years. The median age of the first non-eczema reaction (n= 60) was 12 months (2-182 months). 1.8% had peanut sensitization without clinical symptoms. PST results were mean + 3.4 (scale 0-4, n=76, median 4). Three patients had negative skin tests. The median PN-IgE was 10.5 kUa/L (mean 29 kUa/L, n=108, <0.35 to >100) with 10 < 0.35kUa/L. CONCLUSIONS: The AAP guidelines for high-risk infants, postponing introduction of peanut products during breast-feeding and first three years of life were not followed in our population and may be associated with early peanut sensitization.

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Development of an ELISA for Digestion-Resistant Ara h 2 Peptide: Monitoring the Peptide in Body Fluids of Healthy Volunteers Who Consumed Peanut J. L. Baumert1, K. A. Peeters2, A. C. Knulst2, S. J. Koppelman2, S. J. Maleki3, E. Knol2, S. L. Hefle1; 1Food Allergy Research & Resource

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Program, University of Nebraska, Lincoln, NE, 2Department of Dermatology/Allergology, University Medical Center, Utrecht, THE NETHERLANDS, 3Agricultural Research Service, Southern Regional Research Center, U.S. Department of Agriculture, New Orleans, LA. RATIONALE: Studies have examined the levels of peanut protein in some body fluids using commercially available ELISA kits, but the antibodies in these kits are directed against intact peanut proteins. Since peanut allergens are affected by digestion, results from these kits may vastly underestimate the amount of allergenic peanut protein transported across the gut epithelium. Ara h 2 has been shown to be the most important peanut allergen. Antibodies directed against the digestion-resistant portion of Ara h 2 may allow more sensitive detection of allergenic peanut proteins transported into blood, breast milk, and saliva. METHODS: Ara h 2 was isolated from defatted peanut, digested with trypsin for 90 minutes, then purified to obtain the 10-kD digestion-resistant peptide (DRP-Ara h 2). The DRP-Ara h 2 was used to immunize rabbits and obtain antibodies. An ELISA was constructed to detect DRP-Ara h 2 in body fluid samples (blood and saliva) of non-allergic human volunteers who had consumed peanut. RESULTS: The ELISA indicated the presence of peanut proteins in breast milk and saliva, however, detectable levels of Ara h 2 were not found blood serum. CONCLUSIONS: The use of ELISA detection assays using antibodies directed against digestion-resistant portions of peanut allergens allow for more sensitive detection of transported allergenic fractions across the gut epithelium. This information may shed light on the quantity of allergen entering blood circulation which could lead to sensitization of the individual or an infant via breast milk or saliva. Funding: University of Nebraska-Lincoln Risk of Peanut Allergy Associated with High Household Exposure to Peanut in Infancy A. T. Fox1, G. L. du Toit1, H. Syed2, P. Sasieni2, G. Lack1; 1Paediatric Allergy, Imperial College, London, London, UNITED KINGDOM, 2Cancer Research UK Centre of Epidemiology, Mathematics and Statistics, Wolfson Institute of Preventive Medicine, London, UNITED KINGDOM. RATIONALE: Over 90% of peanut allergic children react on their first known oral exposure. The route by which sensitisation has occurred is unclear. Recent data suggest low-dose cutaneous exposure as a likely route of sensitization. METHODS: Retrospective dietary questionnaire in cohort of children with suspected allergy and age-matched controls investigating the role of infants’ environmental peanut exposure on later allergy. Questionnaires were completed before subjects were aware of allergic status, avoiding recall bias. Questionnaires asked about maternal peanut consumption during pregnancy, breast-feeding and the remainder of the child’s first year of life. Similarly, information was obtained about peanut consumption amongst all other household members, enabling quantification of overall exposure to peanut in the child’s household. Exposure was compared in 3 groups of age-matched children: children with peanut allergy, children with egg allergy (but not peanut sensitised) and non-allergic children. RESULTS: median weekly household peanut consumption in the peanut allergic cases (n=126) was 77.2g as compared with 29.1g in the normal controls (n=150) and only 8.1g in the egg allergic controls (n=160). Pair-wise comparisons between the three groups each gave significant differences with a p-value <0.0001. Differences in maternal peanut consumption during pregnancy and lactation are less significant and become non-significant after adjusting for other dietary factors. CONCLUSIONS: data suggest that exposure to environmental peanut during infancy promotes sensitisation and that low levels may be protective in atopic children. No special effect of maternal consumption during pregnancy or lactation is observed. This supports the hypothesis that peanut sensitization occurs as a result of environmental exposure. Funding: Food Standards Agency

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Abstracts S35

J ALLERGY CLIN IMMUNOL VOLUME 117, NUMBER 2