Non-immunoglobulin E-mediated gastrointestinal food allergic disorders (non-IgE-GI-FA) include food protein-induced enterocolitis syndrome (FPIES), food protein-induced enteropathy (FPE) and food protein-induced allergic proctocolitis (FPIAP), which present with symptoms of variable severity, affecting the gastrointestinal tract in response to specific dietary antigens. The diagnosis of non-IgE-GI-FA is made clinically, and relies on a constellation of typical symptoms that improve upon removal of the culprit food. When possible, food reintroduction should be attempted, with the documentation of symptoms relapse to establish a conclusive diagnosis. Management includes dietary avoidance, nutritional counselling, and supportive measures in the case of accidental exposure. The prognosis is generally favorable, with the majority of cases resolved before school age. Serial follow-up to establish whether the acquisition of tolerance has occurred is therefore essential in order to avoid unnecessary food restriction and potential consequent nutritional deficiencies. The purpose of this review is to delineate the distinctive clinical features of non-IgE-mediated food allergies presenting with gastrointestinal symptomatology, to summarize our current understanding of the pathogenesis driving these diseases, to discuss recent findings, and to address currents gaps in the knowledge, to guide future management opportunities.
Peanut IgE‐mediated food allergy is one of the most common food allergies in children with a prevalence that has increased in the past decades in Westernized countries. Peanut allergies can trigger severe reactions and usually persist over time. Peanut‐allergic children and their families are often confronted to processed foods with precautionary allergen labeling (PAL) such as “may contain traces of peanuts,” which are frequently used by the food industry. Patients are generally confused as to whether eating such foods entails a risk of allergic reaction, which can ultimately lead to dietary restrictions and decreased quality of life. Thus, guidance toward eviction of foods with PALs such as “may contain traces of peanuts” is a recurring problem that peanut‐allergic patients address during pediatric allergy consultations with varying attitudes among allergists. Many studies have evaluated peanut contamination in foods with PALs, with generally less than 10% of foods containing detectable levels of peanuts, albeit heterogeneous amounts, with in rare occasions levels that could trigger allergic reactions in certain patients. The risk of reacting to foods with traces varies significantly with threshold, with patients with the lowest reaction thresholds at highest risk, and a dramatic reduction of risk as threshold increases. Thus, risk stratification based on individual reaction threshold may help stratify patients’ risk of reacting to foods with PAL. In clinical practice, a single‐dose 30 mg peanut protein oral food challenge may be an option to stratify peanut‐allergic patients’ risk when introducing foods with PAL, as illustrated by three clinical cases.
Purpose of review
To present the most recent evidence on atopic dermatitis and its relation to food allergy.
Recent findings
Atopic dermatitis is a chronic inflammatory disorder of the skin characterized by impaired skin barrier because of multifactorial causes including genetic factors, immune dysregulation, and skin microbiome dysbiosis. Infants with temporary skin barrier disruption and/or persistent atopic dermatitis are particularly at risk of developing food allergy (during the so-called atopic march), with up to half of patients demonstrating positive food-specific IgE and one-third of severe cases of atopic dermatitis having positive symptoms on oral food challenge. A high proportion of children with atopic dermatitis exhibit asymptomatic sensitization to foods, and skin testing to identify potential food triggers is not recommended unless the patient has a history suggestive of food allergy and/or moderate-to-severe atopic dermatitis unresponsive to optimal topical care. Indeed, indiscriminate testing can lead to a high proportion of false-positive tests and harmful dietary evictions. Promising strategies to prevent food allergy in children with atopic dermatitis include early skincare with emollients and treatment with topical steroid, and early introduction of highly allergenic foods.
Summary
Further studies are required to identify risk factors for atopic dermatitis to help prevent the development of food allergy in this high-risk population.
There is an increased risk of anaphylaxis upon peanut introduction in siblings of children with peanut allergy, and parents are reluctant to introduce at home without testing. Allergy testing prior to introduction is negative in over 90% of cases and carries a high negative predictive value.
Further studies are needed for the standardization of DPT protocols and to confirm the favourable natural history of beta-lactam drug allergies in children. In addition, multicentric studies are required to confirm the increasingly accepted position of performing DPTs without skin tests in nonimmediate mild reactions to beta-lactams and to further evaluate the possibility of performing DPTs in benign immediate reactions to beta-lactams in children.
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