Abstract PDF

Allergy, Asthma & Clinical Immunology 2014, Volume 10 Suppl 1
http://www.aacijournal.com/supplements/10/S1
ALLERGY, ASTHMA & CLINICAL

IMMUNOLOGY
MEETING ABSTRACTS
Open Access
Canadian Society of Allergy and Clinical

Immunology Annual Scientific Meeting 2013
Toronto, Canada. 3-6 October 2013
Published: 3 March 2014
These abstracts are available online at http://www.aacijournal.com/supplements/10/S1
MEETING ABSTRACT
A1
MHC class II deficiency in the Dene native population: a case report
highlighting pitfalls in diagnosis and treatment
Alex Lyttle1*, Chaim Roifman2, Harjit Dadi2, Nicola Wright1, Fotini Kavadas1
1
Alberta Childrens Hospital, Calgary, Alberta, Canada; 2The Hospital for Sick
Children, Toronto, Ontario, Canada
E-mail: alex.lyttle@gmail.com
Allergy, Asthma & Clinical Immunology 2014, 10(Suppl 1):A1
Background: Bare lymphocyte syndrome (BLS) is a rare, hereditary
immunodeficiency characterized by the absence of major histocompatibility
complex (MHC) class II leading to a form of severe combined
immunodeficiency (SCID). Here we present a case introducing BLS in a novel
population and emphasize some of the difficulties faced in diagnosing and
treating this condition.
Case: Our patient was a male of Dene native background from the
Northwest Territories of Canada. Between the ages of 2 weeks to 6 months
of age he had multiple bouts of both viral and bacterial pneumonia, two
episodes of bacteremia, and showed poor growth. Despite a low
lymphocyte count of 0.9 x 109 cells/L and undetectable immunoglobulins,
an immunologist was not initially consulted.
Finally, after his fifth episode of pneumonia he was referred to the
Immunology Department in Edmonton and then transferred to the Alberta
Childrens Hospital in Calgary. Initial testing revealed IgG levels < 2 g/L,
undetectable IgM/IgA and poor response to the diphtheria and tetanus
vaccines. Flow cytometry revealed low CD3, CD4 and CD19 counts but
normal NK and CD8 counts. Thymidine mitogen testing for T-cell function
was low however T-cell receptor excision circle (TREC) analysis was normal.
An open thymic biopsy showed evidence of CD4+ maturation arrest. Based
on this, MHC class II expression was investigated looking for HLA-DR
proteins by flow cytometry and were found to be absent.
A suitable bone marrow donor could not be found. Due to the patients
deteriorating course, a high resolution hematopoietic stem cell
transplantation using a 5/6 umbilical cord donor was performed.
Unfortunately, engraftment failed and the child passed away at 19 months
of age secondary to respiratory failure.
The genetic testing came back posthumously showing MHC class II
deficiency with a RFX5 gene mutation (R400X (1198 c>t).
Discussion: BLS is extremely rare with less than 200 reported cases
worldwide [1] and can result from mutations in one of four regulatory
proteins necessary for MHC-II production: CIITA, RFX5, RFXANK and RFXAP
[2]. This condition leads to severe CD4+ T-cell dysfunction and thus
recurrent bacterial, viral and protozoal infections. Recently TREC studies have
begun to be used as part of newborn screening programs for SCID. While
sensitive for nearly all forms of SCID [3,4], TREC studies may be normal
in BLS [5].
Our case is the first of BLS identified in the Dene native population. Given that
early BMT has been shown to have better success rates in treating BLS [6], a
screening program may be beneficial in this population.
Acknowledgments: The authors of this paper thank the immunology
laboratory at The Hospital for Sick Children in Toronto for their assistance
with the diagnostic work-up of this patient. We also thank Dr. Capucine
Picard at Centre detude des deficits immunitares, Paris, France for her
contribution in the genetic analysis of this patient.
Disclosure: No outside sources of funding were used in the creation of this
abstract.
References
1. Ouederni, et al: Major histocompatibility class II expression deficiency
caused by RFXANK founder mutation: a survey of 35 patients. Blood
2011, 118(19):5108-18.
2. Krawczyk M, Reith W: Regulation of MHC class II expression, a unique
regulatory system identified by the study of primary immunodeficiency
disease. Tissue Antigens 2006, 67:183-197.
3. Somech, et al: T-cell receptor excision circles in primary
immunodeficiencies and other T-cell immune disorders. Curr opinion
Allergy Clin Immunol 2011, 11:517-524.
4. Puck, et al: Neonatal screening for severe combined immunodeficiency.
Curr Opin Pediatr 2011, 23:667-673.
5. Lev, et al: Thymic function in MHC class II-deficiency patients. Journal of
Allergy and Clinical Immunology 2012.
6. Siepermann, et al: MHC class II deficiency cured by unrelated mismatched
umbilical cord blood transplantation: case report and review of 68 cases
in the literature. Pediatric Transplantation 2011, 15(4):E80-6.
A2
Chronic Spontaneous Urticaria an evaluation of an indirect
immunofluorescence method for detecting anti-mast cell IgG
antibodies
Bahar Bahrani*, Natasha Gattey, Peter Hull
Department of Medicine, University of Saskatchewan, Saskatoon,
Saskatchewan, Canada, S7N 0W8
E-mail: Bab210@mail.usask.ca
Background: An autoimmune basis is believed to be responsible for about
half of all cases of chronic spontaneous urticaria (CSU) with specific IgG
antibodies directed at the high affinity receptor sites for IgE on the mast cell.
The autologous serum skin test (ASST) is used to identify this autoimmune
form of CSU. Currently, basophil histamine release assay and basophil
2014 various authors, licensee BioMed Central Ltd. All articles published in this supplement are distributed under the terms of the
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Page 2 of 36
activation test (BAT) have been used as an alternative to the ASST. These tests
are not widely available and are limited in that they only provide evidence
that the patients serum is capable of inducing basophil degranulation.
We have developed an indirect immunofluorescence method to
demonstrate the presence of anti-mast cell antibodies using skin sections
from a patient with severe bullous mastocytosis.
Methods: Sections were cut from paraffin embedded blocks from skin
biopsied infant with bullous mastocytosis. An EDTA buffer solution for heatinduced epitope retrieval was used. Serum from 69 patients with CSU was
used, and fluorescein conjugated human IgG was used to label fixed
antibody. An ASST had been previously performed on 66 of the patients with
severe urticaria and was found to be positive in 45.45%. 27 of these patients
were receiving intravenous immunoglobulin (IVIG) or had received in the past.
Results: A positive indirect immunofluorescence was found in half the
patients. It was positive in 22.73% of the patients with a positive ASST,
but was also positive in 25.76% with a negative ASST. The sensitivity and
specificity of ASST were calculated to be 46.88% and 52.94%, respectively.
We considered the possibility that the use of IVIG might interfere with
indirect immunofluorescence, and this subset was omitted giving a
sensitivity and specificity of 34.62% and 77.27%, respectively.
Conclusion: Positive indirect immunofluorescence was found in half the
patients with CSU. When IVIG treated patient were excluded the ASST
was associated with is a high specificity but with low sensitivity. Indirect
immunofluorescence should be considered as better indicator of the
autoimmune form of urticaria.
A3
Calcitriol reduces eosinophil cytolysis and release of cytotoxic granules
in vitro
Caroline Ethier1*, Yingqi Wu1, Paige Lacy1, Lisa Cameron1, Francis Davoine1,2
1
Pulmonary Research Group - Department of Medicine, Edmonton, Alberta,
Canada; 2Campus Saint-Jean, University of Alberta, Edmonton, Alberta,
Canada, T6G 1A6
E-mail: cethier@ualberta.ca
Background: Epidemiological studies show a strong correlation between
vitamin D deficiency and asthma severity. Genetic studies have identified
vitamin D receptor polymorphisms as a risk factor for asthma in diverse
human populations. Calcitriol (1,25-dihydroxyvitamin D3), the physiologically
active metabolite of mammalian vitamin D, is able to modulate receptor and
cytokine expression as well as cell differentiation and maturation of various
leukocytes in an anti-inflammatory manner. Despite the role of eosinophils
in allergic asthma pathology, little is known about the effects of calcitriol on
eosinophil biology. Calcitriol has a direct modulatory effect on eosinophil
survival and effector functions in vitro.
Methods: Human peripheral blood eosinophils from atopic donors were
isolated and incubated with calcitriol (VD) and interleukin-5 (IL-5). Doseresponse assays tested physiological doses of calcitriol (0.01-100 nM). The
potentiating effect of calcitriol (10 nM) on eosinophil survival with IL-5
(1 ng/mL) was investigated on a 14-day time course. Viability/apoptosis/
necrosis levels were obtained using an Annexin-V/PI flow cytometry
assay. Eosinophil crystalloid granules and EPX release were measured by
CD63 and EPX monoclonal antibody staining using flow cytometry. EPX
activity was determined using an OPD substrate colorimetric assay.
Results: Eosinophil survival increased after 24 h of calcitriol treatment in a
dose-dependent manner (Fig1. n = 5). Calcitriol alone yielded similar
eosinophil survival rates (Fig2.4.5 1.5%, n = 11) after 7 days compared to
control media (Fig2. 2.1 2.1%, n = 11). In contrast, calcitriol potentiated the
survival effect of IL-5 starting from day 7. At 14 days, 66 7% of eosinophils
were still intact when treated with calcitriol and IL-5, compared to IL-5 alone
(Fig2. 34 8%, p < 0.05, n = 4). Cells treated with IL-5 alone showed
increased necrosis from day 7 onward with 32% additional necrotic
eosinophils at day 14, compared to the combined treatment. As cell debris
increased in correlation with necrosis (Fig3 A&B.), low-SSC/FSC events
stained positive for CD63 and EPX confirming whole, intact crystalloid
granules along with free EPX in media (Fig4.). Moreover, EPX activity in
media was reduced on days 4 and 7 following calcitriol and IL-5 treatment
(Fig5.). Overall, reduced spontaneous EPX release strongly correlated with
increased eosinophil survival (Fig6. r2 = 0.96, n = 4-11).
Figure 1(abstract A3)
Conclusions: These findings support the hypothesis that calcitriol plays

an anti-inflammatory role by decreasing cytotoxic granule release into
airway mucosal tissues during allergic inflammatory responses, therefore
reducing mucosal inflammation and tissue damage.

Page 3 of 36
A4
Social media; a tool for retention?
Claire R Unruh*, Allan Becker
Department of Pediatrics and Child Health, University of Manitoba,
Winnipeg, Canada
E-mail: cunruh@mich.ca

Page 4 of 36
research are involved in recruiting participants for studies. Social media

provides an exploratory and informative environment for families
involved in longitudinal studies. Researchers and study families can
mutually share information creating a web of connections through the
internet. Such engagement may help in the retention of participants in a
longitudinal study.
Methods: Facebook: Keep connections with study families in a timely
fashion. Facebook is able to show what a research team does on a
regular basis. Researchers can share information regarding recent and
related publications. Because of the many connections of those signed in
to Facebook, communities are built [2] and users become engaged.
Facebook has the ability to poll the public on different issues and gives
insights and data to group administration.
Twitter: Keep connections with other health care professionals,
researchers and members of the general public. There is a potential for
collaboration. Talks directly to experts and clients and gives all the
ability to connect to each other.
Pinterest: Share allergy and asthma news with the public in one area.
Pinterest is a collection of links to articles and websites about information
surrounding research in pediatric allergy and asthma.
Instagram: The sharing of photos. Researchers can share photos of the lab
environment; including how to capture data and measurements. This aids
in daily contact with the families of research studies. Benefits the families;
allows the kids to see the testing environment and opens up links of
communication.
The ability to link social media sites to each other offers the availability of
information to be accessed in different means, furthering the webs of
connection.
Results: There are no results yet from the usage of social media for the
retentions of a longitudinal cohort like CHILD. With more time and analysis,
significant results are anticipated.
Conclusions: There are limitations to using social media for a research
study. There must be time allocated to updating each site as regularly as
possible. The Internet is still not accessible to all despite being accessible to
many. Information is only shared with those engaged in social media. In
these cases, research studies must find other ways to ensure that the
information is equally distributed. With the help of social media, longitudinal
research studies are able to keep a presence in the daily lives of
participating families. This helps to strengthen connections for the study
and may ultimately help in retention. When looking at conducting a study,
researchers should not shy away from social media sites.
References
1. Rajic A, Young I, McEwen SA: Improving the Utilization of Research
Knowledge in Agri-food Public Health: A Mixed-Method Review of
Knowledge Translation and Transfer. Foodborne Pathog Dis 2013,
10(5):397-412.
2. Horbal J: Safe, Savvy, Social: Using Social Media Responsibly for your
Organization. Public Presentation, ChangeMakers Communications 2013.
A5
Biphasic anaphylaxis: a systematic review of the literature
Douglas P Mack
Department of Pediatrics, McMaster University, Hamilton, Ontario, Canada
E-mail: dougpmack@gmail.com
Background: Social media sites are becoming more and more popular
within the healthcare industry. There is a huge potential in research for
using different social media sites for retention and looking at their long
term effects in a longitudinal study like the CHILD study something not
yet looked into at depth [1]. At present, most social media sites in
Background: Biphasic anaphylaxis is a poorly understood allergic

phenomenon with significant variation in causative agent, time to onset,
outcome and overall frequency. The aim of this review is to better
determine the clinical characteristics of this type of allergic reaction.
Methods: A systematic review was performed identifying case reports and
retrospective and prospective studies reporting biphasic allergic reactions.
Biphasic anaphylaxis (BA) was defined as an anaphylactic reaction
consisting of 2 distinct phases separated by at least 1 hour, with both
phases meeting internationally recognized diagnostic criteria for
anaphylaxis. Pediatric and adult cases were evaluated. Biphasic and
uniphasic data was compared using the Chi2 test.
Results: 28 articles included descriptions of patients having biphasic
reactions with sufficient information for evaluation of clinical characteristics.
In total, 150 patients were identified as having biphasic reactions. 84 of
these patients met clinical criteria for true BA. Of these, 28 were pediatric

cases and 56 were adult. Overall frequency of biphasic reactions was

7.36% of anaphylactic reactions with prospective studies reporting a
frequency of 9.07%. Mean time to the second phase of BA was 8.13
hours (95% CI, 6.13-10.14) with similar times between both pediatric
and adult populations. The range of reported times to onset of the
second phase of biphasic reactions was 1 72 hours. 8 articles allowed
comparison of medication use and likelihood of biphasic reactions
suggesting that the use of epinephrine in the initial treatment may
predict the presence of the biphasic reaction (p=0.19). Fatal biphasic
reactions were described in 5 patients. Significant limitations were
encountered because of inconsistent definition of BA and inadequate
reporting of individual patient data.
Conclusions: Biphasic reactions are common presentations of anaphylaxis
with both pediatric and adult patients being affected. Mean and median
times to onset of the second phase are variable, but are longer than most
emergency department observation time recommendations. Carefully
designed prospective studies with clear definitions of BA are necessary
to accurately determine the characteristics of these life-threatening
reactions.
A6
C-CARE: comparing two years of anaphylaxis in children treated at the
Montreal Childrens Hospital
Elana Hochstadter1*, Ann Clarke2,3, Sebastien LaVieille4, Reza Alizadehfar5,
Christopher Mill3, Yuka Asai6, Harley Eisman2, Moshe Ben-Shoshan5
1
Department of Pediatrics, London Childrens Hospital, Western University,
London, ON, Canada; 2Division of Allergy and Clinical Immunology,
Department of Medicine, McGill University Health Center, Montreal, Quebec,
Canada; 3Division of Clinical Epidemiology, Department of Medicine, McGill
University Health Center, Canada; 4Food Directorate, Health Canada, Ottawa,
ON, Canada; 5Division of Pediatric Allergy and Immunology, Department of
Pediatrics, Montreal Childrens Hospital, McGill University Health Center,
Canada; 6Division of Dermatology, Department of Medicine, McGill University
Health Centre, Canada
E-mail: ehochsta@uwo.ca
Background: Studies suggest that rates of anaphylaxis, the most severe
form of an allergic reaction, are increasing in Pediatric Emergency
Departments (PED). Significant gaps still exist regarding the prevalence,
triggers and temporal trends of anaphylaxis in Canada. The Cross-Canada
Anaphylaxis Registry (C-CARE) was created with the primary goal of
determining the societal burden of anaphylaxis in Canada; our aim was
to use C-CARE to examine temporal trends in anaphylaxis rates.
Methods: Over a 2-year period (April 2011 to April 2013), children
presenting to the Montreal Childrens Hospital PED with anaphylaxis were
recruited. The treating physician documented characteristics and triggers of
anaphylactic reactions using a standardized data entry form. Charts of all
PED patients were reviewed to identify anaphylactic cases that were missed
in prospective recruitment.
Results: Among 81,677 PED visits in Year 1, 168 anaphylaxis cases were
identified (0.21%) versus 218 anaphylaxis cases among 78,650 PED visits in
Year 2 (0.27%), yielding a difference of 0.06% (95% CI, 0.02%, 0.12%)
between the two years. The median age of anaphylaxis was 4.8 years (IQR:
2.3-10.1) in Year 1 and 5.9 years (IQR 2.1-11.1) in Year 2. There was a slightly
higher male predominance in cases of anaphylaxis in both Year 1 (51.8%;
95% CI, 44%, 59.5%) and Year 2 (61%; 95% CI, 54.2%, 67.4%). The major
triggers in both years were food allergens (87.5% and 80.6% respectively)
with peanut being the most predominant (29.5% and 20.6%) followed by
tree nuts (15.5% and 14.8%). Severe anaphylaxis (hypoxia, cyanosis,
circulatory collapse, incontinence or neurological symptoms) was found in
7.1% (95% CI, 3.9%, 12.4%) of patients from Year 1 versus 3.7% (95% CI,
1.7%, 7.4%) in Year 2.
Conclusions: There was a greater rate of anaphylaxis in the second year
of the C-CARE study. In both years, food allergens were found to be the
most common trigger with peanuts being the most common food.
These results are comparable to the increasing rates of anaphylaxis
seen in other westernized countries. Future studies in the Montreal
Childrens Hospital as well as in other centers are required to establish
temporal trends in anaphylaxis rates, triggers and reaction
characteristics.
Page 5 of 36
A7
Peanut allergy may be overdiagnosed in younger siblings of those with
confirmed peanut allergy
Elana Lavine1*, Reza Alizadehfar2, Yuka Asai3, Gregory Shand4, Laurie Harada5,
Mary Allen6, Moshe Ben Shoshan2, Ann Clarke4,7
1
Humber River Regional Hospital, Toronto, ON, Canada; 2Division of Pediatric
Allergy and Clinical Immunology, Department of Pediatrics, McGill University
Health Centre, Montreal, QC, Canada; 3Division of Dermatology, Department
of Medicine, McGill University Health Centre, Montreal, QC, Canada; 4Division
of Clinical Epidemiology, Department of Medicine, McGill University Health
Centre, Montreal, QC, Canada; 5Anaphylaxis Canada (AC), Toronto, ON,
Canada; 6Allergy/Asthma Information Association (AAIA), Toronto, ON,
Canada; 7Division of Clinical Immunology and Allergy, Department of
Medicine, McGill University Health Center, Montreal, QC, Canada
E-mail: e.lavine@utoronto.ca
Background: Siblings of children with peanut allergy (PNA) are reported
to have a higher prevalence of PNA than the general population. This
prevalence may have both genetic and environmental influences, but
may also reflect incorrect PNA diagnoses with less rigorous usage of
confirmatory tests in siblings. The Peanut Allergy Registry (PAR), a
Canadian database of individuals with PNA, was used to assess whether
siblings born after the diagnosis of PNA in the index case (i.e., child with
PNA) were more likely to have never been exposed to peanut (PN) and
to be diagnosed without an appropriate clinical history or testing.
Methods: A questionnaire was distributed to all PAR families with at least
one child with confirmed PNA. Data were collected on siblings history of
exposure or allergic reaction to PN, and on the results of any confirmatory
tests. Univariate and multivariate logistic regressions were performed to
examine the association between characteristics of the index case/ siblings
and the following outcomes in siblings: i) complete PN avoidance and
ii) parent-reported diagnosis of PNA without corroborating positive
diagnostic tests. Predictors included sibling age and gender; index case
age at PNA diagnosis, co-morbidities, and severity of allergic reaction;
parental education level and marital status, province of residence, and
sibship size. A hierarchical model was generated using the WinBUGS
program to account for potential clustering effects within families.
Results: Among 935 PAR families surveyed, 748 (80%) responded,
representing 922 siblings, with median age 11.7 (IQR 7.4-16.3) years; 56.9%
of siblings were younger than index cases. Eighty-three percent of siblings
had been exposed to PN. Eighty (of 922) siblings were reported as having
PNA (8.8%, CI 6.9,10.6). Of 80, 34 (42%) had no preceding allergic reaction
to PN; in 5 of these 34, testing was either not performed or not supportive
of the diagnosis. In multivariate analysis, siblings born after the diagnosis
in the index PNA case were more likely (Odds Ratio (OR) 5.2, 95% CI 2.2,
12.9) to have completely avoided peanut. In univariate analysis, siblings
born after the diagnosis in the index case were more likely to be
diagnosed with PNA without a history or confirmatory testing (OR, 12.7
95% CI, 1.3, 120.7). This association was not significant in the multivariate
analysis.
Conclusions: Younger siblings of children with PNA may be at risk of
being labeled with PNA without sufficient confirmatory testing. It is crucial
to develop guidelines for both physicians and families that would prompt
use of confirmatory tests to establish the diagnosis of PNA and advocate
against unjustified PN avoidance.
A8
Longitudinal associations between neighbourhood walkability and
incident childhood asthma
Elinor Simons1,2*, Sharon Dell1,2,3, Rahim Moineddin4, Teresa To1,2
1
Clinical Epidemiology, Department of Health Policy, Management and
Evaluation, University of Toronto, Toronto, ON, Canada; 2Child Health
Evaluative Sciences, Hospital for Sick Children, Toronto, ON, Canada, M5G
1X8; 3Respiratory Medicine, Hospital for Sick Children, Toronto, ON, Canada,
M5G 1X8; 4Department of Family and Community Medicine, University of
Toronto, Toronto, ON, Canada, M5G 1V7
E-mail: elinor.simons@sickkids.ca

Background: Low neighbourhood walkability has been associated with

chronic conditions such as obesity and diabetes, but the relationship
between neighbourhood walkability and incident childhood asthma has
not been determined.
Methods: We evaluated the association between neighbourhood
walkability and incident childhood asthma using prospectively-collected
administrative data at the Institute for Clinical Evaluative Sciences. Among
the 1997-2003 birth cohorts of children living in Toronto, neighbourhood
quintile of walkability was reported using a validated walkability index
with 4 dimensions: population density, dwelling density, access to services
and street connectivity. Incident asthma was defined by the time of entry
into the Ontario Asthma Surveillance Information System (OASIS) database,
requiring 2 outpatient visits for asthma within 2 consecutive years or any
hospitalization for asthma. Sex and neighbourhood income quintile were
obtained from the Registered Persons Database. Histories of preterm
delivery, obesity and other atopic conditions were obtained from Ontario
Health Insurance Plan records. We calculated the associations between
incident childhood asthma and the two lowest versus the two highest
neighbourhood walkability quintiles using Cox proportional and discretetime hazard models.
Results: Twenty-one percent of the 326 383 children met the OASIS
criteria for asthma. After adjusting for sex, preterm delivery, obesity,
atopic conditions and neighbourhood income quintile, children with low
home neighbourhood walkability at birth were at increased risk of
asthma development [hazard ratio (HR) 1.11; 95% confidence interval (CI),
1.08-1.14], and the association did not change for children with
healthcare visits for asthma in the past year (HR 1.10; 95% CI, 1.04-1.16).
When walkability in each year of the childs life was considered, low
neighbourhood walkability was associated with increased odds of
incident childhood asthma (odds ratio 1.12; 95% CI, 1.09-1.15). These
associations were not substantially affected by year of birth within the
cohort.
Conclusions: Children living in neighbourhoods with low walkability are at
increased risk of incident childhood asthma after adjusting for
neighbourhood and individual characteristics. The association persists for
children with visits for asthma within the past year. Possible mechanisms
of this association include more physical activity, fewer weight problems
and decreased exposure to traffic-related air pollution in more walkable
neighbourhoods. Our findings suggest that promotion of neighbourhood
walkability may offer a strategy for primary asthma prevention. Walkability
of existing neighbourhoods may be improved by encouraging greater
placement of services such as banks and grocery stores within walking
distance of residential neighbourhoods and adding pedestrian paths
between roads to improve street connectivity.
A9
Life threatening shrimp allergy cross reacting with mite allergy : a case
report
Farag I Farag-Mahmod1,2*, Waheed I Hessam1
1
Suez Canal University Hospital, Faculty of Medicine, Allergy & Immunology
Unit, Egypt; 2Omega laboratories Ltd, Montreal, Quebec, Canada
E-mail: ffarag112@yahoo.com
Background: Food allergy is apparently increasing and it is estimated that
34% of adults have food allergy. Shrimp is one of the most common
causatives in seafood allergy. Patients with shrimp allergy may exhibit life
threatening anaphylactic reactions. Tropomyosin is a known important
allergen in shrimp. The IgE-binding epitope in shrimp tropomyosin, crossreacts with other allergenic invertebrate tropomyosins in house dust mites
(Der p 10, Der f 10) and cockroaches (Per a 7).
Objective: This study was undertaken to evaluate the results of
immunotherapy to Mites upon allergic reactions to shrimp allergen in a
40 years old female suffering from combined allergy to mites and shrimp.
The patient had a 10 years history of severe allergic reactions after eating
shrimp; for which she was hospitalized several times to receive
intravenous steroids and antihistamines. Despite avoiding consumption of
shrimp for several years she continued to have allergic rhinitis symptoms.
The last episode of allergic reactions to shrimp occurred while cooking
shrimp not eating it.
Page 6 of 36
Materials and methods: Allergy skin prick testing against a panel of 30

common allergens including Mites and shrimp ( Omega, Montreal,
Canada) revealed a strong positive wheal and erythema reaction to both
shrimp and D. farinae (13mm, 9 mm for wheal and 2.5 cm, 2.3 cm for
erythema respectively). Allergen specific serum IgE testing also revealed
elevated serum specific IgE to both allergens. The patient started
subcutaneous allergen specific immunotherapy (ASIT) against D. farinae
using Omega labs allergy shots. Six months after ASIT there was a
significant reduction in the size of the wheal and erythema and also
significant decrease of serum specific IgE values for both allergens.
Conclusion: Subcutaneous immunotherapy against mites may desensitize
patients against shrimp allergy.
A10
Administration and burden of subcutaneous immunotherapy for
allergic rhinitis in clinical practice in Canada
Steven W Blume1, Karen Yeomans2, Harold Kim1, Sunning Tao2,
Stephanie M Hubbard3, Felicia Allen-Ramey4*
1
Evidera, Bethesda, MD, 20814, USA; 2United BioSource Corporation,
Montreal, QC, H9S 5J9, Canada; 3United BioSource Corporation, Lexington,
MA, 02420, USA; 4Merck & Co., Inc., West Point, PA, 19486, USA
E-mail: felicia.ramey@merck.com
Background: Allergic rhinitis (AR) has been estimated to affect
approximately 2025% of Canadians. [1] Management of AR encompasses
allergen avoidance, use of symptomatic medications, and allergen
immunotherapy for patients unresponsive to other pharmacotherapy. [2,3]
This study was conducted to characterize patients receiving subcutaneous
immunotherapy (SCIT) and the SCIT administration process in Canada and
the United States; Canadian results are presented.
Methods: A multi-center, prospective, observational study was conducted
at 5 allergy clinics in Quebec and Ontario and 1 primary care clinic in
Quebec from March-September 2012. Patients 6 years who were
scheduled for SCIT on study days were invited to participate in the study.
Patients enrolled in a clinical trial, receiving sublingual immunotherapy or
allergic only to insect venom, latex, food, or drugs were excluded. Site and
patient-specific information were captured via direct observation,
questionnaires, and medical chart review. Costs were estimated from time
and supply observation and query.
Results: A total of 294 patients were enrolled with a mean age of 44
years (4% <18 years and 9% 65 years). Of these, 59% were female, 81%
Caucasian, 57% employed full-time and 30% reported household income
$100,000. Concomitant allergy medications were reported by 66% of
patients; 25% used asthma medications. Two-thirds of patients reported
initiating SCIT because they desired a cure once and for all for their
allergies. Primary symptoms at initiation of SCIT were nasal congestion
(62%), rhinorrhea (59%), sneezing (35%) and itchy eyes (32%). Chart data
indicated that patients received treatment for several different antigens
(mean: 4; SD: 3); those most commonly noted were ragweed (82%),
house dust mites (55%), grass (48%) and tree (48%). Sites reported a SCIT
build-up phase requiring one injection/week over 12-52 weeks. The SCIT
maintenance phase was reported as one injection/month over 4-5 years.
Site-specific means (SDs) for total patient time in the clinic for SCIT
ranged from 32 (11) to 49 (10) minutes, including a 30-minute required
post-injection observation at all but one site. Average patient travel time
to the office for SCIT was 20 (SD: 14) minutes. Mean time missed from
work in the previous week was 0.7 hours. The direct costs of an injection
ranged from $14 to $41 by site, with extract preparation or acquisition
and administrative tasks the largest components.
Conclusions: Patients initiated SCIT to permanently resolve allergy
symptoms. SCIT requires a long-term commitment, resulting in considerable
direct and indirect costs.
References
1. Canadian Allergy, Asthma and Immunology Foundation. 2013 [http://
www.allergyfoundation.ca/website/asthma_allergies_brochure.pdf],
Accessed July 11.
2. Bahls C: In the clinic. Allergic rhinitis. Ann Intern Med 2007, 146(ITC4):1-13.
3. Price D, Bond C, Bouchard J, et al: International Primary Care Respiratory
Group (IPCRG) Guidelines: management of allergic rhinitis. PrimCare
Respir J 2006, 15:58-70.

A11
Sublingual or Subcutaneous immunotherapy for Seasonal Allergic
Rhinitis (AR): an indirect analysis of efficacy, safety and cost
George Dranitsaris1*, Anne K Ellis2
1
Augmentium Pharma Consulting, Toronto, M4K 3H4, ON, Canada; 2Division
of Allergy, Department of Medicine, Queens University, Kingston, K7L 3N6,
ON, Canada
E-mail: george@augmentium.com
Background: The current standard of preventive care for poorly controlled
seasonal AR symptoms is subcutaneous immunotherapy (SCIT) with allergen
extracts, administered in a physicians office. As an alternative to SC
administration, sublingual immunotherapy (SLIT) is now an option for
patients. Oralair and Grazax are two SLIT agents currently available in
many countries. However, head to head comparative data between the
three options are not available. In this study, an indirect comparison on
efficacy, safety and cost was undertaken between Oralair, Grazax and
SCIT.
Methods: A systematic review of major databases was conducted from
January 1980 to December 2012 for double blind placebo controlled
randomized trials evaluating Oralair, Grazax or SCIT in patients with
grass-induced seasonal AR. Using placebo as the common control, an
indirect statistical comparison between treatments was performed using
meta regression analysis with active drug as the primary independent
variable. Other variables considered in the regression model included
year of study publication, geographic region where the trial was
conducted, trial duration, duration of immunotherapy, number of
asthmatic patients enrolled in the trial, number of allergens and patient
type (adults vs. children). A cost comparison, which included costs for
drug therapy, pharmacy fees, physician visits and indirect costs (i.e.
patient travel and lost productivity) was also undertaken.
Results: Overall, 20 placebo-controlled trials met the inclusion criteria for
indirect analysis. Keeping in mind the caveats associated with comparisons
across clinical trials, the indirect analysis suggested a possibility for improved
efficacy with Oralair over SCIT (standardized mean difference [SMD] in AR
symptom control = - 0.21; p = 0.007) and Grazax (SMD = - 0.18; p = 0.018).
In addition, the meta regression analysis did not identify significant
differences in the risk of discontinuation due adverse events between the
three therapies. Oralair was also associated with cost savings against year
round SCIT ($2,471), seasonal SCIT ($948) and Grazax ($1,168) during the
first year of therapy.
Conclusions: Through an indirect comparison of placebo controlled trials,
the evaluation suggested that Oralair has at least non-inferior efficacy
and comparable safety against SCIT and Grazax at a lower annual cost.
A12
Skin prick tests to multiple pollens and prevalence of IgE specific to
profilin
Greg Plunkett1*, Domingo Barber2, Eliseo M Villalobos3, Joshua S Jacobs4,
Jeffrey S Hallett5, Tara Mostofi4, Agustin Galan Nieto6, Tricia Moore1
1
ALK-Abell, Inc, Round Rock, TX, 78664, USA; 2Institute of Applied Molecular
Medicine, CEU San Pablo University, 28003 Madrid, Spain; 3Allergy Institute of
San Antonio, PA, San Antonio, TX, 78231 USA; 4Allergy and Asthma Medical
Group of the Bay Area, Walnut Creek, CA, 94598, USA; 5Dr. Jeffery Hallett,
Round Rock, TX, 78681, USA; 6ALK-Abell, E-28037 Madrid, Spain
E-mail: greg.plunkett@alk.net
Background: Panallergens like profilin are proteins that have very similar
sequences and structure. People can develop IgE specific to these highly
cross reactive panallergens. The purpose of this study was to determine
the prevalence of profilin sensitivity and the contribution to multiple
allergen skin test responses. Sensitivity to profilin was established by IgE
binding to purified profilins. Possible effects on skin test results were
studied by including Queen Palm (QP) allergen in the skin prick testing
panel as a possible source of profilin. QP is a species with a low probability
of pollen exposure.
Methods: 65 subjects from Central Texas and Northern California were
recruited for SPT with Multi-TestII to a panel of up to 51 allergens.
Page 7 of 36
Several extracts were tested for profilin and spanned a range of 0 14

microgram/mL. QP containing 10ug/mL profilin was added to the panel
as a possible source of panallergen. IgE to various purified component
major allergens and profilin was determined using Thermo Fisher ISAC
microarray or ADVIA Centaur.
Results: 23 of 65 subjects (35%) had a positive IgE to at least one profilin.
Of these, 9 had a >3mm wheal to QP. 20 of 65 subjects (32%), had a
positive QP SPT, a similar prevalence of positive SPT as either Timothy
grass (43%) or birch (34%) pollen. Subjects reacting by SPT to QP also
reacted to multiple allergens, 21 100% of allergens tested (average 58%).
The multiple allergen SPT sensitivity (percent of 16 allergens) correlated
with in vitro profilin IgE binding, QP SPT+, sIgE+, 75%; QP SPT+, sIgE-, 56%;
QP SPT-, sIgE+, 40%; QP SPT-, sIgE-, 32%.
Conclusions: Prevalence of IgE to profilin in the current study is similar
to reports from European studies. The association of IgE specific to
profilin and Queen Palm pollen skin responses suggests this low
probability allergen may be useful to identify panallergen responses
responsible for multiple sensitivities.
A14
Efficacy and safety of standardized short ragweed sublingual
immunotherapy tablet (SLIT-T) treatment in Canadian subjects with
ragweed pollen-induced rhinitis with or without conjunctivitis
Michael Blaiss1, Peter Creticos2, Jacques Hbert3*, Amarjot Kaur4, Harold Kim5,6
, Jennifer Maloney4, Harold Nelson7, Hendrik Nolte4, Susan Waserman6
1
University of Tennessee Health Science Center, Memphis, TN, 38163, USA;
2
Johns Hopkins University School of Medicine, Division of Allergy & Clinical
Immunology, Baltimore, MD, 21205, USA; 3Centre de Recherche Applique
en Allergie de Qubec, Qubec, QC, G1V 4T3, Canada; 4Merck, Whitehouse
Station, NJ, 08889, USA; 5Western University, London, Ontario, N6A 3K7,
Canada; 6McMaster University, Hamilton, Ontario, L8S 4L8, Canada; 7National
Jewish Health, Denver, CO, 80206, USA
E-mail: hebert.j@videotron.ca
Background: Efficacy of standardized short ragweed sublingual
immunotherapy tablet (SLIT-T), MK-3641 (Merck/ALK; 12 Amb a 1-U of
Ambrosia artemisiifolia) treatment on Canadian ragweed-allergic subjects
was assessed using subgroup analysis of data from 2 multinational,
randomized, double-blind, placebo-controlled clinical trials designed to
evaluate ragweed SLIT-T efficacy and safety in adults with ragweed
pollen-induced allergic rhinitis with or without conjunctivitis (AR/C), with
or without asthma.
Methods: We conducted pooled subgroup analysis of data from 2 studies
(P05234, n=784; P05233, n=565) investigating efficacy and safety of oncedaily ragweed SLIT-T [1,2]. In both trials, subjects were randomized to
receive ragweed SLIT-T (of multiple doses tested, 12 Amb a 1-U was
found most effective and is included here) or placebo. Treatment was
started approximately 16 weeks before ragweed pollen season (RS) and
continued during and after RS (total, approximately 52 weeks). Subjects
recorded AR/C symptoms in daily e-diaries from randomization to end of
RS. During RS, subjects also recorded AR/C rescue medication use. The
primary efficacy endpoint was the average total combined score (TCS),
the sum of the daily symptom score (DSS) and daily medication score
(DMS) during peak RS (the 15 consecutive days within RS with the
highest 15-day moving average pollen count).
Results: In the pooled study population of the 2 trials, approximately 80%
of subjects were polysensitized and approximately 20% had asthma; mean
age was approximately 36 years. The pooled Canadian subpopulation
included 104 and 94 subjects receiving placebo and 12 Amb a 1-U SLIT-T
respectively. Average pollen count for Canadian sites was approximately 100
grains/m3 during peak RS. Canadian subjects receiving 12 Amb a 1-U SLIT-T
had a mean TCS of 5.13 over peak RS, representing a 42% reduction vs 8.90
for placebo (3.77; 95% CI, 5.16 to 2.39). Reductions in the primary
endpoint with 12 Amb a 1-U SLIT-T were supported by reductions in
components DSS and DMS in the pooled population. Treatment-emergent
adverse events (AEs) were reported for 80.9% and 94.5% of Canadian
subjects in placebo and 12 Amb a 1-U SLIT-T groups respectively; treatmentrelated AEs were reported for 33.9% and 80.9% respectively. The majority of
treatment-related AEs were mild, local, application-site reactions with no
reports of serious treatment-related AEs or systemic allergic reactions.

Conclusions: In pooled subgroup analysis from 2 trials, ragweed SLIT-T

therapy reduced symptom and medication scores in Canadian subjects
with ragweed pollen-induced AR/C with or without asthma.
Trial registration: ClinicalTrials.gov Identifiers NCT00783198, NCT00770315
Acknowledgements: These studies were funded by Merck, Whitehouse
Station, NJ, USA. Medical writing and editorial assistance was provided by
Rob Coover, MPH, of Adelphi Communications, New York, NY. This
assistance was funded by Merck, Whitehouse Station, NJ, USA. Editorial
assistance was also provided by Jorge Moreno-Cantu, PhD, Global Scientific
and Medical Publications, Office of the Chief Medical Officer, Merck,
Whitehouse Station, NJ, USA.
References
1. Creticos PS, Maloney J, Bernstein DI, et al: Randomized controlled trial of a
ragweed allergy immunotherapy tablet in North American and
European adults. J Allergy Clin Immunol 2013, 131:1342-1349.e6.
2. Nolte H, Hbert J, Berman G, et al: Randomized controlled trial of ragweed
allergy immunotherapy tablet efficacy and safety in
North American adults. Ann Allergy Asthma Immunol 2013, 110:450-456.e4.
A15
A series of NSAID-induced anaphylactic response to immunotherapy
and a proposal to include NSAIDS avoidance in future immunotherapy
guidelines
Jennifer YF Chen1, Jason K Lee2,3*
1
Faculty of Medicine and Dentistry, University of Alberta, Edmonton, AB,
Canada; 2Division of Clinical Immunology and Allergy, University of Toronto,
Toronto, ON, Canada; 3St. Michaels Hospital, Toronto, ON, Canada
E-mail: jasonk.lee@utoronto.ca
A review of anaphylaxis in a clinic over three years was performed. A cofactor for anaphylaxis stood out as a commonality to all reactions. All five
patients had a non steroidal anti-inflammatory drug (NSAID) 24 hours
prior to immunotherapy.
Among symptoms, urticaria was the commonest; others included cough,
angioedema, dyspnea, nausea, vomiting, hypotension and tachycardia.
The symptoms appeared within 5 minutes to two hours post-injection. All
reactions resolved after few hours. In all cases, NSAID use pre-injection
was the only common factor. Two patients also had moderate exercise
post-injection, but previous immunotherapy was without incident. All but
one patient were administered epinephrine in clinic and recovered
without significant morbidity, some were also given cetirizine as adjunct
treatment and all were observed until symptoms resolved. While two
patients stopped immunotherapy, three patients continued without
incident and are now on maintenance dose. The one patient who did not
receive epinephrine presented to a walk in clinic for her reaction and
received antihistamine treatment alone.
NSAID use, although overlooked in the literature, is a common cofactor in
anaphylaxis in response to immunotherapy. At Torontoallergists, a clinic
with three allergists in practice, 5 such cases among approximately 3 600
injections in the last three years were noted after extensive chart review.
Therefore an NSAID was associated with anaphylaxis in 0.0014% of the
immunotherapy injections, whereas two cases of anaphylaxis involved
NSAID and exercise involvement. No cases implicating other risk factors or
co-factors for anaphylaxis during immunotherapy, such as dosage errors, or
injection during asthma exacerbation were present [1].
It is speculated that aspirin and other NSAIDS lower the threshold for
anaphylaxis after allergen injections through their COX-inhibiting
mechanism of action [2]. The COX pathway synthesizes, from arachidonic
acids, prostaglandin D2 and E2, are repressors of inflammatory mediator
release from basophils and mast cells [3]. Therefore, NSAIDS increases the
likelihood of anaphylaxis after immunotherapy by suppression of
prostaglandin D2 and E2, which would normally inhibit histamine release.
Supporting this mechanism is Marone et als study where higher
concentration of NSAIDS and more inhibition of COX activity correlated with
higher release of histamine [2].
However, in spite of the data about NSAID acting as a co-factor for
anaphylaxis, NSAID avoidance around immunotherapy cannot be found in
practice parameters from the AAAAI, ACAAI, and CSACI [4,5].
Therefore, as a patient safety precaution, we highly encourage NSAIDS
avoidance to be included for future immunotherapy practice guidelines.
We welcome other centers to corroborate.
Page 8 of 36
References
1. Borchers AT, Keen CL, Gershwin ME: Fatalities following allergen
immunotherapy. Clin Rev Allergy Immunol 2004, 27:147-58.
2. Marone G, Kagey-Sobotka A, Lichtenstein LM: Effects of arachidonic acid
and its metabolites on antigen-induced histamine release from human
basophils in vitro. J Immunol 1979, 123:1669-77.
3. Hogaboam CM, Bissonnette EY, Chin BC, Befus AD, Wallace JL:
Prostaglandins inhibit inflammatory mediator release from rat mast
cells. Gastroenterology 1993, 104:122-9.
4. Cox L, Nelson H, Lockey R, Calabria C, Chacko T, Finegold I, Nelson M,
Weber R, Bernstein DI, Blessing-Moore J, et al: Allergen immunotherapy: a
practice parameter third update. J Allergy Clin Immunol 2011, 127:S1-55.
5. Leith E, Bowen T, Butchey J, Fischer D, Kim H, Moote B, Small P, Stark D,
Waserman S: Consensus Guidelines on Practical Issues of
Immunotherapy-Canadian Society of Allergy and Clinical Immunology
(CSACI). Allergy Asthma Clin Immunol 2006, 2:47-61.
A16
Attrition in the Canadian Healthy Infant Longitudinal Development
(CHILD) study
JC Venevongsa1,2*, R Chooniedass1,2, AL Kozyrskyj3,4, CD Ramsey4,5,
AB Becker1,2
1
Department of Pediatrics and Child Health, University of Manitoba, Winnipeg,
MB, Canada; 2Manitoba Institute of Child Heath, Winnipeg, MB, Canada;
3
Department of Pediatrics, University of Alberta, Edmonton, AB, Canada;
4
Community Health Sciences, University of Manitoba, Winnipeg, MB, Canada;
5
Department of Medicine, University of Manitoba, Winnipeg, MB, Canada
E-mail: jluo@mich.ca
Background: Studies have shown that retention of study subjects is a
major challenge in research. Longitudinal studies provide a wealth of
information over time, but participants need to continue until the study is
complete. Study participants have the right to withdraw.
Objective: 1. To determine the attrition rate across study sites in the
CHILD study.
2. To document the principle reasons for attrition.
3. To identify maternal factors associated with attrition
Methods: CHILD is a study assessing the environmental impact on
childrens health. The study includes 4 recruitment sites across Canada
(Vancouver, Edmonton, Manitoba, and Toronto). Women enrolled while
pregnant will be followed, along with their child for 5 years. Home
assessments were done at 3 months, clinical assessments at 1, 3, and
5 years of age, and questionnaires are administered every 6 months. If
a study participant withdraws, staff completes a one page questionnaire
to determine reasons for withdrawal. The checklist incudes: no reason
given, father not interested, family lacks time, family concern regarding
privacy, expense to family, inconvenient to travel, complicated family
situation, testing difficult, enrolled in another study, too many
questionnaires, separation, personal health issue and others. Maternal
factors included: history of asthma or food allergy, marital status,
socioeconomic status (post secondary education, income),
ethnic/cultural group, being born in Canada, age, and stress measured
by a Perceived Stress Scale.
Results: CHILD recruited 3628 participants at 4 sites (Vancouver 816,
Edmonton 840, Manitoba 1107, and Toronto 865). Of the 316 participants
withdrawn from the study, 149 were not eligible due to birth issues and
167 withdrew). Attrition rates for those 167 who declined further study
were 4.5% (37/816) in Vancouver, 6.2% (52/840) in Edmonton, 2.3%
(25/1107) in Manitoba, and 6.1% (53/865) in Toronto. Of the 167, further
information is available only for 100. 81% (81/100) withdrew due to a lack
of time, 17% (17/100) withdrew due to family issues, and 16% (16/100) due
to other reasons, such as moving away, religions reason, etc. We compared
2698 participants with available data with 167 withdrawn active
participants. Perceived stress was high in 99% withdrawn vs. 69% of active
participants (p=0.02). Other important factors for withdrawing include
single mother status (12% vs. 6%, p=0.03), maternal history of asthma
(13% vs. 23%, p=0.03), and maternal food allergy (11% vs. 22%, p=0.009).
Conclusion: Lack of time and family issues were the main reasons for
withdrawal. There was greater attrition among mothers who were single
parents, had greater stress, and who did not have asthma and allergy.
There were no significant differences for education, income, cultural
group, being born in Canada or maternal age.

Relevance: It is important to retain families for longitudinal studies.

Researchers must be aware of the main reasons and factors associated
with attrition before designing longitudinal studies, and implement
retention effective strategies.
A17
Regional diagnostic panels for aeroallergens in Canada
Joshua Young*, Robert Erskine, Tricia Moore, Greg Plunkett
ALK, Inc. Round Rock, TX, USA
E-mail: joshua.young@alk.net
Background: Prevalence of allergenic plants varies by geographic region
and climate, which affects the level of allergen exposure experienced by
patients in different parts of the country. Because of these variations in
exposure it is recommended that allergy practices use customized regional
diagnostic panels based on the prevalence and significance of various
aeroallergens. However, gathering this information can be difficult for new
physicians. The purpose of these recommendations is to provide a
foundation for new physicians to begin building a custom aeroallergen
panel for all regions of Canada.
Methods: Clinical, geographical and botanical references were evaluated and
compiled to determine the prevalence and impact of various aeroallergens
across Canada. These recommendations were discussed with regional allergy
practices and other clinical authorities for consensus on recommendations.
Results: Aeroallergen recommendations were compiled into a prevalence
map and table that was organized by the major geographic regions of
Canada. Allergens were categorized as (1) high allergenicity & high
prevalence, (2) high allergenicity & low prevalence, (3) low allergenicity &
high prevalence, or (4) low allergenicity & low prevalence. A significant
degree of allergen similarity across all regions was recognized although
specific differences in species selection and general distribution patterns
were identified for each region.
Conclusions: Gathering clinical and botanical prevalence data for
aeroallergens across different regions can be time consuming and difficult.
These recommendations were compiled from many years of industry
experience working with allergy specialists across the country and were
verified by the literature. It is hoped that this knowledge can provide a
foundation for new physicians trying to understand which aeroallergens to
target for allergy diagnostic panels specific to their region.
A18
Specific IgEs passively transferred through a platelet transfusion caused
two discrete allergic reactions to food
Joyce CY Ching1*, Wendy Lau2,3, Barbara Hannach3, Julia EM Upton4
1
Department of Pediatrics, Rouge Valley Health System, Toronto, Ontario, Canada,
M1E 4B9; 2Transfusion Medicine, Pediatric Laboratory Medicine, University of
Toronto, Hospital for Sick Children, Toronto, Ontario, Canada, M5G 1X8;
3
Canadian Blood Services, Toronto, Ontario, Canada, M5G 2M1; 4Department of
Pediatrics, Division of Clinical Immunology and Allergy, University of Toronto,
Hospital for Sick Children, Toronto, Ontario, Canada, M5G 1X8
E-mail: scarboroughallergyclinic@gmail.com
Background: An unusual cause of an allergic reaction to food is the
passive transfer of specific IgE through blood product transfusions. We
report two separate allergic reactions due to passive transfer of food
specific IgE from a pooled platelet transfusion.
Case report: A non-atopic 8 year old boy received multiple blood product
transfusions as part of his treatment for meduloblastoma. He subsequently
experienced anaphylaxis to salmon. Within minutes of eating salmon, he
developed angioedema of the lip, facial erythema, throat discomfort and low
blood pressure. Before this episode, he regularly ate fish with no reaction.
The passive transfer of food specific IgE was suspected and he was advised
to carry an epinephrine auto-injector and avoid all vertebrate fish. Specific
IgE to salmon by ImmunoCAP was positive. Follow-up was arranged to
follow his specific IgE to salmon with the expectation that his allergy would
resolve. One week after his anaphylactic episode to fish, he developed an
allergic reaction to peanuts. He ate a chocolate peanut butter cup and within
10 minutes he vomited, developed angioedema of the lip and experienced
lethargy. Previously, he routinely ate peanuts without any symptoms. Skin
prick testing showed positive results to peanut, salmon, mixed fish, and tree
Page 9 of 36
nut mix. He had a positive ImmunoCAP to peanut. Approximately 6 months

later, he had undetectable ImmunoCAP results to both salmon and peanut.
He resumed consumption of salmon and peanuts with no reaction. As part
of the adverse event investigation by Canadian Blood Services all donors
associated with the reaction were contacted and one donor stated that they
have a severe allergy to peanuts, tree nuts, shellfish, and all fish including
salmon. This information implicated one specific pooled platelet transfusion
in which the platelets were suspended in the plasma of the atopic donor.
The donor has been excluded from future donations.
Conclusions: To our knowledge, this is the first reported case of two
allergic reactions to food documented to be caused by passive transfer of
food-specific IgE from pooled platelets. This case shows that if a passive
allergy from a transfusion occurs, consideration should be given to look for
additional passively transferred specific IgE. Knowledge of the allergies in
the blood donors can assist in the investigations and avoidance instructions.
A19
Do epinephrine auto-injectors have an unsuitable needle length for
young children?
Laura Kim1*, Immaculate FP Nevis2, Gina Tsai3, Arunmozhi Dominic3,
Ryan Potts4, Jack Chiu3, Harold Kim2,3
1
Department of Anatomy and Cell Biology, McGill University, Montreal, Quebec,
Canada, H3A 0G4; 2Michael DeGroote School of Medicine, McMaster University,
Hamilton, Ontario, Canada, L8S 4L8; 3Schulich School of Dentistry and Medicine,
Western University, London, Ontario, Canada, N6A 3K7; 4Department of Biology,
University of Waterloo, Waterloo, Ontario, Canada, N2L 3G1
E-mail: laurakimkw@gmail.com
Background: Epinephrine delivered by an auto-injector to the anterolateral
aspect of the thigh is the standard of care for the emergency treatment of
anaphylaxis. For most pediatric patients in Canada, the EpipenJr is
prescribed, which has a needle length of 12.7mm. The route of epinephrine
administration affects its onset of action, and intramuscular delivery is
recommended for rapid absorption. If epinephrine is injected subcutaneously,
the absorption will be slower. Conversely, if it is injected into the bone, the
absorption will be unpredictable. There are no published clinical studies
assessing whether the needle length of the EpipenJr is adequate to deliver
epinephrine intramuscularly in pediatric patients at risk of anaphylaxis.
Methods: Consecutive pediatric patients under 15kg with confirmed food
allergy who required prescriptions or refills of EpipenJr at an allergists
office were included in this study. An ultrasound of the anterolateral
aspect of the mid thigh was performed under minimal (min) and maximal
(max) pressure. Measurements of skin-to-muscle depth (STMD) and skin-tobone depth (STBD) were completed. Baseline characteristics between two
patient groups were compared: patients with STBDmax less than 12.7mm
and patients with STBDmax greater than or equal to 12.7mm. Multivariable
linear regression was performed including variables such as age, sex, BMI
and race. The likelihood of the STBD max of less than 12.7 mm was
calculated for the weight groupings of <9kg,<11kg and <15kg.
Results: A total of 75 participants were included in this study. There
were 21 patients (28%) that had STBD max less than 12.7mm. Baseline
characteristics differed significantly for height and weight of the participants
between the two groups (p<0.05). Multivariable linear regression showed
that age (p=0.0002) and BMI (p=0.00008) were significantly associated with
STBDmax, following adjustment for sex and race. For patients under 9kg,
90% had STBDmax less than 12.7mm. For patients under 11kg, 53% had
STBDmax less than 12.7mm.
Conclusions: Based on this study, there are a significant number of
children under 15kg at risk of receiving an epinephrine auto-injector into
the bone. Because of this risk, epinephrine auto-injectors should be
prescribed with caution in this population.
A20
Optimizing subject retention in a longitudinal birth cohort study:
lessons learned from the Vancouver site of the CHILD Study
Linda Warner*, Mary Ann Mauro, Susan Menzies, Ghazal Assadian,
Robby Mamonluk, Claire Lepine, Stuart E Turvey
Department of Pediatrics, University of British Columbia, Vancouver, BC, V6T
1Z4, Canada
E-mail: lwarner@cw.bc.ca

Background: The Canadian Healthy Infant Longitudinal Development

(CHILD) study is a multicentre birth cohort study following children for
the first five years of life to determine how environmental and genetic
variables impact early life health, particularly the development of asthma
and allergies. Optimal subject retention is essential for scientific integrity,
budget containment and ultimately, for continuity of data collection.
We completed an analysis of participants from the Vancouver general
cohort after their first year in the study to address retention challenges
related to urban mobility, time constraints, and stressful life situations
while considering their socio-economic status (SES) in regards to family
income and parents education level.
Methods: Reasons for voluntary participant withdrawals were identified
by questionnaires and by direct participant feedback. Anonymous surveys
were administered to parents to evaluate clinical practice, and provide
insight on changes that could be implemented.
Results: Out of 706 participants the CHILD study successfully retained 93%
of participants with 3% excluded at birth due to exclusion criteria (e.g.
premature birth, significant medical complication) and another 4 % of the
cohort voluntarily withdrawing. 11% of active participants were identified
as participants at risk of withdrawing. Issues putting these participants at
risk included: lack of time (25%), difficulty with testing (23%) and
inconvenience of travel (24%) with a remaining 28% divided into smaller
categories affecting the participants such as divorce or health concerns.
The administered anonymous surveys indicated that staff professionalism
and ability to establish good rapport, while expressing value and
appreciation, were the most important characteristics of the staff to parent
participants. The confidentiality of the survey provided an honest outlet for
parents to empower them in giving direct feedback, thus improving staff
availability and ease of clinic process and procedures. Scheduling
flexibility, the use of birthday cards and other monetary reimbursements,
as well as the dissemination of knowledge and test results were noted by
parents as positive methods that increased participation and retention
rates.
Conclusion: Successfully engaging and retaining study participants are
crucial to achieving study objectives and collection of quality of data.
Recruitment and retention obstacles should be identified at the onset of a
longitudinal study. Adapting to these challenges requires implementation
of new strategies and a flexible approach. Continuity of staff service, as
well as participant involvement, enhances both the quality of data and the
value participants place on study.
A21
Anaphylactic death due to bee sting a comparison case study
Lindsay Douglas2*, Shahin Zanganeh1,2
1
Schulich School of Medicine and Dentistry Western University, Windsor,
Ontario, Canada; 2Windsor Allergy Asthma Associates, Windsor, Ontario,
Canada
E-mail: lindsayedouglas@hotmail.com
Introduction: In 2000 the World Health Organization reported that in the
USA there were 54 deaths attributed to bee stings from a population of
281 million. Only 0.4% of the population is allergic to stings. First line
treatment of stings is Epinephrine best delivered when anaphylactic
symptoms are first noted. In the spring of 2012 two males were stung in
Windsor Essex County resulting cardiac arrest.
Methods: We describe a comparison case study of two patients.
Patient A: A 45 Year-old male was stung by a wasp as he was putting on his
shirt. Patient complained of chest pain and soon collapsed. Past medical
history is unremarkable.
Patient B: A 48-Year old male stung multiple times while working outside.
Patient became light-headed and passed out. Past history is significant for a
venom allergy and left eye injury as a child.
Results: Patient A: EMS notified, epinephrine administered with delay.
Patient transferred to local hospital pulseless on arrival. He was
resuscitated over a period of 45 minutes where he developed a poor pulse.
Total IgE and specific IgE revealed an IgE of 149kU/L, Common Wasp 1.50
kU/L, Honey Bee 0.55 kU/L, Paper Wasp 2.83 kU/L, White-Faced Hornet
1.08 kU/L and Yellow Hornet 0.57 kU/L. Nine days after sting patient had
worsening neurological status. A repeat CT of the head revealed a new left
Page 10 of 36
thalamic intracranial hemorrhage with mass effect. The following day

support was withdrawn and the patient expired shortly after.
Patient B: EMS notified, epinephrine administered. Patient transferred to
local hospital PEA on arrival. He was resuscitated and transferred to ICU.
Specific IgE revealed Common Wasp 0.70 kU/L, Honey Bee <0.35 kU/L, Paper
Wasp 0.35 kU/L, White-Faced Hornet 0.35 kU/L and Yellow Hornet <0.35 kU/L.
Patient discharged home 11 days after sting. Patient noted to be
neurologically stable with some short-term memory loss.
Conclusion: Early recognition and treatment is crucial to patient survival
with venom allergy. People at risk of insect sting anaphylaxis should be
educated regarding measures to avoid insect stings. It is advised that an
epinephrine auto injector be immediately available and administered as
soon as a severe reaction is suspected.
A22
Kounis syndrome and systemic mastocytosis: one step from elective
lipoma resection to cardiac arrest
Marina Lerner1*, Raveen Pal2, FRCPC1, Rozita Borici-Mazi3
1
Department of Respirology, McMaster University, Hamilton, ON, Canada, L8S
4L8; 2Department of Cardiology, Queens University, Kingston, ON, Canada,
K7L 3N6; 3Department of Allergy and Immunology, Queens University,
Kingston, ON, Canada, K7L 3N6
E-mail: marina.lerner@yahoo.com
Background: Kounis Syndrome manifests as unstable vasospastic or
nonvasospastic angina and is caused by the release of inflammatory
mediators following an allergic reaction. A variety of causes have been
reported including antibiotics, general anesthetics, latex, insect stings, drug
eluting stents, etc. To the best of our knowledge, Kounis syndrome in the
setting of systemic mastocytosis has not been previously published. We
describe the case of a 52- year- old male, who developed Kounis syndrome
perioperatively and was subsequently diagnosed with systemic mastocytosis.
Methods: Case report and literature review.
Results: A 52-year-old man was brought to operating room for an elective
lipoma resection. Shortly after receiving cefazoline intravenously he
developed generalized skin pruritus, flushing and dyspnea. He was treated
with intravenous Benadryl and the lipoma site was infiltrated with
combination of local anesthetics. He became increasingly agitated, hypoxic
and the monitor showed development of ST elevation followed by
ventricular fibrillation. The patient sustained a cardiac arrest and required
full resuscitation. Return of circulation was achieved and ST segment
elevation resolved within minutes of treatment with epinephrine.
The procedure was abandoned. He was transferred to our hospital and
subsequent angiography showed mild coronary artery disease.
A transthoracic ECHO yielded a LVEF of 70% with no wall motion
abnormality. His past medical history was remarkable for OSA, hypertension,
dyslipidemia, obesity and allergic rhinitis. He reported allergies to insect
stings and Terramycin. Blood work obtained one week after the episode
showed an elevated baseline tryptase level of 29.3 ng/ml suggesting
ongoing mast cell degranulation. He was assessed in Allergy Clinic 3 months
later and reported a few years history of symptoms suggestive of Systemic
Mastocytosis. His tryptase level was 31.2 ng/ml. RAST for penicillin allergens
was negative. Skeletal survey was negative for lytic bone lesions. A working
diagnosis of systemic mastocytosis was made and further confirmatory tests
are pending. He was started on a combination H1 and H2 antihistamines,
leukotriene antagonist and mast cell stabilizer.
Conclusion: Kounis syndrome is one of the manifestations of anaphylactic
reaction. This case report emphasizes the importance of recognizing
Kounis syndrome in the setting of anaphylaxis. Effective management of
Kounis syndrome should focus on the investigation and treatment of the
acute coronary event as well as suppression of the allergic reaction. The
flare of underlying systemic mastocytosis due to perioperative stress,
rather than a true allergic reaction to cephalosporin, could have caused
this reaction; however, further investigations are required.
References
1. Marcoux V, Nosib S, Bi H, Brownbridge B: Intraoperative myocardial
infarction: Kounis syndrome provoked by latex allergy. BMJ Case Rep
2013, 2013.
2. Kounis Nicholas G, et al: Kounis Syndrome: A new twist on an old
Disease. Future Cardiol 2011, 7(6):805-824.

3.
4.
Cevik C, Nugent K, Shome GP, Kounis NG: Treatment of Kounis syndrome.

Int J Cardiol 2010, 143(3):223-6.
Schwartz Lawrence B: Diagnostic value of tryptase in anaphylaxis and
masctocytosis. Immunol. Allergy Clin N Am 2006, 26:451-463[http://www.
uptodate.com/home].
A23
Presentation and management of ACE-I induced angioedema in the
Emergency Department: an observational study
R Mason Curtis1*, Sarah L Felder2, Rozita Borici-Mazi2, Ian M Ball1,3,4
1
Department of Emergency Medicine, Queens University, Kingston, Ontario,
Canada; 2Division of Allergy and Immunology, Queens University, Kingston,
Ontario, Canada; 3Program in Critical Care Medicine, Queens University,
Kingston, Ontario, Canada; 4Department of Biomedical and Molecular
Sciences, Queens University, Kingston, Ontario, Canada
E-mail: rcurtis@qmed.ca
Background: Angioedema of the upper airway is a life-threatening
Emergency Department (ED) presentation with many etiologies. Angiotensin
converting enzyme-inhibitor (ACE-I) use is one cause of non-mast cell
mediated angioedema. As the use of this medication class increases with
our aging population, it is important to characterize the presentation and
management of ACE-I induced angioedema (AAE), a rare but potentially
severe side effect of this commonly prescribed medication class. The
objectives of this study were to describe the incidence and management of
AAE in the ED and to identify any epinephrine-induced morbidity.
Methods: A retrospective medical record review was conducted of all
patients presenting to two Canadian tertiary care EDs between July 2007
and March 2012. Patients were identified for inclusion using the
International Classification of Diseases, 10th revision discharge diagnostic
codes of T782, T783, T784, T886, T887 and D841. Records were excluded
from study if there was no visible swelling documented on the medical
record, or if swelling was found to be secondary to non-systemic reaction to
an insect sting, trauma or irritant exposure.
Results: Of 1702 medical records identified through our inclusion criteria,
1175 were excluded for reasons cited above. Of the remaining 527 ED visits,
an inciting cause was identified in 48.8% (n=257), based on our a priori
definitions. Of these, the most common identifiable etiology was AAE
(33.1%, n= 85). The most common locations of swelling in patients with AAE
were the tongue or lips, found in 51% and 40% of subjects, respectively.
Common ED medications used to manage AAE included diphenhydramine
(63.5%, n=54), corticosteroids (50.6%, n=43) and ranitidine (31.8%, n= 27).
Epinephrine was administered in 18 AAE patients (21.2%), 5 of whom
received repeated doses. In two of these patients, morbidity developed
shortly after epinephrine administration, causing myocardial ischemia or
dysrhythmia. Four AAE patients (4.7%) required admission to hospital and
one required endotracheal intubation. There was no associated mortality.
Conclusions: Our study demonstrates that AAE is the most common
identifiable etiology of angioedema of patients presenting to the ED.
Management of AAE commonly includes antihistamines and corticosteroids.
Concerningly, epinephrine use is common. Many patients started on ACE-Is
are at high risk for developing complications from epinephrine
administration, which has limited physiologic rationale for use in the setting
of AAE. More research is required to better delineate epinephrines role in
this vulnerable patient population and identify other therapeutic options.
A24
Impact of cesarean section delivery and breastfeeding on infant gut
microbiota at one year of age
Meghan B Azad1*, Theodore Konya2, David S Guttman3, Catherine J Field4,
Radha S Chari5, Malcolm R Sears6, Allan B Becker7, James A Scott2,
Anita L Kozyrskyj1, the CHILD Study Investigators8
1
Pediatrics, University of Alberta, Edmonton, Alberta, Canada; 2Dalla Lana
School of Public Health, University of Toronto, Toronto, Ontario, Canada;
3
Cell & Systems Biology, University of Toronto, Toronto, Ontario, Canada;
4
Agriculture, Food & Nutritional Sciences, University of Alberta, Edmonton,
Alberta, Canada; 5Obstetrics & Gynecology, University of Alberta, Edmonton,
Alberta, Canada; 6Department of Medicine, McMaster University, Hamilton,
Ontario, Canada; 7Pediatrics & Child Health, University of Manitoba,
Page 11 of 36
Winnipeg, Manitoba, Canada; 8Canadian Healthy Infant Longitudinal

Development Study, Canada
E-mail: meghan.azad@ualberta.ca
Background: The gut microbiota is essential to human health, playing

central roles in host metabolism and immunity. In a pilot study, we
previously demonstrated that mode of delivery and breastfeeding influence
the infant gut microbiota at 4 months of age. Here, we examine the impact
of these critical early-life exposures in a larger cohort at 12 months of age.
Methods: The study comprised a sub-sample of 190 healthy term infants
from one centre participating in the Canadian Healthy Infant Longitudinal
Development (CHILD) birth cohort study. Mode of delivery was determined
from hospital records, and mothers reported infant diet at 3, 6 and
12 months postpartum. Antibiotic exposure was documented from hospital
and prescription records. Gut microbiota was characterized by Illumina 16S
rRNA sequencing of fecal samples collected at 12 months.
Results: Delivery and breastfeeding practices significantly influenced
infant gut microbiota composition and diversity at one year of age.
Regardless of breastfeeding or antibiotic exposure, infants delivered by
emergency cesarean section had higher gut microbiota diversity compared
to infants delivered vaginally or by elective cesarean section (p<0.001).
Consistent with our pilot results at 4 months, emergency cesarean delivery
was associated with lower relative abundance of Bacteroides (p<0.001); this
difference was attenuated in breastfed infants. Independent of delivery
mode or antibiotic exposure, and contrary to our findings at 4 months,
breastfeeding exclusivity (none, partial or full) and duration (never, < 6
months, 6 months) were associated with progressively higher diversity,
and increasing relative abundance of Bifidobacteria (p for trends all <0.01).
Other taxa influenced by mode of delivery and breastfeeding included the
Family Lachnospiraceae (increased following emergency cesarean delivery)
and the Genera Veillonella, Lactobacillus and Megasphera (all increased
among breastfed infants).
Conclusions: Mode of delivery and breastfeeding are strong
determinants of the infant gut microbiota, with persistent and potentially
interactive effects throughout the first year of life. Breastfeeding appears
to influence microbiota diversity differently at 4 versus 12 months of age,
indicating that measures of diversity require cautious interpretation
(including consideration of age at assessment), and that a single measure
of nutrition may not adequately reflect the diverse exposures that occur
during the weaning period. Ongoing research in the CHILD study will
address the cumulative and long-term impact of these and other earlylife exposures, and associated changes to the gut microbiota, on the
development of allergic disease and other health outcomes.
A25
Probiotic supplementation during pregnancy or infancy for the
prevention of asthma and wheeze: a systematic review and metaanalysis
Meghan B Azad1*, J Gerard Coneys2, Anita L Kozyrskyj1, Catherine J Field4,
Clare D Ramsey2,3, Allan B Becker5,6, Carol Friesen7,8, Ahmed M Abou-Setta7,
Ryan Zarychanski2,3,7
1
Pediatrics, University of Alberta, Edmonton, Alberta, Canada; 2Department of
Internal Medicine, University of Manitoba, Winnipeg, Manitoba, Canada;
3
Department of Community Health Sciences, University of Manitoba,
Winnipeg, Manitoba, Canada; 4Department of Agriculture, Food & Nutritional
Sciences, University of Alberta, Edmonton, Alberta, Canada; 5Manitoba
Institute of Child Health, Winnipeg, Manitoba, Canada; 6Pediatrics and Child
Health, University of Manitoba, Winnipeg, Manitoba, Canada; 7George & Fay
Yee Centre for Healthcare Innovation, University of Manitoba / Winnipeg
Regional Health Authority, Winnipeg, Canada; 8Neil John Maclean Health
Sciences Library, University of Manitoba Libraries, Winnipeg, Canada
E-mail: meghan.azad@ualberta.ca
Background: Often preceded by early-life wheezing, asthma is the most
common chronic disease of childhood. In view of the emerging microflora
hypothesis of allergic disease, probiotics have been proposed for the
prevention and treatment of allergic disorders including asthma, but
clinical studies have yielded conflicting results. We undertook a systematic
review and meta-analysis of randomized controlled trials to evaluate the

association of probiotic use during pregnancy or infancy with childhood

asthma and wheeze.
Methods: Following a registered protocol (PROSPERO CRD42013004385),
we searched MEDLINE, EMBASE, and CENTRAL from inception to February
2013, plus the World Health Organizations International Clinical Trials
Registry Platform and relevant conference proceedings for the preceding 5
years. Included trials and relevant reviews were forward searched in Web
of Science. Two reviewers independently identified randomized controlled
trials evaluating probiotics administered during pregnancy or the first year
of life. The primary outcome was clinician-diagnosed asthma; secondary
outcomes included wheeze and lower respiratory tract infection.
Results: We identified 20 eligible trials involving 4866 children. Studies were
heterogeneous in the type and duration of probiotic supplementation, and
duration of follow up. Two trials conducted follow-up at or beyond 6 years
of age, and no trials were powered for asthma detection. We adjudicated
most trials (16/20) to be of unclear or high risk of bias. Among 2781 infants
enrolled in 8 studies contributing asthma data, the risk ratio of cliniciandiagnosed asthma in participants randomized to receive probiotics was 0.96
(95% confidence interval [CI] 0.71 to 1.29, I2 = 13%). The risk ratio of incident
wheeze was 0.95 (95%CI 0.85 to 1.07, I2 = 0%, 8 trials, 1770 infants). Among
1364 infants enrolled in 6 trials, the risk ratio of lower respiratory tract
infection following probiotic use was 1.26 (95%CI 0.99 to 1.61, I2 = 0%).
Conclusions: We found no evidence to support a protective association
between perinatal administration of probiotics and clinician-diagnosed
asthma or childhood wheeze. There is currently insufficient evidence from
randomized controlled trials to recommend probiotics for the primary
prevention of these disorders. Extended follow up of existing trials, along
with further clinical and basic research, are required to accurately define
the role of probiotics in the prevention of childhood asthma.
A26
Corn-dependent exercise-induced anaphylaxis
Mitra Abaeian*, Rozita Borici-Mazi
Department of Medicine, Queens University, Kingston ON, Canada
E-mail: mitra.abaeian@medportal.ca
Background: Exercise-induced anaphylaxis is a rare disorder characterized
by the development of a severe allergic response occurring after mild- tostrenuous physical activity. Food-dependent exercise-induced anaphylaxis
(FDEIA) comprises 30-50% of all cases of exercise-induced anaphylaxis [2].
Diagnosis involves careful history and appropriate skin prick testing and
food specific IgE levels [4,6]. However, food dependent exercise challenges
may be required to confirm the diagnosis [6]. We describe the case of a 51
year old male, diagnosed with corn dependent exercise anaphylaxis via
serial exercise challenges.
Methods: Case report and literature review.
Results: A 51 year old male military pilot described the following symptoms
10 minutes after running on the treadmill: sudden onset palm pruritus,
bilateral arm tingling, urticarial rash on his arms and chest, tongue and
eyelid swelling, and difficulty speaking/swallowing. He denied wheezing,
shortness of breath, gastrointestinal symptoms, or light-headedness. He was
self-treated with 50 mg of diphenhydramine and loratadine. His symptoms
resolved in 2-3 hours. He had consumed a Shepherds Pie approximately
45 minutes prior to exercise. The ingredients included beef, potato, corn,
wheat, flour, and Worchestershire sauce. He denied ingestion of ASA/NSAIDS
or alcoholic beverages prior to the event. His past medical history was
remarkable for hypercholesterolemia and diet-controlled Diabetes Mellitus.
He had a history of seasonal allergies for which he was on maintenance
allergen immunotherapy. His medications included Crestor, Coenzyme Q10,
and a fiber supplement. Physical examination was unremarkable. Skin prick
testing to the individual ingredients of the Shepherds Pie were negative. IgE
levels were positive for corn and wheat, and negative to the other
ingredients. Patient was advised a wheat and corn free diet and was able to
resume his exercise routine. Subsequently, he underwent serial food
dependent exercise challenges. The exercise challenges verified that corn
was the culprit food. The patient was advised to stop eating corn, introduce
wheat, and resume his regular exercise routine. He had two minor episodes
of urticaria with exertion in the following year, confirmed to be from
accidental exposure to corn.
Page 12 of 36
Conclusions: This case demonstrated that, although wheat is one of the

most common triggers of food dependent exercise induced anaphylaxis,
corn was the culprit for this patients exercise induced symptoms. Food
dependent exercise challenges can be time consuming and associated
with risks, but yet important to verify the diagnosis when multiple
triggers are suspected.
References
1. Maulitz RM, Pratt DS, Schocket AL: Exercise-induced anaphylactic reaction
to shellfish. J Allergy Clin Immunol 1979, 63:433-434.
2. Dascola CP, Caffarelli C: Exercise-induced anaphylaxis: a clinical view. Ital J
Pediatr 2012, 38:43.
3. Miller CWT, et al: Exercise-induced anaphylaxis: a serious but preventable
disorder. Phys Sportsmed 2008, 36(1):87-94.
4. Barg , et al: Exercise-Induced Anaphylaxis: an update on diagnosis and
treatment. Curr Allergy Asthma Rep 2011, 11(1):45-51.
5. Sheffer , et al: Exercise-induced anaphylaxis: a serious form of physical
allergy associated with mast cell degranulation. J Allergy Clin Immunol
1985, 75(4):479-84.
6. Robson-Ansley P, DuToit G: Pathophysiology, diagnosis, and management
of exercise-induced anaphylaxis. Curr Opin Allergy Clin Immunol 2010,
10(4):312-7.
A27
Chronic Spontaneous Urticaria the Saskatchewan experience and
questionnaire survey
Natasha Gattey*, Bahar Bahrani, Peter Hull
Department of Medicine, University of Saskatchewan, Saskatoon,
Saskatchewan, Canada, S7N 0W8
E-mail: Nrg977@mail.usask.ca
Background: Chronic spontaneous urticaria (CSU) is defined as urticaria
persisting for more than 6 weeks. An autoimmune basis is held
responsible for more than half the cases. In this questionnaire study, we
examined responses to treatment, current urticarial activity, effect on
lifestyle, frequency of hospital visits, beliefs of causation, and satisfaction
with treatment method.
Methods: The patients were ascertained from the patients seen in the
Division of Dermatology at the University of Saskatchewan. 173 patients
with CSU had been seen between 2003 and 2013 and an autologous
serum skin test (ASST) had been performed on 138 patients. 101
participants responded.
Results: In the original cohort there were significantly more females than
males (130:43). The ASST was positive in 58 patients (42.02%), and only a
quarter of these were men (M: F; 12:46).
Of the respondents, 80 were women and 21 men. The age range was 1
year to 81. The mean age was 36 years. The average duration of
symptoms was 9.3 years. They included 40 patients who were ASST
positive (M: F; 8:32) and 49 negative M:F; 12:37 ). 50 participants no
longer had hives. Patients reported being most bothered by pruritus,
disturbed sleep, anxiety and their physical appearance including facial
swelling. Many (71.2%) had missed work or school because of the
urticaria. Almost 22% of participants attributed stress to be a major cause
of their CSU.
Twenty-nine patients found antihistamines alone gave adequate relief of
urticaria. Prednisone, as prescribed by emergency room physicians and
family practitioners, was added as treatment in about a fifth of all the
participants.
Twenty ASST positive patients with severe uncontrollable hives were
treated with intravenous immunoglobulin (IVIG) available to the patients
at no cost through Canadian Blood Transfusion Services. 85.0% of these
patients had improved quality of life, with 13 of these patients were now
free of urticaria and no longer receiving IVIG. Three patients who did not
benefit from IVIG did respond to methotrexate. None of the ASST
negative patients received IVIG.
Conclusion: In this follow-up questionnaire study, about 30% of patients
found antihistamines gave effective control. Half the patients had been
free of urticaria for at least 3 months. About 40% of patients with CSU
had an autoimmune basis as assessed by the ASST and IVIG was a highly
effective treatment for this group.

A28
Diagnostic yield of allergy testing in Pediatric Eosinophilic Esophagitis:
a 10 year experience at a tertiary care centre
Perri R Tutelman1*, Jason Ohayon2, Jefferson Terry3, Mary E Sherlock1
1
Pediatric Gastroenterology and Nutrition, McMaster Childrens Hospital,
McMaster University, Hamilton, Ontario, Canada; 2Department of Pediatrics,
McMaster Childrens Hospital, McMaster University, Hamilton, Ontario,
Canada; 3Department of Pathology and Molecular Medicine, McMaster
Childrens Hospital, McMaster University, Hamilton, Ontario, Canada
E-mail: tutelmp@mcmaster.ca
Background: Eosinophilic Esophagitis (EoE) is a disease in children
characterized by esophageal dysfunction and eosinophilic infiltration [1].
Patients frequently present with an atopic history; therefore, allergy
testing by both skin prick and food patch testing are often performed.
However, the utility of allergy testing remains unclear [1,3]. Treatment
with topical corticosteroids may be needed for clinical and histologic
improvement if allergic triggers are not identified [1,2]. However, the
natural history of EoE suggests that this condition is chronic and may
recur when corticosteroids are withdrawn [2]. Therefore, treatment with
dietary/aeroallergen avoidance is preferable to reduce the need for oral
corticosteroids, while preventing exacerbation of EoE [3]. This study aims
to describe the atopic characteristics of a pediatric cohort with EoE over a
10 year period at a tertiary care center.
Methods: All children (< 18 years) who had esophagogastroduodenoscopy
with biopsy proven EoE (15+ eosinophils per high power field) at McMaster
Childrens Hospital between January 2003 and December 2012 were
identified and their medical records reviewed. Data pertaining to patient
demographics, symptoms at diagnosis, atopic history, endoscopic and
histologic findings, results of allergy testing (skin prick, patch and
immunoCAP) and treatment outcomes were extracted.
Results: A total of 96 cases were identified. The median age at diagnosis
was 13.2 years (IQR=8.6-15.7), and 72 of the identified cases were male
(74.2%). Seventy-four of 91 (81%) and 62 of 79 (78%) patients with data
available reported a history of personal and family atopy, respectively. Six
patients (7%) had a first degree family member diagnosed with EoE.
Patients who reported a history of food allergy were significantly more
likely to present with a food bolus impaction at diagnosis (p=0.035,
OR=3.056). Sixty-nine patients underwent allergy testing as part of a
standard EoE workup, of which, 60 (87.0%) had a positive test result. Ten
(14.5%) patients who had identifiable allergies were positive only to
environmental allergens. The top identified food and environmental
allergens were recorded by allergy test type (Figs 1, 2, 3, 4).
Figure 1(abstract A28) (N=69) underwent skin prick testing
Page 13 of 36
Conclusions: Pediatric EoE is considered to be an allergic disease with

both environmental and food allergen triggers in many patients. A
majority of patients present with a history of atopy and show positive
allergy test results to both foods and aeroallergens. Both environmental
and food allergen elimination should be considered a part of a therapeutic
program. Identification of offending allergens by allergy skin and patch
testing can be an important factor in guiding clinical decision making.
References
1. Liacouras CA, Furuta GT, Hirano I, Atkins D, Attwood SE, Bonis PA, et al:
Eosinophilic esophagitis: updated consensus recommendations for
children and adults. J Allergy Clin Immunol 2011, 128:3-20.
2. Helou EF, Simonson J, Arora AS: 3-Yr-Follow-Up of Topical Corticosteroid
Treatment for Eosinophilic Esophagitis in Adults. Am J Gastroenterol 2008,
103:2194-2199.
3. Henderson CJ, Abonia JP, King EC, Putnam PE, Collins MH, Franciosi JP,
et al: Comparative dietary therapy effectiveness in remission of pediatric
eosinophilic esophagitis. J Allergy Clin Immunol 2012, 129:1570-1578.
A29
Bloodworm induced Anaphylaxis
Peter Ho*, Chrystyna Kalicinsky
Section of Allergy and Clinical Immunology, Department of Internal
Medicine, University of Manitoba, Winnipeg, Manitoba, Canada, R3A 1R9
E-mail: hop@cc.umanitoba.ca
Introduction: Bloodworms are a group of bristle worms found at the
bottom of marine waters. They have pale skin, which allows their red
body fluid, which contains hemoglobin, to show through, hence the
name bloodworm. Bloodworms are often used as bait in fishing and are
also available commercially as a food-source for aquarium fish [1,2].
This case report describes a patient who experienced repeated allergic
reactions after feeding her fish.
Case report: A 21 year old female student was seen in the Adult Allergy
and Immunology clinic for evaluation of hives. Eleven months ago, the
patient experienced three distinct episodes where she experienced hives
and itching affecting her neck. The first episode lasted for 30 minutes
and then spontaneously resolved. Her second episode was similar to the
first, but she also experienced the sensation of throat closing. She denied
tongue or lip swelling and resolution occurred within 30 minutes. Her
third episode was similar to her second episode and in addition she
experienced itchy eyes. When the patient was asked about any suspected
triggers, should reported that these symptoms occurred shortly after
feeding her fish with bloodworms. After she suspected bloodworms as

Figure 2(abstract A28) N=69 underwent skin prick testing
Figure 3(abstract A28) N=35 underwent patch testing
Figure 4(abstract A28) N=14 underwent ImmunoCAP testing.
Page 14 of 36

the etiology for her reactions, she switched fish food to mosquito larvae
and has had no further recurrence.
The patient had epicutaneous skin testing to a solution of bloodworms in
saline, which was positive.
Discussion: This patient had recurrent urticaria as well as subjective
respiratory compromise and conjunctivitis which occurred shortly after
contact with bloodworms, with positive epicutaneous skin test. She meets
the clinical diagnosis of anaphylaxis [3]. A literature search conducted in
Pubmed with the keywords Bloodworm Allergy in July 2013 identified a
case report of blood-worm induced asthma, but did not reveal any
published reports of blood-worm induced anaphylaxis [4]. We counseled the
patient to avoid any further contact with Bloodworms and to continue with
an alternative fish food.
References
1. Bloodworm facts. 2013 [http://www.mainebloodworms.com/facts.html],
Accessed July 20.
2. Bloodworm: Complete Guide to Fishing Uses & Applications. 2013
[http://www.ccmoore.com/bait-blog/bloodworm-complete-guide-fishinguses-applications/], Accessed July 20.
3. Lieberman P, Nicklas R, Oppenheimer J, et al: The diagnosis and
management of anaphylaxis practice parameter: 2010 update. J Allergy
Clin Immunol 2010, 126(3):477-80, e1-42.
4. Wu KC, Rsnen K, Hudson TJ:.
A30
Enigmas of primary immunodeficiency and mycobacterial infection in
our territory
Roya Sherkat
Acquired Immunodeficiency Research Center, Isfahan University of Medical
Sciences, Isfahan, Iran
E-mail: sherkat@med.mui.ac.ir
Introduction: Defects of the immune system in Primary immunodeficient
diseases (PIDs) predispose individuals to recurrent infections. Complex
genetic components for susceptibility to mycobacterial disease have been
suggested. Natural human immunity to the mycobacteria group, including
Mycobacterium tuberculosis(MTB), Bacille Calmette-Gurin (BCG) or
nontuberculous mycobacteria (NTM) relies on the functional IL-12/23-IFN-g
integrity of macrophages (monocyte/dendritic cell) connecting to
T lymphocyte/NK cells [1]. Restricted defective molecules in the circuit and
recently discovered CYBB responsible for autophagocytic vacuole and
proteolysis have been identified in around 60% of patients with the
Mendelian susceptibility to the mycobacterial disease (MSMD) phenotype [2].
Primary defects in oxidase activity in chronic granulomatous disease (CGD)
lead to severe, life-threatening infections. The role of phagocytic
respiratory burst in host defense against mycobacterium tuberculosis was
controversial. Previous studied showed that the critical role at reactive
oxidants is to serve as intracellular signals for activation of microbicidal
enzymes, rather than excretions a microbicidal effect perse [3]. The role of
phagocytic respiratory burst in host defense against M. TB is further
supported by recent studies discovered immunological defects secondarily
affecting phagocyte respiratory burst function and resulting in primary
immunodeficiencies with varied phenotypes, including susceptibilities to
pyogenic or mycobacterial infections [4].
The patients with severe PIDs like SCID have broader diverse infections
susceptibility and mycobacterial infections as well, however, Common
variable immunodeficiency (CVID) mostly characterized by a deficiency of
immunoglobulins and recurrent sinopulmonary infections.
Method: We overview the clinical rate of mycobacterial disease in our
PID cases and evaluate the complex cases.
Results: Two hundred PID cases were evaluate between 1996-2013 in our
clinic, Among 5% of them which diagnosed as MSMD nearly all presented
with mycobacterial infection. 8% diagnosed as CGD and interestingly 60%
of them have been experienced mycobacterial disease sometimes in their
life, as disseminated BCG or late onset complications of BCG including
osteomyelitis or MTB once or more than one episode through their life.
Also we have presented a CVID patient with disseminated TB and
granulomatouse hepatitis, TB arthritis and peritonitis.
Conclusion: PID cases Like CGD, MSMD or CVID which are living in areas
with high prevalence of mycobacterial infection could have quiet different
Page 15 of 36
presentations and the study of these complex cases has provided essential
insights into the functioning of the immune system. Despite the
conventional view we have confirmed that the generation of ROIS by
phagocytic respiratory burst may play a role in the defense of the host
against M. tuberculosis by clinical evidence.
References
1. Salem S, Gros P: Genetic determinants of susceptibility to Mycobacterial
infections: IRF8, a new kid on the block. Adv Exp Med Biol 2013, 783:45-80.
2. Lee WI, Huang JL, Yeh KW, Jaing TH, Lin TY, Huang YC, Chiu CH: Immune
defects in active mycobacterial diseases in patients with primary
immunodeficiency diseases (PIDs). J Formos Med Assoc 2011,
110(12):750-8.
3. Reeves EP, Lu H, Jacobs HL, et al: Killing activity of neutrophils is
mediated through activation of proteases by K+ flux. Nature 2002,
416:291-7.
4. De Oliveira-Junior EB, Bustamante J, Newburger PE, Condino-Neto A: The
human NADPH oxidase: primary and secondary defects impairing the
respiratory burst function and the microbicidal ability of phagocytes.
Scandinavian Journal of Immunology 2011, 73(5):420-427.
A31
Impact of perinatal antibiotic exposure on the infant gut microbiota at
one year of age
Ryan Persaud1*, Meghan B Azad2, Theodore Konya3, David S Guttman4,
Radha S Chari5, Malcolm R Sears6, Allan B Becker7, James A Scott3,
Anita L Kozyrskyj2, the CHILD Study Investigators8
1
Pharmacy, University of Manitoba, Winnipeg, Manitoba, Canada; 2Pediatrics,
University of Alberta, Edmonton, Alberta, Canada; 3Dalla Lana School of
Public Health, University of Toronto, Toronto, Ontario, Canada; 4Cell &
Systems Biology, University of Toronto, Toronto, Ontario, Canada; 5Obstetrics
& Gynecology, University of Alberta, Edmonton, Alberta, Canada;
6
Department of Medicine, McMaster University, Hamilton, Ontario, Canada;
7
Pediatrics & Child Health, University of Manitoba, Winnipeg, Manitoba,
Canada; 8Canadian Healthy Infant Longitudinal Development Study
E-mail: umpersar@cc.umanitoba.ca
Background: Disruption of the infant gut microbiota has been linked to
long-term health outcomes, including obesity and allergic disease [1].
Antibiotics can significantly alter the microbiota [2], but evidence is scarce
for the long-term effect of antibiotic exposure during the perinatal period
(shortly before or after delivery). Our research aimed to determine the
impact of infant and maternal perinatal antibiotic exposure on the infant gut
microbiota at 1 year of age.
Methods: Antibiotic exposure in the perinatal period was documented by
retrospective hospital chart review of 184 Manitoban infants enrolled in
the Canadian Healthy Infant Longitudinal Development (CHILD) Study.
Data on mode of delivery, indications for treatment, and maternal health
status were also collected. Gut microbiota composition (relative abundance
of select taxa chosen for their previous association with antibiotic exposure
or health outcomes) was determined by Illumina 16S rRNA sequencing of
fecal samples collected at 1 year of age. Microbiota diversity was
characterized using Chao1 Richness Estimator, Shannon Diversity Index,
and Simpson Diversity Index.
Results: Of the 184 infants, 8 (4.4%) received intravenous antibiotics
during the perinatal period for suspected sepsis. Seventy-two (39.1%)
mothers received antibiotics shortly before or after delivery, resulting in
indirect antibiotic exposure of the infant via placental transfer or breast
milk. Indirect perinatal antibiotic exposure did not alter the 1 year old
infants overall microbiota diversity; however, these infants had an
increased relative abundance of Clostridium (p=0.04). Infants who were
both directly and indirectly exposed to antibiotics had increased
microbiota diversity at 1 year of age (p<0.03 for Shannon and Simpson
diversity indices computed at Family and Genus levels). These infants also
had a lower relative abundance of the phylum Bacteriodetes (p=0.03), and
increased relative abundance of the genus Akkermansia (p=0.03) and the
phylum Proteobacteria (p=0.02). Similar trends were observed following
stratification by mode of delivery, premature rupture of membranes,
presence of Group B Streptococcus, breastfeeding, and postnatal antibiotics
(throughout the first year); except for the decrease in Bacteroidetes, which
was attenuated in breastfed infants.

Page 16 of 36
Conclusions: Antibiotics administered at birth are associated with longlasting changes to the infant gut microbiota, increasing overall diversity
and modifying community composition until at least 1 year of age.
Maternal perinatal antibiotics may also influence infant gut microbiota
composition. Going forward, we will conduct comprehensive microbiota
analyses and investigate how antibiotic-associated changes ultimately
influence health outcomes during later childhood.
References
1. Penders J, Thijs C, van den Brandt PA, Kummeling I, Snijders B, Stelma F,
Adams H, van Ree R, Stobberingh EE: Gut microbiota composition and
development of atopic manifestations in infancy: the KOALA Birth
Cohort Study. Gut 2007, 56:661-7.
2. Willing BP, Russell SL, Finlay BB: Shifting the balance: antibiotic effects on
hostmicrobiota mutualism. Nature Reviews Microbiology 2011, 9:233-243.
Reference
1. Nguyen-Luu , Ben-Shoshan , Clarke : Inadvertent exposures in children
with peanut allergy. Pediatric Allergy and Immunology 2012, 23(2):133-9.
A32
Accidental exposure (AE) to peanut in a large cohort of Canadian
children with peanut allergy
Sabrine Cherkaoui1*, Moshe Ben-Shoshan2, Reza Alizadehfar2, Yuka Asai3,
Greg Shand4, Yvan St-Pierre4, Laurie Harada5, Mary Allen6, Ann Clarke4,7
1
Division of Internal Medicine, Department of Medicine, University of
Montreal, Montreal, QC, Canada; 2Division of Pediatric Allergy and Clinical
Immunology, Department of Pediatrics, McGill University Health Center,
Montreal, QC, Canada; 3Division of Dermatology, Department of Medicine,
McGill University Health Center, Montreal, QC, Canada; 4Division of Clinical
Epidemiology, Department of Medicine, McGill University Health Center,
Montreal, QC, Canada; 5Anaphylaxis Canada (AC), Toronto, ON, Canada;
6
Allergy/Asthma Information Association (AAIA), Toronto, ON, Canada;
7
Division of Clinical Immunology and Allergy, Department of Medicine,
McGill University Health Center, Montreal, QC, Canada
E-mail: sabrine.cherkaoui@umontreal.ca
Background: Cows milk allergy is the most common food allergy among
children. Previous studies have reported that up to 75% of children may
tolerate baked milk goods. Various forms of baked milk challenges have
been used in the literature such as muffins, pizza, and waffles. However,
the food used for baked milk challenge is often prepared in a nonstandardized manner by the parents at home, raising concerns with
regards to validity, reproducibility and convenience. Instant skim milk
powder is made by a food process that involves heating skim milk to up to
200C for up to 30 minutes which should be sufficient to denature thermolabile proteins.
Objective: To evaluate the usefulness of skim milk powder as a
convenient standardized form of baked milk challenge.
Methods: All challenges to instant skim milk powder (cumulative dose of
4g proteins) performed at Sainte-Justine Hospital in Montreal, Canada
between November 2008 and January 2013 were retrospectively reviewed.
Observed reaction rates to challenge and to subsequent home
introduction were compared to previous literature using different forms of
baked milk. Demographic data, clinical characteristics, skin prick tests (SPT)
and specific IgE levels were compared between those that passed and
those that failed the challenge.
Results: Thirty-nine children underwent an open food challenge to instant
skim milk powder and thirty patients (76,9%) passed the challenge. All of
those who passed the challenge successfully introduced baked milk
products at home. Compared to those who were baked milk tolerant,
baked milk reactive children had higher median specific IgE levels to cows
milk (P < .0005), casein (P < .001), a-lactalbumin (P < .001) and blactoglobulin (P < .04). Both cohort reaction rates and characteristics were
comparable to previous literature using other forms of baked milk product
for challenge.
Conclusion: Challenge with instant skim milk powder is a safe,
convenient and easily standardized alternative to home baked food for
baked milk challenge.
Background: We have previously estimated that the annual rate of

accidental exposure (AE) to peanut in a Canadian cohort of 1411 children
with peanut allergy, followed for 2227 patient-years, was 11.9% [1]. The
cohort has increased to 1825 children, with 4134 patient-years of followup, and we determined the incidence of AE in this expanded cohort and
described the severity, management, and location of the AE.
Methods: Children with physician-confirmed peanut allergy were
identified from the Montreal Childrens Hospital and food allergy advocacy
organizations from 2004 to May 2013. Parents completed a questionnaire
at study entry and every two years regarding their childs AE to peanut
over the preceding year; starting in 2010, follow-up questionnaires were
administered annually.
Result: The mean age (SD) was 2.4 (2.1) years at diagnosis and 7.0 (4.0)
years at the time of the initial questionnaire completion. Patients were
predominantly boys (61.8%) and Caucasians (89.5%). When all children were
included, regardless of length of observation interval, 456 AE occurred in
336 children over 4134 patient-years, yielding an annual incidence rate of
11.0 % (95 % CI, 9.0 - 13.1%). Because the rate of AE may vary with
observation interval length, the rate was calculated excluding AE occurring
after the initial questionnaire and excluding those providing <1 year of
observation; this yielded 164 AE in 141 children over 1405 patient-years, for
an annual incidence rate of 11.7% (95 % CI, 9.7 % - 13.6%). One hundred
forty-seven AE were mild, 242 moderate, and 67 severe. Among 429 AE
preceded by an initial reaction, 22.4 % of AE were more severe than the
initial reaction. No treatment was administered for 41 (27.9 %) mild AE,
40 (16.5%) moderate and 4 (6.0%) severe. Of 309 AE that were moderate/
severe, only 93 (30.1%) sought medical attention and among these, only
30.1% received epinephrine. Of the 153 moderate/severe AE treated at
home, only (11.8%) received epinephrine. Thirty-nine percent of AE occurred
at home, 17.3% at relatives/friends home, 11.4% in restaurants, 7.5% at
schools/day-cares prohibiting peanut, 3.7% at schools/day-cares allowing
peanuts, and 20.6% at other or unknown places.
Conclusion: Despite increasing efforts to provide information on the
management of food allergy, AE continue to occur, mainly in the childs
home but also in peanut free schools/day-cares. Most moderate/severe AE
are managed inappropriately by caregivers and physicians. Consequently,
more education is required on the importance of strict allergen avoidance
and the need for prompt and correct management of anaphylaxis.
A33
Powder milk as a user-friendly tool for baked milk challenge
Sabrine Cherkaoui1, Louis Paradis2,3, Philippe Bgin2,3, Anne Des Roches2*
1
Division of Internal Medicine, Department of Medicine, University of
Montreal, Montreal, QC, Canada; 2Divisions of Pediatric Allergy and
Immunology, Department of Pediatrics, Sainte-Justine Hospital, Montreal, QC,
Canada; 3Divison of Clinical Immunology and Allergy, Department of
Medicine, University of Montreal, QC, Canada
E-mail: a.des.roches@umontreal.ca
A34
Angioedema in the emergency department: clinical presentation and
outcomes
Sarah L Felder1*, R M Curtis1, Ian Ball2, Rozita Borici-Mazi3
1
School of Medicine, Queens University, Kingston, Ontario, K7L 3N6, Canada;
2
Department of Emergency Medicine, Queens University, Kingston, Ontario,
K7L 3N6, Canada; 3Division of Allergy/Immunology, Department of Internal
Medicine, Queens University, Kingston, Ontario, K7L 3N6, Canada
E-mail: sfelder@qmed.ca
Rationale: Angioedema is an acute, potentially life-threatening presentation
with multiple mechanistically distinct causes. We hypothesized that the
clinical features of angioedema correlate with the cause of angioedema and
may predict the outcomes of angioedema in the emergency department
(ED).
Methods: A retrospective data review of all ED visits to two academic
tertiary care centers over the period of July 1, 2007 to March 31, 2012 was
conducted. Records selected for full review met the inclusion criteria of
documented visible swelling and one of the ICD-10 diagnostic codes for
anaphylactic shock, angioneurotic edema, allergy unspecified, defects in the
complement system, or unspecified drug adverse effect. Age, sex, cause and

site of swelling, comorbidities, medications, allergies, admissions, etc. were

collected via a standardized form. Bivariate and multivariate analyses were
performed using chi-square tests. Potential predictors for admission were
identified using a multivariate logistic regression model. A p value less than
0.05 was considered significant. This study was approved by Queens
University Ethics Committee.
Results: Medical records from 527 ED visits by 455 patients were included
in the study, and 21 patients were admitted. Angioedema was encountered
at annual rate of 10 per 10000 ED visits. Patients who presented with
urticaria (29.8%) were significantly more likely to present with lip swelling
(p=0.001) and extremity swelling (p=0.008), while the absence of urticaria
correlated with tongue swelling (p=0.001). The mean duration of stay in ED
was significantly longer in patients with urticaria (p<0.001), but the presence
of urticaria did not predict admission. A probable cause was identified in
48.8% of visits. Periorbital angioedema was associated with environmental,
contact, and insect sting allergy (p<0.001). 58.3% of patients with
angioedema due to drug allergy had lip angioedema (p=0.032). C1 esterase
inhibitor deficiency was most frequently associated with a history of
previous episodes. Several factors were found to predict admission,
including NSAID-induced angioedema (OR=15.3), epinephrine treatment
(OR=8.34), hypotension (OR=15.7), multiple site angioedema (OR=4.25),
pharyngeal angioedema (OR=1.23), and tongue angioedema (OR=4.62).
Conclusions: This large cohort retrospective review confirms causeclinical associations in angioedema and demonstrates novel predictors of
morbidity, with implications in clinical practice.
Acknowledgments: This work was funded by Summer Studentship
Awards from CSL Behring.
References
A35
Infant gut microbiota and the development of wheeze in early
childhood
Scarlet M Salas1,2*, Meghan B Azad3, Tedd Konya4, David S Guttman5,
Allan B Becker1,2, Malcolm R Sears6, James A Scott4, Anita L Kozyrskyj1,3,
the CHILD Study Investigators7
1
Manitoba Institute of Child Health, Winnipeg, Manitoba, R3E 3P4, Canada;
2
Pediatrics and Child Health, University of Manitoba, Winnipeg, Manitoba,
R3E 3P4, Canada; 3Pediatrics, University of Alberta, Edmonton, Alberta, T6T
1C9 Canada; 4Dalla Lana School of Public Health, University of Toronto,
Ontario, M5T 1R4, Canada; 5Cell & Systems Biology, University of Toronto,
Toronto, Ontario, M5S 3B2, Canada; 6Medicine, McMaster University,
Hamilton, Ontario L8S 4K1, Canada; 7Canadian Healthy Infant Longitudinal
Development Study, Canada
E-mail: ssalas@mich.ca
Background: Commensal gut microbes play an important role in human
development and lifelong health. There is increasing evidence that
disruption of the infant gut microbiota may be linked to the development
of childhood allergy and asthma-related outcomes, including wheezing.
Our objective was to investigate the association of infant gut microbiota
diversity and composition with development of wheeze in early childhood.
Methods: The study population included 160 infants enrolled at the
Winnipeg site of the Canadian Healthy Infant Longitudinal Development
Study (CHILD) population-based birth cohort. Standardized questionnaires
were completed by mothers at 3, 6 and 12 months after birth, and reported
on breastfeeding and occurrence of infant wheezing. Wheezing (defined as
a whistling sound in the chest lasting more than 15 minutes and occurring
with or without a cold) was classified according to the number of episodes
in the first year of life: 0, 1, 2 or 3. Mode of delivery and use of antibiotics
were documented from hospital and medical records. Fecal samples were
collected at one year of age and microbiota composition (relative
abundance of select taxa) was characterized by high-throughput Illumina
sequencing of the 16S rRNA gene. Biodiversity was evaluated using the
Chao1 richness estimator and the Shannon & Simpson diversity indices.
Results: In the first year of life, any wheezing as defined above was
reported for 36/160 infants (22.5%). Sixteen infants (10.0%) wheezed on
more than one occasion, and 12 infants (7.5%) experienced 3 or more
wheezing episodes. Selected taxa were chosen for composition analysis,
based on their established associations with other allergic disease outcomes.
The genus Clostridium was under-represented among infants with two or
Page 17 of 36
more wheezing episodes (p=0.04). Preliminary comprehensive analyses

revealed that operational taxonomic units (OTUs) belonging to the Families
Ruminococcaceae, Rikenellaceae and Lachnospiraceae were overrepresented among wheezing infants (all p<0.01). Gut microbiota diversity
and richness were not significantly associated with wheeze; these findings
were unchanged following adjustment for gender, mode of delivery,
breastfeeding, and antibiotic exposure.
Conclusions: In this preliminary analysis, we identified several crude
differences in microbiota composition among wheezing infants, although a
significant association with overall biodiversity was not observed. The
long-term clinical relevance of these changes will be the focus of ongoing
studies within the CHILD cohort. Detailed and extended assessment of
wheeze (including its severity and association with infection and allergic
disease), gut microbiota, and relevant environmental exposures will be
conducted at different ages throughout childhood.
A36
Systematic review of outcome measures in trials of pediatric
anaphylaxis treatment
Tamar Rubin1, Jacqueline Clayton1, Denise Adams1,2, Hsing Jou1,2,
Sunita Vohra1,2,3*
1
Department of Pediatrics, University of Alberta, Edmonton, Alberta, Canada;
2
CARE Program, University of Alberta, Edmonton, Alberta, Canada;
3
Department of Public Health Sciences, University of Alberta, Edmonton,
Alberta, Canada
E-mail: svohra@ualberta.ca
Background: Considerable heterogeneity has been observed in the
selection and reporting of disease-specific pediatric outcome measures in
randomized controlled trials (RCTs) [1]. This makes interpretation of
results and comparison across trials challenging [2]. Outcome measures in
pediatric anaphylaxis trials have never previously been systematically
assessed [3]. This systematic review (SR) will identify and assess outcome
measures used in RCTs of anaphylaxis treatment in children. As a
secondary objective, this SR will assess the evidence for current treatment
modalities for anaphylaxis in the pediatric population.
Methods: We searched MEDLINE, EMBASE, The Cochrane Library, Cochrane
Central Register of Controlled Trials (CENTRAL), and CINAHL from 2001 until
December 2012. We also searched websites listing ongoing trials. We
included randomized and controlled trials of anaphylaxis treatment in
patients 0-18 years of age. Two authors independently assessed articles for
inclusion.
Results: No published studies fulfilled the inclusion criteria (Fig 1).
Conclusions: There is an alarming absence of RCTs evaluating the
treatments for anaphylaxis in children. High quality studies are needed and
are possible to design, despite the severe and acute nature of this condition.
Consensus about the selection and validation of appropriate outcome
measures will enhance the quality of research and improve the care of
children with anaphylaxis.
Systematic review registration: CRD42012002685.
References
1. Clarke M: Standardising outcomes for clinical trials and systematic
reviews. Trials 2007, 8:39.
2. Williamson PR, Gamble C, Altman DG, Hutton JL: Outcome selection bias
in meta-analysis. Stat Methods Med Res 2005, 14:515-524.
3. Sinha I, Jones L, Smith RL, Williamson PR: A systematic review of studies
that aim to determine which outcomes to measure in clinical trials in
children. PLoS Med 2008, 5(4):e96.
A37
IgE Mediated allergy to wheat in a child with celiac disease
Tiffany Wong*, Edmond S Chan
Department of Pediatrics, Division of Allergy & Immunology, Faculty of
Medicine, University of British Columbia, Vancouver, BC, Canada
E-mail: tiffany.wong@cw.bc.ca
Introduction: Celiac disease and immediate type hypersensitivity to
wheat are immune responses with different pathogenic mechanisms.

Page 18 of 36
Figure 1(abstract A36) Search Flow Diagram
Both diseases are well known entities but their coexistence in the same
patient is rarely reported.
Case presentation: We report the case of a girl with celiac disease who
subsequently developed IgE mediated hypersensitivity to wheat. The
patient is a Caucasian female who was diagnosed with celiac disease at
18 months of age after presenting with recurrent vomiting and failure to
thrive. Her anti-tTG antibody level was greater than 200 E.U. and biopsy
results from endoscopy were consistent with celiac disease. Specific IgE
antibody to wheat was negative at 2 years of age. Around seven years of
age, she developed immediate symptoms of urticaria, cough and
shortness of breath with accidental exposures to wheat. Specific IgE
antibody testing was repeated and positive to wheat (42.5 kU/L), as well
as rye (33.9 kU/L), barley (53.4 kU/L) and oat (11.3kU/L). At 9 years of age,
skin prick testing was positive to wheat, barley and rye but negative to
oat. The patient has subsequently tolerated an open oral food challenge
to oat. She continues to avoid wheat, rye and barley and carries an
epinephrine autoinjector at all times.
Conclusion: To our knowledge, this is the first report of a patient with
celiac disease and concomitant IgE-mediated allergy to wheat presenting
with immediate symptoms in two body systems. Although the
pathophysiology of these diseases is different, this case demonstrates
that they are not exclusive of one another. In clinical assessment of celiac
disease over time, development of IgE mediated allergy is possible and
should be considered.
A38
Anaphylaxis to Celebrex during an oral challenge
Vaishaali Manga1*, Gordon Sussman2
1
Department of Internal Medicine, Memorial University, St. Johns,
Newfoundland and Labrador, A1B3V6, Canada; 2Department of Clinical
Immunology and Allergy, University of Toronto, Toronto, Ontario M4V 1R2,
Canada
E-mail: vmanga@munmed.ca
Case: We report a case of a 65-year-old female with an anaphylactic type
reaction during a graded oral celecoxib challenge. She was previously
using NSAIDS and Celebrex (celecoxib) for analgesia in 2005. However,

due to the side effect profile of COX2 inhibitors, Celebrex was
discontinued. The patients primary analgesic was ibuprofen. Upon
reintroduction of Celebrex, the patient developed urticaria after the
second dose and urticaria with angioedema after the third dose. When
the patient presented to the allergy clinic, it was felt that the urticaria
and angioedema were secondary to ibuprofen. Because she had a
negative crude prick skin test to Celebrex, an oral challenge to Celebrex
was done. One hour after the 200 mg cumulative challenge, the patient
was asymptomatic and an additional 200 mg was given. Twenty minutes
later the patient developed facial flushing, angioedema, respiratory
distress and hypotension, with her blood pressure dropping to 78/53
mmHg from a baseline of 120/80 mmHg. The patient was treated with
epinephrine 0.1 mg subcutaneously, without recovery. After 5 and 15
minutes additional 0.2 mg subcutaneous epinephrine injections were
administered. She was also treated with Reactine 20mg and prednisone
50mg. The patient was stabilized within thirty minutes.
The patient was able to tolerate ibuprofen and sulfonamide antibiotics
without any side effects. She was also taking hydrochlorothiazide on a
daily basis for hypertension. She does not have any previously
documented allergies or adverse reactions to medications.
Discussion: Our patient had an anaphylactic type reaction to celecoxib.
Most patients that have a reaction to celecoxib are thought to have a
hypersensitivity to the sulfonamide moiety. There are two types of
sulfonamide moieties in medications. Antibiotics that contain sulfonamide
have the arylamine moiety, whereas other medications such as
hydrochlorothiazide contain the nonarylamine moiety. Usually patients
with a hypersensitivity to the arylamine sulfonamide can tolerate
medications with the nonarylamine sulfonamide, as they do not typically
cross react. In our case, the patient tolerated sulfonamide antibiotics
(arylamine) and hydrochlorothiazide (nonarylamine) meaning that she is
not reacting to either of the sulfonamide groups, but rather another
component of Celebrex.
Conclusion: Anaphylaxis to Celebrex, although rare, has been reported in
the literature. We report a case of anaphylactic reaction to Celebrex in a
patient that tolerated both arylamines and nonarylamines sulfonamides,
suggesting that our patient has a hypersensitivity to a different
component of Celebrex. This requires further study and demonstrates
necessary caution when challenging with COX2 inhibitors.

A39
Unusual presentation of a patient with complement deficiency and
immunoglobulin deficiency
Vaishaali Manga1*, Donald Stark2
1
Department of Internal Medicine, Memorial University, St. Johns,
Newfoundland and Labrador, A1B3V6, Canada; 2Department of Clinical
Immunology and Allergy, University of British Columbia, Vancouver, British
Columbia, V6Z1Y6, Canada
E-mail: vmanga@munmed.ca
Background: The complement system is a vital component of innate
immunity. Deficiencies in any part of the complement pathway
characteristically present with recurrent infections. C2 factor deficiency is
the most common complement deficiency. The presentation can vary from
being asymptomatic to developing recurrent infections. Thus empiric
vaccinations have been recommended, despite the lack of substantial
evidence to support this practice. Recently, Jonnson and colleagues
revisited this controversial topic and demonstrated the importance of
vaccinations in this patient population. They further established that C2
deficient patients can mount an immune response to vaccination, undergo
class-switching and develop a more efficient phagocytosis.1
C2 deficiency is inherited in an autosomal recessive pattern. Homozygotes
generally present with increased severity of disease as compared to
heterozygotes. Alper and colleagues state that 25% of C2-deficient
homozygotes have increased susceptibility to severe bacterial infections.2
Furthermore, they found that these C2-deficient patients had significantly
lower mean levels of IgG4 and IgA than those patients that did not
demonstrate an increased susceptibility for recurrent infections.
Case: We report a case of a 59-year-old female with a history of C2
deficiency presenting with recurrent upper and lower respiratory tract
infections. Although she received the pneumococcal vaccine, she failed to
mount a response based on her post-vaccination titers. Further workup
revealed a borderline low IgG. Due to her having recurrent infections and
a borderline low IgG, the patient was started on subcutaneous
immunoglobulin (SCIG) therapy as a trial. While on the treatment, she did
not develop any new infections.
Discussion: In the cohort by Jonnson, post-vaccination C2 deficient
patients mounted a good response to vaccination along with a more
efficient phagocytosis via increased opsonin production secondary to a
possible c1q dependent C2-independent pathway [1]. This pathway may
not be effectively activated in post vaccinated C2 patients who are IgG
deficient because of the role IgG plays in the c1q dependent pathway.
Therefore, C2 deficient patients that have a concomitant immunoglobulin
deficiency may respond differently to vaccination than the C2 deficient
patient with normal immunoglobulins. We postulate that our patient did
not respond to antigenic stimulations because she may fall in the 25% C2
deficient homozygous category in which the IgG levels are decreased [2].
Conclusion: Further studies are requires to determine the effectiveness
of vaccination in these two different C2 deficient patient populations and
to help guide vaccination protocols.
References
1. Jonsson, et al: Vaccination against encapsulated bacteria in hereditary C2
deficiency results in antibody response and opsonization due to
antibody-dependent complement activation. Clinical Immunology 2012,
144:214-227.
2. Alper, et al: Immunoglobulin deficiencies and susceptibility to infection
among homogyzotes and heterozygotes for C2 deficiency. Journal of
Clinical Immunology 2003, 4:297-305.
A40
Regulation of Proteinase Activated Receptor-2 on airway epithelium
Vivek Gandhi*, Harissios Vliagoftis
Pulmonary Research Group, Department of Medicine, University of Alberta,
Edmonton, Alberta, T6G 2S2, Canada
E-mail: vivekdip@ualberta.ca
Background: The prevalence of allergic asthma has increased dramatically
over the last 20 years. Environmental allergens such as house dust mites
Page 19 of 36
(HDM), cockroach, fungi and pollens are major asthma triggers. Recent
studies indicate that the serine proteinase activity of these allergens is an
important factor contributing to their ability to induce airway
inflammation. Allergen serine proteinases can activate Proteinase Activated
Receptor -2 (PAR-2), a G protein coupled receptor, which is upregulated on
the airway epithelium of asthmatics. PAR-2 activation is pro-inflammatory
in many biological systems. PAR-2 polymorphisms are associated with the
development of atopy. We have shown that allergic sensitization and
inflammation in mouse models of asthma is PAR-2 dependent. We
have proposed that PAR-2 on the airway epithelium is a sensor for
environmental allergens and leads to allergic inflammation. However, the
regulation of PAR-2 expression on airway epithelium is poorly studied. As
asthmatic airways are under various types of cellular stress, we
hypothesized that cellular stress regulates PAR-2 on airway epithelium.
Methods: To study the effect of cellular stress on PAR-2 expression, Normal
Human Bronchial Epithelial (NHBE) cells were exposed to various stressors
such as inflammatory mediators, hypoxia, growth factor deprivation, ROS
(Reactive Oxygen Species) and RNS (Reactive Nitrogen Species) for various
time periods and PAR-2 mRNA levels were studied by real time PCR. PAR-2
function in stressed cells was assessed by measuring IL-8 release following
activation with PAR-2 specific activating peptide (PAR-2 AP).
Results: Growth factor deprivation significantly upregulated PAR-2 mRNA
(2.25 +/- 0.2 fold), while all the other studied cellular stress stimuli did
not modulate PAR-2 expression on airway epithelial cells. Growth factor
deprived cells showed significantly upregulated PAR-2 mediated IL-8
release (2.1 +/- 0.2 fold) compared to cells grown with growth factors.
Addition of epinephrine, a growth medium supplement used for airway
epithelial cells, prevented the effects of growth factors deprivation on
PAR-2 expression.
Conclusion: Cellular stress could be the driving force for increased PAR-2
expression in asthmatic airways. Further activation of this upregulated
PAR-2 can perpetuate inflammation by releasing higher levels of
inflammatory mediators. Epinephrine, an adrenergic agonist, neutralizes
stress effect on PAR-2 expression. Understanding the mechanisms of these
effects could lead to the development of more specific treatments for
preventing PAR-2 mediated airway inflammation.
A41
Neutropenia in patients with adenosine deaminase deficiency
Vy HD Kim*, Chaim R Roifman, Eyal Grunebaum
Division of Clinical Immunology and Allergy, Department of Paediatrics,
Hospital for Sick Children and University of Toronto, Toronto, Ontario,
Canada
E-mail: vy.kim@sickkids.ca
Background: Adenosine deaminase (ADA) deficiency is a disorder where
the accumulation of purine metabolites, which are particularly toxic to
lymphocytes, can lead to severe, life threatening infections. In addition, ADA
deficiency also affects other tissues. Few reports describe the presence of
neutropenia in these patients, primarily in older patients after hematopoietic
stem cell transplantation (HSCT) or gene therapy. We hypothesized that
abnormal purine metabolism could also affect granulopoiesis.
Objective: The objective of the study was to assess the frequency and
nature of neutropenia in patients with ADA deficiency in the first 180 days
of life.
Methods: This retrospective study analyzed all patients who were
diagnosed with ADA deficiency at the Hospital for Sick Children between
1984 and 2012 and had at least one documented complete blood count
with differential in the first 180 days of life.
A diagnosis of ADA deficiency was made when erythrocytes ADA enzyme
activity was less than 1-2% of control and/or demonstration of mutations
in the ADA gene.
Neutropenia was defined as the absolute neutrophil count of less than
6.0 x 109/L for ages 6 days, less than 1.5 x 109/L for ages 7-13 days, less
than 1.0 x 109/L for ages 14-89 days and less than 1.5 x 109/L for ages
90 days. Patients were excluded if neutropenia was first documented after
chemotherapy for HSCT.
Results: Thirteen patients with ADA deficiency were included in the
study. Nine of the 13 patients had neutropenia that was first documented
within the first 180 days of life (median age of first neutropenia 70 days,

range 1-176 days). In 5 patients, the neutropenia was not present on the
initial blood count but developed over time. The lowest neutrophil counts
ranged from 0.11-1.08 x 10 9 /L (median 0.5 x 10 9 /L). The neutropenia
developed in 7 patients prior to the onset of cotrimoxazole or other
medications that commonly have myelosuppressive effects. The neutropenia
was not associated with infections commonly causing neutropenia or with
autoimmune manifestations. Bone marrow examinations in 2 patients with
neutropenia were reported as normal. The neutropenia improved
spontaneously in 3 patients, while in 4 additional patients it resolved after
initiation of PEG-ADA replacement therapy or HSCT.
Conclusions: Neutropenia occurs commonly in patients with ADA
deficiency. Further studies are required to determine the pathogenesis of
the neutropenia in ADA deficiency.
Page 20 of 36
3.
Martin A, Lavoie L, Goetghebeur M, Schellenberg R: Economic benefits of

subcutaneous rapid push versus intravenous immunoglobulin infusion
therapy in adult patients with primary immune deficiency. Transfus Med
2013, 23:55-60.
A43
Abstract withdrawn
Abstract withdrawn
A42
Implications to payers of switch from hospital-based intravenous
immunoglobulin (IVIg) to home-based subcutaneous immunoglobulin
(SCIg) therapy in patients with primary immunodeficiencies (PID) and
secondary immunodeficiencies (SID) in Canada
William C Gerth1*, Stephen D Betschel2, Arthur S Zbrozek3
1
W. C. Gerth & Associates, Shrewsbury, New Jersey, 07702, USA; 2University
of Toronto, Toronto, Ontario, Canada, M5B 1W8; 3CSL Behring, King of
Prussia, Pennsylvania, 19406, USA
E-mail: gerthw@verizon.net
A44
Migration of the contractile phenotype of human airway smooth
muscle cells in response to supernatants from rhinovirus infected
human bronchial epithelial cells
Abid Qureshi*, Sami Shariff, Sergei Nikitenko, Jason Arnason, Chris Shelfoon,
Suzanne Traves, David Proud, Richard Leigh
Snyder Institute for Chronic Diseases, University of Calgary, Calgary, Alberta,
T2N 4N1, Canada
E-mail: agquresh@ucalgary.ca
Background: A nurse shortage in Canada is contributing to large

amounts of paid/unpaid overtime and increased labor-related
expenditures. Shifting PID/SID patients from hospital-based IVIg to less
labor-intensive home-based SCIg can improve their quality of life and
treatment satisfaction [1] and may improve efficient allocation of nurse
staff. The objectives for this study were to estimate the return on
investment in the upfront cost in nursing time for patient training and
the number of PID/SID patients needed to be switched to SCIg to gain
one full-time nurse equivalent (FTE).
Methods: The return on investment was estimated by multiplying the
hourly nurse compensation ($57.58 = $104,440 1,813) for wage and
benefits for a general duty nurse in British Columbia by the number of
nursing hours in year 1 and subsequent years required for each route of
administration. The number of patients needed to be switched to SCIg to
gain one nurse FTE was estimated by dividing the number of work hours in
a typical year for publicly-employed nurses (1,813 = 37 hours x 49 weeks),
based on a report prepared for the Canadian Federation of Nurses Unions
[2], by the average annual savings in nursing time over 3 years in Canada
based on Martin et al [3]. (49.2 hours). Sensitivity analyses were performed
adjusting the number of hours in a typical year and nurse compensation.
Results: The initial investment in year 1 for nurse time to switch one
patient to home-based SCIg care would be $691 (6 hours training, 6 hours
monitoring) and $345 (6 hours monitoring only) annually thereafter to
offset $3,294 (57.2 hours set-up and monitoring) of hospital-based nursing
time annually. There would need to be 37 IVIg patients switched to homebased SCIg to gain one nurse FTE annually. The annual net saving for these
37 patients in nursing time in year 1 would be $96,297 and $109,080
annually in subsequent years. Sensitivity analysis show that as the number
of hours in a work year decline, as a consequence of a shorter work week
and/or fewer weeks in the year, the number of switched patients needed
to gain one FTE decreases.
Conclusions: The shift from labor-intensive hospital-based IVIg to less
labor-intensive home-based SCIg therapy has the potential to reduce
overall healthcare costs, alleviate nurse shortages, and improve efficient
allocation of nurse staff in Canada. Health care professionals should
consider advocating for home-based SCIg therapy for PID/SID patients
when clinically appropriate.
References
1. Jones C, Rojavin M, Baggish J: Patients with primary immunodeficiency
receiving subcutaneous immune globulin Hizentra maintain health-related
quality of life and treatment satisfaction in a multicentre extension study
of efficacy, tolerability and safety. J Health Serv Res 2012, 3: 41-47.
2. Lasota M: Trends in own illness or disability-related absenteeism and
overtime among publicly-employed registered nurses - summary of key
finding. Report prepared by Informetrica Limited for Canadian Federation of
Nurses Union Ottawa 2009.
Rationale: Human rhinovirus (HRV) infections during early childhood are

associated with a significantly increased risk of developing asthma in
subsequent years [1]. There is published evidence that airway remodeling
is present in pre-school children, often before the diagnosis of asthma is
established [1]. It is thought that this increased risk relates to the fact
that HRV infections facilitate airway remodeling in asthma [2]. A feature
of airway remodeling is the proximity of airway smooth muscle (ASM) to
the subepithelial region among other pathological changes [3]. Smooth
muscle is also known to exist in two distinct phenotypes: secretory and
contractile [4]. We have recently shown that HRV infection of Human
Bronchial Epithelial Cells (HBEC), both in vitro and in vivo, results in the
up-regulation of a number of airway remodeling mediators [5]. We now
sought to determine which ASM phenotype (contractile or secretory)
results in migration to supernatants from HRV infected HBE cells.
Methods: Primary HBE cells were cultured in growth medium until
confluent, pre-treated with 1% insulin, transferrin, and selenium (ITS) medium
for 24 hours and then stimulated with media-control or purified HRV-16. The
ASM D9 cell-line was obtained from Dr. Andrew Halaykos laboratory and
cultured in T-175 flasks in 10% serum containing Dulbeccos Modified Eagle
Medium (DMEM; Gibco; secretory phenotype) or 1% ITS F-12 media (Gibco;
contractile) until they reach ~90-100% confluence. HBEC supernatants were
used as chemo-attractants for ASM (4hrs) migration through 8 m pore
polycarbonate filter in a 48-well Boyden Chamber. Migrated cells on filter
were fixed/stained via Diff-quick and counted at 200x view.
Results: ASM D9 cells treated with 1% ITS F12 media showed significantly
higher levels of migration to fetal bovine serum (FBS) compared to ASM
D9 cells treated with serum (n=3, p < 0.001). Preliminary data indicate that
HRV-16 infected HBEC supernatants resulted in greater ASM migration
compared to HBEC supernatant from media alone in the ASM D9
contractile phenotype but not the secretory phenotype.
Conclusions: These findings support our hypothesis that the contractile
phenotype of ASM D9 cells, which is more representative of ASM cells in
vivo, migrate better than the secretory phenotype. Additionally, strong
preliminary data indicate that supernatants from HRV infected HBE cells
promotes ASM chemotaxis, and provides additional evidence for the role of
contractile ASM, and HRV infections, in the pathogenesis of airway
remodeling. Ongoing studies will examine protein expression between the
two different phenotypes.
Acknowledgements: This abstract was funded in part thanks to the
AllerGen NCE., and the GSK-CIHR Professorship in inflammatory lung disease.
References
1. Lemanske RF: The childhood origins of asthma (COAST) study. Pediatr
Allergy Immunol 2002, 13:38-43.
2. Proud D, Leigh R: Epithelial cells and airway diseases. Immunological
reviews 2011, 242:186-204.
3. Gerthoffer WT: Migration of airway smooth muscle cells. Proc Am Thorac
Soc 2008, 5:97-105.

4.
5.
Sharma P, et al: Expression of the dystrophin-glycoprotein complex is a

marker for human airway smooth muscle phenotype maturation. Am J
Physiol Lung Cell Mol Physiol 2008, 294:L57-L68.
Leigh R, et al: Human rhinovirus infection enhances airway epithelial cell
production of growth factors involved in airway remodeling. J Allergy
Clin Immunol 2008, 121:1238-1245.e4.
A45
Maternal early life trauma and wheeze in young children: could there
be an association?
Alicia N Pawlowski1*, Anita L Kozyrskyj1, Suzanne C Tough1,2, Sandra A Wiebe1
, Lionel J Dibden1
1
Pediatrics, University of Alberta, Edmonton, AB, Canada, T6T 1C9; 2Pediatrics,
University of Calgary, Calgary, AB, Canada, T3B 6A8
E-mail: apawlows@ualberta.ca
Background: Chronic trauma in childhood can program an abnormal stress
reaction in affected children, resulting in lifelong difficulties with stress
management and poor health outcomes linked to changes in the immune
system. At the same time, maternal stress during pregnancy and the
postpartum period has been linked to a number of diseases in childhood,
including wheeze and asthma. Given the potential for her own
maltreatment in childhood to shape a mothers later response to stress
during pregnancy, it seems plausible that children may demonstrate
inheritance of their mothers childhood trauma through their own health
issues. We hypothesize that preschool children are more likely to have a
wheeze or allergic disorder if their mother has a history of childhood abuse,
independent of her distress during pregnancy and postnatally.
Methods: The Community Perinatal Care (CPC) Study of Calgary provides
extensive data on 791 medically low risk mothers, of whom 61 (7.7%) and
77 (9.7%) had children with a wheezing disorder and allergies, respectively,
at age 3. In order to investigate how past maternal maltreatment might be
associated with wheeze and asthma in young children, a number of
validated questionnaires within the CPC study were used to measure and
categorize past maternal trauma . The abuse variables produced were used
in logistic regression models, adjusted for relevant confounding factors, to
determine their association with the development of wheeze or allergies in
preschool children.
Results: Calgary women fell within reported Canadian norms in their
experience of childhood maltreatment, as did their children in their reports
of wheeze and allergy. After adjustment, multiple logistic regression revealed
associations between different maternal childhood abuse types and wheeze
or allergies at age 3. There was a significant association between a mothers
experience of household dysfunction before age 5 (defined as having
parents who fought frequently and violently, and at least one parent who
had a substance abuse problem) with childhood wheeze (adjusted OR: 5.01,
95%CI: 1.41-17.84). Given sex interactions of a moderate strength, we
decided to also perform an analysis centered on gender. In women who
were sexually abused before age 8, their sons were more likely to have
allergies (adjusted OR: 2.96, 95%CI: 1.09-8.08). Experiencing more than
2 types of maternal childhood abuse before age 5 increased the likelihood
of daughters having a wheeze disorder (OR: 6.92, 95% CI: 1.39-34.49).
Conclusions: Stressful maternal childhood experiences are associated
with the development of wheeze and allergy in children.
A46
Th17/Treg ratio derived using DNA methylation analysis discriminates
allergen-induced early from dual asthmatic responses
Amrit Singh1*, Masatsugu Yamamoto1, Jian Ruan1, Jung Young Choi1,
Gail M Gauvreau2, Paul M OByrne2, Sven Olek3, Ulrich Hoffmueller3,
Christopher Carlsten4, J Mark FitzGerald4, Louis-Philippe Boulet5,
Scott J Tebbutt1
1
James Hogg Research Centre, St. Pauls Hospital, University of British Columbia,
Vancouver, British Columbia, V6Z 1Y6, Canada; 2Department of Medicine,
McMaster University, Hamilton, Ontario, L8S 4L8, Canada; 3Epiontis GmbH, Berlin,
Germany; 4Vancouver Coastal Health Research Institute, Vancouver General
Hospital, Vancouver, British Columbia, V5Z 1M9, Canada; 5Centre de
Pneumologie de LHopital, Universit Laval, Sainte-Foy, Quebec, G1V 0B4, Canada
E-mail: amrit.singh@hli.ubc.ca
Page 21 of 36
Background: Atopic allergic asthmatic individuals experience acute

bronchoconstriction (early response) upon allergen exposure. Several
hours after the initial exposure, some individuals exhibit a chronic late
phase (dual responders, DRs) whereas others do not (early responders,
ERs). The purpose of this study is to determine changes in Th17 and
regulatory T (Treg) cell numbers and their associated gene expression
profiles in whole blood between allergen-induced ERs and DRs.
Methods: 14 participants with mild, atopic asthma (8 ERs and 6 DRs)
underwent a cat allergen inhalation challenge as part of the AllerGen
Clinical Investigator Collaborative. Whole blood was collected immediately
prior to challenge (pre) and 2 hours post-challenge. DNA methylation
analysis was used to measure the frequency of Th17, Treg, B and T cells
(Epiontis, Germany). Whole blood transcriptome profiling was performed
using Affymetrix GeneChip Human Gene 1.0 ST Arrays. Statistical analysis
was performed using R.
Results: Sum of the T cell and B cell frequencies obtained using the
methylation assays strongly correlated (r = 0.95) with the lymphocyte
frequency obtained using a hematolyzer. Allergen inhalation did not
significantly (p>0.05) change Th17, Treg, B and T cell counts between ERs
and DRs. However, the Th17/Treg ratio was significantly (p=0.03) different
between ERs and DRs post challenge. 199 genes positively correlated with
Th17 cells at an FDR of 5%. 463 genes positively correlated with Treg cells
at an FDR of 5%. Th17 genes were inversely correlated with Treg genes.
Conclusions: Th17/Treg ratio derived using DNA methylation analysis
discriminates allergen-induced early from dual asthmatic responses. The
inverse correlation between Th17 genes and Treg genes may be
indicative of the inflammatory or suppressive phenotypes of these cells.
A47
The effects of poly I:C stimulation of primary bronchial epithelial cells
and TSLP secretion on CD34+ progenitor cell eosinophil and basophil
differentiation
Ashley Yu*, Claudia CK Hui, Judah A Denburg
Department of Medicine and Clinical Immunology, McMaster University,
Hamilton, Ontario, L8S 4L8, Canada
E-mail: yuam@mcmaster.ca
Background: In asthmatic lungs, elevated levels of thymic stromal
lymphopoetin (TSLP) are linked to eosinophilic inflammation and disease
severity [1]. TSLP is involved in initiating a TH2 inflammatory response,
through activation of T cells, and recently, CD34+ hemopoietic progenitor
cells [2,3]. However, the biological effects of epithelial-derived TSLP on
human peripheral blood (PB) CD34+ progenitor eosinophil-basophil (Eo/B)
lineage commitment have not been described. The aim of the current
study is to examine the effects of primary bronchial epithelial cell-derived
TSLP on CD34+ hemopoietic progenitor differentiation.
Methods: Primary bronchial epithelial cells (PBEC) grown in air-liquid
interface were apically stimulated with media or varying doses of
polyinosinic:polycytidylic acid (Poly I:C; 1, 10, 25, and 50g/mL) and
cultured in the presence or absence of PB CD34+ cells in the basolateral
compartment overnight. Supernatant was collected and analyzed for
cytokine/chemokine secretion using Luminex assays. Overnight
co-cultured PB CD34+ cells were (1) cultured in methylcellulose colony
assays to assess for the mean numbers of Eo/B colony-forming units
(CFU) (colonies were defined as 40 cells) after 14 d; or (2) assessed for
TSLPR expression using flow cytometry.
Results: Preliminary data demonstrates that overnight stimulation of PBEC
with poly I:C in the absence of PB CD34+ cells induced a dose-dependent
release of IL-4, IL-5, IL-13, TNF eotaxin-1, and MCP-1; however, failed to
secrete detectible levels of IL-1b and IFN-. Poly I:C at 10g/mL enhanced
TSLP and TARC secretion while at 50g/mL, poly I:C enhanced IL-33
secretion from PBEC compared to unstimulated control. Furthermore, basal
levels of IL-3, IL-6, IL-8, MDC, and RANTES were detected from rested PBEC,
with no observable trend in secretion following poly I:C stimulation. Finally,
PB CD34+ cells co-cultured overnight with poly I:C-stimulated PBEC have
been cultured in methylcellulose colony assays and waiting for Eo/B CFU
to be counted.
Conclusions: In conclusion, our co-culture system will allow for the
establishment of epithelial-derived TSLP activity and its influence on
CD34+ progenitor Eo/B differentiation. In the future, we would like to

examine whether PBEC obtained from atopic vs. non-atopic individuals

results in distinct progenitor response.
Acknowledgements: I would like to thank the AllerGen Network for the
AllerGen Summer Studentship, and the members of the Denburg lab.
References
1. Shikotra A, Choy DF, Ohri CM, Doran E, Butler C, Hargadon B, et al: Increased
expression of immunoreactive thymic stromal lymphopoietin in patients
with severe asthma. J Allergy Clin Immunol 2012, 129:104-11, e1-9.)rinters.
2. Wang WL, Li HY, Zhang MS, Gao PS, He SH, Zheng T, Zhu Z, Zhou LF:
Thymic Stromal Lymphopoietin: A Promising Therapeutic Target for
Allergic Diseases. Int Arch Allergy Immunol 2013, 160:18-26.
3. Kimura S, Pawankar R, Mori S, Nonaka M, Masuno S, Yagi T, Okubo K:
Increased Expression and Role of Thymic Stromal Lymphopoietin in
Nasal Polyposis. Allergy Asthma Immunol Res 2011, 3:186.
Page 22 of 36
Table 1(abstract A48)

Variable
Testing
Time Point
Prenatal Smoke
Exposure
3 months
Postnatal Smoke
Exposure
Background: Exhaled nitric oxide (FENO) is a biomarker for eosinophilic

airway inflammation [1]. Elevated FENO has been proposed as a marker
for diagnosing asthma and predicting asthma exacerbations [2]. We
wished to examine the association between known asthma risk factors
and FENO. A sub cohort of children (n=222) participating in the Canadian
Healthy Infant Longitudinal Development (CHILD) study underwent infant
pulmonary function tests (IPFTs) during the first year of life.
Methods: Risk factors were obtained from a subset of available CHILD
questionnaires administered prenatally and 3 times during the first year
of life. FENO was collected using a multiple-breath sampling technique
during quiet tidal breathing at the 3 month visit, 1 year visit, or both
visits. Prenatal smoke exposure was defined as any maternal smoking,
including mothers who stopped or cut down on smoking during
pregnancy. Postnatal smoke exposure was defined as any exposure in or
away from the home up to 1 year of age. Parental asthma was defined as
self-reported or doctor diagnosed asthma. Parental atopic status was
confirmed by allergy skin tests. T-tests with Bonferroni correction for
multiple comparisons were used to compare FE NO in the exposed and
unexposed groups (a=0.004).
Results: At the 3 month visit, 134 infants attended the IPFT lab, and 84
of 117 attempted eNO tests were successfully analyzed; mean FENO was
16.88.1ppb. At the 1 year visit, 181 infants attended the IPFT lab and
138 of 158 attempted eNO tests were successfully analyzed; mean FENO
was 15.39.7ppb. Prenatal smoking rates were low (3% and 6%) and
showed no association with FE NO (Table 1). Postnatal smoke exposure
was also not associated with FENO. FENO was not statistically different in
infants whose mothers or fathers had a history of asthma or atopic
status, compared to those without. Having siblings was not significantly
associated with FENO after applying the Bonferroni correction.
Conclusions: Smoke exposure was not related to FE NO , however no
nicotine biomarker was assessed and smoking rates were low. Maternal and
paternal histories were not associated with FENO levels in healthy children
up to 1 year of age. None of the risk factors were statistically significantly
associated with FENO, however infants with siblings were observed to have a
lower FENO than infants without siblings at the 1 year visit. A larger sample
size is required to increase the power of these tests. Further factors must be
studied to explain the variation in FENO measures seen.
References
1. Gabriele C, Jaddoe VW, van Mastrigt E, Arends LR, Hofman A, Moll HA, de
Jongste JC: Exhaled nitric oxide and the risk of wheezing in infancy: the
Generation R Study. Eur Respir J 2012, 39:567-572.
2. American Thoracic Society: ATS/ERS Recommendations for Standardized
Procedures for the Online and Offline Measurement of Exhaled Lower
Respiratory Nitric Oxide and Nasal Nitric Oxide, 2005. Am J Respir Crit
Care Med 2005, 171:912-930.
Maternal Atopic
Status
15.40 7.7
21.12 14.6
15.63 9.5
0.405
3 months
Yes 14
15.13 7.5
0.471
No 64
16.76 7.6
3 months
3 months
3 months
1 Year
Paternal Asthma
3 months
1 Year
Sibling
0.072
Yes 6
No 100
1 Year
Paternal Atopic
Status
13.12 0.8
No 57
1 Year
Maternal Asthma
Yes 2
P value
1 Year
1 Year
A48
Are known biomarkers for asthma present in early infancy?
M Ayanna Boyce1*, Sanja Stanojevic2, Krzysztof Kowalik3, Susan Balkovec2,
Felix Ratjen2, Malcolm R Sears4, Padmaja Subbarao2
1
Faculty of Applied Health Sciences, University of Waterloo, Waterloo,
Canada; 2Respiratory Medicine, Hospital for Sick Children, Toronto, Canada;
3
Department of Physiology, McGill University, Montreal, Canada;
4
Department of Medicine, McMaster University, Hamilton, Canada
E-mail: maboyce@uwaterloo.ca
Sample Mean SD
Size
(ppb)
3 months
1 Year
Yes 38
13.72 8.2
No 99
15.73 10.1
Yes 47
16.72 7.5
No 19
15.19 7.5
0.233
0.458
Yes 87
15.11 10.0
No 40
15.94 8.9
Yes 16
No 49
17.23 8.2
15.62 7.5
0.495
0.460
Yes 29
14.50 7.9
No 88
15.86 10.3
Yes 55
16.32 7.4
No 12
16.07 8.4
Yes 87
15.13 9.4
No 21
19.24 9.5
0.638
0.925
0.085
Yes 10
15.45 10.0
No 48
15.28 7.2
Yes 20
No 80
19.42 10.1
14.89 9.5
0.081
Yes 30
13.54 8.2
0.065
No 29
17.17 6.5
Yes 46
13.27 10.0
No 60
17.98 9.4
0.962
0.015
A49
Human rhinovirus infection of human bronchial epithelial cells results
in migration of human bronchial fibroblast cells
Christopher Shelfoon*, Sami Shariff, Suzanne Traves, Jason Arnason,
Sergei Nikitenko, Richard Leigh, David Proud
Snyder Institute for Chronic Disease, University of Calgary, Calgary, Alberta,
T2N 4N1, Canada
E-mail: cjshelfo@ucalgary.ca
Background: Recent studies have demonstrated that structural changes in
the airways characteristic of asthma, collectively referred to as airway
remodeling, occur in young children even prior to the diagnosis of asthma.
Young children who experience human rhinovirus (HRV)-associated
wheezing illness within the first three years of life are at increased risk for
the subsequent development of asthma. This association, together with
evidence that HRV-infected epithelial cells release a number of growth
factors and cytokines, has led to the hypothesis that HRV infection may be
involved in the pathogenesis of airway remodeling. Thickening of the
lamina reticularis found below the true basement membrane in the human
airway is a characteristic feature of airway remodeling in asthma. The human
bronchial fibroblast (HBF) is believed to contribute to this thickening by
moving closer to the laminar reticularis and producing matrix proteins. We

hypothesized that HRV infection of human bronchial epithelial (HBE) cells

induces production of chemoattractants that can induce HBF migration.
Methods: Primary HBE cells were grown in bronchial epithelial growth
medium (BEGM). Cells were incubated for 2 h in bronchial epithelial basal
media (BEBM) prior to experiments. Cells were exposed to BEBM alone
(control) or purified HRV-16 (MOI: 1) for 24 hours. HBE cell supernatants from
several donors were then recovered, centrifuged, pooled and studied as
chemoattractants for HBF chemotaxis. HBF migration was examined using
both a 48-well modified Boyden chamber and a 16-well xCELLigence
apparatus (ACEA Biosciences, Inc., San Diego, USA). In the latter, migration to
HBE supernatants was measured via electrical impedance, as per
manufacturers instructions, and compared to medium control.
Results: Using the xCELLigence system to measure migration in real time,
it was found that migration to HBE supernatants and platelet derived
growth factor (positive control) was maximal within 6h. Supernatants from
HRV-16 infected HBE cells resulted in greater HBF migration compared to
supernatants from HBE cells exposed to medium alone (negative control)
in both the Boyden chamber and the xCELLigence system. Migration to
supernatants from HRV-16 infected cells was concentration dependent.
Conclusions: These data provide the first demonstration that HRV
infection of HBE produces soluble factor(s) that cause migration of HBF
cells. This provides further evidence for a potential role of HRV infection
in the pathogenesis of airway remodeling in asthma.
A50
Peripherally induced Foxp3+ regulatory T cells mediates the
immunomodulatory effect of intravenous immunoglobulin in an
experimental model of allergic airway disease
Amir H Massoud1,3*, Gabriel Kaufman1, Madelaine Taylor1, Marianne Beland1,
Ciriaco A Piccirillo2, Walid M Mourad3, Bruce D Mazer1
1
McGill University, Dept. of Experimental Medicine, Montreal, QC, Canada,
H2X 2P2; 2McGill University Dept. of Microbiology and Immunology,
Montreal, QC, Canada, H3G 1A4; 3Universite de Montral, Dept. Microbiologie
et Immunologie Montreal, QC, Canada, H2X 3J4
E-mail: amir.hossein.massoud@umontreal.ca
Background: IVIg is a polyclonal IgG preparation with potent immunemodulating properties. We demonstrated that IVIg protects against airway
hyperreactivity (AHR) and airway inflammation in mouse models of allergic
airway disease, accompanied by peripheral induction of Foxp3+regulatory
T-cells (iT reg). The requirement of IVIg-induced iT reg and their antigenspecificity in attenuation of AHR and airway inflammation remains unknown.
Methods: We utilized DEREG mice, carrying a transgenic diphtheria toxin
receptor under the control of the Foxp3 promoter, allowing for selective
depletion of Foxp3+Treg by the application of diphtheria toxin (DT). Mice
were sensitized and challenged with ovalbumin (OVA) and treated with
IVIg. AHR was measured using a FlexiVent small animal ventilator. Total
and antigen-specific IgE, as well as pro-inflammatory cytokines levels
were determined in serum and alveolar lavage, using ELISA.
Results: In the absence of Treg, due to multiple DT doses before and after
the treatment, IVIg was not able to attenuate AHR, diminish IgE levels and
Th-2 type cytokine production, nor alleviate airway inflammation. However,
mice in which the pre-established Treg cells (nTreg) were depleted before
but not following IVIg treatment demonstrated an induction of Foxp3+Treg
to IVIg therapy and did not develop AHR and airway inflammation to
allergen-challenge. Adoptive transfer of enriched IVIg-induced iTreg from
OVA-IVIg treated mice failed to transfer protection to mice exposed to
ragweed, but was protective in OVA-sensitized and challenged mice.
Conclusions: Treg can be induced from effector CD4+T-cells in the absence
of nTreg. IVIg-induced antigen specific Treg are capable of suppressing all
aspects of antigen-driven airway inflammation in an antigen-specific manner.
A51
Thymic stromal lymphopoietin promotes human eosinophil-basophil
lineage commitment: a key role for tumor necrosis factor-alpha
Claudia CK Hui*, Sina Rusta-Sallehy, Delia Heroux, Judah A Denburg
Department of Medicine, McMaster University, Hamilton, ON, Canada
E-mail: huicck@mcmaster.ca
Page 23 of 36
Background: Allergic diseases are characterized by tissue eosinophilic and

basophilic inflammation. Both epithelial-derived thymic stromal
lymphopoietin (TSLP) and eosinophil/basophil (Eo/B) lineage-committed
progenitor cells are upregulated and found at sites of allergic inflammation
[1-3]. We have previously shown that TSLP mediates the differentiation of
peripheral blood (PB) CD34+ progenitor cells into eosinophils and basophils.
However, the specific mechanisms through which TSLP promotes this
lineage commitment are unclear. The aim of this study is to characterize the
intracellular mechanisms by which TSLP mediates Eo/B differentiation.
Methods: Purified PB CD34+ progenitors were stimulated overnight with
media, IL-3 (1ng/mL), TSLP (10ng/mL), or IL-3/TSLP and assessed for cytokine
and chemokine secretion using Luminex assays. Alterations in Eo/B colony
forming units (CFU) and surface expression of TSLPR post-stimulation with
IL-3/TSLP (and/or neutralizing anti-TNFa Ab) were assessed by
methylcellulose cultures and flow cytometry respectively.
Results: TSLP alone induced significant levels of IL-1b, IL-6, TNFa, and
CXCL8 from PB CD34+ cells, compared to unstimulated controls (p<0.05).
IL-3/TSLP-stimulated CD34+ cells released significant levels of IL-1b, IL-6,
IL-13, TNFa, CXCL8 and CCL2, but failed to secrete detectable levels of IL-4,
IL-9, GM-CSF, IFNg, and eotaxin. Blockade of TNFa in vitro in the
differentiation assays inhibited both TSLPR expression (p<0.05) and
IL-3-responsive Eo/B CFU formation (p<0.05). Overnight stimulation of PB
CD34+ cells with IL-3 (10ng/mL) and TNFa (50pg/mL) enhanced surface
expression of TSLPR to comparable levels post TSLP/IL-3-stimulation.
Moreover, pre-stimulating CD34+ cells with IL-3/TNFa prior to culturing in
methylcellulose cultures resulted in enhanced sensitivity to TSLP-mediated
Eo/B colony formation at lower concentrations of TSLP.
Conclusions: We have previously shown that stimulation of human PB
CD34+ cells with TSLP promotes Eo/B differentiation through upregulation
of IL-3Ra and TSLPR. Our current study demonstrates that TSLP can
modulate Eo/B lineage commitment, by inducing PB CD34+ cells to actively
secrete chemokines and cytokines (key among which is TNFa), which,
together with IL-3, induce the upregulation of TSLPR, leading to the
subsequent amplification of Eo/B CFU. The novel role of TSLP-induced Eo/B
differentiation points to the importance of the epithelium, and its responses
to environmental stimuli, in the development of allergic diseases.
Acknowledgements: This work is funded by CIHR, AllerGen NCE
(CAIDATI Award), McMaster University (Medicine Graduate Initiative Fund).
References
1. Ying S, OConnor B, Ratoff J, Meng Q, Mallett K, Cousins D, et al: Thymic
stromal lymphopoietin expression is increased in asthmatic airways and
correlates with expression of Th2-attracting chemokines and disease
severity. J Immunol 2005, 174:8183-90.
2. Robinson DS, Damia R, Zeibecoglou K, Molet S, North J, Yamada T, et al:
CD34(+)/interleukin-5Ralpha messenger RNA+ cells in the bronchial
mucosa in asthma: potential airway eosinophil progenitors. Am J Respir
Cell Mol Biol 1999, 20:9-13.
3. Kim YK, Uno M, Hamilos DL, Beck L, Bochner B, Schleimer R, et al:
Immunolocalization of CD34 in nasal polyposis. Effect of topical
corticosteroids. Am J Respir Cell Mol Biol 1999, 20:388-97.
A52
Mapping of novel chromosomal regions associated with atopy
Cynthia Kanagaratham1*, John Ren2, Pierre Camateros3, Rafael Marino3,
Rob Sladek1, Silvia Vidal1, Danuta Radzioch1,3
1
Department of Human Genetics, McGill University, Montreal Quebec,
Canada; 2Department of Microbiology and Immunology, McGill University,
Montreal, Quebec, Canada; 3Faculty of Medicine, Division of Experimental
medicine, McGill University, Montreal, Quebec, Canada
E-mail: cynthia.kanagaratham@mail.mcgill.ca
Background: A panel of recombinant congenic strains (RCS) of mice can be
used to study an array of disease related phenotypes [1]. We have used a
panel of 33 AcB/BcA RCS, derived from parental strains A/J and C57BL/6J
(Figure 1), to study phenotypes of allergic asthma that are difficult to
segregate in the human population, such as airway hyperresponsiveness [2].
Each recombinant strain is fully inbred and contains approximately 12.5% of
the genome from one parental strain on the background of the other
parental strain. Here we present our findings for mapping chromosomal
regions associated with atopy, another phenotype of allergic asthma.

Page 24 of 36
Figure 1(abstract A52) Generation of 33 RCS from atopic A/J and nonatopic C57BL/6J strains (adapted from [2])
Figure 2(abstract A52) Strain distribution pattern of parental strains A/J and C57BL/6J (red bars), 12 AcB strains (white bars), and 21 BcA strains (black
bars). Significance was calculated by one-way ANOVA by comparing each RCS to its major genetic donor parental strain. *, ** and *** represents p<0.05,
p<0.01 and p<0.001, respectively, post Bonferroni correction.

Methods: Nave mice from each RCS were phenotyped for atopy by
measuring plasma IgE concentration by ELISA. RCS mice were genotyped at
1215 markers that spanned the entire genome. Using the log transformed
phenotype values and genotyping data, a marker-by-marker association
analysis was performed to identify associations between the strain phenotype
and genotype, while correcting for major background strain. Within the
phenotype associated loci, candidate genes were selected based on the
presence of coding mutations between the sequences of the two parental
strains.
Results: A/J and C57BL/6J strains have significantly different plasma IgE
concentrations. A/J mice have higher plasma IgE levels, making them a
good model of atopic individuals. Among the 33 RCS, a wide distribution
in plasma IgE concentrations was observed (Figure 2). Genotypephenotype analysis identified one region on chromosome 3 as
significantly associated with atopy. This region contains a total of six
protein coding genes of which four have coding variants in their
sequences between A/J and C57BL/6J strains.
Conclusions: To the best of our knowledge, we have identified a novel
candidate loci associated with atopy. Future plans of our study include
functionally validating the importance of our candidate genes, candidate
locus, and of chromosome 3 in atopy. Our results demonstrate that using a
genetically unique panel of RCS we can identify candidate genes that are
in common and unique to the various phenotypes of allergic asthmatics.
References
1. Fortin A, Diez E, Rochefort D, Laroche L, Malo D, Rouleau GA, et al:
Recombinant congenic strains derived from A/J and C57BL/6J: a tool for
genetic dissection of complex traits. Genomics 2001, 74:21-35.
2. Camateros P, Marino R, Fortin A, Martin JG, Skamene E, Sladek R, et al:
Identification of novel chromosomal regions associated with airway
hyperresponsiveness in recombinant congenic strains of mice. Mamm
Genome 2010, 21:28-38.
A53
Induction of human airway epithelial to mesenchymal transition upon
rhinovirus infection
Danielle Minor*, Suzanne Traves, David Proud, Richard Leigh
T2N 4N1, Canada
E-mail: dmminor@ucalgary.ca
Background: Structural changes of the airway, collectively referred to as
airway remodeling are believed to be the underlying cause of the
airway hyperresponsiveness that is characteristic of asthma. Airway
remodeling is characterized by thickening of the subepithelial
membrane, goblet cell hyperplasia, angiogenesis, increased smooth
muscle mass, and epithelial fragility. Thickening of the subepithelial
membrane, due to increased deposition of matrix proteins by
fibroblasts/myofibroblasts, has been observed in children even prior to
the formal diagnosis of asthma. Recent data have shown that young
children who experience episodes of human rhinovirus (HRV)-induced
wheezing in early childhood are at increased risk of subsequently
developing asthma. The primary site of infection of HRV is the
airway epithelium. Recent evidence suggests that the molecular
reprogramming of epithelial cells through a process called epithelial to
mesenchymal transition (EMT) may contribute to increases in fibroblast/
myofibroblast in the asthmatic airway. Therefore, we hypothesize that
HRV infection plays a role in early airway remodeling by triggering EMT
to produce fibroblasts/myofibroblasts that cause thickening of the
subepithelial membrane by depositing matrix proteins.
Methods: The BEAS-2B human bronchial epithelial cell line was grown in
6-well plates in bronchial epithelial growth medium (BEGM). Prior to
experiments, cells were grown for 24 h in BEGM from which hydrocortisone
was removed. Cells were exposed to medium (control), or purified HRV-16
alone or in the presence of various growth factors for 120 hours with media
and growth factor replacement at 48 and 96 hours. Cell lysates were
collected and then analyzed by western blot for protein expression of
epithelial and mesenchymal markers.
Results: BEAS-2B cells that were infected with HRV in the presence of
epidermal growth factor (EGF) showed decreased expression of the
Page 25 of 36
epithelial marker E-cadherin, and increased expression of the mesenchymal

marker vimentin.
Conclusions: HRV infection, particularly in combination with EGF causes
changes characteristic of EMT. I will confirm and extend these
observations by looking at other epithelial and mesenchymal markers
and looking for phenotypic changes. Future studies will examine
the mechanisms underlying HRV induced EMT using siRNA and
pharmacologic approaches.
A54
Parental inheritance and perinatal tobacco smoke exposure increase
the gender-dependent risk of physician diagnosed asthma at
preschool age
Chih-Chiang Wu1,2,3, Te-Yao Hsu4*, Ho-Chang Kuo5, Chia-Yu Ou4,
Jen-Chieh Chang6,7, Chieh-An Liu8, Chih-Lu Wang8, Hua Chuang7,
Hsiu-Mei Liang4, Kuender D Yang2,3,9*
1
Department of Pediatrics, Show Chwan Memorial Hospital, ChangHua,
Taiwan; 2Department of Medical Research, Show Chwan Health Care System
in Chang Bing, Changhua, Taiwan; 3Institute of Clinical Medicine, National
Yang-Ming University, Taiwan; 4Department of Obstetrics and Gynecology,
Kaohsiung Chang Gung Memorial Hospital, Taiwan and Chang Gung
University College of Medicine, Kaohsiung, Taiwan; 5Department of
Pediatrics, Kaohsiung Chang Gung Memorial Hospital and Chang Gung
University College of Medicine, Kaohsiung, Taiwan; 6Division of Dermatology,
Department of Medicine, McGill University Health Centre, CanadaInstitute of
Biomedical Sciences, National Sun Yat-Sen University, Kaohsiung, Taiwan;
7
Genomic and Proteomic Core Laboratory, Department of Medical Research,
Kaohsiung Chang Gung Memorial Hospital and Chang Gung University
College of Medicine, Kaohsiung, Taiwan; 8Department of Pediatrics, Po-Jen
Hospital, Kaohsiung, Taiwan; 9Department of Pediatrics, Po-Jen Hospital,
Kaohsiung, Taiwan
E-mail: phachang@gmail.com
Background: Genetic inheritance and perinatal tobacco smoke exposure
(TSE) have been proven to be critical for the development of childhood
allergic diseases [1, 2]. This study investigated the interactive roles of
parental allergic histories and TSE on the development of childhood
asthma at 6 years old.
Methods: A birth cohort in southern Taiwan was studied. Information
about parental allergic histories, gender, prematurity, TSE, and childhood
allergic disease ever diagnosed by a physician were acquired from
questionnaire during follow up. Children were asked to follow up at 6
years of age for allergic questionnaire and sensitization examination (CAP
system).
Results: In this cohort study, 748 of the children with complete data
were analyzed. 217 (29%) of children had positive parental allergic
history, 191 (25.5%) of children had TSE history, and 186 (24.9%) of
children had been diagnosed as asthma by a physician in the first 6 years
of life. In a regression analysis, physician diagnosed asthma ever in the
first 6 years of life were significantly associated with male gender (OR:
1.941, 95% CI: 1.371-2.748, p<0.001), either parent with allergic diseases
(OR: 1.548, 95% CI: 1.047-2.288, p=0.028), and TSE (OR: 1.504, 95% CI:
1.038-2.179, p=0.031), but not significantly associated with preterm
(p=0.801). TSE with more than 20 cigarettes per day made children
significantly higher risky to have physician-diagnosed-asthma than those
with smoke exposure less than 20 cigarettes per day or those without
smoke exposure (35%, 25% and 22.7% respectively, p=0.003). TSE was
not related to physician diagnosed rhinitis, dermatitis or allergic
sensitization by 6 years of age (p>0.5). Besides, TSE and parental allergic
history had synergistic influence on the physician diagnosed asthma ever
in the 6 years of life. This synergistic influence was significant in girls,
rather than in boys (Table 1).
Conclusions: In the prospective cohort study, we found that male
gender, parental allergic history, and TSE were significantly associated
with physician diagnosed asthma by 6 years of age. TSE and parental
allergic history had synergistic effect on the physician diagnosed asthma
by 6 years of age. This synergistic influence was significant in girls, rather
than boys.

Page 26 of 36
Table 1(abstract A54) TSE and parental allergic history had synergistic influence on the physician diagnosed asthma
ever in the 6 years of life. This synergistic influence was significant in girls, rather than boys
All
physician diagnosed asthma
parent allergic disorder -, TSE- (A)
30/161
18.60%
OR
1
95%CI
p (compared with A)
parent allergic disorder +, TSE-
97/396
24.00%
parent allergic disorder -, TSE+

parent allergic disorder +, TSE+
13/56
46/135
23.20%
34.10%
1.417
0.896-2.240
0.135
1.32
2.257
0.632-2.757
1.325-3.846
0.459
0.002
4/72
5.60%
38/196
19.40%
4.089
1.404-11.905
3/23
13.00%
2.55
0.526-12.353
0.231
20/61
32.80%
8.293
2.649-25.964
<0.001
parent allergic disorder -, TSE- (A2)
28/89
29.20%
59/200
29.50%
1.014
0.586-1.755
10/33
30.30%
1.054
0.441-2.519
0.907
26/74
35.10%
1.313
0.678-2.541
0.419
Girls
parent allergic disorder -, TSE- (A1)
p (compared with A1)
Boys
0.006
p (compared with A2)
A55
Real-life effectiveness of montelukast administered as monotherapy or
in combination with inhaled corticosteroid (ICS) in pediatric patients
with uncontrolled asthma
Denis Brub1, Michel Djandji2, John S Sampalis3,4*, Allan Becker5
1
Centre Hospitalier Universitaire (CHU) Sainte-Justine, Universit de Montral,
Montral, Qubec, H7M 5M2, Canada; 2Merck Canada Inc., Kirkland, Qubec,
H9H 3L1, Canada; 3McGill University, Montral, Qubec, H3G 1Y6, Canada;
4
JSS Medical Research, St-Laurent, Qubec, H4S 1N8, Canada; 5Section of
Allergy and Clinical Immunology, Department of Pediatrics and Child Health,
University of Manitoba, Winnipeg, Manitoba, R3A 1S1, Canada
E-mail: submission@jssresearch.com
Background: The efficacy of montelukast in the treatment of asthma has
been demonstrated in numerous controlled clinical trials. The aim of this
study was to assess the real-life effectiveness of montelukast
administered as monotherapy or in combination with current ICS in
children with uncontrolled asthma.
Methods: Twelve-week open-label, phase IV, multicenter, prospective
cohort study. Eligible patients included children aged 2-14 years
diagnosed with asthma for =6 months who were: (i) uncontrolled as per
the Canadian Asthma Consensus Guidelines, and; (ii) either untreated,
using a short-acting 2agonist as-needed or using any dose ICS. In this
analysis, patients with Asthma Control Questionnaire (ACQ) score >0.75
were included. Patients 6-14 and 2-5.9 years old were treated once-daily
with montelukast 5mg and 4mg, respectively. Primary outcome measure
was the proportion achieving asthma control (ACQ=0.75). Secondary
outcomes were the absolute change in ACQ and in the Pediatric Asthma
Caregivers Quality of Life Questionnaire (PACQLQ) over time.
Results: Among the 328 patients included, 76 (23.2%) were treated with
montelukast monotherapy and 252 (76.8%) with montelukast combined
with ICS. By 4 weeks of treatment 61.3% and 52.9% of patients in the
monotherapy and combination group, respectively, achieved asthma
control. These proportions increased to 75.0% and 70.9%, respectively, at
week-12. Clinically and statistically (P<0.001) significant improvements
were observed in ACQ (monotherapy: mean (SD) of 1.67 (0.69) at baseline
and 0.50 (0.52) at week-12; combination therapy: 2.02 (0.83) and 0.64
(0.86), respectively) and PACQLQ (monotherapy: mean (SD) of 5.34 (1.14)
at baseline and 6.51 (0.85) at week-12; combination therapy: 4.42 (1.35)
and 6.21 (1.03), respectively) in both patient subgroups. After a 12-week
montelukast add-on therapy, 22.6% of patients reduced their ICS dosage.
Conclusions: Montelukast as monotherapy or in combination with ICS
represents an effective treatment strategy for achieving asthma control in
pediatric patients and improving caregivers quality of life.
0.961
Acknowledgements: On behalf of the ACTION3 investigators.

Trial registration: Clinicaltrials.gov: 00832455.
A56
Phthalate exposures in a Canadian birth cohort at three months
of age: the CHILD study
Huan Shu1,2*, Ryan Allen2, Carl-Gustaf Bornehag1, Michael Brauer3, Jeff Brook4,
Bruce Lanphear2, Sheela Sathyanarayana5, Malcolm Sears6, Leilei Zeng7,
Tim Takaro2, the CHILD Environmental Working Group4
1
Department of Health Sciences, Karlstad University, Karlstad, Sweden;
2
Faculty of Health Sciences, Simon Fraser University, Burnaby, Canada;
3
School of Population and Public Health, University of British Columbia,
Vancouver, Canada; 4Environment Canada, Canada; 5Department of
Pediatrics, University of Washington, Seattle, USA; 6Department of Medicine,
McMaster University, Hamilton, Canada; 7Department of Statistics and
Actuarial Science, University of Waterloo, Waterloo, Canada
E-mail: huanshu@kau.se
Background: Exposure to phthalates has been associated with the
development of wheeze and asthma. While infants may be exposed via
multiple routes, the sources of infant exposure arent fully understood.
Methods: We employed the Canadian Healthy Infant Longitudinal
Development (CHILD) Study, a multicentre, longitudinal, population-based
birth cohort with 3,300 children to identify sources of phthalate
exposures in infants. For the first 1,539 CHILD participants we examined
associations between 6 urinary phthalate metabolites, measured at 3
months of age and corrected for specific gravity, with 90 variables
characterizing the indoor environment, including furnishings, household
care products and personal care products. Univariate, Bivariate, and Tobit
regression were used for modeling. We also examined the relationship of
urinary phthalates with socio-demographic characteristics and
breastfeeding.
Results: Overall, there were 32 variables associated with higher
concentrations and 20 inverse associations. We found higher urinary
phthalates among children whose families used oven cleaners (Mono-nbutyl phthalate (b=7%, 95%CI: 2-15%), Mono-benzyl phthalate (b=15%, 526%), and Mono-ethyl phthalate (15%, 5-26%)) and air fresheners (Mono-nbutyl phthalate (4%, 2-10%), Mono-benzyl phthalate (10%, 5-15%), and
Mono-ethyl phthalate (10%, 5-17%)), or who heated food in hard plastic
(Mono-n-butyl phthalate (32%, 15-48%), Mono-2-ethyl-5-hydroxylhexyl
phthalate (29%, 7-51%). Soft vinyl flooring was highly correlated with Monobenzyl phthalate (58%, 35-91%). Mono-2-ethylhexyl phthalate, Mono-2-ethyl5-hydroxylhexyl phthalate, and Mono-2-ethyl-5-oxohexyl phthalate
concentrations were lower in children who were breastfed. Household

income was inversely associated with Mono-2-ethyl-5-oxohexyl phthalate

concentrations.
Conclusions: Our analysis demonstrated higher levels of phthalate
metabolites associated with use of household product and plastics. The
identification of these exposures as possible contributors to phthalate
body burden in three-month-old children is an important step in
exposure categorization and supports efforts to reduce exposure.
A57
Pre-existing human rhinovirus infection modulates host response to
secondary bacterial infections
Jason Arnason*, Kyla Jamieson, Cora Kooi, Sergei Nikitenko, Sami Shariff,
Chris Shelfoon, David Proud, Richard Leigh
Snyder Institute for Chronic Disease, University of Calgary, Calgary, Alberta,
T2N 4N1, Canada
E-mail: jwarnaso@ucalgary.ca
Background: Secondary bacterial infections following viral infections of
the airways are well documented and are associated with increased
severity of respiratory disease compared to virus or bacterial infections
alone. Human rhinovirus (HRV) infections are the most common causes of
exacerbations in individuals with chronic airways diseases such as asthma
and COPD. Moreover, bacterial colonization is commonly found in the
airways of patients experiencing exacerbations of these chronic airways
diseases and linked to increased severity and duration of these
exacerbations. The mechanisms underlying the increased prevalence of
secondary bacterial infections and the association with more severe
outcomes following viral infections is not known. It has been suggested
that viral infection of the airways cause dysregulation of innate host
defense mechanisms, such as, impaired antimicrobial peptide expression
of the airways. Antimicrobial peptides are key components of the innate
immune response after infection and are important in efficient clearance
of microbial colonization to prevent infection. We sought to determine
whether HRV modulates the innate host defense response to secondary
bacterial infections of the airways.
Methods: Studies performed using primary human bronchial epithelial
cells (HBECs). Cells grown in monolayer to confluence (80-90%).
Antibiotics and Hydrocortisone were removed from the media 48 h and
24 h prior to infection respectively. On day of infection, cells were
stimulated with purified HRV-16 or bacteria (H. influenzae/P. aeruginosa)
alone, or treated in combination of HRV-16 then subsequently bacteria.
TLR5 agonists (Flagella) also used alone and in combination with HRV-16.
The protein and mRNA levels of different antimicrobial peptides
(b-defensin, LL-37, lysozyme, lactoferrin, and SLPI) measured using ELISA
(R&D Systems) and real-time RT-PCR (Applied Biosystems), respectively.
Results: Preliminary data indicate supernatants from HRV-16/bacterial coinfection resulted in synergistic trend in b-defensin levels compared to
HRV and bacteria alone. A synergistic increase in b-defensin levels was also
seen with TLR5 agonist when combined post HRV-16 infection compared
to TLR5 or HRV-16 alone. Minimum inhibitory concentration results
showed b-defensin (1mg/ml), Lysozyme (30g/ml), Lactoferrin (1mg/ml)
and LL-37 (460g/ml) were able to inhibit growth of NTHi and PAO.
Conclusions: The data provide the first demonstration that there is a
dysregulation of antimicrobial levels in HRV infected HBECs when
encountered with a secondary bacterial infection. This provides evidence
to why individuals with chronic airways diseases have a prolonged and
more severe disease state than normal individuals. It could also lead to a
new targeted therapy of people with diseases such as asthma or COPD
to decrease severity of exacerbations.
A58
The Allergic Rhinitis Clinical Investigator Collaborative nasal allergen
induced eosinophilia
Jenny Thiele1*, Lisa Steacy2, Marie-Eve Boulay3, Ann Efthimiadis4,
Susan Waserman5, Paul Keith5, Harissios Vliagoftis6, Louis-Philippe Boulet3,
Helen Neighbour4, Anne K Ellis1,2
1
Departments of Medicine and Biomedical & Molecular Science, Queens
University, Kingston, ON, K7L 3N6, Canada; 2Allergy Research Unit, Kingston
General Hospital, Kingston, ON, K7L 2V7, Canada; 3Institut Universitaire de
Page 27 of 36
Cardiologie et de Pneumologie de Quebec, Quebec City, QC, G1V 4G5,

Canada; 4Firestone Institute for Respiratory Health, McMaster University,
Hamilton, ON, L8N 4A6, Canada; 5Department of Medicine, McMaster
University, Hamilton, ON, L8N 3Z5, Canada; 6Pulmonary Research Group,
University of Alberta, Edmonton, AB, Canada
E-mail: jenny.thiele@queensu.ca
Background: The Allergic Rhinitis Clinical Investigator Collaborative (ARCIC) is a Canadian multi-center initiative with the primary goal of
performing standardized nasal allergen challenge (NAC) to study the antiallergic effects of novel therapeutic agents for allergic rhinitis (AR). The
model further allows identification of potential mechanisms of allergic
disease and biomarkers. In this study we examined differential counts,
more specifically eosinophil numbers, in nasal lavage samples before, 1
hour (1H) and 6 hours (6H) after direct nasal allergen challenge.
Methods: Thirty-three atopic and five non-atopic participants were
enrolled at four study centers. All atopic participants had AR symptoms
following exposure to environmental allergens and a supportive skin test
response. Using the Pfeiffer Bidose Nasal Delivery Device 100l allergen
solution was delivered to each nostril. Atopic pilot study participants
were challenged with a threshold dose of allergen determined via
titration 1 week prior to NAC, non-atopic participants were challenged
with a 1:2 allergen dose. The allergens used included either ragweed,
grass, D. farina, D. pteronyssinus and cat hair. Nasal lavage samples
were collected at baseline, 1H and 6H post NAC. Total cell counts (TCC)
were determined on unstained samples prior to cytospin. Cytospin slides
were prepared and differentially stained (i.e. DiffQuick).
Results: Atopic individuals exhibited eosinophilia at 1H and 6H post NAC
when compared to baseline samples. Non-atopic participants did not
display a significant increase in eosinophils at any time point. Furthermore,
TCCs were increased at 1H post NAC in atopic participants. This trend was
not observed in non-atopic samples.
Conclusions: Differences were noted in eosinophil numbers (elevated)
between baseline, 1H and 6H post direct NAC only in participants with
AR. Nasal lavage collection for differential count analysis is a robust assay
that can be integrated into clinical trials conducted using the AR-CIC.
A59
Diagnosis of nasal and eye allergies: the Allergies, Immunotherapy, and
RhinoconjunctivitiS (AIRS) patient survey
Michael Blaiss1*, Mark Dykewicz2, Bryan Leatherman3, David Skoner4,
Nancy Smith5, Felicia Allen-Ramey5
1
Allergy & Asthma Care, Germantown, TN, 38138, USA; 2Wake Forrest Baptist
Health, Winston-Salem, NC, 27157, USA; 3Coastal ENT Associates, Gulfport,
MISS, 39501, USA; 4West Penn Allegheny Health System, Cranberry, PA,
16066, USA; 5Merck & Co, Inc, West Point, PA 19486, USA
Background: Knowledge and avoidance of allergies can lead to better
allergy symptom control. The AIRS study assessed approaches to diagnosis
of nasal and eye allergies or allergic rhinoconjunctivitis in the US.
Methods: A national sample of 34,030 households using a dual frame
approach of random digit dialing and cell phone sample were targeted.
Patients aged =5 years with a health care professional diagnosis of hay
fever, allergic rhinitis, rhino-conjunctivitis, nasal or eye allergies and
symptoms or medication for condition in past 12 months were surveyed.
Data on specific diagnosis and allergy testing were collected.
Results: Based on screening land-line sample of 20,835 households, 18%
of individuals were diagnosed with one of conditions of interest. Of the
2765 surveyed patients, 86% were diagnosed with nasal allergies, 59%, hay
fever, 54% eye allergies, 30%, allergic rhinitis and 13%, rhinoconjunctivitis.
Four percent of respondents reported they were given an allergy test by
doctor or health professional in past four months, 3% in past year, 7%,
1-2 years ago, and 37%, 3 or more years ago. Of those, 71% reported that
they had a skin prick test, 13% had blood test and 12% had both blood
and skin prick test. 47% report they never received an allergy test.
Conclusions: The AIRS survey demonstrated that 18% of individuals > 5
years were diagnosed with an above allergic condition. Although these
respondents had been diagnosed by a health care professional with

Page 28 of 36
allergies, almost half never had any allergy testing to determine the
triggers of their condition.
A60
Comparison of questionnaire responses with biomarkers of tobacco
smoke exposure in a Canadian birth cohort at three months of age
Kathleen McLean1*, Bruce Lanphear1, Amanda J Wheeler2, Jeff Brook3,
James Scott4, Ryan Allen1, Michael Brauer5, Malcolm Sears6,
Padmaja Subbarao7, Stuart Turvey8, Allan Becker9, Piush Mandhane10,
Tim Takaro1
1
Faculty of Health Sciences, Simon Fraser University, Burnaby, Canada; 2Air
Health Science Division, Health Canada, Ottawa, Canada; 3Air Quality
Research Division, Environment Canada, Toronto, Canada; 4Dalla Lana School
of Public Health, University of Toronto, Toronto, Canada; 5School of
Population and Public Health, University of British Columbia, Vancouver,
Canada; 6Department of Medicine, McMaster University, Hamilton, Canada;
7
Department of Pediatrics, Hospital for Sick Children, Toronto, Canada;
8
Department of Pediatrics, University of British Columbia, Vancouver, Canada;
9
Department of Pediatrics & Child Health, University of Manitoba, Winnipeg,
Canada; 10Faculty of Medicine and Dentistry, University of Alberta,
Edmonton, Canada
E-mail: kathleen_mclean@sfu.ca
Background: Exposure to tobacco smoke increases the risk for several
adverse health effects in children including wheeze, asthma, and asthma
exacerbation [1,2]. Accurately assessing tobacco smoke exposure is
important for understanding and preventing these health effects.
Questionnaires are a flexible and relatively inexpensive method of assessing
exposure, but biomarkers of tobacco smoke exposure are considered more
accurate. We developed questionnaire-based exposure models predicting
urinary levels of biomarkers cotinine and trans-3-hydroxycotinine (3HC)
(metabolites of nicotine) in 3-month old infants using parent-reported
questionnaire responses about tobacco smoke exposure from the Canadian
Healthy Infant Longitudinal Development (CHILD) Study.
Methods: We used a manual model building process to build multiple
linear regression models predicting urinary concentrations of cotinine,
3HC, and the sum of cotinine and 3HC on a molar basis (Cot+3HC) for
987, 1003, and 983 infants, respectively. Questions were included on the
infants exposure assessed at 3 months of age and tobacco smoke odour
in the home. We also included questions on maternal smoking status and
history, passive exposure, and family socio-economic status assessed
during pregnancy, as potential indirect measures of the infants exposure
at 3 months. Adjusted R2 values were maximized in the final models.
Results: During pregnancy, the prevalence of maternal smoking was 2.4
%, and 115 (11.4 %) mothers reported smoking by at least 1 person at
home. Of the 144 (14.3 %) infants whose mothers reported that smoking
occurred at home when their child was 3 months, 129 (89.6%) and 136
(94.4%) had cotinine and 3HC levels above the detection limit (0.03 ng/
mL), respectively. Of the 811 infants who had no parent-reported
exposure at 3 months, 538 (66.3%) and 715 (88.2%) had detectable
cotinine and 3HC levels, respectively. After correcting for urine dilution,
the geometric mean levels were 0.085 ng/mL for cotinine, 0.20 ng/mL for
3HC, and 1.62 picomole/mL for Cot+3HC. The final questionnaire models
explained 43.4%, 41.0%, and 42.9% of the variance in cotinine, 3HC, and
Cot+3HC levels, respectively.
Conclusions: Our results indicate that exposure of these infants to
tobacco smoke is not completely captured by questionnaires, suggesting
that exposure assessment could be improved by using a combination of
biomarker and questionnaire methods. Though more detectable, the
inclusion of 3HC did not increase the ability of the questionnaires to
explain variance in metabolite levels, but 3HC may be important since
the ratio of 3HC to cotinine can be used to quantify the rate of nicotine
metabolism and variation within populations [3,4].
References
1. Committee on the Assessment of Asthma and Indoor Air, Division of Health
Promotion and Disease Prevention, Institute of Medicine: Clearing the Air:
Asthma and Indoor Air Exposures. Washington, DC: National Academy
Press 2000.
2. U.S. Department of Health and Human Services: The Health Consequences
of Involuntary Exposure to Tobacco Smoke. A Report of the Surgeon
3.
4.
General Atlanta, GA: U.S. Department of Health and Human Services,

Centers for Disease Control and Prevention, Coordinating Center for Health
Promotion, National Center for Chronic Disease Prevention and Health
Promotion, Office on Smoking and Health 2006, [Publications and Reports
of the Surgeon General].
Dempsey D, Tutka P, Jacob P 3rd, Allen F, Schoedel K, Tyndale RF,
Benowitz NL: Nicotine metabolite ratio as an index of cytochrome P450
2A6 metabolic activity. Clin Pharmacol Ther 2004, 76:64-72.
Johnstone E, Benowitz N, Cargill A, Jacob R, Hinks L, Day I, Murphy M,
Walton R: Determinants of the rate of nicotine metabolism and effects
on smoking behavior. Clin Pharmacol Ther 2006, 80:319-330.
A61
Cytokine profiling of umbilical cord blood plasma
Katrina K Au1*, Jenny Thiele2, Anne K Ellis1,2
1
Department of Biomedical Sciences, Queens University, Kingston, Ontario,
K7L 3N6, Canada; 2Department of Medicine, Queens University, Kingston,
Ontario, K7L 3N6, Canada
E-mail: 9ka19@queensu.ca
Background: Cytokines have been shown to be important signal molecules
in the development of allergy and asthma, especially the regulatory cytokine
IL-10, which has been shown to correlate with higher risk of allergy
development in children [1]. Research results regarding cytokine levels in
umbilical cord blood plasma vary greatly; some studies find the
concentration of cytokines detectable whereas other studies do not. The
purpose of this pilot study was to determine if cytokines could be measured
from cord blood plasma using IL-10 ELISAs and xMAP Luminex assay.
Methods: Umbilical cord blood was collected into EDTA vacutainer tubes
(BD) from mothers who underwent an elective Caesarean section at
Kingston General Hospital and gave written informed consent. Twenty
minutes post collection, plasma was separated by centrifugation at 1300 g
for 10 minutes and 500 l aliquots were temporarily stored at -80 C. One
aliquot was assayed using the human IL-10 ELISA (EBiosciences). In a
follow up analysis, a second plasma sample aliquot was examined using
the Milliplex map kit (Millipore) that targeted human IL-1b, IL-2, IL-4, IL-5,
IL-6, IL-7, IL-8, IL-10, IL-12(p70), IL-13, IFN-g, GM-CSF, and TNF-a.
Results: The IL-10 ELISA showed that IL-10 was present in 1 of 6 the
plasma samples examined. Using the Milliplex assay, IL-1b was detectable
in 60% of the samples; IL-2 in 50% of the samples; IL-4 and IL-5 in 90% of
the samples; IL-6, IL-7 and IL-8 in 100% of the samples; IL-10 in 90% of the
samples; IL-12(p70) in 80% of the samples; IL-13 in 100% of the samples;
IFN-g and GM-CSF in 80% of the samples; TNF-a in 100% of the samples.
Conclusions: The ELISAs lower detection limit of 2 pg/ml was not
sensitive enough to measure IL-10 accurately in these cord blood plasma
samples. The lower limit of detection of the Milliplex map kit assay ranged
from 0.01 pg/ml for IL-5 to 0.48 pg/ml for IL-13, and was sufficient to
determine the cytokines concentrations in most of the samples. The
variation observed in the measurement of the cytokine levels may have
been due to the hemolysis of two of the samples as well as the samples
being stored at -80 C instead of -20 C. Future research will compare
cytokine levels in umbilical cord blood plasma from atopic mothers
compared to non-atopic mothers.
Reference
1. Hrd J, Kocourkov I, Prokeov L: Impaired function of regulatory T cells
in cord blood of children of allergic mothers. Clinical & Experimental
Immunology 2012, 170:10-17.
A62
Estimating the impact of temperature and air pollution on
cardiopulmonary and diabetic health during the TORONTO 2015 Pan
Am/Parapan Am Games
Laura Feldman1,2*, Jingqin Zhu1,3, Jacqueline Simatovic1, Teresa To1,2,3
1
Child Health Evaluative Sciences, The Hospital for Sick Children, Toronto,
ON, Canada, M5G 1X8; 2University of Toronto, Toronto, ON, Canada, M5S
1A1; 3Institute for Clinical Evaluative Sciences, North York, ON, Canada,
M5T 3M6
E-mail: l.feldman@mail.utoronto.ca

Page 29 of 36
Figure 1(abstract A62) The geospatial distribution of temperature, humidity and Air Quality Health Index (AQHI)a in Pan Am and Parapan Am regions of
Ontario in July 2010. aA composite measure of NO2, PM2.5 and O3 where 1-3=low health risk, 4-6=medium health risk, 7-10=high health risk.
Background: The TORONTO 2015 Pan Am/Parapan Am Games will attract

thousands of visitors to Ontario, many of whom may suffer from chronic
disease. It has been shown that those with asthma, asthma-related
conditions, hypertension and diabetes are particularly sensitive to worsening
air quality [1].
Objective: To predict patterns of temperature, humidity and air quality,
as well as health service use for cardiopulmonary conditions and diabetes
in July 2015.
Methods: Exposure data (temperature, humidity and air pollution) were
obtained from Environment Canada for years 2003 to 2010. Using ArcGIS,
the geospatial patterns of exposures were described for regions of
Ontario hosting Pan Am events. A linear trend was used to forecast
expected exposures for Pan Am regions in July 2015. Health outcomes
(hospitalizations, emergency department visits and outpatient claims) for
all-cause morbidity, asthma, asthma-related conditions, diabetes and
hypertension were measured using data provided by the Institute for
Clinical Evaluative Sciences. Associations between exposures and health
outcomes were obtained from regression models. Health outcomes were
predicted for July 2015 using scenarios of 5% and 10% higher exposure
levels than forecasted.
Results: Figure 1 shows the geospatial differences in temperature,
humidity and air quality across Pan Am regions of Ontario in July 2010.
Predicted daily rates of hospitalization and outpatient claims showed the
largest increase under scenarios of increased exposure levels (Table 1).
Given a 10% higher temperature than forecasted, predicted daily
outpatient claims rates were 15% higher for all causes (Table 1), 20%
higher for asthma and 20% higher for hypertension, compared to
predicted rates using the forecasted temperature. Given a 10% higher Air
Quality Health Index (AQHI) level than forecasted, predicted daily
hospitalization rates were 6% higher for all causes (Table 1), 4% higher for
asthma and 4% higher for asthma-related conditions, compared to
predicted rates using the forecasted AQHI level.
Conclusions: With thousands more people being exposed to Ontarios
weather and air pollution in July 2015, it is especially important to
consider strategies to minimize the environmental impact of human
activities. This will lessen the potential burden on individuals, especially
those living with chronic disease.
Reference
1. To T, Licskai C, Dell S, Su J, Foty R, Feldman L, Moores G: Using the Air
Quality Health Index to measure the impact of poor air quality on
chronic diseases in Ontario. The Hospital for Sick Children Toronto (ON):
Child Health Evaluative Sciences 2012, 53, Supported by the Ontario

Ministry of the Environment.
A63
The impact of the intestinal microbiome on human immune
development and atopic disease
Leah T Thomas*, Marie-Claire Arrieta, Pedro A Dimitriu, Lisa Thorson,
William W Mohn, B Brett Finlay, Stuart E Turvey
Department of Microbiology & Immunology and Pediatrics, University of
British Columbia, Vancouver, BC V6T 1Z4, Canada
E-mail: leahscapades@gmail.com
Background: Asthma is a chronic inflammatory disease characterized by
bronchial hyper-responsiveness [1]. As the most endemic of all childhood
diseases, asthma accounts for the majority of hospitalizations and school
absences in children [2]. Exciting new research focuses on the involvement
of the gut microbiome in asthma development. Murine studies support the
hypothesis that the administration of probiotics or antibiotics during postnatal life alters the gut microbiome and ultimately the asthmatic
symptoms of these mice [3-5]. This study will translate these findings into
humans using stool samples obtained from the Canadian Healthy Infant
Longitudinal Development (CHILD) study.
Hypothesis: The composition of the human gut microbiome in early life
influences immune system development specifically related to asthma
susceptibility, and specific microbial populations protect against or
promote asthma development.
Methods: 1262 children enrolled in the CHILD study with valid skin prick
test and wheeze data (determined by questionnaire/clinical assessment)
were grouped into four clinically relevant phenotypes: atopic wheeze,
atopic non-wheeze, non-atopic wheeze, and non-atopic non-wheeze.
Individuals who test positive for both wheeze and atopy are known to be
at the highest risk for developing asthma versus those of the other three
phenotypes [6,7]. 16S rDNA extracted and amplified from 3-month and 1year stool samples of children in these four phenotypes was subjected to
high throughput Illumina sequencing to identify common/predominant
microbial populations among these children during the first year of life.
Principle coordinate analysis (PCoA) will be applied to compare the
microbial taxa among the four phenotypes and assess the effect of
confounding factors.
Table 1(abstract A62) For Pan Am regions: observed and forecasted exposures, with predicted daily health service use
rates for all-cause morbidity in July 2015 under scenarios of 5% and 10% higher exposure levels than forecasted
Exposures
Temperature (C)
Humidity (%)b
AQHIa
a
Hospitalizationsc
Emergency Department Visitsc
Outpatient Claimsc
Observed
Forecasted
(July 03-10)
(July 15)
Forecasted
5%
10%
Forecasted
5%
10%
Forecasted
5%
10%
25.66
25.74
3.36
3.62
3.88
10.95
10.99
11.02
253.46
272.30
291.15
71.2
4.2
69.5
2.6
3.67
2.84
3.90
2.93
4.13
3.01
10.99
10.90
11.03
10.91
11.07
10.92
275.91
216.85
293.36
222.85
310.82
228.86
Monthly average of daily maximums. bMonthly average of daily averages. cPer 10,000 general population.

Results: PCoA will be used to compare the microbial populations among

these four phenotypes. This analysis will be extended to examine the
effects of confounding factors such as, mode of delivery, antibiotic
exposure, feeding methods (breast milk vs. formula/solid food diet), and
furred pet exposure on the gut microfloral diversity and composition
relative to asthma development. These data will ultimately be compared
alongside murine model data already established in the Finlay lab as well
as with additional clinical data from the CHILD study regarding asthma/
allergy development in these subjects at 3- and 5-years of age.
Conclusions: This study could potentially identify the gut microbiome as
a therapeutic target to prevent the development of asthma in children,
perhaps through the addition of specific probiotic regimens during the
first year of life [4].
References
1. Mazzarella G, Bianco A, Catena E, De Palma R, Abbate F: Th1/Th2
lymphocyte polarization in asthma. Allergy 2000, 55(Suppl 61):6-9.
2. World Health Organization: Asthma. 2011.
3. Arnold IC, Dehzad N, Reuter S, Martin H, Becher B, Taube C, Muller A:
Helicobacter pylori infection prevents allergic asthma in mouse models
through the induction of regulatory T cells. J Clin Invest 2011,
121:3088-3093.
4. Forsythe P, Inman MD, Bienenstock J: Lactobacillus reuteri inhibits the
allergic airway response in mice. Am J Respir Crit Care Med 2007,
175:561-569.
5. Russell SL, Gold MJ, Hartmann M, Willing BP, Thorson L, Wlodarska M, Gill N,
Blanchet MR, Mohn WW, McNagny KM, Finlay BB: Early life antibioticdriven changes in microbiota enhance susceptibility to allergic asthma.
EMBO Rep 2012, 13:440-447.
6. Gong H: Wheezing and Asthma. Clinical Methods The History, Physical, and
Laboratory Examinations Boston: Butterworths: Walker, H. K., Hall, W. D.,
Hurst, J. W. , 3 1990, Ch. 37.
7. Rochetti R, Jesenak M, Rennerova Z, Barreto M, Ronchetti F, Villa MP:
Relationship between atopic asthma and the population prevalence
rates for asthma or atopy in children: atopic and nonatopic asthma in
epidemiology. Allergy Asthma Proc 2009, 30(1):55-63.
A64
Evaluating preferences for long term wheeze following RSV infection
using TTO and best-worst scaling
Lilla MC Roy1*, Nick Bansback2, Carlo Marra1, Roxane Carr3, Mark Chilvers3,
Larry D Lynd1
1
Faculty of Pharmaceutical Sciences, University of British Columbia,
Vancouver, Canada, V6T 1Z3; 2School of Population and Public Health,
University of British Columbia, Vancouver, Canada, V6T 1Z3; 3British Columbia
Childrens Hospital, Vancouver, Canada, V6H 3E8
E-mail: lillaroy@mail.ubc.ca
Background: Respiratory Syncytial Virus (RSV) infects 70% of infants
under one year, and is a leading cause of infant bronchiolitis-related
hospitalizations [1,2]. RSV is a relatively benign, temporary condition, and
therefore likely to have limited impact on quality adjusted life years,
however, it has potential for long-term consequences such as asthma and
wheeze [3,4]. Preferences related to the trade-offs between different long
and short term aspects of RSV have not been explored previously,
however, deriving preferences for infant health states is very challenging
as infants require proxy elicitation of preferences [5-8].
Methods: The objectives of this study were to explore preferences
surrounding attributes of RSV using proxy- and self-perspectives. Time tradeoff (TTO) and best-worst scaling were used to derive utilities for health
states of RSV and determine relative preferences for different levels of
disease attributes. Vignettes were constructed from focus group data and
expert opinion. Respondents were randomized to either a child perspective
(imagine that your child has RSV), or an adult perspective (imagine that
you have RSV). Experimental design for the BWS was developed using
Sawtooth Software. 1000 Canadians were recruited through a market
research panel facilitating a societal perspective. Five attributes were used
hospitalization status, oxygen support, presence of tubes (IV/NG), breathing
symptom severity, and risk of long term wheeze. Ethics approval
was obtained from the UBC BREB. Respondents completed both TTO and
BWS tasks.
Page 30 of 36
Results: Disutility associated with the short term health state of RSV was
significant. Disutility followed an expected gradient, with more time traded
for more severe RSV, and less time traded for less severe RSV (mean range:
0.57 0.14). Utilities were lower in the child perspective than the adult
perspective. 0% risk of long term risk of wheeze was most preferred over
all other attributes, and respiratory failure was least preferred (-4.7). Strong
negative preferences were similar for IV/NG (-3.3), ICU admission (-3.5),
mechanical ventilation (-3.6), and severe breathing problems (-3.6). Utility
associated with risk of wheeze became lower as risk increased, with a
relative preference for 80% risk of wheeze (-2.8) between moderate (-1.5)
and severe (-3.7) breathing problems.
Conclusions: Preferences indicate societal willingness to accept immediate,
short term, potentially clinically significant consequences to avoid long term
risk of wheeze. This study provides utilities that can be utilized for the
evaluation of any potential or proposed treatment of RSV in children, and is
important to understanding and applying priorities in health care.
Acknowledgments: This study is funded by Abbott Laboratories and
AllerGen NCE Canada.
References
1. Chidgey SM, Broadley KJ: Respiratory syncytial virus infections:
characteristics and treatment. J Pharm Pharmacol 2005, 57:1371-1381.
2. Holberg CJ, Wright AL, Martinez FD, Ray CG, Taussig LM, Lebowitz MD: Risk
factors for respiratory syncytial virus-associated lower respiratory
illnesses in the first year of life. Am J Epidemiol 1991, 133:1135-1151.
3. Stensballe LG, Ravn H, Kristensen K, Agerskov K, Meakins T, Aaby P,
Simes EAF: Respiratory syncytial virus neutralizing antibodies in cord
blood, respiratory syncytial virus hospitalization, and recurrent wheeze.
J Allergy Clin Immunol 2009, 123:398-403.
4. Bont L, Steijn M, van Aalderen WMC, Kimpen JLL: Impact of Wheezing
After Respiratory Syncytial Virus Infection on Health-Related Quality of
Life. Pediatr Infect Dis J 2004, 23:414-417.
5. Prosser LA: Current Challenges and Future Research in Measuring
Preferences for Pediatric Health Outcomes. J Pediatr 2009, 155:7-9.
6. Griebsch I: Quality-Adjusted Life-Years Lack Quality in Pediatric Care: A
Critical Review of Published Cost-Utility Studies in Child Health.
PEDIATRICS 2005, 115:e600-e614.
7. Petrou S: Methodological issues raised by preference-based approaches
to measuring the health status of children. Health Econ 2003, 12:697-702.
8. Ungar WJ: Challenges in health state valuation in paediatric economic
evaluation: are QALYs contraindicated? Pharmacoeconomics 2011,
29:641-652.
A65
Is response to IVIG in Chronic Idiopathic Urticaria related to presense
of autoantibodies?
Lana Rosenfield1*, Chrystyna Kalicinsky2, Richard Warrington2
1
Department of Internal Medicine, University of Manitoba, Winnipeg,
Manitoba, Canada; 2Section of Allergy and Clinical Immunology ,Department
of Internal Medicine, University of Manitoba, Winnipeg, Manitoba, Canada
Background: Treatment of Chronic Idiopathic Urticaria (CIU) may be
challenging, as patients can be refractory to various treatments. This may
be due to an autoimmune mechanism in its pathogenesis. CIU has been
shown to be associated with autoantibodies to IgE or IgE receptor and
with thyroid autoimmunity [1,2]. Treatments targeting this autoimmune
pathogenesis are now being used, such as intravenous immunoglobulin
(IVIG). We reviewed patients with CIU treated with IVIG to see if response
to treatment correlated with presence of autoimmunity (antibodies to
IgE/IgE receptor or Thyroidperoxidase (TPO) antibodies).
Methods: A retrospective chart review of patients seen in Allergy and
Clinical Immunology clinics at Health Sciences Centre and Grace Hospital
in Winnipeg was completed. Inclusion criteria included treatment with IVIG
with a clinical diagnosis of CIU. There were a total of 21 patients identified.
13 patients were treated with protocol A, 2g/kg load split between 4 doses
given within a two week period followed by maintenance of 0.5 g/kg.
Protocol B was used for 8 patients consisting of monthly IVIG (60-80g).
Autoimmune blood work was recorded for Histamine Release Assay (HRA)
and TPO. HRA testing implies the presence of antibodies to IgE or IgE
receptor. Patients response to IVIG was recorded.

Results: HRA was done on 15 /21 patients and 5 of these patients tested
positive. 3/5 were able to maintain remission with continued IVIG
treatment, one relapsed after discontinuing IVIG following remission and
one was unresponsive to IVIG. Anti-TPO was tested in 11 patients of which
3 were positive. Of these three patients, one was responsive to IVIG, one
relapsed after initially being responsive and one was unresponsive. Overall
13/21 patients were responsive to IVIG. Of those who were responsive to
IVIG 6 were HRA negative and 3 HRA positive of the 9 tested, and 4 TPO
negative and 1 TPO positive of the 5 tested for TPO. When comparing
protocols, 7/13 patients who underwent protocol A responded without
relapse compared to 6/8 treated with protocol B.
Conclusion: IVIG can be effective in some patients with CIU who are
unresponsive to antihistamine treatment. A greater number of patients
who were responsive to IVIG had negative results for the autoimmune
tests we conducted. Therefore, based on our data, the response to IVIG
cannot be determined by the presence of positive HRA or TPO
antibody.
A66
Tryptase levels in children presenting with anaphylaxis to the Montreal
Childrens Hospital
Michelle Halbrich1*, Ann Clarke2,3, Sebastian La Vieille4, Harley Eisman5,
Reza Alizadehfar1, Joseph Lawrence2,6, Chris Mill2, Judy Morris7,
Moshe Ben-Shoshan1
1
Division of Paediatric Allergy and Clinical Immunology, Department of
Paediatrics, McGill University Health Centre, Montreal, Quebec, Canada;
2
Division of Clinical Epidemiology, Department of Medicine, McGill University
Health Centre, Montreal, Quebec, Canada; 3Division of Allergy and Clinical
Immunology, Department of Medicine, McGill University Health Centre,
Montreal, Quebec, Canada; 4Food Directorate, Health Canada, Ottawa,
Ontario, Canada; 5Montreal Childrens Hospital, Emergency Department,
McGill University Health Centre, Montreal, Quebec, Canada; 6Departments of
Epidemiology and Biostatistics, McGill University, Montreal, Quebec, Canada;
7
Department of Emergency Medicine, Hpital du Sacr-Coeur de Montral,
Universit de Montral, Qubec, Canada
E-mail: michelle.halbrich@hotmail.com
Rationale: There are little data on the role of tryptase in the diagnosis of
anaphylaxis. We aimed to assess the sensitivity of elevated tryptase levels
(>11.4) as defined in the current medical literature to diagnose
anaphylaxis and to identify factors associated with elevated tryptase
levels.
Methods: Children presenting with anaphylaxis to the Montreal Childrens
Hospital Emergency Department (ED) between April 2011 and April 2013
were recruited. The treating physician documented symptoms, triggers,
and management of the anaphylactic reactions. Total tryptase levels were
measured 30-120 minutes following onset of symptoms. Charts of all ED
patients were reviewed to identify cases that were missed in prospective
recruitment. Multivariate logistic regression was used to examine the
association between an elevated tryptase level and age, gender, reaction
trigger, reaction severity, and history of atopy.
Results: Of 398 anaphylaxis cases (203 of whom were recruited
prospectively), 84 children had serum tryptase levels measured. Age, gender,
anaphylactic trigger, and severity of reaction were comparable between
cases with and without tryptase measurements. However, there was higher
percentage of patients treated with epinephrine in hospital in the group
with tryptase measurements. The median age of these 84 children was 5.1
years (IQR 1.3, 12.3), 40.4% were females, 78.6% identified food as the
potential anaphylactic trigger, and 7.1% experienced a severe reaction.. The
mean tryptase level was 6.9 ng/mL (4.5, 8.0). Only 13 patients [15.5% (95%CI,
8.8,25.4)] had elevated levels. Severe reactions and history of eczema were
associated with elevated levels ( OR =115.4 (95%CI,8.7,1527.8) and 14.2(95%
CI,2.6,78.5) respectively.
Conclusions: Our results do not support the use of total tryptase as a
diagnostic tool in children with anaphylaxis. Given the poor sensitivity (13/
84 = 15%) of the current tryptase threshold, new laboratory tests need to be
developed to help establish the diagnose of anaphylaxis accurately. Severe
reactions and presence of eczema are associated with high levels, but wide
confidence intervals preclude definitive conclusions for the other risk factors
we investigated.
Page 31 of 36
A67
Genomewide DNA methylation dynamics upon diesel exhaust exposure
in asthmatics
Ruiwei Jiang1*, Francesco Sava2, Michael S Kobor3, Christopher R Carlsten2
1
Genome Sciences and Technology, College for Interdisciplinary Studies,
University of British Columbia, Vancouver, British Columbia, Canada, V6T 1Z4;
2
Department of Medicine, Division of Respiratory Medicine, University of
British Columbia, Vancouver, British Columbia, Canada, V5Z 1M9;
3
Department of Medical Genetics, University of British Columbia, Vancouver,
British Columbia, Canada, V5Z 4H4
E-mail: ruiwei06@gmail.com
Background: Particulate air pollution can induce epigenetic changes
and regulate gene expression relevant to the pathophysiology of
asthma and allergic diseases. Recently, epidemiologic data suggests that
there are observable acute effects of air pollution on peripheral blood
DNA methylation levels of genomewide Alu and LINE-1 repeat
elements, as well as certain genes involved in oxidative stress response
and innate immunity. In this study, we hypothesized that in a
controlled exposure setting, diesel exhaust (as a model of particulate air
pollution) can induce DNA methylation changes that are detectable on
the genomewide level.
Methods: We recruited 16 subjects with asthma, and/or airway hyperresponsiveness. They were exposed to both diesel exhaust (DE) and filtered
air (FA) following a randomized crossover design. Peripheral blood
mononuclear cells (PBMCs) were collected at baseline, 6 hours, and 30 hours
post-exposure. Methylation at 415,382 CpG sites covering 39,136 genes was
measured using the Illumina Infinium 450K bead chip methylation array. To
detect effects of the diesel exposure, we conducted a principal component
analysis (PCA) , resulting in principal components with common patterns of
methylation variation across samples. Using this method we were able to
pinpoint one principal component that was significantly associated with
diesel exhaust exposure, from which we then selected a subset of probes
that possessed that specific pattern of variation.
Results: Whole genome analysis using PCA followed by denoising
revealed that principal component 22, which accounted for 0.5% of the
total variance, was significantly associated with the treatment variable:
[DE 6hr and 30hr] versus [DE 0hr, FA 0hr, 6hr, and 30hr] (Figure 1). Using
loading cutoff of 6 standard deviations, we found 89 CpG sites to
possess the specific pattern of variation (Figure 2). These include genes
whose expression is associated with exposure to either diesel exhaust or
components of diesel exhaust as reported by literature: CASP7, ATCAY,
ABCA1, JAK3, CYFIP2, and NOX2 [1-6].
Conclusions: These results suggest that short-term exposure to diesel
exhaust in a controlled setting has minimal but detectable effects on a
genomewide level in PBMCs. We are currently applying mixed effects
modeling and intraclass correlation to our identified hits to further
substantiate the association of these hit probes to the treatment
variable.
References
1. Amara N, Bachoual R, Desmard M, Golda S, Guichard C, Lanone S, Aubier M,
Ogier-Denis E, Boczkowski J: Diesel exhaust particles induce matrix
metalloprotease-1 in human lung epithelial cells via a NADP(H) oxidase/
NOX4 redox-dependent mechanism. Am J Physiol Lung ell Mol Physiol
2007, 293(1):L170-181.
2. Cao D, Tal TL, Graves LM, Gilmour I, Linak W, Reed W, Bromberg PA,
Samet JM: Diesel exhaust particulate-induced activation of Stat3 requires
activities of EGFR and Src in airway epithelial cells. Am J Physiol Lung Cell
Mol Physiol 2007, 292(2):L422-429.
3. Hirano M, Tanaka S, Asami O: Classification of polycyclic aromatic
hydrocarbons based on mutagenicity in lung tissue through DNA
microarray. Environ Toxicol 2011, DOI: 10.1002/tox.20761.
4. Lee SE, Lee SH, Ryu DS, Park CS, Park KS, Park YS: Differentially-expressed
genes related to atherosclerosis in acrolein-stimulated human umbilical
vein endothelial cells. BioChip J 2010, 4(4):264-271.
5. Simkhovich BZ, Kleinman MT, Mehrian-Shai R, Hsu YH, Meacher D,
Gookin G, Kinnon MM, Salazar K, Willet P, Feng G, Lin SM, Kloner RA:
Chronic exposure to ambient particulate matter alteres cardiac gene
expression patterns and markers of oxidative stress in rats. Air Qual
Atmos Health 2011, 4:15-25.

Page 32 of 36
Figure 1(abstract A67) Impact values of each sample in principal component 22. Samples were separated into DEP 6hr and 30hr, followed by FAP 0hr,
6hr and 30hr, and DEP 0hr.
Figure 2(abstract A67) Distribution of probe loading values for principal component 22. The values located at 3 and 6 standard deviations are
marked.

6.
Steiner S, Mueller L, Popovicheva OB, Raemy DO, Czerwinski J, Comte P,

Mayer A, Gehr P, Rothe-Rutishauser B, Clift MJ: Cerium dioxide
nanoparticles can interfere with the associated cellular mechanistic
response to diesel exhaust exposure. Toxicol Lett 2012, 214(2):218-225.
A68
Double blind randomized crossover trial of PF-03654764 + fexofenadine
in the environmental exposure unit (EEU)
Michelle L North1,2*, Terry Walker2, Lisa M Steacy2, Barnaby G Hobsbawn2,
Richard J Allan3, Frances Hackman3, Xiaoqun Sun4, Andrew G Day4,
Anne K Ellis1,2,5
1
Department of Biomedical and Molecular Sciences, Queens University,
Kingston, Ontario, Canada, K7L 2V5; 2Allergy Research Unit, Kingston General
Hospital, Kingston, Ontario, Canada, K7L 2V7; 3Pfizer Ltd., Sandwich, Kent,
CT13 9NJ, UK; 4Clinical Research Centre, Kingston General Hospital, Kingston,
Ontario, Canada, K7L 2V7; 5Division of Allergy and Immunology, Department
of Medicine, Queens University, Kingston, Ontario, Canada, K7L 2V7
Background: Oral histamine receptor1 antagonists, such as fexofenadine,
offer suboptimal relief of allergic rhinitis-associated nasal congestion.
Combinations with oral sympathomimetics, such as pseudoephedrine,
relieve congestion but produce side effects. Histamine receptor-3
antagonists, such as PF-03654764, reduce congestion in animals and have
been proposed as novel therapeutics. Previous nasal allergen challenge
studies of similar H1+H3 receptor antagonist combinations demonstrated
reduced congestion. Herein we employ the Environmental Exposure Unit
(EEU) to conduct the first randomized controlled trial of PF-03654764 in
allergic rhinitis. The primary objective was to compare the effect of
PF-03654764+fexofenadine to pseudoephedrine+fexofenadine on the
subjective measures of congestion and Total Nasal Symptom Score (TNSS).
The objective of post-hoc analyses were to compare all treatments to
placebo and determine the onset of action (OA).
Methods: 64 participants were randomized in a double-blind, placebocontrolled 4-period crossover study. Participants were exposed to ragweed
pollen for 6 hours post-dose in the EEU.
Results: PF-03654764+fexofenadine was not superior to pseudoephedrine
+fexofenadine. In post-hoc analyses, PF-03654764+fexofenadine
significantly reduced TNSS, relative to placebo, and OA was 60 minutes.
Pseudoephedrine+fexofenadine significantly reduced congestion and
TNSS, relative to placebo, with OA of 60 and 30 minutes, respectively. All
PF-03654764-treated groups experienced an elevated incidence of
adverse events.
Conclusions: PF-03654764+fexofenadine failed to provide superior relief
of allergic rhinitis-associated nasal symptoms upon exposure to ragweed
pollen compared to fexofenadine+pseudoephedrine. However, PF03654764+fexofenadine improved TNSS compared to placebo. Side
effects were not insignificant.
A69
Human rhinovirus infection of human bronchial epithelial cells results
in migration of human airway smooth muscle cells
Sami Shariff*, Sergei Nikitenko, Abid Qureshi, Jason Arnason, Chris Shelfoon,
Suzanne Traves, David Proud, Richard Leigh
T2N 4N1, Canada
E-mail: sami.shariff@gmail.com
Background: Young children who experience human rhinovirus (HRV)associated wheezing illnesses are more likely to develop subsequent
asthma [1]. This has led to the hypothesis that HRV infection may be
involved in the pathogenesis of airway remodeling in asthma [2].
Increased airway smooth muscle (ASM) mass, in which ASM cells are in
close proximity to the subepithelial region, is a characteristic feature of
airway remodeling [3]. We have shown that HRV infection of human
bronchial epithelial (HBE) cells, both in vitro and in vivo, results in the
upregulation of airway remodeling mediators [4]. We now sought to
determine whether HRV infection of HBE cells is associated with airway
smooth muscle (ASM) chemotaxis.
Page 33 of 36
Methods: Primary HBE cells pre-treated with medium containing 1% insulin,

transferrin, and selenium (ITS) for 24 hours were exposed to medium
(control) or purified HRV-16 (MOI: 0.3-1) for 24 hours. HBE cell supernatants
were then studied as chemoattractants for ASM chemotaxis. ASM migration
was examined using both a 48-well modified Boyden chamber and a 16well xCELLigence apparatus (Roche, Laval, Canada). In the latter case,
migration to HBE supernatants was measured via electrical impedance, as
per manufacturers instructions, and compared to medium control.
Chemotactic gradient was abolished by addition of chemoattractants to top
and bottom wells of the apparatuses. Additionally, the effects of filtered
supernatants and pre-treatment with Pertussis toxin (PTX) on ASM
chemotaxis were studied using the xCELLigence apparatus.
Results: Supernatants from HRV-16 infected HBE cells resulted in
significantly greater ASM cell directional migration, compared to
supernatants from HBE cells exposed to medium (negative control) in both
the Boyden chamber (n=3; p<0.01) and the xCELLigence system (n=3;
p<0.001); relationship was concentration-dependent (n=3; p<0.05). Time
course experiments demonstrated that rate of migration was maximal at
4 hours. Migration was significantly attenuated when the chemotactic
gradient was abolished, indicating that directional cell migration is due to
chemotaxis and not chemokinesis (n=3; p<0.001). ASM migration
significantly increased even after filtration of HRV and proteins greater
than 100,000 MW (n=3; p<0.05). However, pretreatment with PTX
abrogated HRV-induced ASM chemotaxis (n=3, p<0.05). Pretreatment with
dexamethasone, formoterol, or combination, abolished ASM chemotaxis
(n=4, p<0.05).
Conclusions: These data provide the first demonstration that HRV infection
of airway epithelial cells produces soluble factor(s) that cause directional
migration of ASM cells. Moreover, migration appears to be dependent on a
PTX sensitive pathway. Taken together, they provide further evidence for a
role of HRV infection in the pathogenesis of airway remodeling in asthma.
Acknowledgements: This abstract was funded in part thanks to AllerGen
NCE., the Queen Elizabeth II scholarship, Canadian Institutes of Health
Research, and GSK-CIHR Professorship in inflammatory lung disease.
References
1. Lemanske RF: The childhood origins of asthma (COAST) study. Pediatr
Allergy Immunol 2002, 13:38-43.
2. Proud D, Leigh R: Epithelial cells and airway diseases. Immunological
reviews 2011, 242:186-204.
3. Gerthoffer WT: Migration of airway smooth muscle cells. Proc Am Thorac
Soc 2008, 5:97-105.
4. Leigh R, et al: Human rhinovirus infection enhances airway epithelial cell
production of growth factors involved in airway remodeling. J Allergy
Clin Immunol 2008, 121:1238-1245.e4.
A70
Systematic review of outcome measures in randomised controlled trials
of pediatric eosinophilic esophagitis (EoE) treatment
Tamar Rubin1, Jacqueline Clayton1, Denise Adams1,2, Rabin Persad1,4,
Sunita Vohra1,2,3*
1
Department of Pediatrics, University of Alberta, Edmonton, Alberta, Canada;
2
CARE Program, University of Alberta, Edmonton, Alberta, Canada;
3
Department of Public Health Sciences, University of Alberta, Edmonton,
Alberta, Canada; 4Department of Pediatric Gastroenterology, University of
Alberta, Edmonton, Alberta, Canada
E-mail: svohra@ualberta.ca
Background: Heterogeneity has been noted in the selection and reporting
of disease-specific pediatric outcomes in randomized controlled trials (RCTs)
[1]. The consequence may be invalid results from RCTs, or difficulty in
comparing results across trials [2,3]. The primary objective of this systematic
review was to assess the heterogeneity of outcome measures selection and
reporting in recent pediatric EoE treatment trials. As secondary objectives,
we assessed the heterogeneity of disease definition and resolution across
studies compared to established concensus guidelines, as well as the
evidence for current EoE treatments.
Methods: We searched MEDLINE, EMBASE, The Cochrane Library,
Cochrane Central Register of Controlled Trials (CENTRAL), and CINAHL from
the last ten years, including randomized controlled trials of EoE treatment

Page 34 of 36
Figure 1(abstract A70) Flow Diagram
in patients 0-18 years. Two authors independently assessed articles

for inclusion.
Results: A total of 11 studies met inclusion criteria (Fig 1). Numerous
outcome measures were selected and reported in these trials, with
certain measures, such as esophageal eosinophilia, clinical symptoms,
safety, histologic features, and endoscopic features, re-occurring
frequently, but not universally. Uptake of consensus-established
diagnostic criteria for EoE (FIGER criteria) was 30% in trials published after
2007. Due to the small number and heterogeneity of studies obtained, no
conclusions regarding treatment efficacy could be made.
Conclusions: The results of this study confirm the need for universally
reported, pediatric-specific, standardized outcome measures in EoE trials.
Adherence to standardized disease definitions will enhance the utility of
outcome measures. Consistent disease definition and standardized
outcome reporting will allow for meta-analyses across similar trials and
thus inform future clinical decision-making in pediatric EoE.
Systematic review registration: CRD42013003798
References
1. Clarke M: Standardising outcomes for clinical trials and systematic
reviews. Trials 2007, 8:39.
2. Sinha I, Jones L, Smith RL, Williamson PR: A systematic review of studies
that aim to determine which outcomes to measure in clinical trials in
children. PLoS Med 2008, 5(4):e96.
3. Williamson PR, Gamble C, Altman DG, Hutton JL PR: Outcome selection
bias in meta-analysis. Stat Methods Med Res 2005, 14:515-524.
A71
Cyclic stretch augments human rhinovirus induced inflammatory
responses in airway epithelial cells
Sergei Nikitenko*, Sami Shariff, Jason Arnason, Chris Shelfoon, Cora Kooi,
David Proud, Richard Leigh
T2N 4N1, Canada
E-mail: snikiten@ucalgary.ca
Background: Structural cells of the airways are subject to normal

mechanical stretch during respiration [1]. Mechanical stretch acts as a
mechanism of cell activation, and mechanotransduction pathways have
been shown to activate pro-inflammatory genes [2]. Human rhinovirus
(HRV) infections are a major cause of asthma exacerbations, and
mechanical forces are likely to be more pronounced during asthma
exacerbations [3]. Moreover, smoking is associated with worse clinical
outcomes in asthma. Previous studies have shown that HRV infection,
cigarette smoke extract (CSE), or mechanical stretch each induce CXCL8
production in bronchial epithelial cells [4-6]. In this study, we sought to
determine whether mechanical stretch interacts with HRV infection and
CSE to further upregulate airway inflammation.
Methods: Studies were performed using primary human bronchial
epithelial cells (HBEC), the human bronchial epithelial cell line BEAS-2B. Cells
were treated with CS (FlexCell FX-4000), HRV-16 or with a combination of CS
+HRV-16. Protein and mRNA levels were measured using ELISA (R&D
Systems) and real-time RT-PCR (Applied Biosystems).
Results: Mechanical stretch and HRV infection each significantly increased
CXCL8 release in BEAS-2B and HBE cells compared to static controls
(p<0.001). When studied in combination, there was a significant synergistic
increase in CXCL8 in BEAS-2B (p<0.001). Ultraviolet (UV) inactivation of HRV
attenuated this increase in CXCL8 release. Mechanical stretch and HRV
infection each increased CXCL8 mRNA levels compared to static controls,
with the combination resulting in further enhanced induction (p<0.01).
CSE alone did not significantly increase CXCL8 production in BEAS-2B.
However, the combination of CSE+HRV significantly enhanced CXCL8
release compared to medium control (p<0.001) and HRV alone (p<0.05),
and this increase was significantly further augmented by mechanical
stretch (p<0.001).
Conclusions: Mechanical stretching of BEAS-2B and HBE cells increased
HRV-induced CXCL8 mRNA and protein levels, confirming that this effect
is, at least in part, regulated at the transcriptional level. Moreover, the
combination of mechanical stretch and HRV infection, as might occur
during asthma exacerbations, resulted in a synergistic enhancement of
CXCL8 expression, compared to either stimulus alone. CSE further
enhanced HRV-induced and stretch-induced CXCL8 release, and the

combination of all three variables potentiated this effect. Since levels of

CXCL8 have been linked to increased airway neutrophils and symptom
severity, mechanical stretch, if it also enhances CXCL8 production induced
during HRV infections in vivo, may contribute to the pathogenesis of
airway inflammation in HRV-induced asthma exacerbations.
Acknowledgements: The funding sources for this study include AllerGen
NCE Inc., Queen Elizabeth II Masters Scholarship, Canadian Institutes of
Health Research, and the GSK-CIHR Professorship in Inflammatory Lung
Disease.
References
1. Lionetti V, Recchia FA, Ranieri VM: Overview of ventilator-induced lung
injury mechanisms. Curr Opin Crit Care 2005, 11:82-6.
Page 35 of 36
2.
3.
4.
5.
6.
Trepat X, Deng L, An SS, Navajas D, Tschumperlin DJ, Gerthoffer WT,

Butler JP, Fredberg JJ: Universal physical responses to stretch in the
living cell. Nature 2007, 447:592-5.
Arden KE, Mackay IM: Rhinoviruses. eLS 2001, 33:1-12.
Proud D, Leigh R: Epithelial cells and airway diseases. Immunol Rev 2011,
242:186-204.
Fahy V, Kim KW, Liu J, Boushey HA: Prominent neutrophilic inflammation
in sputum from subjects with asthma exacerbation. J Allergy Clinical
Immunol 1995, 95:843-52.
Jatakanon A, Uasuf C, Maziak W, Lim S, Chung KF, Barnes PJ: Neutrophilic
inflammation in severe persistent asthma. Am J Respir Crit Care Med 1999,
160:1532-9.
Figure 1(abstract A72) IDO1 gene expression fold changes relative to plain media control. IDO1 expression levels were normalized to HPRT1 expression.
The error bars represent the standard error of the mean. Numbers per stimulation group are as indicated beneath the graph. Cultures of atopic and nonatopic AMNCs were plated at 7.5x106 cells per condition. Following 5.5 hours incubation with either plain media, 1 g/ml IFN-g, or 1 g/ml IFN-g and 10
ng/ml CSE, cells were lysed for RNA extraction. RNA was reverse transcribed and cDNA levels were analyzed.
Figure 2(abstract A72) Supernatant cytokine level change relative to plain for Th2 cytokines IL-4 (A), IL-5 (B) and IL-13 (C). Error bars represent the
standard error of the mean. Cultures of atopic and non-atopic AMNCs were plated at 5x106 cells per condition. Following 5.5 hours incubation with
either plain media, 1 g/ml IFN-g, or 1 g/ml IFN-g and 10 ng/ml CSE, supernatants were collected and analyzed. A=high atopic risk, NA=low atopic risk.
Each condition/atopic risk group contains a minimum of 6 samples.

Page 36 of 36
Figure 3(abstract A72) Supernatant cytokine level change relative to plain for pro- and anti-inflammatory cytokines TNF-a (A), IL-6 (B) and IL-10 (C). Error
bars represent the standard error of the mean. Cultures of atopic and non-atopic AMNCs were plated at 5x106 cells per condition. Following 5.5 hours
incubation with either plain media, 1 g/ml IFN-g, or 1 g/ml IFN-g and 10 ng/ml CSE, supernatants were collected and analyzed. A=high atopic risk,
NA=low atopic risk. Each condition/atopic risk group contains a minimum of 6 samples.
A72
Analysis of indoleamine 2,3-dioxygenase 1 (IDO1) expression of cultured
cord blood adherent mononuclear cells as an indicator of atopic risk
Yifei Zhu*, Jenny Thiele, Anne K Ellis
Department of Biomedical and Molecular Sciences/Medicine, Queens
University, Kingston, ON, K7L 3N6, Canada
E-mail: 8yz7@queensu.ca
Background: Maternal atopy is a known risk factor for allergy development
in children. This link can be studied to find potential indicators of atopic risk
by examining umbilical cord blood. Indoleamine 2,3-dioxygenase 1 (IDO1),
the initiator of the IDO pathway, plays a regulatory role in the immune
response and may differ in expression in the adherent mononuclear cells
(AMNC) of atopic and non-atopic individuals. Supernatants of these AMNC
cultures may also exhibit different cytokine profiles.
Methods: Cord blood samples were collected from consenting women
undergoing elective Caesarian-sections and atopic status was selfreported. Mononuclear cells were isolated and cryopreserved. Once
thawed, AMNCs were cultured and stimulated with interferon-gamma
(IFN-g 1g/ml or 1ng/ml) with or without control standard endotoxin (CSE
10ng/ml). In each condition, 7.5x106 cells were seeded for gene analysis
and 5x106 cells were seeded for cytokine analysis. Cells were lysed for
RNA isolation, reverse transcribed and cDNA levels were analyzed using
qPCR. Supernatant cytokine levels were analyzed using the Luminex
xMAPTM Technology.
Results: IDO1 expression was significantly increased in all stimulated
conditions (P<0.05) except for the CSE only condition. The high atopic
risk group displayed trend towards decreased IDO1 expression, however,
high and low atopic risk groups did not show significant differences
(Figure 1). Supernatant cytokine analysis show heightened levels of Th2
cytokines IL-4, IL-5, IL-13 (Figure 2). Similarly, heightened levels of TNF-a
and IL-6 were observed, while levels of IL-10 were decreased in the high
atopic risk samples in all stimulated conditions (Figure 3).
Conclusions: Preliminary differences detected suggest that further
research could elucidate a suitable biomarker to predict atopic risk. Due
to the lack of significant differences between high and low atopic risk
groups for IDO1 expression and cytokine expression, a reliable biomarker
was not determined in this study.
Cite abstracts in this supplement using the relevant abstract number,

e.g.: Zhu et al.: Analysis of indoleamine 2,3-dioxygenase 1 (IDO1)
expression of cultured cord blood adherent mononuclear cells as an
indicator of atopic risk. Allergy, Asthma & Clinical Immunology 2014,
10(Suppl 1):A72

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Allergy, Asthma & Clinical Immunology 2014, Volume 10 Suppl 1

ALLERGY, ASTHMA & CLINICAL

Canadian Society of Allergy and Clinical

Allergy, Asthma & Clinical Immunology 2014, Volume 10 Suppl 1

Figure 1(abstract A3)

Figure 2(abstract A3)

Conclusions: These findings support the hypothesis that calcitriol plays

Allergy, Asthma & Clinical Immunology 2014, Volume 10 Suppl 1

Figure 4(abstract A3)

Figure 3(abstract A3)

Allergy, Asthma & Clinical Immunology 2014, Volume 10 Suppl 1

Figure 5(abstract A3)

research are involved in recruiting participants for studies. Social media

Figure 6(abstract A3)

Background: Biphasic anaphylaxis is a poorly understood allergic

Allergy, Asthma & Clinical Immunology 2014, Volume 10 Suppl 1

cases and 56 were adult. Overall frequency of biphasic reactions was

Allergy, Asthma & Clinical Immunology 2014, Volume 10 Suppl 1

Background: Low neighbourhood walkability has been associated with

Materials and methods: Allergy skin prick testing against a panel of 30

Allergy, Asthma & Clinical Immunology 2014, Volume 10 Suppl 1

Several extracts were tested for profilin and spanned a range of 0 14

Allergy, Asthma & Clinical Immunology 2014, Volume 10 Suppl 1

Conclusions: In pooled subgroup analysis from 2 trials, ragweed SLIT-T

Allergy, Asthma & Clinical Immunology 2014, Volume 10 Suppl 1

Relevance: It is important to retain families for longitudinal studies.

nut mix. He had a positive ImmunoCAP to peanut. Approximately 6 months

Allergy, Asthma & Clinical Immunology 2014, Volume 10 Suppl 1

Background: The Canadian Healthy Infant Longitudinal Development

thalamic intracranial hemorrhage with mass effect. The following day

Allergy, Asthma & Clinical Immunology 2014, Volume 10 Suppl 1

Cevik C, Nugent K, Shome GP, Kounis NG: Treatment of Kounis syndrome.

Winnipeg, Manitoba, Canada; 8Canadian Healthy Infant Longitudinal

Background: The gut microbiota is essential to human health, playing

Allergy, Asthma & Clinical Immunology 2014, Volume 10 Suppl 1

association of probiotic use during pregnancy or infancy with childhood

Conclusions: This case demonstrated that, although wheat is one of the

Allergy, Asthma & Clinical Immunology 2014, Volume 10 Suppl 1

Figure 1(abstract A28) (N=69) underwent skin prick testing

Conclusions: Pediatric EoE is considered to be an allergic disease with

Allergy, Asthma & Clinical Immunology 2014, Volume 10 Suppl 1

Figure 2(abstract A28) N=69 underwent skin prick testing

Figure 3(abstract A28) N=35 underwent patch testing

Figure 4(abstract A28) N=14 underwent ImmunoCAP testing.

Allergy, Asthma & Clinical Immunology 2014, Volume 10 Suppl 1

Allergy, Asthma & Clinical Immunology 2014, Volume 10 Suppl 1

Background: We have previously estimated that the annual rate of

Allergy, Asthma & Clinical Immunology 2014, Volume 10 Suppl 1

site of swelling, comorbidities, medications, allergies, admissions, etc. were

more wheezing episodes (p=0.04). Preliminary comprehensive analyses

Allergy, Asthma & Clinical Immunology 2014, Volume 10 Suppl 1

Figure 1(abstract A36) Search Flow Diagram

using NSAIDS and Celebrex (celecoxib) for analgesia in 2005. However,

Allergy, Asthma & Clinical Immunology 2014, Volume 10 Suppl 1

Allergy, Asthma & Clinical Immunology 2014, Volume 10 Suppl 1

Martin A, Lavoie L, Goetghebeur M, Schellenberg R: Economic benefits of

Allergy, Asthma & Clinical Immunology 2014, 10(Suppl 1):A43

Background: A nurse shortage in Canada is contributing to large

Rationale: Human rhinovirus (HRV) infections during early childhood are

Allergy, Asthma & Clinical Immunology 2014, Volume 10 Suppl 1

Sharma P, et al: Expression of the dystrophin-glycoprotein complex is a

Background: Atopic allergic asthmatic individuals experience acute