Bridging knowledge gaps in paediatric chronic urticaria through a video-based educational tool.

BACKGROUND: There is a lack of patient educational resources about chronic urticaria (CU). AIMS: To develop and test the effectiveness of an education tool to help paediatric patients and their families better understand CU and its management. METHODS: From July 2020 to May 2022, paediatric patients with a history of CU who presented to the allergy outpatient clinics at our institution were recruited. Consenting families and patients were asked to complete five questions related to the definition, causes and management of CU at the time of presentation to the clinic. Participants were shown a 5-min animated video addressing the main knowledge gaps about CU. At the end of the video, participants were redirected to the same five questions to respond again. The scores were recorded as a proportion of correct answers (range 0·0-1·0). RESULTS: In total, 53 patients [30 girls (56·6%), 23 boys (43·4%); mean age 9·7 ± 5·1 years, range 1·4-18·5 years] were recruited. The mean baseline pre-video education questionnaire score was 0·67 ± 0·2 (range 0·2-1·0), while the mean post-video score was 0·94 ± 0·1 (range 0·4-1·0), a mean score difference of 0·27, which was statistically significant (P < 0·001). At the 1-year follow-up, 14 (26·4%) patients answered the questionnaire again to assess retention of knowledge; the mean score was 0·83 ± 0·2 (range 0·2-1·0). CONCLUSIONS: Our educational video was successful in educating patients and their families to better understand urticaria. Future studies should aim to optimize patient education through nontraditional tools such as videos, and compare knowledge gain using different methods of education.

Epinephrine autoinjectors: individualizing device and dosage to optimize anaphylaxis management in the community setting.

Background: Anaphylaxis is the most severe manifestation of a systemic allergic reaction, and, in the community setting, the immediate administration of an epinephrine autoinjector (EAI) can be life-saving. Physicians are tasked with selecting the most appropriate EAI for each individual and counseling patients and/or their caregivers to maximize the likelihood of successful deployment of the EAI. Objective: To offer an evidence-based expert clinical perspective on how physicians might best tailor EAI selection to their patients with anaphylaxis. Methods: A group of eight adult and pediatric allergists with expertise in anaphylaxis management reviewed and assessed the published data and guidelines on anaphylaxis management and EAI device selection. Results: Personalized EAI selection is influenced by intrinsic individual factors, extrinsic factors such as the properties of the individual EAI (e.g., dose, needle length, overall design) as well as cost and coverage. The number and the variety of EAIs available have expanded in most jurisdictions in recent years, which provide a greater diversity of options to meet the characteristics and needs of patients with anaphylaxis. Conclusion: There currently are no EAIs with customizable dose and needle length. Although precise personalization of each patient's EAI remains an optimistic future aspiration, careful consideration of all variables when prescribing EAIs can support optimal management of anaphylaxis.

Nasal Nitric Oxide in Primary Immunodeficiency and Primary Ciliary Dyskinesia: Helping to Distinguish Between Clinically Similar Diseases.

PURPOSE: Primary ciliary dyskinesia (PCD) is a rare disorder of the mucociliary clearance leading to recurrent upper and lower respiratory tract infections. PCD is difficult to clinically distinguish from other entities leading to recurrent oto-sino-pulmonary infections, including primary immunodeficiency (PID). Nasal nitric oxide (nNO) is a sensitive and specific diagnostic test for PCD, but it has not been thoroughly examined in PID. Past publications have suggested an overlap in nNO levels among subjects with PCD and PID. We sought to determine if nNO measurements among patients diagnosed with PID would fall significantly above the established PCD diagnostic cutoff value of 77 nL/min. METHODS: Children > 5 years old and adults with definitive PID or PCD diagnoses were recruited from outpatient subspecialty clinics. Participants underwent nNO testing by standardized protocol using a chemiluminescence analyzer and completed a questionnaire concerning their chronic oto-sino-pulmonary symptoms, including key clinical criteria specific to diagnosed PCD (neonatal respiratory distress at term birth, year-round cough or nasal congestion starting before 6 months of age, any organ laterality defect). RESULTS: Participants included 32 patients with PID, 27 patients with PCD, and 19 healthy controls. Median nNO was 228.9.1 nL/min in the PID group, 19.7 nL/min in the PCD group, and 269.4 in the healthy controls (p < 0.0001). Subjects with PCD were significantly more likely to report key clinical criteria specific to PCD, but approximately 25% of PID subjects also reported at least 1 of these key clinical criteria (mainly year-round cough or nasal congestion). CONCLUSIONS: While key clinical criteria associated with PCD often overlap with the symptoms reported in PID, nNO measurement by chemiluminescence technology allows for effective discrimination between PID and PCD.

Modulation of the Interleukin-21 Pathway with Interleukin-4 Distinguishes Common Variable Immunodeficiency Patients with More Non-infectious Clinical Complications.

PURPOSE: Common variable immunodeficiency (CVID) is characterized by hypogammaglobulinemia and clinical manifestations such as infections, autoimmunity, and malignancy. We sought to determine if responsiveness to interleukin-21 (IL-21), a key cytokine for B cell differentiation, correlates with distinct clinical phenotypes in CVID. METHODS: CVID subjects were recruited through the Canadian Primary Immunodeficiency Evaluative Survey registry. Peripheral blood mononuclear cells were cultured with anti-CD40 ± interferon-gamma, interleukin-4 (IL-4), IL-21, and/or IL-4+IL-21. B cell subpopulations and IgG production were determined at baseline and day 7 by flow cytometry and ELISA. Clinical complications were compared using contingency tables. RESULTS: CVID subjects exhibited decreased CD27+ B cells and IgG production after 7 days of stimulation with anti-CD40+IL-21 (p < 0.05). In a subset of subjects [CVID responders (R)], the addition of IL-4 led to significant increases in CD27+ B cells and IgG (p < 0.05). In CVID non-responders (NR), CD27+ B cells and IgG remained lower despite the addition of IL-4. CVID NR experienced significantly more non-infectious clinical complications of CVID than R [OR 8.8, 95% confidence interval (CI) 1.6 to 48.13]. Previous studies reported that CVID subjects with ≤ 2% class-switched memory B cells were more at risk of these complications, but no significant association was found among this cohort of subjects [OR 3.5, CI 0.9 to 13.3]. In fact, 34.6% of CVID NR had > 2% class-switched memory B cells at baseline. CONCLUSIONS: The IL-4 and IL-21 in vitro assays distinguish two groups of CVID subjects and can be used with baseline B cell subpopulation phenotyping to better identify patients experiencing more vs. fewer clinical non-infectious complications and potentially to modulate therapy.

The Risk of Recurrent Anaphylaxis.

OBJECTIVES: To determine the recurrence rate of anaphylaxis in children medically attended in an emergency department (ED), we performed a prospective cohort study to evaluate prehospital and ED management of children with recurrent anaphylaxis and to assess factors associated with recurrent anaphylaxis. STUDY DESIGN: As part of the Cross-Canada Anaphylaxis Registry, parents of children with anaphylaxis identified prospectively in 3 EDs and through an emergency medical response service were contacted annually after presentation and queried on subsequent reactions. Cox regression analysis determined factors associated with recurrence. RESULTS: Among 292 children who were registered as having had medical attended anaphylaxis, 68.5% completed annual follow-up questionnaires. Forty-seven patients experienced 65 episodes of anaphylaxis during 369 patient-years of follow-up. Food was the trigger in 84.6% of cases, and epinephrine was used in 66.2%. In 50.8%, epinephrine was used outside the health care facility, and 81.7% were brought to a health care facility for treatment. Asthma, reaction triggered by food, and use of epinephrine during the index episode increased the odds of recurrent reaction. Patients whose initial reaction was triggered by peanut were less likely to have a recurrent reaction. CONCLUSIONS: We report a yearly anaphylaxis recurrence rate of 17.6% in children. There is substantial underuse of epinephrine in cases of anaphylaxis. Educational programs that promote effective avoidance strategies and prompt use of epinephrine are required.

Novel 3q27.2-qter deletion in a patient with Diamond-Blackfan anemia and immunodeficiency: Case report and review of literature.

3q27.2-qter deletion syndromes feature an overlapping set of terminal and interstitial deletions with variable congenital malformations. Diamond-Blackfan anemia (DBA) is etiologically heterogeneous disorder in which one cause is dominant mutations of the RPL35A gene on 3q29. We report a child with a 3q27.2-qter deletion that contains the RPL35A gene. She had clinical and laboratory features consistent with DBA and as well, an unexplained immunodeficiency disorder. Given these unusual findings, we reviewed other patients in the literature with overlapping genomic deletions. In addition, we evaluated our patient for the immunodeficiency disorder, RIDDLE syndrome, due to recessive mutations in the RNF168 gene on 3q29. A PubMed search for case reports of 3q27.2-qter overlapping deletions was performed. To determine if RPL35A was in the deletion region, the chromosomal regions reported were mapped to genomic regions using the UCSC Genome Browser. We identified 85 overlapping deletions, of which six included the RPL35A gene and all should be had DBA. Interestingly, none of the reported cases had immunodeficiency. To evaluate RIDDLE syndrome (radiosensitivity, immunodeficiency, dysmorphic features, and learning difficulties), we sequenced the remaining RNF168 gene and examined her fibroblast culture for a DNA double strand break repair deficiency. These results were normal, indicating that the immunodeficiency is unlikely to result from a RNF168 deficiency. We show that RPL35A haploinsufficiency is a cause of DBA and we report a novel case with 3q27.2-qter deletion and immunodeficiency. The etiology for the immunodeficiency remains unsolved and could be caused by an unknown gene effect or consequent to the DBA phenotype.

Tryptase levels in children presenting with anaphylaxis: Temporal trends and associated factors.

BACKGROUND: The diagnosis of anaphylaxis currently relies on suggestive clinical history after exposure to a potential triggering factor because no reliable diagnostic marker is available to confirm the diagnosis. OBJECTIVES: We aimed to evaluate tryptase levels in children with anaphylaxis and to examine predictors of elevated tryptase level (defined as ≥11.4 µg/L during reaction and for those with a baseline level, defined as a reaction level of at least 2 ng/mL + 1.2 × [postreaction tryptase level]). METHODS: Children presenting with anaphylaxis to the Montreal Children's Hospital were recruited over a 4-year period. Symptoms, triggers, and management of anaphylaxis were documented. Levels during the reaction and approximately 9 months after the reaction were compared on the basis of paired means using the t distribution. Multivariate linear and logistic regressions were used to evaluate the association between tryptase levels and risk factors. RESULTS: Over a 4-year period, 203 children had serum tryptase levels measured. Among these, 39 children (19.2%; 95% CI, 14.1%-25.4%) had elevated levels. Only severe reactions were associated with reaction levels of 11.4 µg/L or more (odds ratio, 6.5; 95% CI, 2.2-19.0). Milk-induced anaphylaxis and severe reactions were more likely associated with increased tryptase levels (beta-adjusted, 4.0; 95% CI, 0.95-7.0, and 7.5; 95% CI, 4.8-10.3, respectively). Reaction levels exceeding the threshold level of 2 ng/mL + 1.2 × (postreaction tryptase level) detected most of the anaphylactic reactions, particularly if baseline levels were taken within 2 months of the reaction. CONCLUSIONS: Tryptase levels are particularly useful for the diagnosis of severe and/or milk-induced anaphylaxis. Assessing the difference between reaction and postreaction tryptase levels may improve diagnostic sensitivity.

Humoral Primary Immunodeficiencies in Chronic Rhinosinusitis.

Chronic rhinosinusitis (CRS) may be the primary presenting symptom for primary immunodeficiencies (PID). PID can affect the humoral or the cellular immune system. This paper provides an overview of PID which affect the humoral immune system, with details around the diagnostic criteria, the epidemiology, the subtypes, the clinical manifestations, underlying molecular mechanisms, methods to screen for PID and the management of CRS in the context of PID. A high clinical suspicion of PID is required when assessing patients with CRS who are refractory to maximal medical therapy.

Rate, triggers, severity and management of anaphylaxis in adults treated in a Canadian emergency department.

BACKGROUND: The Cross-Canada Anaphylaxis Registry (C-CARE) assesses the triggers and management of anaphylaxis and identifies predictors of the development of severe allergic reactions and of epinephrine use. Here, we present data from an urban adult tertiary care emergency department (ED) in Montreal, Canada. METHODS: Potential anaphylaxis cases were identified using ICD-10 codes related to anaphylaxis or allergic reactions. Putative cases underwent chart review to ensure they met anaphylaxis diagnostic criteria. Demographic, clinical and management data were collected. Multivariate logistic regressions were conducted to assess the effect of demographic characteristics, triggers, and comorbidities on severity and management of reactions. RESULTS: Among 37,730 ED visits, 0.26% (95% CI 0.21, 0.32) fulfilled the definition of anaphylaxis. Food was the suspected trigger in almost 60% of cases. Epinephrine was not administered in almost half of moderate-to-severe cases, and similar numbers of individuals with moderate-to-severe reactions were not prescribed an epinephrine autoinjector. Reaction to shellfish was associated with more severe reactions (OR 13.9; 95% CI 2.2, 89.4). Older individuals and those not receiving steroids were more likely managed without epinephrine (OR 1.04; 95% CI 1.01, 1.07 and OR 2.97; 95% CI 1.05, 8.39, respectively). CONCLUSIONS: Anaphylaxis accounted for a substantial number of ED visits in adults, and the most common trigger was food. There is non-adherence to guidelines recommending epinephrine use for all cases of anaphylaxis. We postulate that this may be related to concerns regarding the side effects of epinephrine in adults.

Autosomal dominant cases of chronic mucocutaneous candidiasis segregates with mutations of signal transducer and activator of transcription 1, but not of Toll-like receptor 3.

We report a family with autosomal dominant chronic mucocutaneous candidiasis as well as recurrent viral infections that segregate with a novel signal transducer and activator of transcription 1 (STAT1) mutation. Prophylactic treatment with fluconazole and immunoglobulin replacement has been initiated, with good clinical response.

Inadvertent exposures in children with peanut allergy.

OBJECTIVES: To determine the annual incidence, characterize the severity and management, and identify predictors of accidental exposure among a cohort of children with peanut allergy. METHODS: From 2004 to November 2009, parents of Canadian children with a physician-confirmed peanut allergy completed entry and follow-up questionnaires about accidental exposures over the preceding year. Logistic regression analyses were used to examine potential predictors. RESULTS: A total of 1411 children [61.3% boys, mean age 7.1 yr (SD, 3.9)] participated. When all children were included, regardless of length of observation, 266 accidental exposures occurred over 2227 patient-years, yielding an annual incidence rate of 11.9% (95% CI, 10.6-13.5). When all accidental exposures occurring after study entry and patients providing <1 yr of observation were excluded, 147 exposures occurred over a period of 1175 patient-years, yielding a rate of 12.5% (95% CI, 10.7-14.5). Only 21% of moderate and severe reactions were treated with epinephrine. Age ≥13 yr at study entry (OR, 2.33; 95% CI, 1.20-4.53) and a severe previous reaction to peanut (OR, 2.04; 95% CI, 1.44-2.91) were associated with an increased risk of accidental exposure, and increasing disease duration (OR, 0.88; 95% CI, 0.83-0.92) with a decreased risk. CONCLUSION: The annual incidence rate of accidental exposure for children with peanut allergy is 12.5%. Children with a recent diagnosis and adolescents are at higher risk. Hence, education of allergic children and their families is crucial immediately after diagnosis and during adolescence. As many reactions were treated inappropriately, healthcare professionals require better education on anaphylaxis management.

Oral immunotherapy for milk allergy.

BACKGROUND: The mainstay of treatment of IgE-mediated cow milk allergy (IMCMA) is an avoidance diet, which is especially difficult with a ubiquitous food like milk. Milk oral immunotherapy (MOIT) may be an alternative treatment, through desensitization or induction of tolerance. OBJECTIVES: We aim to assess the clinical efficacy and safety of MOIT in children and adults with IMCMA as compared to a placebo treatment or avoidance strategy. SEARCH METHODS: We searched 13 databases for journal articles, conference proceedings, theses and unpublished trials, without language or date restrictions, using a combination of subject headings and text words. The search is up-to-date as of October 1, 2012. SELECTION CRITERIA: Only randomised controlled trials (RCT) were considered for inclusion. Blinded and open trial designs were included. Children and adults with IMCMA were included. MOIT administered by any protocol were included. DATA COLLECTION AND ANALYSIS: A total of 2111 unique records were identified and screened for potential inclusion. Studies were selected, data extracted and methodological quality assessed independently by two reviewers. We attempted to contact the study investigators to inquire about data not published that was required for the analysis. Statistical heterogeneity was assessed using the I² test. We estimated a pooled risk ratio (RR) for each outcome using a Mantel-Haenzel fixed-effect model if statistical heterogeneity was low as evaluated by an I² value less than 50%. MAIN RESULTS: Of 157 records reviewed, 16 were included, representing five trials. In general, the studies were small and had inconsistent methodological rigor. Overall, the quality of evidence was rated as low. Each study used a different MOIT protocol. A total of 196 patients were studied (106 MOIT, 90 control) and all were children. Three studies were blinded and two used an avoidance diet control.  Sixty-six patients (62%) in the MOIT group were able to tolerate a full serving of milk (about 200 mL) compared to seven (8%) of the control group (RR 6.61, 95% CI 3.51 to 12.44). In addition, 27 (25%) in the MOIT group could ingest a partial serving of milk (10 to 184 mL) while none could in the control group (RR 9.34, 95% CI 2.72 to 32.09). None of the studies assessed the patients following a period off immunotherapy. Adverse reactions were common (97 of 106 MOIT patients had at least one symptom), although most were local and mild. Because of variability in reporting methods, adverse effects could not be combined quantitatively. For every 11 patients receiving MOIT, one required intramuscular epinephrine. One patient required it on two occasions. AUTHORS' CONCLUSIONS: Studies to date have involved small numbers of patients and the quality of evidence is generally low. The current evidence shows that MOIT can lead to desensitization in the majority of individuals with IMCMA although the development of long-term tolerance has not been established. A major drawback of MOIT is the frequency of adverse effects, although most are mild and self-limited. The use of parenteral epinephrine is not infrequent. Because there are no standardized protocols, guidelines would be required prior to incorporating desensitization into clinical practice.

Loss-of-function variants in the filaggrin gene are a significant risk factor for peanut allergy.

BACKGROUND: IgE-mediated peanut allergy is a complex trait with strong heritability, but its genetic basis is currently unknown. Loss-of-function mutations within the filaggrin gene are associated with atopic dermatitis and other atopic diseases; therefore, filaggrin is a candidate gene in the etiology of peanut allergy. OBJECTIVE: To investigate the association between filaggrin loss-of-function mutations and peanut allergy. METHODS: Case-control study of 71 English, Dutch, and Irish oral food challenge-positive patients with peanut allergy and 1000 non peanut-sensitized English population controls. Replication was tested in 390 white Canadian patients with peanut allergy (defined by food challenge, or clinical history and skin prick test wheal to peanut ≥ 8 mm and/or peanut-specific IgE ≥ 15 kUL(-1)) and 891 white Canadian population controls. The most prevalent filaggrin loss-of-function mutations were assayed in each population: R501X and 2282del4 in the Europeans, and R501X, 2282del4, R2447X, and S3247X in the Canadians. The Fisher exact test and logistic regression were used to test for association; covariate analysis controlled for coexistent atopic dermatitis. RESULTS: Filaggrin loss-of-function mutations showed a strong and significant association with peanut allergy in the food challenge-positive patients (P = 3.0 × 10(-6); odds ratio, 5.3; 95% CI, 2.8-10.2), and this association was replicated in the Canadian study (P = 5.4 × 10(-5); odds ratio, 1.9; 95% CI, 1.4-2.6). The association of filaggrin mutations with peanut allergy remains significant (P = .0008) after controlling for coexistent atopic dermatitis. CONCLUSION: Filaggrin mutations represent a significant risk factor for IgE-mediated peanut allergy, indicating a role for epithelial barrier dysfunction in the pathogenesis of this disease.

Bridging Knowledge Gaps in Anaphylaxis Management Through a Video-Based Educational Tool.

Introduction: We aimed to develop and test the effectiveness of an education tool to help pediatric patients and their families better understand anaphylaxis and its management, and to improve current knowledge and treatment guidelines adherence. Methods: From June 2019 to May 2022, 128 pediatric patients with history of food-triggered anaphylaxis who presented to the allergy outpatient clinics at the study institution were recruited. Consenting families were asked to complete 6 questions related to the triggers, recognition, and management of anaphylaxis at the time of presentation to the clinic. Participants were shown a 5-min animated video on the causes, presentation, and management of anaphylaxis. At the end of the video, the participants were redirected to the same 6 questions to respond again. The scores were recorded in proportion of correct answers (minimum 0.0; maximum 1.0). Results: The mean age of the patients was 5.8 ± 4.5 years (range: 0.5-18.8 years). The majority were males (70 patients; 54.7%). The mean baseline prevideo education questionnaire score was 0.76 ± 0.2 (range: 0.3-1.0), whereas the mean follow-up score was 0.82 ± 0.2 (range: 0.3-1.0). This score difference of 0.06 was statistically significant (P < 0.001). There were no significant associations between change in scores and age or gender of the participants. Conclusion: Our video teaching method was successful in educating patients and their families to better understand anaphylaxis and its management at the moment of the clinical encounter. Retention of knowledge at long-term follow-up should be assessed.

Life-threatening viral disease in a novel form of autosomal recessive IFNAR2 deficiency in the Arctic.

Type I interferons (IFN-I) play a critical role in human antiviral immunity, as demonstrated by the exceptionally rare deleterious variants of IFNAR1 or IFNAR2. We investigated five children from Greenland, Canada, and Alaska presenting with viral diseases, including life-threatening COVID-19 or influenza, in addition to meningoencephalitis and/or hemophagocytic lymphohistiocytosis following live-attenuated viral vaccination. The affected individuals bore the same homozygous IFNAR2 c.157T>C, p.Ser53Pro missense variant. Although absent from reference databases, p.Ser53Pro occurred with a minor allele frequency of 0.034 in their Inuit ancestry. The serine to proline substitution prevented cell surface expression of IFNAR2 protein, small amounts of which persisted intracellularly in an aberrantly glycosylated state. Cells exclusively expressing the p.Ser53Pro variant lacked responses to recombinant IFN-I and displayed heightened vulnerability to multiple viruses in vitro-a phenotype rescued by wild-type IFNAR2 complementation. This novel form of autosomal recessive IFNAR2 deficiency reinforces the essential role of IFN-I in viral immunity. Further studies are warranted to assess the need for population screening.

Good's Syndrome: Time to Move on From Reviewing the Past.

For seven decades, the pathophysiology of Good's syndrome (GS) has remained a mystery, with few attempts to solve it. Initially described as an association between hypogammaglobulinemia and thymoma, controversy exists whether this is a unique disease, or a subgroup of Common Variable Immune Deficiency (CVID). Recently, some distinguishing aspects of both syndromes have come to light reflecting fundamental differences in their underlying pathophysiology. GS and CVID differ in demographic features and immune phenotype. GS is found almost exclusively in adults and is characterized by a significantly reduced or absence of peripheral B cells. In CVID, which also occurs in children, most patients have normal or slightly reduced peripheral B cells, with a distinguishing feature of low memory B cells. Similarly, differences in T cell dysregulation and manifestations of hematologic cytopenias may further distinguish GS from CVID. Knowledge of the clinical phenotype of this rare adult immune deficiency stems from individual case reports, retrospective, and cross-sectional data on a few cohorts with a limited number of well characterized patients. The understanding of pathophysiology in GS is hampered by the incomplete and inconsistent reporting of clinical and laboratory data, with a limited knowledge of its natural history. In this mini review, we discuss current state of the art data and identify research gaps. In order to resolve controversies and fill in knowledge gaps, we propose a coordinated paradigm shift from incidence reporting to robust investigative studies, addressing mechanisms of disease. We hope this novel approach sets a clear direction to solve the current controversies.

Establishing the diagnosis of peanut allergy in children never exposed to peanut or with an uncertain history: a cross-Canada study.

The diagnosis of peanut allergy (PA) can be complex especially in children never exposed to peanut or with an uncertain history. The aim of the study is to determine which diagnostic algorithms are used by Canadian allergists in such children. Children 1-17 yrs old never exposed to peanut or with an uncertain history having an allergist-confirmed diagnosis of PA were recruited from the Montreal Children's Hospital (MCH) and allergy advocacy organizations. Data on their clinical history and confirmatory testing were compared to six diagnostic algorithms: I. Skin prick test (SPT) >or=8 mm or specific IgE >or=5 kU/l or positive food challenge (+FC); II. SPT >or=8 or IgE >or=15 or +FC; III. SPT >or=13 or IgE >or=5 or +FC; IV. SPT >or=13 or IgE >or=15 or +FC; V. SPT >or=3 and IgE >or=5 or IgE >or=5 or +FC; VI. SPT >or=3 and IgE >or=15 or IgE >or=15 or +FC. Multivariate logistic regression analysis was used to identify factors associated with the use of each algorithm. Of 497 children recruited, 70% provided full data. The least stringent algorithm, algorithm I, was applied in 81.6% (95% CI, 77-85.6%) of children and the most stringent, algorithm VI, in 42.6% (95% CI, 37.2-48.1%).The factor most associated with the use of all algorithms was diagnosis made at the MCH in those never exposed to peanut. Other factors associated with the use of specific diagnostic algorithms were higher paternal education, longer disease duration, and the presence of hives, asthma, eczema, or other food allergies. Over 18% (95% CI, 14.4-23.0%) of children were diagnosed with PA without fulfilling even the least stringent diagnostic criteria.

Is the prevalence of peanut allergy increasing? A 5-year follow-up study in children in Montreal.

BACKGROUND: Studies suggest that peanut allergy prevalence might be increasing, but these results have not yet been substantiated. OBJECTIVE: We conducted a follow-up study to determine whether peanut allergy prevalence in Montreal is increasing. METHODS: Questionnaires regarding peanut ingestion were administered to parents of children in randomly selected kindergarten through grade 3 classrooms between December 2000 and September 2002 and between October 2005 and December 2007. Respondents were stratified as (1) peanut tolerant, (2) never/rarely ingest peanut, (3) convincing history of peanut allergy, or (4) uncertain history of peanut allergy. Children in group 3 with positive skin prick test responses were considered to have peanut allergy. Children in groups 2 and 4 with positive skin prick test responses had peanut-specific IgE levels measured, and if the value was less than 15 kU/L, an oral peanut challenge was performed. Multiple imputation was used to generate prevalence estimates that incorporated respondents providing incomplete data and nonrespondents. RESULTS: Of 8,039 children surveyed in 2005-2007, 64.2% of parents responded. Among those providing complete data, the prevalence was 1.63% (95% CI, 1.30% to 2.02%) in 2005-2007 versus 1.50% (95% CI, 1.16% to 1.92%) in 2000-2002. After adjustment for missing data, the prevalence was 1.62% (95% credible interval, 1.31% to 1.98%) versus 1.34% (95% credible interval, 1.08% to 1.64%), respectively. The differences between the prevalences in 2005-2007 and 2000-2002 were 0.13% (95% credible interval, -0.38% to 0.63%) among those providing complete data and 0.28% (95% credible interval, -0.15% to 0.70%) after adjustment for missing data. CONCLUSIONS: This is the first North American study to document temporal trends in peanut allergy prevalence by corroborating history with confirmatory tests. The results suggest a stable prevalence, but wide CIs preclude definitive conclusions.