scholarly journals Clinical manifestations of immunoglobulin E‐mediated food allergy, including pollen‐food allergy syndrome

2020 ◽  
Vol 2 (1) ◽  
pp. 22-25
Author(s):  
Pooja Varshney ◽  
Jacqueline A. Pongracic

Immunoglobulin E-(IgE) mediated food allergy affects people of all ages but does not have a consistent presentation and may result in various manifestations, even for an individual. The onset of symptoms is usually quite rapid, minutes to a few hours after consumption of the allergen, although exceptions exist. Cutaneous and gastrointestinal symptoms are the most common clinical manifestations; however, they are not present in all allergic reactions. Clinicians, particularly those in emergency care settings, need to be aware that the lack of cutaneous manifestations does not exclude the possibility of anaphylaxis. It is extremely unusual for food allergy reactions to present with isolated upper or lower respiratory symptoms, nor is chronic urticaria a manifestation of food allergy. Clinical manifestations of IgE-mediated food allergy range from mild to severe and, in rare cases, can be fatal. Mild, localized reactions, such as those that occur in pollen‐food allergy syndrome, occur in individuals with sensitization to pollens. A small proportion of patients with this syndrome develop anaphylaxis. Alcohol, medications (nonsteroidal anti-inflammatory drugs, antacids), physical exertion, increased body temperature, acute infection, and menstruation are factors that are known to augment the severity of food-induced allergic reactions.

2020 ◽  
Vol 2 (1) ◽  
pp. 99-103
Author(s):  
Jennifer Pier ◽  
Kirsi M. Järvinen

Breast-feeding is currently recommended as the optimal source of nutrition for infants; however, it is known that some individuals can excrete enough food antigens in breast milk to result in allergic reactions in infants, especially those already highly sensitized. These reactions can include non‐immunoglobulin E (IgE) mediated reactions, such as atopic dermatitis or gastrointestinal symptoms, and IgE-mediated reactions, such as anaphylaxis, although rare. Food reactions in infants who are breast-fed is a unique challenge because identifying the culprit foods may be more difficult and special consideration must be taken in ensuring proper nutrition during periods of food avoidance for both the infant and mother. This article reviews what is currently known about food allergy in infants who are breast-fed as well as offers insights into a proposed evaluation.


F1000Research ◽  
2016 ◽  
Vol 5 ◽  
pp. 2660 ◽  
Author(s):  
Yui-Hsi Wang

Immunoglobulin E (IgE)-mediated food allergy is an adverse reaction to foods and is driven by uncontrolled type-2 immune responses. Current knowledge cannot explain why only some individuals among those with food allergy are prone to develop life-threatening anaphylaxis. It is increasingly evident that the immunologic mechanisms involved in developing IgE-mediated food allergy are far more complex than allergic sensitization. Clinical observations suggest that patients who develop severe allergic reactions to food are often sensitized through the skin in early infancy. Environmental insults trigger epidermal thymic stromal lymphopoietin and interleukin-33 (IL-33) production, which endows dendritic cells with the ability to induce CD4+TH2 cell-mediated allergic inflammation. Intestinal IL-25 propagates the allergic immune response by enhancing collaborative interactions between resident type-2 innate lymphoid cells and CD4+TH2 cells expanded by ingested antigens in the gastrointestinal tract. IL-4 signaling provided by CD4+TH2 cells induces emigrated mast cell progenitors to become multi-functional IL-9-producing mucosal mast cells, which then expand greatly after repeated food ingestions. Inflammatory cytokine IL-33 promotes the function and maturation of IL-9-producing mucosal mast cells, which amplify intestinal mastocytosis, resulting in increased clinical reactivity to ingested food allergens. These findings provide the plausible view that the combinatorial signals from atopic status, dietary allergen ingestions, and inflammatory cues may govern the perpetuation of allergic reactions from the skin to the gut and promote susceptibility to life-threatening anaphylaxis. Future in-depth studies of the molecular and cellular factors composing these stepwise pathways may facilitate the discovery of biomarkers and therapeutic targets for diagnosing, preventing, and treating food allergy.


2019 ◽  
Vol 40 (6) ◽  
pp. 450-452 ◽  
Author(s):  
Ashley L. Devonshire ◽  
Rachel Glick Robison

Primary prevention and secondary prevention in the context of food allergy refer to prevention of the development of sensitization (i.e., the presence of food-specific immunoglobulin E (IgE) as measured by skin-prick testing and/or laboratory testing) and sensitization plus the clinical manifestations of food allergy, respectively. Until recently, interventions that target the prevention of food allergy have been limited. Although exclusive breast-feeding for the first 6 months of life has been a long-standing recommendation due to associated health benefits, recommendations regarding complementary feeding in infancy have significantly changed over the past 20 years. There now is evidence to support early introduction of peanut into the diet of infants with egg allergy, severe atopic dermatitis, or both diagnoses, defined as high risk for peanut allergy, to try to prevent development of peanut allergy. Although guideline-based recommendations are not available for early introduction of additional allergenic foods, this topic is being actively studied. There is no evidence to support additional dietary modification of the maternal or infant diet for the prevention of food allergy. Similarly, there is no conclusive evidence to support maternal avoidance diets for the prevention of food allergy.


Pharmaceutics ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 1104
Author(s):  
Flavia Lozzi ◽  
Cosimo Di Raimondo ◽  
Caterina Lanna ◽  
Laura Diluvio ◽  
Sara Mazzilli ◽  
...  

Photosensitivity induced by drugs is a widely experienced problem, concerning both molecule design and clinical practice. Indeed, photo-induced cutaneous eruptions represent one of the most common drug adverse events and are frequently an important issue to consider in the therapeutic management of patients. Phototoxicity and photoallergy are the two different pathogenic mechanisms involved in photosensitization. Related cutaneous manifestations are heterogeneous, depending on the culprit drug and subject susceptibility. Here we report an updated review of the literature with respect to pathogenic mechanisms of photosensitivity, clinical manifestations, patient management, and prediction and evaluation of drug-induced photosensitivity. We present and discuss principal groups of photosensitizing drugs (antimicrobials, nonsteroidal anti-inflammatory drugs, anti-hypertensives, anti-arrhythmics, cholesterol, and glycemia-lowering agents, psychotropic drugs, chemotherapeutics, etc.) and their main damage mechanisms according to recent evidence. The link between the drug and the cutaneous manifestation is not always clear; more investigations would be helpful to better predict drug photosensitizing potential, prevent and manage cutaneous adverse events and find the most appropriate alternative therapeutic strategy.


Nutrients ◽  
2019 ◽  
Vol 11 (10) ◽  
pp. 2402 ◽  
Author(s):  
Silvia Salvatore ◽  
Elisabetta Bertoni ◽  
Federica Bogni ◽  
Valentina Bonaita ◽  
Chiara Armano ◽  
...  

The diagnosis of cow’s milk allergy (CMA) is particularly challenging in infants, especially with non-Immunoglobulin E (IgE)-mediated manifestations, and inaccurate diagnosis may lead to unnecessary dietary restrictions. The aim of this study was to assess the accuracy of the cow’s milk-related symptom score (CoMiSSTM) in response to a cow’s milk-free diet (CMFD). We prospectively recruited 47 infants (median age three months) who had been placed on a CMFD due to persisting unexplained gastrointestinal symptoms. We compared data with 94 healthy controls (median age three months). The CoMiSSTM score was completed at recruitment and while on the exclusion diet. In 19/47 (40%) cases a response to the diet occurred. At recruitment CoMiSSTM was significantly higher in cases compared to controls (median score 8 vs. 3; p-value: <0.05), 9 cases had a score ≥12 and 8/9 normalized on CMFD. An oral milk challenge was performed in all 19 responders and six of these had a positive reaction to cow’s milk (CM). In eight infants IgE allergy tests were positive. The receiver operation characteristic (ROC) curve identified a CoMISSTM score of 9 to be the best cut-off value (84% sensitivity, 85% specificity, 80% positive (PPV) and 88% negative predictive value (NPV)) for the response to CMFD. We found CoMiSSTM to be a useful tool to help identify infants with persisting gastrointestinal symptoms and suspected CMA that would benefit from CMFD.


2020 ◽  
Vol 2 (1) ◽  
pp. 119-123
Author(s):  
Amber N. Pepper ◽  
Panida Sriaroon ◽  
Mark C. Glaum

Food additives are natural or synthetic substances added to foods at any stage of production to enhance flavor, texture, appearance, preservation, safety, or other qualities. Common categories include preservatives and antimicrobials, colorings and dyes, flavorings, antioxidants, stabilizers, and emulsifiers. Natural substances rather than synthetics are more likely to cause hypersensitivity. Although rare, food additive hypersensitivity should be suspected in patients with immunoglobulin E (IgE)-mediated reactions to multiple, unrelated foods, especially if the foods are prepared outside of the home or when using commercial products. A complete and thorough history is vital. Skin prick testing and/or specific IgE blood testing to food additives, if available, additive avoidance diets, and blind oral challenges can help establish the diagnosis. Once an allergy to a food additive is confirmed, management involves avoidance and, if necessary, carrying self-injectable epinephrine.


2020 ◽  
Vol 16 (1) ◽  
Author(s):  
Daniel H. Li ◽  
Andrew Wong-Pack ◽  
Andrea Leilani Macikunas ◽  
Harold Kim

Abstract Background Food protein-induced enterocolitis (FPIES), an entity previously thought to only affect children, has been increasingly described in adults. In this study, we report a Canadian cohort of 19 adolescents and adults with recurrent non-immunoglobulin E (IgE)-mediated gastrointestinal symptoms after crustacean ingestion, consistent with FPIES. Methods We conducted a retrospective chart review of patients in an outpatient allergy clinic from January 2005 to May 2020. Electronic records were searched using keywords for crustaceans and for symptoms consistent with FPIES. We included patients with gastrointestinal symptoms specifically to crustaceans on more than one occasion, who were 14 years or older at the time of index reaction. Exclusion criteria included symptoms suggestive of an IgE-mediated anaphylactic reaction or a likely alternative diagnosis. We identified 19 patients for our cohort who met the criteria. Results Our cohort was 68.4% female (13) and 32.6% (6) male. The average age at first reaction to crustaceans was 34 years old with a range of 14–68 years (median = 28 years; IQR = 32 years). Time from ingestion to beginning of symptoms ranged from 3 min to 6.5 h, with an average of 2.8 h (median = 2 h; IQR = 3.25 h). Duration of reaction ranged from less than a minute to over 48 h, with a mean of 9.4 h (median = 4 h; IQR = 7.75 h). Patients had 4.8 reactions on average; however, number of reactions ranged from 2 to 12.5 (median = 3, IQR = 3). All patients identified a “trigger” food in the crustacean group, and 12 subjects identified additional reactions to other seafood. Conclusions This case series will better characterize and advance our understanding of this disease entity in adults. There are key differences in the presentation of FPIES in adults compared to children, namely female predominance, difference in solid food trigger, and unpredictable time course. Future studies are needed to examine the pathophysiology and natural history of adult FPIES. Specific guidelines should be developed for the diagnosis and management in adults. Trial registration: retrospectively registered.


2020 ◽  
Author(s):  
Kristopher K. Ford ◽  
Timothy M. Loftus ◽  
Joseph J. Moellman

Allergic reactions vary in intensity from mild rash or allergic rhinitis to devastating anaphylactic shock. Anaphylaxis, often underrecognized and undertreated, can be a life-threatening syndrome leading to multiorgan dysfunction. This review covers the etiology, pathophysiology, and treatment of severe allergic reactions and anaphylaxis. It is precipitated by exposure to particular allergens—commonly food, medications, insect stings, and environmental exposures—in a previously sensitized individual. Symptoms develop from an IgE-mediated immune response leading to degranulation of mast cells and basophils and the release of preformed mediators, lipid-derived metabolites, and inflammatory cytokines. First-line treatment for anaphylaxis involves epinephrine. Secondary treatments are antihistamines and corticosteroids. Further treatments for patients refractory to standard therapies involve vasopressor agents, nebulized albuterol, and glucagon. Frequency and duration of biphasic reactions are variable, limiting the development of consensus guidelines for monitoring of anaphylactic reactions. Figures show the immune activity and inflammatory pathways in allergic responses, mast cell degranulation, and a depiction of common organs involved and corresponding clinical manifestations. Tables list the criteria for diagnosis of anaphylaxis, classification of hypersensitivity reactions, common clinical manifestations, and etiology and mediators of anaphylaxis.  This review contains 4 highly rendered figures, 11 tables, and 43 references. Key words: allergy, anaphylaxis, antihistamine, corticosteroid, epinephrine, mast cells


2021 ◽  
Vol 42 (3) ◽  
pp. e59-e70
Author(s):  
Brigitte König ◽  
Anja N. Koch ◽  
Joseph A. Bellanti

Background: Although adverse food reactions are commonly divided into immunoglobulin E (IgE) mediated food allergy (FA), and non-IgE FA, the current literature is providing support for the role of innate immune responses as an important component of non-IgE FA. Using a commercially available leukocyte activation (LA) assay, a recent quantitative study of total extracellular DNA released in cellular supernatants of human peripheral blood mononuclear cells exposed either to positive or negative tested foods demonstrated that leukocytes exposed to foods with positive LA test results showed higher DNA content than those exposed to foods with negative LA test results. In humans, the origin of DNA might be either the nucleus or the mitochondria. Analysis of emerging data from several laboratories, including our own, suggests that mitochondrial DNA induces inflammatory responses through induction of proinflammatory cytokines. Objective: This pilot study was designed primarily to convey the finding, and relevance of, mitochondrial DNA in the form of neutrophil extracellular traps (NET) as a new pathogenetic mechanism for innate immune-mediated non-IgE FA. Methods: The study population consisted of a total of six subjects, four in a major FA study group and two in a subgroup. Neutrophils were isolated and treated with food antigens that elicited positive and negative LA responses, and the released free DNA was analyzed for the cellular site of origin by using real-time polymerase chain reaction and for leukocyte calprotectin and S100 calcium-binding protein A12 (S100A12) proteins as markers of NETs. Results: We showed that cellular supernatants from neutrophils treated with foods that elicit positive LA responses can contain increased DNA levels of nuclear as well as mitochondrial origin. Supernatants from neutrophils treated with negative tested food (LA) responses did not induce the release of nuclear or mitochondrial DNA. Conclusion: Analysis of our data suggested that the induction of NETs that contain proinflammatory mitochondrial DNA may provide the critical link necessary for a better understanding of the pathogenesis of non‐IgE-mediated FA. These discoveries may not only facilitate better diagnostic tests of FA but should also improve clinical management of allergic and other inflammatory diseases.


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