Abstracts AB259
J ALLERGY CLIN IMMUNOL VOLUME 135, NUMBER 2
Successful Specific Oral Tolerance Induction with Hake in an Allergic Child Detecting Fish in Cooking Steam Carmen M. Damelio, MD; Departament of Allergy Clinica Universidad de Navarra, PAMPLONA, Spain. RATIONALE: To describe a specific oral tolerance induction (SOTI) protocol with hake in a child suffering urticaria/angioedema upon fish cooking steam exposure. METHODS: A 6-year old girl who presented at 9 month of age acute urticaria after eating different types of fish (i.e. hake, sole). Skin prick test rendered positive results and since then she avoided fish. Subsequently she suffered several acute urticaria episodes after accidental intakes and even when exposed to tuna fish cooking steam. Comorbidities: mild and controlled atopic dermatitis, no bronchial asthma. A SOTI protocol was decided to apply. Sensitization was evaluated by Prick-to-prick (T1), specific IgE (sIgE) and IgG4 (sIgG4) to hake during the induction phase (T2) and when finalized (T3). SOTI to hake was performed using frozen hake loin, starting with lyophilized hake and when 20gr. were tolerated, we used cooked hake until reaching 40gr. RESULTS: The induction phase of the SOTI lasted 11 months until 40gr of hake were reached suffering one anaphylaxis, related to an infectious process and 5 episodes of abdominal pain requiring antihistamines in only 2 of them. After one month in maintenance-phase, eating 40gr of hake daily without reactions, she tolerated 50gr of bass, 50gr. of tuna, 50gr. of monkfish uneventfully. No atopic dermatitis exacerbation was observed. sIgE against hake (T1:3.31kUA/L; T2: 3.98kUA/L; T3: 2.02kUA/L) and wheal size for hake prick-to-prick (T1: 13x11mm; T2: 10x6mm; T3: 7x5mm) decreased during induction phase whereas hake sIgG4 levels increased (T2: 12.7kU/L, T3: 39.2kU/L). CONCLUSIONS: In our case, SOTI with hake induces tolerance to bass, tuna and monkfish.
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Severe Food Allergy to Cow's Milk Treated with Oral Immunotherapy Along with Omalizumab Giovanni B. Pajno, MD, FAAAAI1, Lucia Caminiti1,2, Giuseppe Crisafulli1,2, Stefania Arasi1,2, Fernanda Chiera3, Giuseppina Salzano4; 1University of Messina, Messina, Italy, 2Dept of Pediatrics, Allergy Unit, University of Messina, 3Department of Pediatrics -University of Messina, Messina, Italy, 4Dept of Pediatrics, Allergy Unit, University of Messina, Italy. RATIONALE: Given the rise in prevalence of food allergy in developed countries, oral immunotherapy (OIT), has given many patients hope for a widely available form of treatment. However some patients are included in the pattern of non-responders because of failure of active therapy. METHODS: Since 2006 we have treated 51children suffering from IgE mediated cow’s milk allergy (CMA) with OIT. Among them three (6%) patients had severe or life-threatening events during up-dosing protocol with cow’s milk (CM). Therefore, we used for these patients an anti –IgE monoclonal antibody(omalizumab) as an adjunct to OIT, in order to enhance both the safety and efficacy of oral immunotherapy. The allergic children with severe food allergy caused by milk were 9,11,and 12 years old respectively. Median CM specific IgE levels 48 (+- 21) kU/L. Median total IgE 650 (+-125) kU/L. The dose of omalizumab was of 0.016 mg/Kg/ IgEU/mL (75-to300mg) every two weeks for 10weeks.Aferwards, specific desensitization phase was started along with omalizumab. RESULTS: The patient n. 1 (male- 9y) after two months of treatment reached the dose of 50ml of CM (1.60g. of proteins) ; the patient n. 2 male (male-11y.) reached the dose of 80ml of CM(2.50g of proteins);the third patient (female-12y) reached 40ml of milk (1.20g of proteins).No moderate to severe side effects were observed at this phase of desensitization. CONCLUSIONS: The treatment of severe food allergy with omalizumab and oral desensitization combination therapy in significant IgE mediated CMA could be an effective treatment in selected patients with severe food allergy non-responders to OIT.
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Correlation Between Palmar Hyperlinearity and Early Childhood Atopic Dermatitis with Filaggrin Gene Null Mutations Tatsuki Fukuie, MD, PhD1, Ryuhei Yasuoka, MD1, Jun-ichi Sakabe, PhD2, Toshiharu Fujiyama, MD, PhD2, Yoshiki Tokura, MD, PhD2, Tomohide Taguchi, MD1; 1Department of Pediatrics, Hamamatsu University School of Medicine, Shizuoka, Japan, 2Department of Dermatology, Hamamatsu University School of Medicine, Shizuoka, Japan. RATIONALE: Filaggrin gene (FLG) null mutations are significantly associated with palmar hyperlinearity; however, this association in early childhood atopic dermatitis (AD) has not been reported. METHODS: This study involved infants and toddlers with moderate to severe AD whose parents gave consent for the mutation analysis and photographic documentation. Each child underwent genotyping to detect the eight most prevalent FLG mutations in the Japanese population (R501X, 3321delA, S1695X, S1701X, S2554X, S2889X, S3296X and K4022X). The features and phenotypes of each patient were examined using photos of patients’ palms by 9 specially trained dermatologists and 2 pediatric allergists who were blinded to the genotyping results. RESULTS: Of the 57 children (age range, 2 months to 5 years; median, 22 months), 13 were heterozygotes and 3 were compound heterozygotes. Palmar hyperlinearity, which was recognized by more than 7 physicians, were significantly associated with FLG null mutations (P <0.001, OR 5 13.4, 95% CI 5 3.17–56.91, Fisher’s exact test). Deepness of the linearity, as determined by a median visual analogue scale (VAS) of more than 6 points out of 10, showed significant correlation with FLG mutations (likelihood ratio, 7.69; positive predictive value, 75.0%). Of the 16 patients with FLG mutations, 8 had a cross-shaped crease of the thenar eminence and 5 had the horizontal line type. CONCLUSIONS: Our study indicates that FLG mutation is associated with clinical phenotypes of early childhood AD. The presence of palmar hyperlinearity should prompt the pediatric clinician to consider the possibility of an inherited barrier abnormality of the skin resulting from FLG mutations.
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