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Food allergy is an increasingly prevalent disease driven by uncontrolled type 2 immune response. Currently, knowledge about the underlying mechanisms that initiate and promote the immune response to dietary allergens is limited. Patients with food allergy are commonly sensitized through the skin in their early life, later on developing allergy symptoms within the gastrointestinal tract. Food allergy results from a dysregulated type 2 response to food allergens, characterized by enhanced levels of IgE, IL‐4, IL‐5, and IL‐13 with infiltration of mast cells, eosinophils, and basophils. Recent studies raised a possible role for the involvement of innate lymphoid cells (ILCs) in driving food allergy. Unlike lymphocytes, ILCs lack They represent a group of lymphocytes that lack specific antigen receptors. ILCs contribute to immune responses not only by releasing cytokines and other mediators but also by responding to cytokines produced by activated cells in their local microenvironment. Due to their localization at barrier surfaces of the airways, gut, and skin, ILCs form a link between the innate and adaptive immunity. This review summarizes recent evidence on how skin and gastrointestinal mucosal immune system contribute to both homeostasis and the development of food allergy, as well as the involvement of ILCs toward inflammatory processes and regulatory mechanisms. [ABSTRACT FROM AUTHOR]

An imbalance between the production of reactive oxygen species and the capacity of antioxidant defense mechanisms favoring oxidants is called oxidative stress and is implicated in asthmatic inflammation and severity. Major reactive oxygen species that are formed endogenously include hydrogen peroxide, superoxide anion, hydroxyl radical, and hypohalite radical; and the major antioxidants that fight against the endogenous and environmental oxidants are superoxide dismutase, catalase, and glutathione. Despite the well‐known presence of oxidative stress in asthma, studies that target oxidative burden using a variety of nutritional, pharmacological, and environmental approaches have generally been disappointing. In this review, we summarize the current knowledge on oxidative stress and antioxidant imbalance in asthma. In addition, we focus on possible biomarkers of oxidative stress in asthma and on current and future treatment strategies using the modulation of oxidative stress to treat asthma patients. [ABSTRACT FROM AUTHOR]

Background While several single nucleotide polymorphisms are known to influence the metabolism of folate, the methylene tetrahydrofolate reductase ( MTHFR) gene has been the most extensively studied. The aim of this study was to investigate the relationship between the MTHFR polymorphisms 1298 A> C and 677 C> T and congenital heart disease. In addition, the relationship between these gene polymorphisms and homocysteine level was determined in Turkish subjects. Methods Patients with non-syndromic congenital heart defects who were admitted to the Pediatric Cardiology Unit at Hacettepe University Ihsan Dogramaci Children's Hospital, Ankara, Turkey between June 2002 and June 2003 were recruited for the study. A total of 163 children with congenital heart defects (mean age, 7.63 ± 6.03 years; M/F, 93/70) and 93 healthy controls were analyzed. Results When evaluated either separately or together, there were no differences in the frequency of MTHFR 677 C> T or 1298 A> C polymorphisms between the children with congenital heart defects and the control group. The results were the same when considering only conotruncal defects. Those with the 677 C> T polymorphism had significantly lower homocysteine level ( P = 0.004), but the 1298 A> C polymorphism was not related to homocysteine level. Conclusion No relationship was found between congenital heart defects and 1298 A> C or 677 C> T polymorphisms. The 677 C> T polymorphism was related to low homocysteine level. Because there is often much heterogeneity between populations, this study should be conducted in different populations and with larger numbers of participants. [ABSTRACT FROM AUTHOR]

Background Legumes, and particularly lentils, are frequently consumed in Mediterranean, Middle Eastern, and some Asian countries. The aim of this study was to document the demographic features of children with lentil allergy and to determine the role of specific Ig E (s Ig E) in predicting the risk of clinical reactivity and disease persistence. Methods Thirty children were enrolled. The diagnosis of lentil allergy was based on convincing history of symptoms or anaphylaxis after the ingestion of lentils, with positive skin tests and/or s Ig E to lentils. To determine the diagnosis and prognosis of lentil allergy, 24 children were evaluated with food challenges. Results The median age at the onset of symptoms was 1.5 yr (0.9-2.3) (inter-quartile range). The most frequent symptoms were immediate cutaneous (97%) and respiratory (30%) reactions, whereas eight patients (27%) reported anaphylactic reactions. The median level of lentil s Ig E at the time of diagnosis was 3 kU/l (1.2-9.6). Of the 24 challenges, 12 were positive. Fifteen patients (50%) outgrew the lentil allergy by the age of 3.5 (2.5-11) years. Children with an initial lentil s Ig E < 4.9 kU/l had a significantly higher likelihood (68.4% vs. 18.2%) of outgrowing the lentil allergy than children with an initial lentil s Ig E ≥ 4.9 k/l (p = 0.008). Conclusions Our results suggest that s Ig E levels may be important for predicting clinical reactivity and persistence of lentil allergy. [ABSTRACT FROM AUTHOR]

Background: Urticaria frequently causes pediatric emergency department (PED) admissions. Children with urticaria may unnecessarily avoid suspected allergens. We aimed to investigate the possible and exact triggers of urticaria in children admitted to the PED. Methods: Medical records of children admitted to the PED within a 1‐year period were evaluated for the International Classification of Diseases 10 (ICD‐10) L50 urticaria code, noting symptoms, and possible triggers of urticaria. We performed telephone interviews to complete the missing data and further diagnostic tests for IgE‐mediated allergies to identify the exact triggers of urticaria. Results: Among 60,142 children, 462 (0.8%) with the L50 code were evaluated. Possible triggers based on the history and physical examination could be identified in 46%: infections (18%), drugs (11%), foods (8%), infections and drugs (3%), insects (3%), pollen (1%), blood products (0.4%), and vaccines (0.4%). The most frequent infections related to urticaria were upper respiratory tract infections (74.5%), urinary tract infections (13.2%), gastroenteritis (8.2%), and otitis media (4.1%). After a diagnostic workup, IgE‐mediated allergic diseases were diagnosed in 6% of patients. Twenty‐two percent of the patients had multiple PED admission for the same urticaria flare. Urticaria severity was found to be the most important risk factor for readmissions to the PED (odds ratio: 3.86; 95% confidence interval: 2.39–6.23; p <.001). No relationship between urticaria severity, duration, and the triggers was present. Conclusions: Despite detailed diagnostic tests, IgE‐mediated allergic triggers were rarely the cause of urticaria in children admitted to the PED. Infections are the most frequent trigger. Severe urticaria causes more frequent readmissions to the PED. [ABSTRACT FROM AUTHOR]

In hypersensitive reactions to native L-asparaginase, either premedication and desensitization or substitution with polyethylene glycol conjugated asparaginase ( PEG-ASP) is preferred. Anaphylaxis with PEG-ASP is rare. An 8-year-old girl and a 2.5-year-old boy, both diagnosed as having acute lymphoblastic leukemia, presented with native L-asparaginase hypersensitivity and substitution with PEG-ASP was preferred. They received a premedication (methylprednisolone, hydroxyzine and ranitidine) followed by desensitization with PEG-ASP infusion. Both patients developed anaphylaxis with peg-asparaginase. These are the first reported cases of anaphylactic reaction to PEG-ASP, despite the application of both premedication and desensitization. Anaphylaxis with PEG-ASP is very rare and premedication and desensitization protocols may not prevent these hypersensitive reactions. [ABSTRACT FROM AUTHOR]

Background: The literature includes scarce data on infants with food‐induced anaphylaxis (FIA). Materials and Methods: Medical records of the patients diagnosed with FIA aged 0‐6 years between 2015 and 2020 were retrospectively analyzed. Results: During the study period, there were 451 instances of FIA in 314 patients, of which 175 (38.8%) occurred in 160 infants (50.9%). The median (IQR) age of infants was 7 months (6‐9 months) with a male predominance (67.5%), of which 7.5% had multiple instances (≥2) and 60% atopic dermatitis. The most common triggers were cow's milk (51.4%), tree nuts (16.6%), and hen's egg (15.4%), whereas tree nut was the most common trigger in toddlers (35.8%) and preschool children (35.2%). Skin and neurologic symptoms, and nausea‐vomiting occurred more frequently (P =.003, P ≤.001, and P =.003, respectively), whereas respiratory symptoms occurred less commonly in infants compared to toddlers and preschool children (P ≤.001). In infants, 65 (37.1%) mild, 92 (52.6 %) moderate, and 18 (10.3%) severe episodes of anaphylaxis were detected. History of recurrent wheezing (OR: 6.837 [95% CI: 1.940‐24.097], P =.003) and tree nut allergy (OR: 2.849 [95% CI: 1.056‐7.688], P =.039) were found to be independent risk factors for moderate‐to‐severe anaphylactic reactions. 40.6% of the infants received adrenaline, which was lower than the toddlers (49.7%) and preschool children (57.6%) (P =.005). Conclusion: There is no doubt that food‐induced anaphylaxis is a medical emergency, specifically in young children. Pediatricians should be aware of the distinct features of infant anaphylaxis, particularly gastrointestinal and neurologic symptoms to provide effective treatment as soon as possible. [ABSTRACT FROM AUTHOR]

Background: The consumption of lentil is common in the Mediterranean area and is one of the causes of IgE‐mediated food allergy in many countries. Len c 1 is a well‐defined allergen of lentil and approximately 80% of the patients with lentil allergy recognize the purified Len c 1 protein. We sought to identify IgE and IgG4 sequential epitopes of Len c 1 in patients with red and/or green lentil allergy. We also aimed to determine IgE and IgG4 binding differences between those patients who had outgrown or remained reactive to lentil. Methods: Children with IgE‐mediated lentil allergy were included in the study. We applied a microarray immunoassay to determine the characterization of positive IgE and IgG4 binding to Len c 1 epitopes in the patients' sera. Results: The peptides specifically recognized by IgE and IgG4 antibodies were mainly detected between peptides 107 and 135 of Len c 1. The signal intensities of positive epitopes were significantly greater in reactive patients than tolerant ones (P =.008 for IgE and P =.002 for IgG4). Moreover, IgE and IgG4 antibodies bound largely the same sequential epitopes in patients who remained reactive or outgrew their allergy. Conclusion: IgG4‐binding epitopes in lentil allergy were identified and IgE and IgG4 binding to epitopes in both red and green lentils was compared. Our data regarding signal intensity differences between reactive and outgrown patients and overlap binding of IgE and IgG4 antibodies may be important for the development of more accurate diagnostic tests and understanding of natural tolerance development. [ABSTRACT FROM AUTHOR]

Background High serum basal tryptase ( sBT) levels have been identified as a risk factor for both venom- and food-induced severe allergic reactions. The aim of this study was to compare sBT levels in children with different severity of actual drug hypersensitivity reactions ( DHRs) with those of age- and sex-matched controls without any history of DHRs. Method Patients between 0 and 18 years of age with a history of immediate-type DHRs manifested in 0-6 h after the culprit drug intake were included. Following ENDA (European Network for Drug Allergy) inquiries, patients were evaluated with skin and/or provocation tests to define the actual drug-hypersensitive patients. Serum BT levels were determined for both patients and controls. Results Of 345 children, 106 patients (30.7%) [(58.5% male), median age (interquartile range) 8.0 years (4.2-12.2)] were diagnosed as drug hypersensitive. Ninety-eight controls were also included. The sBT levels of drug-hypersensitive patients with and without anaphylaxis and the control group were similar [2.6 (2.0-3.6) μg/l vs. 2.8 (1.6-4.3) μg/l vs. 2.6 (1.8-3.6) μg/l, respectively, (p > 0.05)]. The sBT levels of the patients with sole cutaneous symptoms 2.8 (1.6-4.3) μg/l, mild anaphylaxis 3.0 (1.9-4.9) μg/l, and moderate-to-severe anaphylaxis 2.6 (2.0-3.6) μg/l were also comparable (p > 0.05). The onset of DHRs [those occurring in 1 h (n = 87) or in 1-6 h (n = 19) after the drug intake], positive results with skin tests with the culprit drug, or the classification of the patients according to different age groups [(0-2 years), (2-6 years), (6-12 years), (12-18 years)] did not correlate with sBT levels. Conclusion The sBT levels in children with actual drug hypersensitivity would not be a risk factor for severe systemic reactions on the contrary to children with allergic reactions to food or insect venom. [ABSTRACT FROM AUTHOR]