What food allergies can trigger asthma

The way in which food allergens may trigger asthma symptoms is not fully understood. The respiratory symptoms that happen in food allergic reactions commonly include rhinitis, bronchospasm, cough, and laryngeal edema (17). One theory is that particles of ingested food are inhaled into the airway, and exposure of these allergenic proteins to mast cells in the lungs causes inflammation and therefore respiratory symptoms (17, 24).

Commonly documented respiratory reactions from aerosolized food proteins own been well documented over the years, mostly in adults. One of the most commonly described examples is baker&#x;s asthma where exposure to inhaled flour proteins causes an IgE-mediated type reaction, which manifests as asthmatic symptoms. Diagnosis is based on a history of work-related asthma symptoms, skin prick tests, and inhalation challenges to bakery allergens, which is the gold standard test (37). Aerosolized fish protein allergens own also been detected in open-air fish markets and can cause respiratory related symptoms due to inhalation of fish proteins (38).

Similarly, occupational asthma and allergy has been reported in snow crab-processing workers who on cumulative exposure to snow crab own developed symptoms of asthma and allergy (39). With regards to children, Roberts et al. performed bronchial challenges in children with proven IgE-mediated food allergy and asthma using aerosolized foods (40). In this study, despite dietary avoidance of allergens (i.e., fish, milk, eggs, chickpeas, and buckwheat), the children had worse chronic asthma symptoms when there was environmental exposure to the foods (i.e., families cooked with the allergenic foods at home).

However, when the families stopped cooking the allergenic food(s) at home, the child&#x;s symptoms improved, and they needed less inhaled corticosteroid treatment (40).

There has also been research performed on specific food allergens and their association with respiratory symptoms and the development of asthma. For example, in a large birth cohort study, having egg allergy during infancy was predictive of respiratory allergy later in childhood (2).

In fact, they reported a positive predictive worth of 80% if the kid also had eczema (2). Rhodes et al. found that in a study of infants who were deemed at high risk of developing asthma and atopy (i.e., had atopic parents), those who were sensitive to egg and milk in the first year of life was predictive of having asthma as an adult (5). Another study looking at peanut or tree nut allergies showed that patients with a severe history of asthma were at greater risk of life-threatening bronchospasm occurring after ingestion of nuts (p ) (41).

Factors Contributing to the Development of Food Allergy and Asthma

In children, 4&#x;8% of asthmatic patients own food allergies and approximately 50% of those with food allergies own allergic reactions that involve acute respiratory symptoms (24, 42).

Various factors own been found to affect the risk of developing asthma in children with food allergy but some of the key factors include seasonal changes, the host immune response, and the use of anti-IgE treatments. Asthma exacerbations seem to coincide with seasonal changes, for example, increase aeroallergen levels such as grass pollen in the spring (43) and dust mite in the autumn (44). The specific-IgE antigens bind to mast cells and basophils causing an inflammatory response within the airways, which over time can cause airway modeling (45).

The host immune response to allergens activates an inflammatory process causing allergic cytokines to be released and a subsequent rise in IgE levels, which own been shown to be associated with an increased risk of asthma (45, 46). In one study, they found that high IgE levels at 6 months ancient was associated with early-onset of asthma and also a strong relationship with the development of asthma in school-age years (47, 48). Milgrom et al. showed that 90% of children in their study with asthma had positive skin prick tests to common allergens (45). Also, the use of anti-IgE treatment (i.e., monoclonal anti-IgE antibodies such as omalizumab) in asthmatic patients has been successful, which suggests there is a role of IgE in the pathogenesis of asthma.

There own been studies that own shown that omalizumab is effective in reducing the need for corticosteroids including finish withdrawal of corticosteroids compared to placebo, a reduction in asthma-related symptoms, and improvement in quality of life of these patients (45, 49).

Morbidity and Mortality in Asthma

In adults, there is evidence that being allergic to more than one food is associated with an increase frequency of oral steroid use and a higher risk of lifetime hospitalizations and emergency department attendances (50). In children, a study showed that having a milk or peanut allergy was associated with an increased number of hospitalizations (p , ) (51).

More specifically, having a milk allergy was associated with an increased use of systemic steroids (p ) (51). Simpson et al. also showed that children with asthma who also had peanut allergy had a times greater rate of systemic steroid use and times greater rate of hospitalization (52).

There is also evidence that suggests that exposure to food allergens can be a risk factor for life-threatening asthma. For example, in a study of children with peanut allergy, 9% (4/46) of the children died from an exacerbation of asthma that represents a significantly higher fatality rate for an asthmatic population (53).

Roberts et al. compared children aged 1&#x;16 years with life-threatening asthma (defined as requiring admission to pediatric intensive care) to those without non-life-threatening asthma and showed that life-threatening asthma was significantly associated with having food allergy (OR , &#x;) and having multiple previous admissions for asthma (OR , &#x;) (54). Ernst et al. conducted a study in patients aged 5&#x;54 years and of the patients had fatal asthma. The main finding in this study was that over 10 prescriptions or more of bronchodilators was associated with an increased risk of near-fatal asthma, but they also found that food allergy was an independent risk factor for near-fatal asthma (odds ratio , 95% CI &#x;) (55).

What food allergies can trigger asthma

Similarly, a case&#x;control study showed that patients with near-fatal asthma (defined as requiring ventilation on intensive care unit) were more likely to be food allergic (OR , &#x;) and/or own had anaphylaxis (OR , &#x;) (56). Vogel et al. compared children who had ward-based care or ambulatory care (i.e., no hospitalization required) with children with potentially fatal asthma (requiring pediatric intensive care admission) and also found food allergy to be a risk factor for life-threatening asthma (57).

Asthma has also been identified as a risk factor for anaphylaxis and is associated with poorer outcomes in children with food allergy (24).

Boyano-Martínez et al. conducted a study where children with cow&#x;s milk allergy had a 10 times higher chance of a severe reaction if they also had asthma (58). Another study found that the majority of fatal reactions attributed to food allergy were asthmatic reactions that occurred in patients on daily asthma treatment (59). Furthermore, in a series looking at fatalities due to food-induced anaphylactic reactions, the majority of the children were asthmatic, and their respiratory symptoms were identified as the main cause for the severity of their reactions (60).

With this evidence over time, guidelines own been produced by various organizations of which pediatric allergists are recommended to prescribe self-injectable adrenaline devices to patients who own both food allergy and asthma (24, 61, 62).

There own also been studies looking at preventative measures [i.e., home dust mite avoidance measures (i.e., protective mattress covers), allergen food avoidance] to prevent atopy in children, of which there is some evidence showing a reduction in respiratory symptoms (i.e., nocturnal cough, severe wheeze) by 1&#x;2 years of age (63&#x;65).

Some studies propose that immunotherapy to respiratory allergens can prevent allergic sensitization to new allergens, but this has not been observed in every studies (66, 67).

Clinical Implications for Patients

When reviewing food allergic or asthmatic children, a detailed clinical history should be taken to identify potential triggers for both allergic disease and asthma. If a specific trigger can be identified, primary advice is for avoidance of the allergen. Asthmatic patients with food allergies require regular assessments, careful monitoring and dietary and emergency management plans, review of treatment, and medication adherence reviews.

In cases of status asthmaticus, the use of intramuscular adrenaline should be considered if there is a history of food allergies. Equally, patients who own known food allergies with respiratory symptoms should be offered beta-agonist inhalers.


If your kid has symptoms after eating certain foods, he or she may own a food allergy.

A food allergy occurs when the body’s immune system sees a certain food as harmful and reacts by causing symptoms. This is an allergic reaction. Foods that cause allergic reactions are allergens.

History

It is significant to inquire about every suspect foods and to discuss the manner of food preparation (e.g.

cooked, raw, added spices or other ingredients). Time of onset of symptoms in relation to food exposure, symptom duration and severity, as well as reproducibility of symptoms in the case of recurrent exposure should be sure. It is also significant to enquire about factors that can potentiate the allergic reaction, such as exercise or alcohol [2–4].

Non-IgE Mediated Food Allergies

Most symptoms of non-IgE mediated food allergies involve the digestive tract. Symptoms may be vomiting and diarrhea.

The symptoms can take longer to develop and may final longer than IgE mediated allergy symptoms. Sometimes, a reaction to a food allergen occurs up 3 days after eating the food allergen.

When an allergic reaction occurs with this type of allergy, epinephrine is generally not needed. In general, the best way to treat these allergies is to stay away from the food that causes the reaction. Under are examples of conditions related to non-IgE mediated food allergies.

Not every children who react to a certain food own an allergy.

They may own food intolerance. Examples are lactose intolerance, gluten intolerance, sulfite sensitivity or dye sensitivity. Staying away from these foods is the best way to avoid a reaction. Your child’s doctor may propose other steps to prevent a reaction. If your kid has any food allergy symptoms, see your child’s doctor or allergist.

What food allergies can trigger asthma

Only a doctor can properly diagnose whether your kid has an IgE- or non-IgE food allergy. Both can be present in some children.

Eosinophilic Esophagitis (EoE)

Eosinophilic (ee-uh-sin-uh-fil-ik) esophagitis is an inflamed esophagus. The esophagus is a tube from the throat to the stomach. An allergy to a food can cause this condition.

With EoE, swallowing food can be hard and painful. Symptoms in infants and toddlers are irritability, problems with eating and poor weight acquire. Older children may own reflux, vomiting, stomach pain, chest pain and a feeling love food is “stuck” in their throat.

The symptoms can happen days or even weeks after eating a food allergen.

EoE is treated by special diets that remove the foods that are causing the condition. Medication may also be used to reduce inflammation.

Food Protein-Induced Enterocolitis Syndrome (FPIES)

FPIES is another type of food allergy. It most often affects young infants. Symptoms generally don’t appear for two or more hours. Symptoms include vomiting, which starts about 2 hours or later after eating the food causing the condition. This condition can also cause diarrhea and failure to acquire weight or height.

Once the baby stops eating the food causing the allergy, the symptoms go away. Rarely, severe vomiting and diarrhea can happen which can lead to dehydration and even shock. Shock occurs when the body is not getting enough blood flow. Emergency treatment for severe symptoms must happen correct away at a hospital. The foods most likely to cause a reaction are dairy, soy, rice, oat, barley, green beans, peas, sweet potatoes, squash and poultry.

Allergic Proctocolitis

Allergic proctocolitis is an allergy to formula or breast milk.

This condition inflames the lower part of the intestine. It affects infants in their first year of life and generally ends by age 1 year.

The symptoms include blood-streaked, watery and mucus-filled stools. Infants may also develop green stools, diarrhea, vomiting, anemia (low blood count) and fussiness. When properly diagnosed, symptoms resolve once the offending food(s) are removed from the diet.

Medical review December

The diagnosis of a food allergy requires a detailed history and physical examination, and diagnostic tests, such as skin prick tests (SPT) and/or serum-specific IgE testing to foods (ImmunoCAP®). In some cases, oral food challenges may also be required [2–4].

Referral to an allergist is significant to confirm the diagnosis of a suspected food allergy.

Patients should avoid the food in question until assessment, and an epinephrine auto-injector should be prescribed, even if the diagnosis is uncertain [6].

Asthma

Asthma is one of the most common long-term childhood conditions of which approximately 9% of children are affected by it (17). Asthma is defined as a chronic respiratory disease characterized by recurrent attacks of wheeze and breathlessness. These symptoms happen due to irritation that occurs in the airways causing inflammation and swelling resulting in reduced lung airflow (18).

Over time with advances in asthma medicine, management continues to change but treatment primarily focuses on assessment of asthma severity, the use of acute and chronic medications including bronchodilators, anti-inflammatory medication (i.e., steroids), and treatment of comorbidities (19). In the management of acute asthma, the goals are to reverse airflow obstruction, correct significant hypoxia, and prevent future relapses (20). In order to achieve this, management for acute exacerbations includes the use of oxygen, short-acting inhaled beta-agonists, ipratropium bromide, systemic corticosteroids, and magnesium sulfate. With regards to long-term management of asthma, stepwise escalation strategies following regular symptom assessment and lung function tests include using medications such as inhaled long-acting beta-agonists, inhaled and systemic corticosteroids, and leukotriene-receptor antagonists (21).

Food Allergy

In the final three decades, there has been a worldwide increase in the prevalence of food allergy with &#x;8% of children having food allergies (17, 22, 23).

Food allergy is defined as an adverse immunological reaction that occurs on exposure to a food that re-occurs on repeat exposure (22).

What food allergies can trigger asthma

It is generally classified into immunoglobulin-E (IgE)-mediated food allergy, non-IgE-mediated food allergy, or mixed IgE- and non-IgE-mediated allergy. IgE-mediated allergy has an acute onset (within 2 h of exposure), and presenting symptoms are often respiratory, skin, and gastrointestinal in nature, whereas non-IgE-mediated food allergy has a delayed onset of symptoms (from 1 to 24 h), and the symptoms tend to be skin and/or gastrointestinal (24).

The key investigations for diagnosing food allergy include taking a thorough clinical history, skin prick testing, serum-specific IgE, and the double-blinded oral food challenge, which considered the gold standard investigation (25). For food allergies proven by positive oral food challenges, recommendation is for strict avoidance of the causative allergen. For those patients who experience life-threatening symptoms of IgE-mediated food allergy, an emergency self-injectable adrenaline device is often prescribed as well.

However, over the final 10 years, increasing research has been performed looking at the use of oral, sublingual, and epicutaneous immunotherapies to desensitize patients through tolerance induction (26).

Physical examination

The primary purpose of the physical examination is to glance for supporting evidence of atopy and other allergic diseases (e.g., atopic dermatitis, asthma, and allergic rhinitis) and to law out the presence of other conditions that may mimic food allergy. The physical examination is also useful for assessing overall nutritional status and growth in children.

IgE Mediated Food Allergies

The IgE mediated food allergies most common in infants and children are eggs, milk, peanuts, tree nuts, soy and wheat.

The allergic reaction can involve the skin, mouth, eyes, lungs, heart, gut and brain. Some of the symptoms can include:

  1. Shortness of breath, trouble breathing, wheezing
  2. Swelling of the lips, tongue or throat
  3. Feeling love something terrible is about to happen
  4. Immunoglobulin E (IgE) mediated. Symptoms result from the body’s immune system making antibodies called Immunoglobulin E (IgE) antibodies. These IgE antibodies react with a certain food.
  5. Stomach pain, vomiting, diarrhea
  6. Skin rash, itching, hives
  7. Non-IgE mediated. Other parts of the body’s immune system react to a certain food.

    This reaction causes symptoms, but does not involve an IgE antibody. Someone can own both IgE mediated and non-IgE mediated food allergies.

Sometimes allergy symptoms are mild. Other times they can be severe. Take every allergic symptoms seriously. Mild and severe symptoms can lead to a serious allergic reaction called anaphylaxis (anna-fih-LACK-sis). This reaction generally involves more than one part of the body and can get worse quick. Anaphylaxis must be treated correct away to provide the best chance for improvement and prevent serious, potentially life-threatening complications.

Treat anaphylaxis with epinephrine.

This medicine is safe and comes in an easy-to-use device called an auto-injector. You can’t rely on antihistamines to treat anaphylaxis. The symptoms of an anaphylactic reaction happen shortly after contact with an allergen. In some individuals, there may be a delay of two to three hours before symptoms first appear.

Cross-Reactivity and Oral Allergy Syndrome

Having an IgE mediated allergy to one food can mean your kid is allergic to similar foods. For example, if your kid is allergic to shrimp, he or she may be allergic to other types of shellfish, such as crab or crayfish.

What food allergies can trigger asthma

Or if your kid is allergic to cow’s milk, he or she may also be allergic to goat’s and sheep’s milk. The reaction between diverse foods is called cross-reactivity. This happens when proteins in one food are similar to the proteins in another food.

Cross-reactivity also can happen between latex and certain foods. For example, a kid who has an allergy to latex may also own an allergy to bananas, avocados, kiwis or chestnuts.

Some people who own allergies to pollens, such as ragweed and grasses, may also be allergic to some foods.

Proteins in the pollens are love the proteins in some fruits and vegetables. So, if your kid is allergic to ragweed, he or she may own an allergic reaction to melons and bananas. That’s because the protein in ragweed looks love the proteins in melons and bananas. This condition is oral allergy syndrome.

Symptoms of an oral allergy syndrome include an itchy mouth, throat or tongue. Symptoms can be more severe and may include hives, shortness of breath and vomiting.

Reactions generally happen only when someone eats raw food. In rare cases, reactions can be life-threatening and need epinephrine.

Diagnostic tests

In general, diagnostic tests for food allergy (e.g., SPT, serum-specific IgE tests, and oral food challenges) should be performed by an allergist. The SPT is a rapid, safe and sensitive method for diagnosing suspected IgE-mediated food allergy.

A positive SPT appears as a wheal and flare reaction when the responsible food is applied to the skin and pricked. A positive SPT has a sensitivity of approximately 90%; however, its specificity is only around 50%. Therefore, a positive SPT alone is not sufficient for diagnosing food allergy; the patient must also own a supportive history. To minimize untrue positive results, over-testing with SPTs should be avoided. SPT should only be done for those foods that are relevant to the patient’s history. The negative predictive worth of a SPT is greater than 95% and, therefore, a negative SPT generally confirms the absence of IgE-mediated reactions [2, 15].

Although less sensitive and more costly than SPTs, serum-specific IgE tests can also be used for diagnosing food allergy, particularly if SPTs cannot be performed or are not available [4].

If there is still clinical suspicion of food allergy, but the diagnosis is uncertain based on the results of SPT and/or serum-specific IgE testing, than an oral food challenge may be appropriate. Oral food challenges involve gradual feeding of the suspected food with careful, medically-supervised assessment for any symptoms.

In the event of symptoms, feeding is discontinued and the patient is treated where approriate. Food challenges should only be conducted in clinics or hospitals equipped with both the personnel and equipment needed to treat anaphylaxis [18].

Other strategies that can assist help in the diagnosis of food allergy are an elimination diet and food/symptom diaries. The elimination diet can be used for both the diagnosis and treatment of food allergy and requires finish avoidance of suspected foods or groups of foods for a given period of time (usually weeks), while monitoring for an associated decrease in symptoms.

Success of this approach in the diagnosis of food allergy depends on identifying the correct food allergen and completely eliminating it from the diet. It is limited by potential bias in both patients and physicians, and variable patient compliance with the diet. Food/symptom diaries require the patient to hold a chronological record of every foods eaten and any associated adverse symptoms. These records may be helpful for identifying the food implicated in an adverse reaction; however, they are not generally diagnostic, particularly when symptoms are delayed or infrequent [2–4].

Tests such as applied kinesiology, vega machine testing and serum immunoglobulin G (IgG) blood testing own no role in the diagnosis of food allergy.

Again, if food allergy is suspected, the food should be avoided, an epinephrine auto-injector should be prescribed, and the patient should be referred for an allergy assessment.

Background

Diseases including asthma, eczema, allergic rhinitis, and food allergy are typically considered as allergic diseases, although the exact association with atopy is frequently debated for eczema and asthma. Nonetheless, such diseases commonly coexist and are common in pediatric populations worldwide. Children affected with one allergic disease frequently develop other allergic diseases. The sequence of disease progression is often referred to as the atopic march (1).

For example, infants with eczema are at higher risk of developing food allergy, children with egg allergy are at increased risk of developing allergic respiratory diseases, and children with allergic rhinoconjunctivitis are at increased risk of developing asthma. Furthermore, children with a single food allergy frequently develop additional food allergies. The causal relationship between these atopic diseases remains unclear as it is not absolute in every patients and the sequence may vary (2&#x;5). The dual-allergen hypothesis provides a plausible explanation as to how allergic disease may progress.

It describes how early allergic sensitization occurs through breakdown of skin barrier integrity that allows for exposure to food and environmental allergen, an effect that can be moderated be early-life ingestion for foods such as peanut and is some studies hens egg (6&#x;10). Research has shown that the development of eczema can be associated with mutations of the filaggrin gene that is responsible for a major structural protein in the epidermis (11). Thus, children with eczema are at greater risk of developing food allergies due to a weakened skin barrier; for example, a study reported that 50% of children with eczema developed food allergy by 1 year (12).

Similarly, Martin et al. (13) showed that in infants with eczema, the earlier onset and greater severity of their eczema symptoms increased their risk of food allergy.

What food allergies can trigger asthma

This emphasizes the hypothesis that allergen exposure through the cutaneous route contributes to allergic sensitization and highlights the key role of skin barrier integrity in protecting the baby immune system, which has been seen in children sensitized to peanut allergy (14, 15). A review showed that approximately 70% of patients with severe eczema developed asthma or allergic rhinitis later in life, and asthmatic patients who had filaggrin mutations had a hard disease course with more asthma exacerbations (11).

Other work has shown that patients who own filaggrin loss-of-function mutations own a significant association with food challenge confirmed peanut allergy (16).

Two Categories of Food Allergies

  • Immunoglobulin E (IgE) mediated. Symptoms result from the body’s immune system making antibodies called Immunoglobulin E (IgE) antibodies. These IgE antibodies react with a certain food.
  • Non-IgE mediated. Other parts of the body’s immune system react to a certain food. This reaction causes symptoms, but does not involve an IgE antibody. Someone can own both IgE mediated and non-IgE mediated food allergies.

Understanding the Relationship between Food Allergy and Asthma

Asthma and food allergy own been commonly shown to coexist with each other, especially as they often share risk factors (family history of allergy, atopic eczema, and asthma) but the way in which they interact and influence each other is yet to be fully understood.

Studies own shown that food allergies can develop in the first year of life and precede the development of asthma (17, 27). There has also been increasing recognition that there is an allergic component to asthma as a disease with specific focus on the role of environmental allergens (i.e., home dust mite and cat allergens). Exacerbations of asthma can be caused by exposure to inhalant allergens, although avoidance of these allergens on asthma disease is not entirely understood. For example, a study that looked at the effectiveness of avoiding home dust mite allergen on asthma management found that using allergen-impermeable covers to avoid home dust mite allergen did not own a significant effect on clinical asthma (28).

Schroeder et al. showed that there was a higher prevalence of asthma in children with food allergy as well as it occurring at a 7 earlier age compared to children without food allergy (29). Another study showed that compared to children who were not sensitized to common food and aeroallergens, those who were cosensitized had a higher risk of developing respiratory allergic disease (27). Studies own also looked at the timing of when food sensitization occurs and own shown that food sensitization early in life (within the first 2 years of life) is a strong predictor of allergy by school age and also children with food allergy own approximately double the chance of developing asthma and rhinitis (30, 31).

There also seems to be an association between asthma and non-IgE-mediated food allergy, although it is less prevalent than that seen in IgE-mediated allergy (32).

In a study, approximately one-third of children with non-IgE-mediated food allergy had asthma and allergic rhinitis (33). Higher rates of asthma (26&#x;66%) own also been reported in eosinophilic esophagitis, which is considered a food allergy disease (34&#x;36).

Understanding the Relationship between Food Allergy and Asthma

Asthma and food allergy own been commonly shown to coexist with each other, especially as they often share risk factors (family history of allergy, atopic eczema, and asthma) but the way in which they interact and influence each other is yet to be fully understood. Studies own shown that food allergies can develop in the first year of life and precede the development of asthma (17, 27).

There has also been increasing recognition that there is an allergic component to asthma as a disease with specific focus on the role of environmental allergens (i.e., home dust mite and cat allergens). Exacerbations of asthma can be caused by exposure to inhalant allergens, although avoidance of these allergens on asthma disease is not entirely understood. For example, a study that looked at the effectiveness of avoiding home dust mite allergen on asthma management found that using allergen-impermeable covers to avoid home dust mite allergen did not own a significant effect on clinical asthma (28).

Schroeder et al. showed that there was a higher prevalence of asthma in children with food allergy as well as it occurring at a 7 earlier age compared to children without food allergy (29). Another study showed that compared to children who were not sensitized to common food and aeroallergens, those who were cosensitized had a higher risk of developing respiratory allergic disease (27). Studies own also looked at the timing of when food sensitization occurs and own shown that food sensitization early in life (within the first 2 years of life) is a strong predictor of allergy by school age and also children with food allergy own approximately double the chance of developing asthma and rhinitis (30, 31).

There also seems to be an association between asthma and non-IgE-mediated food allergy, although it is less prevalent than that seen in IgE-mediated allergy (32).

In a study, approximately one-third of children with non-IgE-mediated food allergy had asthma and allergic rhinitis (33). Higher rates of asthma (26&#x;66%) own also been reported in eosinophilic esophagitis, which is considered a food allergy disease (34&#x;36).


Funding

There was no funding associated with this publication.


Conclusion

Children who own both food allergies and asthma are at an increased risk of severe asthmatic episodes and may be at greater risk of food-induced anaphylaxis and also food allergen-triggered asthmatic episodes. It is significant that clinicians educate patients appropriately regarding the higher risk of life-threatening asthma and anaphylaxis and ensure they get regular assessments regarding their treatment and management.


Summary of key points

&#x; Food allergic infants are at increased risk of developing asthma.

&#x; Children with both asthma and food allergies are at increased risk of severe asthmatic episodes.

&#x; Children with both asthma and food allergies may be at greater risk of allergen-triggered asthma episodes and food-induced anaphylaxis.

&#x; Patients with known IgE-mediated food allergies and asthma should own immediate access to self-injectable adrenaline and inhaled beta-agonists.



Conflict of Interest Statement

The authors declare no conflicts of interest regarding the writing of this mini-review.


Author Contributions

All the authors (RXF, GdT, and AF) were involved in the writing and editing of the manuscript.


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