Project description:BackgroundFood allergy (FA) is a prevalent condition in the United States, but little is known about its phenotypes in racial minority groups.ObjectiveThe objective of this study was to characterize disease phenotypes and disparities in health care utilization among African American (AA), Hispanic, and white children with FA.MethodsWe conducted a large, 2-center, retrospective cohort study of children aged 0-17 years with FA seen in allergy/immunology clinics at 2 urban tertiary care centers in the United States. We used multiple logistic regression analyses adjusted for age, gender, and insurance.ResultsThe cohort of 817 children was composed of 35% AA, 12% Hispanic, and 53% non-Hispanic white. Compared with non-Hispanic white children, AA children had significantly higher odds of having asthma and eczema (P < .01), and significantly higher odds of allergy to wheat, soy, corn, fish, and shellfish (P < .01). Compared with non-Hispanic white children, Hispanic children had significantly higher odds of allergy to corn, fish, and shellfish (P < .01), and higher odds of eczema (P < .01), but a similar rate of asthma (P = .44). In this cohort, 55%, 18%, and 11% of AA, Hispanic, and white children were covered by Medicaid, respectively (P < .00001). Compared with whites, AA and Hispanic children had a shorter duration of follow-up for FA with an allergy specialist and higher rates of FA-related anaphylaxis and emergency department visits (P < .01).ConclusionsFA phenotypes and health care utilization differ among children of different racial and/or ethnic backgrounds in the United States that put AA and Hispanic children at higher risks of adverse outcome than white children. These differences include coexistent atopic conditions, less well recognized food allergens, and higher rates of anaphylaxis.
Project description:Food allergies affect up to 6% of young children and 3%-4% of adults. They encompass a range of disorders that may be IgE and/or non-IgE mediated, including anaphylaxis, pollen food syndrome, food-protein-induced enterocolitis syndrome, food-induced proctocolitis, eosinophilic gastroenteropathies, and atopic dermatitis. Many complex host factors and properties of foods are involved in the development of food allergy. With recent advances in the understanding of how these factors interact, the development of several novel diagnostic and therapeutic strategies is underway and showing promise.
Project description:BackgroundFood allergy is negatively associated with health-related quality of life (HRQL). Although differences exist between parents and children, less is known about age-specific differences amongst children. As such, we aimed to identify if age, as well as other factors, are associated with food allergy-specific HRQL in an objectively defined population of children.MethodsOverall, 63 children (boys: n = 36; 57.1%) with specialist-diagnosed food allergy to 1 + foods were included. Parents/guardians completed the Swedish version of a disease-specific questionnaire designed to assess overall- and domain-specific HRQL. Descriptive statistics and linear regression were used.ResultsThe most common food allergy was hen's egg (n = 40/63; 63.5%). Most children had more than one food allergy (n = 48; 76.2%). Nearly all had experienced mild symptoms (e.g. skin; n = 56/63; 94.9%), and more than half had severe symptoms (e.g. respiratory; 39/63; 66.1%). Compared to young children (0-5 years), older children (6-12 years) had worse HRQL (e.g. overall HRQL: B = 0.60; 95% CI 0.05-1.16; p < 0.04.). Similarly, multiple food allergies, and severe symptoms were significantly associated with worse HRQL (all p < 0.05) even in models adjusted for concomitant allergic disease. No associations were found for gender or socioeconomic status.ConclusionOlder children and those with severe food allergy have worse HRQL.
Project description:Previous studies have predominately examined associations of respiratory allergy and skin allergy with ADHD, but little is known about the association between food allergy and ADHD. We included 192,573 children aged 4-17 years from the National Health Interview Survey (NHIS), a leading health survey in a nationally representative sample of the US population. Allergy conditions and ADHD were defined based on an affirmative response in the NHIS questionnaire. We used weighted logistic regression to estimate the odds ratio (OR) of ADHD. Among the 192,573 children, 15,376 reported ADHD diagnosis. The prevalence of ADHD was higher among children with allergic conditions: 12.66% vs. 7.99% among children with and without food allergy; 12.16% vs. 7.63% among children with and without respiratory allergy; and 11.46% vs. 7.83% among children with and without skin allergy. After adjusting for covariates, the OR of ADHD was 1.72 (95% CI, 1.55-1.91) comparing children with and without food allergy, 1.50 (95% CI, 1.41-1.59) comparing children with and without respiratory allergy, and 1.65 (95% CI, 1.55-1.75) comparing children with and without skin allergy. The observed associations remained significant after mutual adjustment for other allergic conditions. In a nationally representative sample of US children, we found a significant association of common allergic conditions (food allergy, respiratory allergy, and skin allergy) with ADHD.
Project description:BackgroundEvidence suggests a link between food allergy and poor mental health, however, this may be explained by shared genetic and environmental factors. We aimed to investigate the association between food allergy of different severity and mental health in children, and the role of familial factors.MethodsThis population-based, longitudinal cohort study is based on the Child and Adolescent Twin Study in Sweden with questionnaire data reported by parents and/or children. Food allergy 'ever' and doctor's diagnosis were reported at age 9-12 years, and ≥ 1 recent dispensation of adrenaline was used as a marker for current severe food allergy. Outcomes were identified using validated questionnaires for anxiety; Screen for Child Anxiety Related Disorders (SCARED); Strength and Difficulties Questionnaire (SDQ) and depression; Short Mood and Feelings Questionnaire (SMFQ), Center for Epidemiological Studies Depression Scale (CES-D) and Diagnostic and Statistical manual of Mental Disorders (DSM-IV-MDE) and reported at 9-12, 15 and 18 years of age. Multivariate linear and logistic modelling was applied to the whole cohort and a co-twin control approach to remove confounding by familial factors.ResultsIn total, 3039 (8.9%) children had a parent-reported food allergy. Among these, 1292 (43.5%) had non-severe food allergy without diagnosis, 1490 (49%) had non-severe food allergy with diagnosis and 257 (8.5%) had severe food allergy. Compared to children with no food allergy, non-severe food allergy with diagnosis by 9-12 years was associated with parent-reported anxiety/depression; SCARED (adjOR 2.10, 95% CI 1.48-2.98), SMFQ (adjOR 1.92, 95% CI 1.19-3.10) at 9-12 years and SDQ (adjβ 0.2, 95% CI 0.0-0.4) at 15 years. All other associations were null including for those with severe food allergy. All positive estimates in the full cohort were attenuated using co-twin controls.ConclusionEvidence associating paediatric food allergy severity and poor mental health was weak, and positive associations observed were likely due to familial confounding.
Project description:The effect of food introduction timing on the development of food allergy remains controversial. We sought to examine whether the presence of childhood eczema changes the relationship between timing of food introduction and food allergy. The analysis includes 960 children recruited as part of a family-based food allergy cohort. Food allergy was determined by objective symptoms developing within 2 hours of ingestion, corroborated by skin prick testing/specific IgE. Physician diagnosis of eczema and timing of formula and solid food introduction were obtained by standardized interview. Cox Regression analysis provided hazard ratios for the development of food allergy for the same subgroups. Logistic regression models estimated the association of eczema and formula/food introduction with the risk of food allergy, individually and jointly. Of the 960 children, 411 (42.8%) were allergic to 1 or more foods and 391 (40.7%) had eczema. Children with eczema had a 8.4-fold higher risk of food allergy (OR, 95% CI: 8.4, 5.9-12.1). Among all children, later (>6 months) formula and rice/wheat cereal introduction lowered the risk of food allergy. In joint analysis, children without eczema who had later formula (OR, 95% CI: 0.5, 0.3-0.9) and later (>1 year) solid food (OR, 95% CI: 0.5, 0.3-0.95) introduction had a lower risk of food allergy. Among children with eczema, timing of food or formula introduction did not modify the risk of developing food allergy. Later food introduction was protective for food allergy in children without eczema but did not alter the risk of developing food allergy in children with eczema.
Project description:This article reviews the recent advances in the diagnosis and management of IgE mediated food allergy in children. It will encompass the emerging technology of component testing; moves to standardization of the allergy food challenge; permissive diets which allow for inclusion of extensively heated food allergens with allergen avoidance; and strategies for accelerating tolerance and food desensitization including the use of adjuvants for specific tolerance induction.
Project description:Here we studied the epigenetic regulation of the naïve CD4+ T-cell activation response among children with IgE-mediated food allergy. Using integrated DNA methylation and transcriptomic profiling, we found that food allergy in infancy is associated with dysregulation of T-cell activation genes. Reduced expression of cell cycle related targets of the E2F and MYC transcription factor networks, and remodeling of DNA methylation at metabolic (RPTOR, PIK3D, MAPK1, FOXO1) and inflammatory genes (IL1R, IL18RAP, CD82) were associated with poorer T-lymphoproliferative responses in infancy after polyclonal activation of the T-cell receptor.