Signs and Symptoms of Food Allergy and Food-Induced Anaphylaxis.

Food allergies are increasing in prevalence. In order for pediatric clinicians to appropriately diagnose and manage food allergies, the characteristic signs and symptoms of these potentially severe reactions must be recognized. Unlike nonimmunologic adverse food reactions (such as lactose intolerance and food poisoning), food allergies by definition are immune-mediated responses that occur reproducibly on food ingestion. The varying clinical presentations of food allergy include IgE-mediated disorders, mixed IgE- and cell-mediated disorders, and cell-mediated food allergies. This review describes the clinical manifestations of each of these categories of food allergy, with special emphasis on recognition of food-induced anaphylaxis.

Severe allergic reactions to thiol-based cytoprotective agents mesna and amifostine in a child with a supratentorial primitive neuroectodermal tumor.

Both 2-mercaptoethane sulfonate sodium (mesna) and amifostine's active metabolite WR-1065 are thiol-based cytoprotective agents that are critical components of high-dose chemotherapy regimens used to treat various cancers in both adults and children. This case report describes a patient with a supratentorial primitive neuroectodermal tumor who developed severe drug reactions to both mesna and amifostine/WR-1065, suggesting that the thiol component of these agents triggered the adverse reactions. This report highlights the clinical presentation of drug-induced hypersensitivity syndrome in the context of pediatric oncology and the supportive care measures that, if implemented rapidly, may diminish the reaction severity and allow successful completion of chemotherapy.

A novel subset of CD4(+) T(H)2 memory/effector cells that produce inflammatory IL-17 cytokine and promote the exacerbation of chronic allergic asthma.

The inflammatory cytokine interleukin (IL)-17 is involved in the pathogenesis of allergic diseases. However, the identity and functions of IL-17-producing T cells during the pathogenesis of allergic diseases remain unclear. Here, we report a novel subset of T(H)2 memory/effector cells that coexpress the transcription factors GATA3 and RORγt and coproduce T(H)17 and T(H)2 cytokines. Classical T(H)2 memory/effector cells had the potential to produce IL-17 after stimulation with proinflammatory cytokines IL-1ß, IL-6, and IL-21. The number of IL-17-T(H)2 cells was significantly increased in blood of patients with atopic asthma. In a mouse model of allergic lung diseases, IL-17-producing CD4(+) T(H)2 cells were induced in the inflamed lung and persisted as the dominant IL-17-producing T cell population during the chronic stage of asthma. Treating cultured bronchial epithelial cells with IL-17 plus T(H)2 cytokines induced strong up-regulation of chemokine eotaxin-3, Il8, Mip1b, and Groa gene expression. Compared with classical T(H)17 and T(H)2 cells, antigen-specific IL-17-producing T(H)2 cells induced a profound influx of heterogeneous inflammatory leukocytes and exacerbated asthma. Our findings highlight the plasticity of T(H)2 memory cells and suggest that IL-17-producing T(H)2 cells may represent the key pathogenic T(H)2 cells promoting the exacerbation of allergic asthma.

Identifying an at-risk population of children with recurrent near-fatal asthma exacerbations.

BACKGROUND: Children are frequently admitted to hospitals for treatment of severe asthma exacerbations. Anecdotally, a cohort of these children are thought to have multiple readmissions to the intensive care unit (ICU), yet this group of children has not been characterized. The purpose of this study was to examine the factors related to recurrent ICU admissions in children with asthma. METHODS: The authors conducted a retrospective study of all children admitted to the pediatric ICU for asthma between April 1997 and December 2007. Children with more than one ICU admission were defined as having recurrent near-fatal asthma exacerbations. RESULTS: During this period, 306 children with asthma were admitted to the ICU on 350 occasions; 269 children had only one ICU admission and 33 children (11%) had two or more ICU admissions. To predict who might require readmission, the authors compared the first hospitalization of all children. When compared with children admitted to the ICU only once, children admitted to the ICU more than once were more likely to be overweight (odds ratio [OR] 2.3; 95% confidence interval [CI] 1.1, 4.9), to have public insurance (OR 3.6; 95% CI 1.5, 8.5), and less likely to be Caucasian (OR 0.34; 95% CI 0.14, 0.86). There was no difference in Nation Heart, Lung and Blood Institute (NHLBI) asthma classification, admission illness severity, durations of therapy, or length of stay (LOS) that might identify those who would require readmission. To determine the effect of readmission analysis on subsequent hospitalization, the authors used multiple logistic regression to identify factors associated with increased LOS in all hospitalizations of the subset of children with recurrent near-fatal asthma exacerbations. In this analysis, LOS was most closely associated with admission severity of illness (p = .002), but not with number of hospitalizations. CONCLUSIONS: In this single hospital cohort, there were identifiable factors in children admitted to the ICU that are associated with an increased risk of developing recurrent near-fatal asthma exacerbations. Specifically, overweight children with public insurance were more likely and Caucasian children less likely to be readmitted to the ICU for asthma. These children may represent a group to which specific interventions should be targeted prospectively to prevent readmission.