Abstract: Kiwifruit allergy has been described mostly in the adult population, but immunoglobulin (Ig)E-mediated allergic reactions to kiwifruit appear to be occurring more frequently in children. To date, 13 allergens from kiwifruit have been identified. Our aim was to identify kiwifruit allergens in a kiwifruit allergic-pediatric population, describing clinical manifestations and patterns of recognition. Twenty-four children were included. Diagnosis of kiwifruit allergy was based on compatible clinical manifestations and demonstration of specific IgE by skin prick test (SPT) and/or serum-specific IgE determination. SDS-PAGE and immunoblotting were performed with kiwifruit extract, and proteins of interest were further analyzed by mass spectrometry/mass spectrometry. For component-resolved in vitro diagnosis, sera of kiwifruit-allergic patients were analyzed by an allergen microarray assay. Act d 1 and Act d 2 were bound by IgE from 15 of 24 children. Two children with systemic manifestations recognized a protein of 15 kDa, homologous to Act d 5. Act d 1 was the allergen with the highest frequency of recognition on microarray chip, followed by Act d 2 and Act d 8. Kiwifruit allergic children develop systemic reactions most frequently following ingestion compared to adults. Act d 1 and Act d 2 are major allergens in the pediatric age group.
Abstract: This commentary describes the likely impacts on children's health and wellbeing from climate change, based on the solid science of environmental child health. It describes likely climate change scenarios, why children are more vulnerable than older people to these changes, and what to expect in terms of diseases (e.g., infections, asthma) and problems (e.g., malnutrition, mental illness). The common antecedents of climate change and other detrimental changes to our society mean that in combatting them (such as excessive consumption and greed), we may not only reduce the harmful effects of climate change but also work towards a better society overall—one that values its children and their futures.
Abstract: Objectives: The objectives of this study were to establish the prevalence of positive antibodies to endomysium (EMA) and tissue transglutaminase (tTG) in children with type 1 diabetes living in Newfoundland and Labrador (NL), and to examine clinical features associated with positive antibodies. Methods: Patients were recruited from the pediatric diabetes clinic. One hundred sixty-seven children with type 1 diabetes from the 280 children followed at the clinic were prospectively screened for celiac disease using EMA and tTG. The variables of Irish descent, age at onset of diabetes, duration of diabetes, sex, family history of celiac disease, hemoglobin A1C (A1C), ferritin, gastrointestinal symptoms, and body mass index were compiled for all patients. The group of patients with positive antibodies to EMA and/or tTG was compared to the group with negative antibodies. Results: The prevalence of patients with positive antibodies to EMA and/or tTG was 16.8% (n = 28). One patient had also been previously diagnosed with symptomatic celiac disease. The two statistically significant variables with positive antibodies were an earlier age at onset of diabetes (Mann-Whitney U two-tailed test: mean difference 3.2 years, 95% CI 1.7–4.8 years, p < 0.0001) and longer duration of diabetes (Mann-Whitney U two-tailed test: mean difference 2.9 years, 95% CI 1.3–4.4 years, p < 0.0001). Irish descent was associated with positive antibodies but did not reach statistical significance. On logistic regression analysis performed with these three variables together, only age at onset of diabetes remained significant. Conclusions: There is a high prevalence of celiac disease-associated antibodies in children living in NL with type 1 diabetes. Unlike other clinical features, an earlier age at onset of diabetes was predictive for positive antibodies. As the majority of children with positive antibodies did not have signs or symptoms of celiac disease, routine screening for celiac disease in type 1 diabetes is recommended.
Abstract: Food allergy is a serious public health problem with an increasing prevalence. Current management is limited to food avoidance and emergency treatment. Research into the pathogenesis of food allergy has helped to shape our understanding of how patients become sensitized to an allergen. Classically, food sensitization was thought to occur through the gastrointestinal tract, but alternative routes of sensitization are being explored, specifically through the skin. Damaged skin barrier may play a crucial role in the development of food sensitization. Better understanding of how patients initially become sensitized may help lead to the development of a safe and effective treatment for food allergies or better prevention strategies.
Abstract: Egg allergy is a common pediatric allergy, and is usually outgrown by elementary school age. There is, therefore, a need to perform an oral food challenge (OFC) to establish the presence of food allergy to egg. In this study, we conducted a retrospective review of 2304 OFCs at a pediatric center and analyzed the severity of reactions during egg OFCs and compared them with other foods. The gastrointestinal system (GI) has been reported as more affected in egg food challenge. This study confirmed that 11% of patients undergoing egg OFC had GI symptoms vs. 7% undergoing food challenges for other foods or compared to milk, peanut and tree nut, individually. However, the involvement of lower respiratory tract was less frequent with egg than observed in peanut and tree nut OFC and similar to observed rate in milk. In conclusion, our study confirmed that OFC to egg causes more GI symptoms and less respiratory symptoms compared to other foods, in particular peanuts and tree nuts. However, 27% of children who failed egg OFC had lower respiratory tract reactions and required the use of epinephrine, similarly to children undergoing milk challenge.
Abstract: Over 30,000 patients are permanently dependent on Total Parenteral Nutrition (TPN) for survival with several folds higher requiring TPN for a prolonged duration. Unfortunately, it can cause potentially fatal complications. TPN infusion results in impairment of gut mucosal integrity, enhanced inflammation, increased cytokine expression and trans-mucosal bacterial permeation. It also causes endotoxin associated down regulation of bile acid transporters and Parenteral Nutrition Associated Liver Disease (PNALD), which includes steatosis, disrupted glucose metabolism, disrupted lipid metabolism, cholestasis and liver failure. Despite multiple theories, its etiology and pathophysiology remains elusive and is likely multifactorial. An important cause for TPN related pathologies appears to be a disruption in the normal enterohepatic circulation due to a lack of feeding during such therapy. This is further validated by the fact that in clinical settings, once cholestasis sets in, its reversal occurs when a patient is receiving a major portion of calories enterally. There are several other postulated mechanisms including gut bacterial permeation predisposing to endotoxin associated down regulation of bile acid transporters. An additional potential mechanism includes toxicity of the TPN solution itself, such as lipid mediated hepatic toxicity. Prematurity, leading to a poor development of bile acid regulating nuclear receptors and transporters has also been implicated as a causative factor. This review presents the current controversies and research into mechanisms of TPN associated injury.