Background: Food protein‐induced enterocolitis syndrome (FPIES) is a rare non-IgE mediated food allergy. Objective: To delineate the differences in the spectrum of culprit foods, remission patterns, and predictors among varying cultures.
Methods: We reviewed demographics, culprit foods, outcomes, and predictors in 81 children with a diagnosis of FPIES who were followed up between 2015 and 2020. Results: Eighty-one patients (55.6% boys) were enrolled, including 72 with acute FPIES and 9 with chronic
FPIES. Hen’s egg was the most common culprit food (36.6%), followed by fish (26.9%), and cow’s milk (21.5%). Interestingly, cow’s milk was significantly prevalent in chronic FPIES cases (p = 0.006). The most common clinical symptoms were vomiting (100%), pallor
(63.4%), and lethargy (55.9%). Emergency department visits were noted in 39 patients (41.9%), of whom 37 (39.8%) were treated with intravenous (IV) fluid. The subjects were followed up for a median (interquartile range) of 19.4 months (12.3‐41.2 months), and 26 subjects (32.1%) achieved
tolerance. The median (interquartile range) age at tolerance was 2.5 years (2.1‐3.2 years). With regard to the culprit foods, hen’s egg was observed more frequently in the subjects with resolved FPIES cases (p = 0.008), whereas fish FPIES cases were high in the persistent
group (p = 0.001). IgE sensitization of the culprit food was found to be an independent risk factor for the persistence of FPIES (odds ratio 4.855 [95% confidence interval, 1.131‐20.844]; p = 0.034). Conclusion: In our cohort, unlike other
published series, hen’s egg and fish were the two most common culprit foods. Fish differed from other culprit foods, with significantly delayed onset and persistence, and may create a model that allows for the understanding of the disease.
Although the prevalence of food allergy (FA) peaks in early childhood, there has been a shift in understanding from thinking of FA as a disease that passes over time to understanding that FA can have a heterogeneous natural history. 1 The natural history can range from early/late recovery to permanent disease, and is accompanied by the emergence of new allergies and atopic comorbidities. The focus on FA in early life is largely due to the early onset of the disorder and the disappearance of many FA in early childhood. 2 Persistent FA beyond infancy and toddler is common and clinical appearances may vary between age groups. 3The primary objective of this study is to reveal the spectrum of IgE-mediated FA in preschooler, school age children and adolescents in Turkey. Secondary objectives are to examine the relationship between FA and comorbid atopic diseases and the short-term prognosis of FA.
Material and Methods
Study populationThis study is a retrospective analysis of the characteristics of IgE-mediated FAs in children aged 3-18 years at
The exact rate of prevalence of pediatric angioedema is not well known, and any reported rate will change with the presence of urticaria, or due to a specific cause of angioedema. The lifetime prevalence of non-hereditary angioedema was shown to be 4.9%-7.4% in two large nationwide studies. 1,2 However, information about the prevalence of recurrent histaminergic angioedema (HA) and its clinical presentation in children is limited. Considering only patients with hereditary angioedema (HAE), it has been reported that approximately 1 in 50 000 individuals is affected, with a range of 1:10 000-1:150 000 worldwide. 3 Hereditary angioedema is a rare genetic disease characterized by recurrent episodes of submucosal or subcutaneous swelling. The clinical manifestations are highly variable, from asymptomatic cases to life-threatening attacks. The more common forms, HAE type I (85% of patients) and type 2 are caused by autosomal dominant mutations in the gene encoding the C1 inhibitor (C1-INH), leading
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