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Cow's milk allergy (CMA) is one of the most common presentations of food allergy seen in early childhood. It is also one of the most complex food allergies, being implicated in IgE-mediated food allergy as well as diverse manifestations of non-IgE-mediated food allergy. For example, gastrointestinal CMA may present as food protein induced enteropathy, enterocolitis or proctocolitis. Concerns regarding the early and timely diagnosis of CMA have been highlighted over the years. In response to these, guideline papers from the United Kingdom (UK), Australia, Europe, the Americas and the World Allergy Organisation have been published. The UK guideline, 'Diagnosis and management of non-IgE-mediated cow's milk allergy in infancy-a UK primary care practical guide' was published in this journal in 2013. This Milk Allergy in Primary Care (MAP) guideline outlines in simple algorithmic form, both the varying presentations of cow's milk allergy and also focuses on the practical management of the most common presentation, namely mild-to-moderate non-IgE-mediated allergy. Based on the international uptake of the MAP guideline, it became clear that there was a need for practical guidance beyond the UK. Consequently, this paper presents an international interpretation of the MAP guideline to help practitioners in primary care settings around the world. It incorporates further published UK guidance, feedback from UK healthcare professionals and affected families and, importantly, also international guidance and expertise. [ABSTRACT FROM AUTHOR]

Non-IgE-mediated gastrointestinal food allergic disorders (non-IgE- GI- FA) including food protein-induced enterocolitis syndrome ( FPIES), food protein-induced enteropathy ( FPE), and food protein-induced allergic proctocolitis ( FPIAP) are relatively uncommon in infants and young children, but are likely under-diagnosed. Non-IgE- GI- FA have a favorable prognosis, with majority resolving by age 3-5 years. Diagnosis relies on the recognition of symptoms pattern in FPIAP and FPIES and biopsy in FPE. Further studies are needed for a better understanding of the pathomechanism, which will lead eventually to the development of diagnostic tests and treatments. Limited evidence supports the role of food allergens in subsets of constipation, gastroesophageal reflux disease, irritable bowel syndrome, and colic. The immunologic pathomechanism is not fully understood and empiric prolonged avoidance of food allergens should be limited to minimize nutrient deficiency and feeding disorders/food aversions in infants. [ABSTRACT FROM AUTHOR]

In formula-fed infants, extensively hydrolyzed formula (EHF) is considered the first-line treatment of cow's milk protein allergy (CMPA).[1] The American Academy of Pediatrics (AAP) defines an EHF to be "hypoallergenic" if at least 90% of infants with CMPA tolerate it under double-blind, placebo-controlled conditions.[2] The protein hydrolysis process for EHF has traditionally involved the use of porcine pancreatic enzymes. The diagnosis of IgE-mediated CMPA was accepted for patients with a convincing allergic reaction to cow's milk within 6 months I and i presence of milk-specific serum IgE > 0.7 kU SB A sb /L I or i skin prick test (SPT) > 5mm. No residual protein bands were detected, suggesting absence of intact milk protein or peptides in both formulas. Clearer regulatory definitions for the degree of protein hydrolysis and MW weight profile of cow's milk peptides in EHF are required. [Extracted from the article]

Background Heating destroys many conformational epitopes and reduces allergenicity of some foods. IgE-epitope binding has been shown to be different among patients who outgrew their cow's milk or hen's egg allergy and those who did not. A significant proportion of milk- or egg-allergic children are tolerant to these foods in their baked forms. We sought to explore the effects of heating on milk and egg proteins and to evaluate for differences in immunolabeling among children with regard to reactivity to heated milk or egg. Methods Sera from participants in clinical dietary intervention trials were utilized. Milk and egg samples were variably heated and prepared (at times within a wheat matrix). Sodium dodecyl sulfate ( SDS)-polyacrylamide gel electrophoresis ( PAGE), protein transfer, and Western blot were completed. Results Sera from 20 milk-allergic and 24 egg-allergic children were utilized. Gel electrophoresis showed strongly staining casein bands that persisted for up to 60 min of heating. In contrast, β-lactoglobulin and α-lactalbumin bands became progressiv-ely weaker with increasing heating times, with no detectable β-lactoglobulin after 15-20 min of heating. The ovalbumin band became progressively weaker, whereas ovomucoid remained stable after 25 min of heating. Immunolabeling revealed that all heated milk-reactive children possessed IgE antibodies that bound the casein fraction regardless of heating time. Presence of wheat during heating resulted in decreased IgE antibody binding to milk and egg white proteins. Conclusion Heating has a different effect on whey and caseins in cow's milk and ovalbumin and ovomucoid in hen's egg white. The effect of heat on protein allergenicity is affected by the temperature and duration, along with the presence of wheat. [ABSTRACT FROM AUTHOR]

Background Studies show that anaphylaxis is under-recognized and epinephrine (adrenaline) is under-used by medical personnel as well as patients and their families. This study assesses the knowledge of food-induced anaphylaxis diagnosis and management across different populations of providers and caregivers and other interested respondents. Methods An online survey embedded in a case discussion of food-induced anaphylaxis was distributed by Medscape to registered members. Results A total of 7822 responders who started the activity chose to answer at least some of the questions presented (response rate 39.5%). Over 80% of responders in all groups correctly identified the case of anaphylaxis with prominent skin and respiratory symptoms; however, only 55% correctly recognized the case without skin symptoms as anaphylaxis. Only 23% of responders correctly selected risk factors for anaphylaxis, with physicians significantly more likely to choose the correct answers as compared to allied health, other health professionals, and medical students (p < 0.001). Ninety-five percent selected epinephrine (adrenaline) as the most appropriate treatment for anaphylaxis, and 81% correctly indicated that there are no absolute contraindications for epinephrine (adrenaline) in the setting of anaphylaxis. When presented a case of a child with no documented history of allergies who has symptoms of anaphylaxis, more physicians than any other group chose to administer stock epinephrine (adrenaline) (73% vs. 60%, p < 0.001). Conclusion Specific knowledge deficits for food-induced anaphylaxis persist across all groups. Further educational efforts should be aimed not only at the medical community but also for the entire caregiver community and general public, to optimize care for food allergic individuals. [ABSTRACT FROM AUTHOR]

Background Food protein-induced enterocolitis syndrome ( FPIES) is a gastrointestinal hypersensitivity disorder with a poorly understood pathophysiology and no biomarkers to aid in diagnosis. Objective To investigate humoral and cellular responses to casein in children with milk- FPIES, including the role of casein-specific (cs) IgA and T-cell mediated TGF-β responses. Patients and methods Thirty-one children previously diagnosed with milk- FPIES were challenged with milk. Twelve age-matched children with FPIES to other foods and 6 milk-tolerant children without a history of FPIES were used as controls. Casein-specific IgE, IgG, IgG4, and IgA were measured in serum and TGF-β levels in supernatants of casein-stimulated PBMCs. Result Twenty-six children with milk- FPIES reacted (active milk- FPIES) and five tolerated milk (milk- FPIES resolved) during food challenge. All of them had significantly lower levels of csIgG, csIgG4, and csIgA than control children (p-value<0.001). There were no TGF-β responses in supernatants of active milk- FPIES children. Conclusion Children with milk- FPIES have low levels of csIgG, csIgG4, and csIgA. In particular, children with active FPIES to cow's milk have deficient T-cell mediated TGF-β responses to casein, rendering TGF-β a promising biomarker in identifying children who are likely to experience FPIES reactions to this allergen. Prospective studies are needed to validate these findings, elucidate their role in FPIES pathophysiology, and establish the diagnostic utility of TGF-β in milk-induced FPIES. [ABSTRACT FROM AUTHOR]

Background Decreased serum food-specific Ig A antibodies have been associated with allergic disease in cross-sectional, case-control studies. The purpose of this study was to prospectively compare egg-white-( EW)-specific Ig A and Ig A2 levels between egg-allergic children and children tolerating egg. Methods Seventeen egg-allergic children were followed prospectively. Total Ig A, EW-specific Ig A, and EW-specific Ig A2 levels were measured in their sera with a sensitive ELISA. As negative controls were used children with no previous history of egg allergy. Egg-allergic children with or without concomitant milk allergy were evaluated as additional controls with measurement of casein-specific Ig A. Results After 2.5 ± 0.9 yrs, nine out of the 17 allergic children became tolerant and eight remained allergic to baked egg. Baseline EW-specific Ig A2 levels were significantly lower in the egg-allergic subjects (median 23.9 ng/ml) compared with the negative control subjects (99.4 ng/ml) and increased significantly by 28% over the study time period in eight out of the nine allergic children that became tolerant to baked egg. There was no significant change over time in EW-specific Ig A in any of the study groups. Non-milk-allergic subjects with concomitant egg allergy had almost threefold higher casein-specific Ig A levels than the milk- and egg-allergic subjects (p = 0.025). Conclusions These results suggest a potential role for allergen-specific Ig A2 antibodies in the induction of food tolerance. Furthermore, they support the hypothesis that immature or impaired production of allergen-specific Ig A2 may be associated with the pathophysiology of food allergy, a defect that seems to be selective for the culprit allergen. [ABSTRACT FROM AUTHOR]

Background Children with food allergy have been shown to have increased small intestinal permeability ( IP) following ingestion of the offending food as well as during elimination diets. We investigated IP in asymptomatic food allergic children during an elimination diet to identify clinical characteristics associated with altered IP. Methods Urinary recovery ratios of lactulose and mannitol ( L/ M) were determined 5 h following ingestion of 7.5 g of lactulose and 2 g of mannitol in 131 cow's milk and egg allergic children. An L/ M ratio of ≥0.025 was considered abnormal based upon previously established laboratory internal references. A chart review was conducted to assess the clinical characteristics of these patients. Results A total of 50 (38%) of the 131 children (median 6.7, range 4.8-8.9 yr; 66.2% male) with food allergy had elevated IP while asymptomatic on strict elimination diets. Age and height negatively correlated with IP. However, in the regression model analysis, abnormal IP was associated with shorter stature independently of age. Otherwise, food allergic patients with increased IP were comparable in gender, nutritional status, age of onset of food allergy, history of reactions, atopic diseases, and family history of food allergies to those with normal IP. Conclusions Elevated IP was found in about one-third of asymptomatic food allergic children on elimination diets and was associated with shorter stature. Our results suggest that increased IP may be an intrinsic trait in a subset of food allergic children. However, large, prospective studies are necessary to determine the role of impaired intestinal barrier in food allergy. [ABSTRACT FROM AUTHOR]

Background Children have increased prevalence of food allergy ( FA) and eosinophilic gastrointestinal disease ( EGID) following liver transplantation. The aim of this study was to identify related risk factors. Methods Chart review of pediatric liver transplant ( LT) recipients with de novo FA and/or EGID post- LT and non-allergic controls. Results We identified 30 (8.5%) children with FA and/or EGID among 352 pediatric LT recipients. Median age at transplant was 0.9 inter-quartile range ( IQR 0.6-2.0) years. FA developed at a median 1.0 ( IQR 0.5-8.2) yr post- LT and manifested with gastrointestinal symptoms (53%) or urticaria/angioedema (40%). Commonly avoided foods included milk (60%), egg (57%), and peanut (47%). Of the 15 children with FA who underwent endoscopy, 11 had eosinophilic infiltrates in multiple segments of the esophagus alone or in combination with other bowel segments. FA and EGID were linked to transplantation at a younger age (median, 0.9 vs. 5.5 yr), higher frequency of blood eosinophilia, and prior history of rhinitis and atopic dermatitis. Tacrolimus use and tacrolimus serum levels were similar between allergic subjects and controls. Conclusions Findings suggest that exposure to tacrolimus alone post- LT is insufficient to initiate de novo allergic disease in LT recipients; rather, younger age and underlying predisposition to atopic disease may play larger roles. [ABSTRACT FROM AUTHOR]

In the original version of this article [1], published on 23 August 2017, an incorrect version of Additional file 4 has been used. The corrected version of Additional file 4 is given in this correction. [ABSTRACT FROM AUTHOR]