AB144 Abstracts
472
Increasing Incidence of Food Allergies in Olmsted County, MN
Erin Willits1, Martha F. Hartz, MD, FAAAAI2, Nancy L. Ott, MD, FAAAAI2, Miguel A. Park, MD3, Avni Y. Joshi, MD2; 1Mayo Clinic, 2 Mayo Clinic, Rochester, MN, 3Department of Internal Medicine: Division of Allergic Diseases, Mayo Clinic, Rochester, MN. RATIONALE: There is a growing epidemic of food allergies in the western hemisphere, with current prevalence estimates of 6-8%. One prior study determined the incidence of peanut allergy to be 68.8/100,000 person-years in 2007. The incidence of all food allergies remains unknown. METHODS: We undertook a historical cohort study to describe the epidemiology of food allergy in Olmsted County, Minnesota using the Rochester Epidemiology Project. RESULTS: There were a total of 513 subjects (222 males, 291 females) with physician diagnosed food allergy over the 2006-2011year period. The overall incidence of food allergy was 61/100,000 person - years. The incidence peaked at 75/100,000 person-years over the study period in 2009 and plateaued to 57/100,000 person-years in 2011. For the pediatric age group (children 518 yrs age), the overall incidence was 195/100,000 person-years, with a higher incidence of 237/100,000 person-years in females and 154/100,000 person-years in males. There was no significant change in antibiotic usage over time; 43% of the cohort was exposed to antibiotics prior to food allergy diagnosis in 2006, versus 69% of the cohort in 2011 (p50.3). 40% of the children also had reactive airway disease/asthma and 54% children had co-existent atopic dermatitis. There was low association with antibiotic allergy in this cohort with only 25/513 ( 5%) children with penicillin allergy and 20/513 (4%) reporting other medication allergy. CONCLUSIONS: This is one of the first population-based studies examining the incidence of all types of food allergies. The food allergy incidence in Olmsted County peaked in 2009 at 75/100,000 person years.
473
SUNDAY
Eczema Is an Independent Risk Factor for Incident Mouse Skin Test Sensitivity Among Employees at a Mouse Production and Research Facility
Torie Grant, MD1, Jennifer Dantzer, MD1, Corinne Keet, MD, PhD1, Roger Peng, PhD2, Mary Krevans, RN3, Karol Hagberg, BSN, FNP3, Jean Curtin-Brosnan, MA1, Wayne Shreffler, MD, PhD4, Elizabeth Matsui, MD, MHS1; 1Division of Pediatric Allergy/Immunology, Johns Hopkins School of Medicine, Baltimore, MD, 2Johns Hopkins School of Public Health, Baltimore, MD, 3The Jackson Laboratory, Bar Harbor, ME, 4Division of Allergy and Immunology, Department of Pediatrics, Massachusetts General Hospital and Harvard Medical School, Boston, MA. RATIONALE: The disrupted skin barrier in eczema has been hypothesized to increase the risk of IgE sensitization. However, it is unclear whether eczema, independent of atopy, is a risk factor for the development of allergic sensitization. METHODS: New employees at The Jackson Laboratory enrolled in a cohort study underwent skin prick testing (SPT) at baseline and every six _3mm5+SPT). months to mouse and a panel of aeroallergens (net wheal > Mouse allergen exposure was measured every six months using personal air monitors. Eczema was defined as self-reported doctor-diagnosed eczema. Cox proportional hazard modeling was used to examine the association between baseline eczema and incident mouse skin test sensitivity and adjust for potential confounders. RESULTS: Participants (n5394) were followed for a median of 24 months. Fifty-four percent were female, 89% were white, and 64% handled mice. At baseline, 7% reported doctor-diagnosed eczema and 9% current asthma; 61% had at least one positive skin test. At 30 months, 36% of those with eczema vs. 14% of those without eczema had developed a positive mouse skin test (log-rank test, p50.02). After adjusting for age, race, sex, smoking status (current, former, never), current asthma, hay fever, number
J ALLERGY CLIN IMMUNOL FEBRUARY 2016
of positive skin tests at baseline, and mouse allergen exposure, doctordiagnosed eczema was an independent risk factor for incident mouse skin test sensitization (HR [95% CI]5 5.6 [2.1-15.2], p50.001). CONCLUSIONS: Doctor-diagnosed eczema was a risk factor for incident mouse sensitization, independent of atopy and allergic respiratory disease, suggesting that a defect in skin barrier alone may increase the risk of skin sensitization.
474
Expression of Filaggrin in Skin Biopsies: Role in Maintenance of Symptoms Among Brazilian Patients with Moderate-to-Severe Atopic Dermatitis
Karine Boufleur, MD1, Renata Nahas Cardili, Sr2, Janaina M. L. Melo, MD3, Adriana S. Moreno, PhD3, Ana Maria Roselino2, Edson Soares2, Luisa Karla P. Arruda, MD, PhD, FAAAAI3; 1Ribeirao Preto Medical School, University of Sao Paulo, Ribeirao Preto, Brazil, 2Ribeirao Preto Medical School- University of Sao Paulo, 3Ribeirao Preto Medical School - University of Sao Paulo, Ribeirao Preto, Brazil. RATIONALE: Atopic dermatitis (AD) is a chronic disease characterized by epidermal barrier failure and immune-mediated inflammation. Loss-offunction mutations within the filaggrin (FLG) gene have been associated with AD in populations from Northern Europe and Asia. We aimed to investigate FLG expression in skin lesions of Brazilian patients with moderate-to-severe AD. METHODS: Skin biopsies of active AD lesions from 20 adult patients, aged 19- 75 years-old (65% female), were obtained. All patients were in treatment with emollients, topical corticosteroids and/or calcineurin inhibitors, and 9/20 patients were taking oral cyclosporine A. SCORAD averaged 44.5 (range 11-75), and no withdrawal of medications was attempted prior to biopsies due to severity of symptoms. Normal skin was available from 20 individuals who underwent plastic surgery, with no history of allergic diseases. Immunohistochemical analysis for FLG expression was performed using mouse monoclonal anti-filaggrin antibody SPM181(ABCAM). RESULTS: Total IgE levels were elevated in all patients (geometric mean 4,224UI/mL, range 145- 63,000IU/mL). IgE to mite>3,5 KU/L was found in 18/18 patients who underwent this evaluation. FLG expression in AD patients was as strong as that observed in normal controls, with no difference on a blind evaluation. CONCLUSIONS: Our results showed that patients with moderate-tosevere AD who remain symptomatic despite anti-inflammatory and immunosuppressant therapy presented FLG expression comparable to control individuals. The results suggested that among patients from southeast Brazil, FLG expression may not be a determinant factor for maintenance of clinical disease. Further studies investigating the presence of FLG loss-of-function mutations will be necessary for better interpretation of these results.