David W. Hauswirth

A survey study of index food-related allergic reactions and anaphylaxis management

To cite this article: Jacobs TS, Greenhawt MJ, Hauswirth D, Mitchell L, Green TD. A survey study of index food‐related allergic reactions and anaphylaxis management. Pediatr Allergy Immunol 2012: 23: 582–589.

Pediatric Allergic Rhinitis: the Stepwise Treatment Approach

Opinion StatementTreatment of allergic rhinitis in children requires a thoughtful, stepwise approach. Before considering medication for rhinitis, possibly chronic medication, you must (1) confirm disease based on symptoms or testing for offending allergens, (2) implement environmental controls when possible, (3) understand how allergy medication will affect children, and (4) recognize the need to use the minimum amount of medicine necessary to treat symptoms. Special attention to the impact of medication on school performance and social interactions is important when treating children. For intermittent symptoms, an oral antihistamine should be tried first. Chronic symptoms will respond best to a topical nasal steroid spray. Spending the time to figure out what most troubles the child will focus therapy (such as an antihistamine eye drop when ocular itching is a primary symptom) and prevent use of unnecessary medication. Moving past medication to immunotherapy is an important next step as we look for ways to change the natural course of atopic disease. There are now multiple approved forms of immunotherapy in the USA; this should allow a tailored approach to treating symptoms that have progressed beyond pharmacologic therapy. These layers of therapy, environmental control, pharmacologic management focused on bothersome symptoms, and immunotherapy, naturally allow for escalation of treatment with increasing symptoms. Working with the parents is imperative to fully understand the impact symptoms are having on the child and to achieve compliance with medications. This combined, stepwise approach will lead to good relief for the child and satisfaction among both parents and treating physician.

The Prevention Pendulum: Avoidance or Introduction

ritant/toxin exposures, and immune responses to infectious agents or components (e.g. viral infections and endotoxin) all impact the beginnings of atopic sensitization. As we continue to grow in our understanding of the origins of atopy, we learn that single-antigen avoidance may not be the key to primary prevention. In this issue of International Archives of Allergy and Immunology , Kuo et al. [2] have put forth a very well-done study of primary prevention. The concept was straightforward: in a large group of formula-fed infants, they were hoping to prevent the onset of atopic disease. Infants with a family history of allergy who were unable to breast feed were offered the opportunity to be enrolled and randomized to a hydrolyzed milk protein-based formula or a standard cow’s milk formula for the first six months of life. The children were then followed until 36 months of life to evaluate dietary avoidance of milk proteins as a primary prevention measure against general atopic disease. Unfortunately, their results are similar to those found in so many primary prevention studies. Avoidance of one specific allergen may lead to decreased sensitization to that particular allergen (in this case milk), but has no bearing on the overall development of atopic disease. Importantly, in the study by Kuo et al. [2] , the authors were able to demonstrate a significant reduction in milk proThe treatment and diagnosis of allergic disease continues to evolve; however, the definitive cure would be prevention. There are many different ways to intervene in the natural history of a disease; the most common strategies describe disease prevention using the terms primary, secondary, and tertiary. Primary prevention aims to prevent the disease from ever occurring; secondary prevention happens after the pathologic origin of the disease, but prior to clinical recognition, and tertiary prevention occurs after the discovery of disease, preventing further suffering and disability [1] . In clinical allergy, primary prevention seems obtainable as the human allergic response is based upon exposure. The formation of allergen-specific IgE occurs, by definition, after exposure to the offending allergen. The timing, route, and amount of allergen exposure are often varied. The concept remains simple: modify exposure and prevent disease. It would seem ‘easy’ to avoid one offending allergen and limit disease; however, the aim of primary prevention in allergy is not to prevent one sensitivity or limit disease from one allergen. The ultimate goal is to prevent atopy and the myriad of diseases and comorbidities that are associated with atopic disease. To further complicate matters, allergen sensitization is not the only variable that relates to allergic disease; atopy has complex and varied origins. Genetics, environmental irPublished online: October 20, 2010