Detection of Specific IgE by a Microarray-Based assay (MBa)

AB108 Abstracts

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Four Clusters were Identified in Abruptly-Increasing Neonates and Infants with Food Protein-Induced Gastrointestinal Syndrome, A Report of Japanese Patients I. Nomura1, H. Morita1, N. Ito1, T. Fukuie1, N. Ohtsuka2, S. Hosokawa2, M. Watanabe2, A. Terada2, H. Hoshina2, T. Takamasu2, Y. Ohya1, H. Saito1, K. Matsumoto1; 1National Center for Child Health and Development, Tokyo, JAPAN, 2Japanese Research Group for Neonatal, Infantile Allergic Disorders, Tokyo, JAPAN. RATIONALE: Food Protein Induced Gastrointestinal Syndrome (FPIGS) is a general term of Cell-mediated food allergy in infancy. FPIGS especially in neonates is markedly increasing in Japan. Those patients show all sorts of gastrointestinal symptoms and characteristic biological data. METHODS: Incidence was determined by sending questionnaires to the all pediatric and/or obstetric facilities of Tokyo area. Case-series study was done by registration of precise patient’s data from the hospitals of the research group. Total 176 patients’ data was submitted to headquarter. Forty-six patients were performed food challenge test. About these 46 diagnosis-confirmed patients, cluster analysis was done by using 5variables (birth weight, onset day, vomiting, bloody stool, milk-specific IgE antibody). RESULTS: Annual incidence of FPIGS was found to be 0.21%. Four clusters (Cluster 1;4) were generated by cluster analysis and vomiting and bloody stool were found to be the strongest discriminatory variables. Cluster 1 had both vomiting and bloody stool. Cluster 2 had vomiting. Cluster 3 showed none of those. Cluster 4 showed bloody stool. Food challenge test provoked almost same symptom as in the onset of disease. Cluster 3 showed significantly lower birth weight and rather highest eosinophil counts. Each Cluster might be assigned to already-established Cellmediated food allergies (Food-Protein Induced Enterocolitis, Proctocolitis and etc.). But several differences were existed. CONCLUSIONS: Clinical picture of abruptly increasing FPIGS became clear. Th2 type immunologic mechanism might be involved in gastrointestinal inflammation. Comparison of patients by an international research setting is also necessary.

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Eosinophilic Cholangiopathy Presenting With Peripheral Eosinophilia and Hepatic Mass M. Ling, J. Begun, S. Patil, D. L. Hamilos; Massachusetts General Hospital, Boston, MA. RATIONALE: Identifying the cause of peripheral eosinophilia often presents a diagnostic challenge to clinicians. Eosinophilic cholangiopathy, which encompasses eosinophilic cholecystitis and cholangitis, is a rare cause of peripheral eosinophilia characterized by eosinophilic infiltration of the gallbladder and/or hepatobiliary tree without a known trigger. We present an unusual case of a 58-year old female with peripheral eosinophilia, hepatic mass, hyperbilirubinemia, and periportal lymphadenopathy who after an extensive workup was diagnosed with eosinophilic cholangiopathy. METHODS: Ultrasound, CT, and MRI were utilized to image the abdomen. Upper endoscopy with ultrasound and retrograde cholangiopancreatography were performed for visualization and tissue sampling. Percutaneous liver biopsy revealed the diagnosis. RESULTS: The patient presented with a 6-day history of fevers, chills, abdominal pain, decreased appetite, scleral icterus, and nausea. Laboratory studies revealed an absolute eosinophil count of 17,730 in association with an elevation of SGOT, SGPT, alkaline phosphatase, and bilirubin. Peripheral smear revealed numerous eosinophils but was otherwise normal with no blasts. Flow cytometry for T and B cell immunophenotyping was normal. FIP1L1/PDGFRA mutation analysis was negative. Imaging revealed gallbladder wall thickening, ductal dilation, 5x4x2 cm porta hepatis mass, and periportal lymphadenopathy. Ultrasound-guided percutaneous liver biopsy revealed diffuse inflammatory infiltrate composed of eosinophils and plasma cells and no evidence of malignancy. There was gradual spontaneous resolution of her eosinophilia.

J ALLERGY CLIN IMMUNOL FEBRUARY 2011

CONCLUSIONS: Eosinophilic cholangiopathy is an unusual cause of peripheral eosinophilia that may mimic primary sclerosing cholangitis, hypereosinophilic syndrome, and malignancy.

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Eosinophilic Esophagitis and IgE Mediated Allergy in Children: Detection of Specific IgE by a Microarray-Based assay (MBa) G. Cavagni, P. De Angelis, L. E. D’Urbano, K. Pellegrino, F. Rea, C. Riccardi, F. Torroni, R. Luciano, F. De Benedetti, L. Dall’Oglio; I.R.C.C.S. Children’s Hospital ‘‘Bambino Gesu’’, Rome, ITALY. RATIONALE: Atopy is prevalent in eosinophilic esophagitis (EE) but the role of inhalant and food allergens in the etiopathogenesis of EE is unknown. We test serum specific IgE (sIgE) with molecoular method, Microarray ImmunoCAP (ISACÒ), to have a broad view of allergens implicated, in pediatric EE and evaluated the correlation between traditional investigations of atopy on allergenic extracts and atopic features. METHODS: In 30 consecutive patients affected by EE (according Furuta GT et al criteria of 2007), traditional test to measurement sIgE (ImmunoCAP System) and skin prick testing (SPT) were performed. Moreover inhalants, foods and panallergens sensitivities were assessed using a protein MBa on 103 recombinant or highly purified molecules. RESULTS: The prevalence of the sensitization to at least one allergen was 65% with ISAC, and this method shows more positive results than SPT (27%) and sIgE (40%); sIgE to inhalant molecules were most common (57% of the patients: pollens 46%, mite 26%, pets 16%, fungi 13%) and respiratory symptoms were reported in 50% of EE; panallergens were frequently involved (40%: LTP 20%, profilins 16%, PR 10 7%, tropomiosine 3%); sIgE to foods were infrequent (cow’s milk caseine 3%, ovomucoide 3%, fish 3%, kiwi 10%, peanut 3%). CONCLUSIONS: By using a MbA for sIgE detection we found:1) EE children are highly atopic with frequent allergic sensitivities, often associated with respiratory symptoms; 2) inhalants and panallergens are more frequently involved than foods; these data improve our understanding of the pathogenesis of EE related to atopy and open more rational approaches.

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Food Sensitization Is Prevalent in Adults With Eosinophilic Esophagitis S. Gottlieb1, B. Green2, R. Sadurski2, M. Bachinski2, A. Ramage2, W. Gilchrist2; 1Carolina Allergy, Sinus & Asthma, Greenwood, SC, 2Digestive Disease Group, Greenwood, SC. RATIONALE: While EE is often food induced in children by IgE and cellmediated mechanisms, its role in adults is less well defined. We report on the prevalence and patterns of food sensitization in 33 adults with EE. METHODS: 33 adults (male:female, 5:6), 19-76yrs, with EE (20-300 eos/ hpf) were evaluated for food sensitization via prick testing (PST) with commercial extracts and fresh foods, atopy patch tests (APT), and in vitro tests for specific IgE. RESULTS: PSTs were positive in 19/32 (59.3%) pts with commercial extracts (1 pt w/negative histamine control), and 9/15 (60%) pts with fresh foods. Fresh food tests uncovered a new sensitivity in 8 of 9 fresh food (1) pts. APTs reacted in 7/24 (29.2%) pts w/new sensitization found in 7/7. Three of 7 pts had (1) in vitro tests. Milk, grains and seeds were the most common reactors along with foods that cross-react with pollens of the oral allergy syndrome. Six of 24 pts were PST 1/APT 1; 10/24 pts were PST 1/APT–; 1/24 pts was PST–/APT1; 7/24 pts were PST–/APT–. CONCLUSIONS: 68.7% of adults with EE had evidence of food sensitization. Multiple testing modalities are necessary to comprehensively evaluate these patients.