Nonimmunoglobulin E–Mediated Immune Reactions to Foods

Abstract

An adverse food reaction is any abnormal response to an ingested food, regardless of the pathophys-iology. One classification scheme separates immunologic from nonimmunologic entities. Non-immune reactions include jitteriness from caffeine and metabolic disorders such as lactase deficiency. Immune reactions are divided into those that are immunoglobulin E (IgE)-mediated and those that are not IgE mediated. IgE-mediated reactions are the classic presentations of food allergy, such as hives or anaphylaxis after inges-tion of the offending food antigen. Non-IgE-mediated food reactions have been described in the last several years and include food protein-induced enterocolitis syndrome and allergic eosinophilic esophagitis. Non-IgE-mediated food reactions are classified as negative skin test results or specific IgE to foods, with positive challenge to the offending food. The reactions can vary by system, from gastrointestinal (GI) to cutaneous to respiratory ; gastrointestinal reactions are the most common reactions (Table 1). In regard to biology and documentation, food-specific non-IgE-mediated reactions are currently not as well understood as IgE-mediated reactions are. The greatest insight into their pathophysiol-ogy comes from the identification of food-specific T cells in atopic dermatitis (AD). Food-specific skin-homing cutaneous lymphocyte antigen (CLA +) T cells have been identified in the lesions of milk-allergic patients who have AD. 1 These patients have a flare of their AD when challenged by milk. Milk-sensitive patients with GI symptoms on challenge or the control group (nonmilk-allergic) patients did not have milk-specific CLA + T cells. Additional evidence of the role of T cells in non-IgE-mediated food allergy is found in atopy food patch testing of persons with AD. Atopy Abstract Adverse food reactions are abnormal responses to ingested foods. Reactions vary from immunologic to nonimmunologic immune reactions and can be either immunoglobulin E (IgE) mediated or non-IgE mediated. Food-induced IgE-mediated reactions range from localized urticaria to anaphylaxis and have been well studied. However, in comparison, there has been significantly less research into non-IgE-mediated food reactions. Non-IgE-mediated reactions can cause respiratory, gastrointestinal, and cutaneous symptoms. The most recent evidence suggests that these reactions are probably T-cell mediated as evidenced in lymphocyte proliferation assays. This review will explore the symptoms and testing methods of the most common non-IgE-mediated reactions.

Viscous Topical Is More Effective Than Nebulized Steroid Therapy for Patients With Eosinophilic Esophagitis

“…Poor correlation between symptoms and histologic/endoscopic findings has been frequently reported. 19, 23–27 One reason for this is that no symptom score, including the MDQ, has been validated in EoE. 1 In addition, in our study there were more dilations at baseline in the NEB group than in the OVB group.…”

Economic Burden of Atopic Manifestations in Patients With Atopic Dermatitis - Analysis of Administrative Claims

“…From theperspectiveo fthe third-party payers, thet reatmentc ostsa ttributablet oA Mi nA Dp atients aree xtrapolated across thee ntirem embership to be $3.81 PMPY.T hese resultss upport thef indingso fp reviouss tudiest hatp atients with AD arep redisposedt ot he subsequent developmento fA Ms,w hich,i nt urn, usesm oreh ealth care resources, andthattreatment of AD patients with ketotifenor cetirizine coulddecreasethe risk of developingAMs. [11][12][13][15][16][17][18] In ours tudy of newlyd iagnosed AD patients of all ages,w e estimated thei ncidence rate of AMst ob e2 1.8%, whichw as significantlyh ighert hant hato ft he matchedn on-ADp atients (16.9%). AD patients hadah igherr iskt hann on-ADp atients of developingt he followingm anifestations:f ood allergy by 2.35 times, followed by 1.50 timesf or allergicc onjunctivitis, 1.35 timesf or allergicr hinitis, and1 .20t imes fora sthma.…”

“…[11][12] Previous researchersreported that patients with AD more commonly presented with atopic manifestations such as asthma (oddsratio [OR] =1.45-2.17), allergicc onjunctivitis( OR =2.10),a llergic rhinitis (OR=1.53-2.51), andf ood allergies (OR=3. 20-6.14),c ompared with patients without AD;h owever, thesef igures representc oncomitant associations,n ot assessmentso fa topic manifestation( AM) emergence in patients whofirst developed AD.…”

“…[8][9] However, ther eduction of AD severity throught reatment intervention with ketotifeno rc etirizinei nc ertain patient groups maydelay theprogressionofAM. 12,[16][17][18] Althoughi ti sap revailing concept, thec ausal relationship betweenADand AM currentlyremains uncertain. Recent reviews question then atureo ft he associationb etween allergic sensitization andchildhood eczema,indicatingthatthe high prevalence of childhood eczema in industrializedc ountries mayb ed ue to spurious factorss ucha sm icrobial stimulationa nd affluent westernl ifestyles, rather thant he direct resultso fa topy.…”

Acidification of stratum corneum prevents the progression from atopic dermatitis to respiratory allergy

“…The clinical manifestations of atopic dermatitis (AD), characterized by xerosis, eczematous lesions, pruritus, epidermal barrier dysfunction, immunodysregulation and IgE-mediated sensitization to exogenous allergens, 1 predate the development of asthma and allergic rhinitis in a serial process called the atopic march, suggesting that AD is an entry point for subsequent allergic disease. 2,3 The development of asthma in individuals with AD is secondary to allergen sensitization through a primarily defective epidermal barrier, which enables allergens such as house dust mites (HDM) to penetrate the skin easily and then make contact with Langerhans cells (LCs) in the skin, which in turn promotes Th2 inflammation leading to systemic allergy. [4][5][6] Meanwhile, thymic stromal lymphopoietin (TSLP) secreted by keratinocytes in the disrupted epidermis activate polyclonal T cells.…”