Lucila C Lopes de Oliveira1, Martina Aderhold2, Marianne Brill3, Gabriele Schulz2, Claudia Rolinck-Werninghaus2, E N Clare Mills4, Bodo Niggemann5, Charles Kirov Naspitz6, Ulrich Wahn2, Kirsten Beyer7. 1. Department of Pediatric Pneumology and Immunology, Charité Universitätsmedizin Berlin, Berlin, Germany; Division of Allergy and Clinical Immunology, Department of Pediatrics, Federal University of São Paulo, São Paulo, Brazil. 2. Department of Pediatric Pneumology and Immunology, Charité Universitätsmedizin Berlin, Berlin, Germany. 3. VBC Genomics, Vienna, Austria. 4. Institute of Food Research, Norwich, United Kingdom. 5. Department of Pediatric Pneumology and Immunology, Charité Universitätsmedizin Berlin, Berlin, Germany; Pediatric Allergology and Pneumology, German Red Cross Hospital Westend, Berlin, Germany. 6. Division of Allergy and Clinical Immunology, Department of Pediatrics, Federal University of São Paulo, São Paulo, Brazil. 7. Department of Pediatric Pneumology and Immunology, Charité Universitätsmedizin Berlin, Berlin, Germany. Electronic address: kirsten.beyer@charite.de.
Abstract
BACKGROUND: To avoid unnecessary oral food challenges, which are time consuming, stressful, and risky, improved in vitro diagnostic methods for food allergy such as component resolved diagnostics are still under investigation. OBJECTIVE: To investigate the role of whole peanut- and peanut-component (Ara h 1, Ara h 2, Ara h 3, Ara h 6 and Ara h 8)-specific IgE levels in the diagnostic procedure of peanut allergy as well as the diagnostic properties of peanut-specific IgG and IgG4. METHODS: Sixty-one children underwent oral peanut challenge tests for diagnostic purposes irrespective of their peanut-specific IgE levels. Peanut-specific serum IgE, IgG, and IgG4 levels were determined by ImmunoCAP FEIA and specific IgE against individual peanut proteins by Immuno Solid-phase Allergen Chip. RESULTS: Thirty-four of 61 patients (56%) had a peanut allergy. No significant difference was observed for peanut-specific IgG or peanut-specific IgG4 levels between patients who were allergic and tolerant patients, whereas peanut-specific IgE was significant higher in patients who were allergic than in tolerant patients (P < .005). Twenty-five of 61 children had peanut-specific IgE above a previously proposed cutoff level of 15 kUA/L; however, 7 of these 25 children (28%) were clinically tolerant. Ara h 2-specific IgE was significantly lower in tolerant than in patients with allergies (P < .0001). Interestingly, 94% of the patients with peanut allergies showed IgE-binding to Ara h 2. Unfortunately, 26% of the sensitized but tolerant patients have shown IgE binding to Ara h 2 too. CONCLUSIONS: Neither the level of specific IgE to peanut nor to Ara h 2 was able to clearly distinguish patients with clinical relevant peanut allergy from those who were clinical tolerant in our population. As expected, peanut-specific IgG and IgG4 did not improve the diagnostic procedure.
BACKGROUND: To avoid unnecessary oral food challenges, which are time consuming, stressful, and risky, improved in vitro diagnostic methods for food allergy such as component resolved diagnostics are still under investigation. OBJECTIVE: To investigate the role of whole peanut- and peanut-component (Ara h 1, Ara h 2, Ara h 3, Ara h 6 and Ara h 8)-specific IgE levels in the diagnostic procedure of peanutallergy as well as the diagnostic properties of peanut-specific IgG and IgG4. METHODS: Sixty-one children underwent oral peanut challenge tests for diagnostic purposes irrespective of their peanut-specific IgE levels. Peanut-specific serum IgE, IgG, and IgG4 levels were determined by ImmunoCAP FEIA and specific IgE against individual peanut proteins by Immuno Solid-phase Allergen Chip. RESULTS: Thirty-four of 61 patients (56%) had a peanutallergy. No significant difference was observed for peanut-specific IgG or peanut-specific IgG4 levels between patients who were allergic and tolerant patients, whereas peanut-specific IgE was significant higher in patients who were allergic than in tolerant patients (P < .005). Twenty-five of 61 children had peanut-specific IgE above a previously proposed cutoff level of 15 kUA/L; however, 7 of these 25 children (28%) were clinically tolerant. Ara h 2-specific IgE was significantly lower in tolerant than in patients with allergies (P < .0001). Interestingly, 94% of the patients with peanutallergies showed IgE-binding to Ara h 2. Unfortunately, 26% of the sensitized but tolerant patients have shown IgE binding to Ara h 2 too. CONCLUSIONS: Neither the level of specific IgE to peanut nor to Ara h 2 was able to clearly distinguish patients with clinical relevant peanutallergy from those who were clinical tolerant in our population. As expected, peanut-specific IgG and IgG4 did not improve the diagnostic procedure.
Keywords:
Ara h 1; Ara h 3; Ara h 6; Ara h 8; Ara h 2; Component-resolved diagnostics; IgE; IgG; IgG(4); Immuno Solid-phase Allergen Chip; Peanut allergy
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