INTRODUCTION
Defining adverse food reactions:
An adverse reaction to food is any undesirable response that happens after eating or being exposed to food
These reactions fall into two main categories:
Food Allergy: These reactions involve the immune system
Food Intolerance: These reactions do not involve the immune system,
Examples of food intolerance:
Metabolic - lactose intolerance where the body lacks sufficient lactase enzyme to break down the sugar lactose leading to symptoms like bloating, gas, and diarrhooea after consuming dairy products.
Pharmacologic - These are reactions are due to the presence of bioactive compounds in foods that have pharmacological effects in sensitive individuals.
Histamine Intolerance: Occurs when there's an imbalance between histamine ingestion and degradation, often due to reduced activity of the enzyme diamine oxidase (DAO). Symptoms can include headaches, flushing, hives, and gastrointestinal discomfort.
Caffeine Sensitivity: Individuals with reduced ability to metabolize caffeine may experience symptoms like jitteriness, insomnia, and palpitations even at low doses.
Tyramine Sensitivity: Tyramine, found in aged cheeses and cured meats, can trigger migraines in susceptible individuals.
Toxic-
Food posioning - Due to ingestion of food contaminated with live bacteria, viruses, or parasites (eg salmonella, campylobacter, norovirus)
Toxin related disease - Ingestion of pre-formed toxins produced by bacteria like Clostridium botulinum in contaminated foods can cause severe foodborne illnesses.
Scromboid poisoning - A toxic reaction from consuming spoiled fish from the scrombidae family (eg tuna and mackerel) and other dark fleshed fish (sardines, anchovies). These fish contain a chemical called histidine. Bacteria in this fish can multiply in fish stored in warm conditions and turn histidine into scrombotoxin which contains histamine. Cooking the fish destroys the bacteria but not the histamine produced by the fish. Symptoms resemble allergic reactions, including flushing, headaches, brochnospasm and gastrointestinal distress. Symptoms usually begin within 90 minutes of ingestion and symptoms usually disapear within 3-36 hours
FOOD ALLERGY INTRODUCTION
Food allergies themselves can be classified based on the immune mechanism involved:
IgE-mediated: These involve IgE antibodies (Type I hypersensitivity reactions)
Non-IgE mediated: These involve other cells of the immune system, such as T cells
Mixed IgE and non-IgE mediated: These involve both IgE and cellular mechanisms
Understanding whether a food reaction is IgE-mediated or non-IgE-mediated is crucial for proper diagnosis and management
TYPE 1 HYPERSENSITIVITY REACTION (IgE MEDIATED)
Mechanism:
This is the classic type of food allergy many people are familiar with.
It occurs when the body's immune system produces IgE antibodies specific to certain food proteins.
Upon subsequent exposure to the food, these IgE antibodies bind to mast cells and basophils, triggering the rapid release of mediators like histamine, which cause immediate symptoms.
Presentation:
This is the commonest type of food allergy (affects about 5% of young Irish children and about 2% of older children and adults). Patients may experience a spectrum of severity, from mild skin symptoms or mouth itching to anaphylaxis, which is a severe, potentially life-threatening systemic reaction.
Timing of Onset:
Symptoms develop very quickly after exposure, typically within minutes, and generally within 2 hours of ingesting the food.
Even very small amounts of the food can elicit a significant reaction
In severe cases a reaction can occur due to airborne exposure
Symptoms:
These reactions can affect one or multiple organ systems
Skin:
Acute urticaria and angioedema are common
Immunologic contact urticaria - Localised contact reactions can occur and you get hives where food touches the skin (eg fish including shellfish, dairy, egg white, wheats and flour)
Gastro-intestinal:
Oral/pharyngeal itching or swelling, immediate vomiting, nausea, abdominal cramps, or diarrhoea
Respiratory:
Rhinitis, hoarseness, stridor/laryngeal oedema, cough, dyspnoea, chest tightness, wheezing
Cardiovascular:
Pallor, cold sweats, heart palpitations, pre-syncope/syncope, tachycardia, hypotension, or shock
Neurological:
Anxiety, a "feeling of impending doom," change in behaviour, irritability, apathy, lethargy, seizures, syncope/loss of consciousness
On their own urticaria and angioedema are ‘minor’ symptoms
Cough/hoarseness (indicating upper airway obstruction) or feeling faint (cardiovascular collapse) should be treated as potentially severe symptoms
Type 1 hypersensitivity reactions can occur in different ways which will be discussed later:
In the image below you can see the 8 common foods implicated in Type I allergy
Nut allergy persists for life in approximately 80% of cases
Milk and egg allergy persists in just 10-20% of cases.
NON-IgE MEDIATED FOOD ALLERGY
These are delayed in onset (usually type IV hypersensitivity)
Mechanism: These reactions do not involve IgE antibodies. Instead, they are mediated by other parts of the immune system, often T cells.
Timing of Onset: Symptoms are delayed, typically occurring hours to days after ingesting the food. This delayed onset can make it more difficult to elicit from the history compared to IgE reactions
Presentation:
A small dose may be tolerated but incremental doses are not tolerated. Symptoms are more diffuse and include GI symptoms and worsening eczema
Non-IgE mediated food allergies lack reliable laboratory tests for diagnosis.
Standard allergy assessments, such as skin prick testing and specific IgE measurements, are not useful.
In cases where there is clinical suspicion exclusion of the food for 2-4 weeks with reintroduction is the only supportable diagnostic and possibly therapeutic intervention
If symptoms get better when the food is removed and then return again when the food is reduced then that is diagnostic for food allergy
Ideally this would be supervised by a dietitian.
Symptoms:
The symptoms are often gastrointestinal. These can include bloating, reflux, colic, persistent crying, diarrhoea (sometimes with blood or mucus), abdominal pain, loose stools, food aversion, failure to thrive.
You do not tend to get acute urticaria or anaphylaxis in non-IgE mediated allergies. However skin symptoms can occur, notably flares of atopic eczema.
This is particularly seen in infants and young children with moderate-to-severe eczema.
There are other GI syndromes that can occur due to delayed type food allergy which I will go into more detail about later:
Food protein-induced enteroloitis syndrome (FPIES)
Food protein-induced allergic proctocoolitis (FPIAP)
Food protein-induced enteropahty
Eosinophilic Oesophagitis (mixed IgE and non-IgE mediated allergy)
MIXED IGE AND NON-IGE MEDIATED FOOD ALLERGY
To further complicate things, some patients with food allergies can have both IgE-mediated and non-IgE-mediated allergies at the same time.
Patients with this may present with immediate reactions like urticaria alongside delayed features such as eczema flares.
Also non IgE mediated allergies can convert to IgE mediated allergies and therefore long term follow up is important.
A structured clinical approach including a careful history, targeted allergy testing, and appropriate use of elimination trials is therefore key to tease out these difficult cases.
FOOD ALLERGIES AND ECZEMA
There is a temporal association between food allergy and atopic eczema
They tend to develop early in life in a majority of patients and they tend to coexist
Multiple studies have shown that the risk of food allergy is increased in children with early-onset eczema (< 6 months)
Similarly, increased severity of eczema also increases the probabilty of food allergy
Atopic march and dual allergen exposure hypothesis:
The atopic march refers to the natural history of atopic manifestations
Initially young atopic patients present with eczema and food allergies
These then become less common with age
Later asthma occurs and in adults atopic patients will most likely have allergic rhinitis
Recent literature supports the idea of a causal link where sensitisation of food happens through the skin
The dual allergen exposure hypothesis proposes that the risk of developing food allergy depends on the balance between cutaneous exposure and oral exposure to the allergen
Cutaneous exposure - especially through inflammed skin in children with eczema - tends to be pro-allergenic, especially when the exposure occuras at low doses via the environment. The combination of skin inflammation and the altered immune environment in eczema promotes an IgE-mediated allergic response
In contrast, oral exposure via the gastrointestinal tract is pro-tolerogenic, particularly when it occurs in high doses and prior to sensitisation through the skin
Once sensitisation has occurred via the skin, the risk of an allergic response increases
So essentially, introducing the allergen to GI immune system creates an appropriate immune response to the allergen however if the allergen is repeatedly introduced through the skin the infant will develop an abnormal immune response to the allergen
LEAP STUDY
The LEAP (Learning Early About Peanut Allergy) study published in NEJM in 2015 was a landmark randomised controlled trial that tested this hypothesis
Early introduction of certain foods (eg peanut) may actually decrease incidence of food allergy
High-risk infants (those with severe eczema and/or egg allergy) were randomised to either consume peanuts regularly from 4-11 months of age or avoid them until age five
The study found an 81% relative reduction in the prevalence of peanut allergy by age five in the group that consumed peanuts regularly compared to the avoidance group
This protective effect of early introduction of peanut was maintained even after a period of subsequent peanut avoidance
Based on the LEAP study results, guidelines have changed internationally
Current recommendations, particularly in countries where peanuts are consumed and for high-risk infants, are to actively introduce peanut into the diet between four and six months of age, ideally before six months, alongside other solid foods and continuing breastfeeding where possible
If the eczema is not severe, around six months is appropriate
CLINICAL WORKUP
The first and most important step in the work up for suspected food allergy is a detailed allergy-focused clinical history
This will guide if any further subsequent tests are required and how we interpret the results
The clinical history for instance can help us estimate the likelihood (pre-test probability) of an IgE mediated food allergy
The food allergy history can be difficult in a child with eczema This is particularly true for the non-IgE delayed reactions. Some of the reasons why food allergy diagnosis and eczema can be difficult include:
Atopic eczema can wax and wane and therefore can be difficult to pin down if a delayed food allergy is causing these flare ups. Reproducibility and consistency are important. If the parents report that sometimes the food seems to cause a reaction but then sometimes it doesn’t then it is unlikely to be the food that is causing the flare
The eczema may often be under treated making it difficult to assess if its the food causing the flares. It may be untreated due to lack of awareness of parents on how to manage it or due to non-adherence, possibly due to concerns about the use of steroids.
There can be diverse patterns of skin reactions to food in children with atopic eczema
In the case of IGE-mediated food allergies. Atopic eczema patients will have high polyclonal IgE anyway and will have raised IgE to speicfic foods when investigated that may not be clincially relevant
Clinical patterns of allergic reactions to food:
A study called ‘Late eczematous reactions to food in children with atopic dermatitis’ preformed by Breur et al was published in 2024 looked at the clinical patterns of allergic reactions to foods in children with atopic eczema who had a suspected food allergy exacerbating the eczema
This was a retrospective analysis of 106 double-blind placebo-controlled food challenges (DBPCFCs)
OFCs to cow’s milk, egg, wheat, or soya was performed in 64 children (median age 2 years) with atopic dermatitis.
57 challenges were positive (54%), and 49 were negative (46%).
Among the positive challenges
43.5% showed only immediate-type reactions.
56.5% exhibited delayed eczematous reactions.
Of these, 45% had delayed eczema following immediate symptoms.
The remaining 12% had isolated delayed eczematous reactions without immediate symptoms.
Need to clean this part up:
Clinical patterns of allergic reactions to foods in children with atopic eczema:
Immediate skin reactions - Happens within minutes up to by definition, two hours, but this is uncommon, so it's usually within a few minutes of exposure to the food. We see urticaria, angioedema, redness on the predilection sites of eczema, and then it can be accompanied by IgE mediated symptoms in other organs or systems.
Immediate erythema and pruritus in predilection sites of eczema - Get this without other IgE mediated manifestations. This is often followed by exacerbation of eczema
Dalayed reactions with eczema exacerbation - We can merely see delayed reactions with exacerbation of eczema, which sometimes is the most most challenging in terms of establishing a causal relationship with the exposure to the foods
History taking:
As mentioned a detailed allergy-focused clinical history is paramount
DIAGNOSIS OF IgE MEDIATED FOOD ALLERGY
After the history you can estimate a ‘pretest probability’ on whether you think they have an allergy to food(s)
If IgE mediated allergy is suspected then you may consider Skin Prick Testing or blood testing for specific IgE to try to confirm or refute the diagnosis
SKIN PRICK TESTING
What it is: This test involves introducing a tiny amount of a suspected food allergen into the skin to see if it causes a localised allergic reaction
How it's done: A small drop of allergen extract (or sometimes fresh food) is placed on the skin, and the skin is then gently pricked through the drop. This allows the allergen to interact with mast cells just below the skin surface. You need to avoid taking antihistamines for about 48 hours before the test, as it can cause a false negative.
What it measures: A positive reaction appears as a raised, red, itchy bump, known as a wheal, surrounded by redness (a flare). The size of the wheal is measured as a diameter.
Interpretation: A positive SPT indicates that the patient is sensitised to the allergen, meaning they have IgE antibodies that react to it. A larger wheal size generally correlates with a higher likelihood of true clinical allergy. Cut-offs are used as guidance; for example, a wheal of 5mm for peanut is considered an optimal cut-off with good sensitivity and specificity, while a larger wheal of 8mm has higher specificity, making it very useful for confirming a diagnosis.
Strengths & Limitations: It's a relatively quick and easy test. However, a positive result only confirms sensitisation, not necessarily a clinical allergy. Many sensitised children are not clinically allergic. Low-level positive results have a lower positive predictive value. It's important to only test for allergens suspected based on the clinical history to avoid false positives and unnecessary food restrictions.
A clear history of a reaction combined with evidence of IgE sensitisation from SPT can be sufficient to confirm a diagnosis
SPECIFIC IgE TESTING
What it is: This is a blood test used to measure the level of IgE antibodies specific to particular food allergens in the patient's serum (previously referred to as RAST)
How it's done: A blood sample is taken and analysed in a laboratory to quantify the amount of IgE antibodies binding to specific food extracts or components
What it measures: The level of specific IgE antibodies, typically reported in kU/L
Interpretation: Similar to SPT, higher levels of specific IgE generally indicate a greater likelihood of clinical allergy. Cut-offs have been determined for various foods that correlate with a high positive predictive value (e.g., 95% PPV)
Strengths & Limitations: Can be done when SPT is not feasible (e.g., due to skin condition or inability to stop antihistamines). Like SPT, a positive result indicates sensitisation, not guaranteed clinical allergy. Broad or "panel" testing is discouraged as it can lead to false positives and unnecessary dietary avoidance.
In general testing for total IgE is not helpful in the diagnosis of food allergy
COMPONENT-RESOLVED DIAGNOSTICS
When we do standard allergy tests (e.g., skin prick testing or specific IgE blood tests to extracts), the extract contains a mix of different proteins:
Some are primary allergens (true causes of allergy).
Some are cross-reactive allergens (proteins that look similar to each other across pollen and food, but don’t always cause real allergic reactions)
Why this matters?
A positive allergy test shows IgE binding to something in the extract, but not all positive tests are clinically relevant.
Sometimes, people test positive because their immune system recognises a similar protein from pollen — but they don’t actually react when eating the food.
Testing for specific proteins (like Ara h 2, Cor a 14, Ana o 3) — called Component-Resolved Diagnostics (CRD) — helps us separate true allergy from harmless sensitisation.
What it is: A blood test that measures IgE antibodies to individual protein components within a food allergen source, rather than the whole extract
How it's done: Similar to standard specific IgE testing, but the lab measures IgE levels against purified individual proteins
What it measures: IgE levels to specific allergenic proteins (e.g., Ara h 2 for peanut, Cor a 14 for hazelnut, Ana o 3 for cashew nut)
Interpretation: Testing for specific components can help distinguish between a true primary food allergy and sensitisation due to cross-reactivity with other allergens, such as pollens.
There are multiple components but some components are highly specific indicators of a genuine food allergy. For example the EEACI guidelines on the management of IgE-mediated food allergy recommends that the best components to test are IgE to Ara h 2 for peanut allergy, Cor A 14 and Ana o 3 for Cashew nuts.
Strengths & Limitations: Improves diagnostic specificity, particularly in complex cases or when cross-reactivity is suspected
Not all foods have well-characterised and informative components available for testing
BASOPHIL ACTIVATION TEST (BAT)
What it is: This is a functional blood test that assesses the response of basophils when exposed to a specific allergen
How it's done: A blood sample is incubated with the suspected allergen in the lab, and then flow cytometry is used to measure the percentage of basophils that become "activated" and express certain markers on their surface
What it measures: The degree to which basophils react to the allergen
Strengths & Limitations: It can provide additional information beyond just detecting the presence of IgE antibodies. Research has shown it performs well for certain allergies, like peanut and sesame seed allergy. However, it is still largely a research test and is not widely available in most clinical practices.
When it's used: Currently, its use in routine clinical practice is limited due to availability. It has been conditionally recommended in recent EACCI guidelines, particularly for peanut and sesame seed allergy where it has shown good diagnostic performance
Putting it Together: The diagnostic process for suspected IgE-mediated food allergy always begins with a thorough clinical history
This helps estimate the likelihood of an allergy33
Based on the history, targeted SPT or specific IgE tests are performed
These tests provide evidence of sensitisation
The results of the tests are then interpreted in the context of the clinical history and symptom patterns
Component testing can be added to refine the diagnosis, especially for specific foods like peanut, hazelnut, and cashew
BAT is a promising test but not yet widely used
If the history and test results are clear, a diagnosis can often be confirmed or ruled out
However, if the results are inconclusive or contradict the history, the gold standard for definitively diagnosing or ruling out a food allergy remains an oral food challenge
It is crucial to avoid ordering broad allergy panels and unnecessary food restrictions based solely on positive test results without a corresponding clinical history
Tests should be only ordered in an appropriate clinical setting such as in the following examples:
Definite history of a reaction to a particular food group
Severe, refractory atopic dermatitis
Exudative unrelenting facial involvement in an infant
MILK ALLERGY
Cow's milk allergy is a very common presentation of food allergy in early childhood, with almost all cases presenting within the first year of life
Prevalence estimates can vary due to potential overestimation due to misinterpretation of symptoms, particularly in non-IgE mediated (delayed) allergy, where common infant issues like eczema, reflux, or abnormal stools might be mistaken for food allergy
The prevalence of CMA in children living in the developed world is approximately 2% to 3%, making it the most common cause of food allergy in the paediatric population
Among breastfed infants the prevalence is lower (0.5 %)
The EuroPrevail study was a big prospective birth cohort study with about 12,000 children across Europe and this reported that milk allergy affects aobut 1% of children in Europe up to the age of 2 years, with the highest prevelence of non-IgE mediated allergy being seen in the UK
The majority of children will outgrow their milk allergy
Non-IgE mediated allergy generally resolves faster than immediate (IgE-mediated) allergy
The EuroPrevail data showed about 70% of IgE mediated allergy was resolved within one year of diagnosis and almost 100% of non-IgE mediated allergy
It was initially felt that milk allergy only persists to preshcool age but it can persist longer into adolescence
It's important to note that milk is now the biggest single food cause of fatal food anaphylaxis
Distinguishing Immediate (IgE-mediated) and Delayed (Non-IgE mediated) Reactions
Diagnosing immediate (IgE-mediated) milk allergy is generally much easier. Reactions occur very quickly after consumption of milk, typically within minutes up to a couple of hour, and can often be confirmed with allergy testing
In contrast, delayed (non-IgE mediated) milk allergy is much trickier to confirm. Symptoms are delayed, and can occur days after exposure
Also the symptoms can be non-specific and include flares of eczema or GI symptoms which can occur in infants without food allergy and can include more vague issues like eczema or non-specific GI symptoms
Diagnosis relies heavily on a clinical history and is primarily confirmed through a strict elimination diet followed by reintroduction
Management of milk allergy:
Management differs significantly based on whether the allergy is IgE-mediated or non-IgE mediated
The mainstay of treatment is to remove cow's milk protein from the diet while ensuring the nutritional adequacy of alternatives
Education is key for managing milk allergy and knowing how to respond to an allergic reaction
If immediate allergy is suspected, referral to an allergy service is recommended
Immediate (IgE-mediated) Allergy:
Managed with milk avoidance
Ensuring the individual has emergency medication is crucial, including antihistamine. Some infants may need adrenaline pens, particularly if they have multiple food allergies or a history of a severe reaction to milk.
A written emergency management plan (e.g., BSACI allergy action plan) should be provided to families and schools
Human breast milk is best for the baby
Majority of infant formulae made using modified cow’s milk and contain cow’s milk protin
Cow’s milk protein allergy varies from 2-7.5%.
Resolution excpected in between 75 and 90% of cases before 5-6 years of age
Rates may be lower in severe cases
The diagnosis of IgE mediated milk allergy is usually quite straightforward
Can be IgE mediated or non IgE mediated:
IgE mediated- rapid onset urticarial, swerlling, airway symptoms
Non IgE mediated- delayed gastrointestinal and skin symptoms
Most children present before 6-7 months of age (during this time milk is major fodd so other food allergies usually don’t need to be considered)
Exclusively breast fed infants with cow’s milk allergy may respond to time defined complete maternal exclusion of cow’s milk (should be supervised by dietician)
Infant formula:
Usually contains cow’s milk protein
Some contain extensively hydrolysed protein- more hypoallergenic
Amino acid based formulas- even more hypoallergenic
So amino acid formulas may be indicated in those presenting younger with severe and persistent allergy
No place for lactose free formula
Other mammalian milk (goat, sheep, camel, donkey, horse etc) and/or plant based milk (soy, rice, oat, almond, coconut) not indicated
-some are not nutritionally complete
-some cross react with cow’s milk and cause reactions
ORAL ALLERGY SYNDROME (POLLEN FOOD SYNDROME)
Oral allergy syndrome (OAS) is an IgE-mediated food allergy
Typically affects individuals who have allergic rhinitis to pollen (eg birch, grass, ragweed)
Symptoms typically occur within minutes with itching, tingling or mild swelling in the lips, mouth and throat
The condition is usually mild and self-limited, but rarely, more serious reactions (eg anaphylaxis) can occur
OAS is a type of cross-reactivity where the immune system mistakes proteins in the fruit/vegetable for similar proteins in pollen
Common triggers include:
Birch pollen allergy → apple, pear, carrot, celery, hazelnut.
Grass pollen allergy → melon, tomato, orange.
Ragweed pollen allergy → banana, cucumber, melon.
Cooking the food often prevents the reaction, as the proteins causing the problem are broken down by heat
Peeling the fruit can help as in fruits like apples, peaches and pears where the proteins that cross-react with pollen allergens are often most abundant in the peel and outer layers
In some foods (like celery or nuts) the allergenic proteins can be more stable and present throughout the food so peeling or cooking may not always prevent reactions
Diangosis is usually based on history but can be supported by skin prick testing or specific IgE testing
Management includes avoiding the raw triggering foods, eating them cooked if possible, and having antihistamines available if needed.
CONTACT URTICARIA
Contact urticaria is the rapid development of wheals (hives), redness, and sometimes swelling at the site where the skin touches a triggering substance.
It is classified into two types:
Immunological contact urticaria: IgE-mediated hypersensitivity (true allergy, e.g., latex, raw foods).
Non-immunological contact urticaria: Direct histamine release without immune sensitization (e.g., from chemicals like benzoic acid, nettle stings).
Symptoms typically appear within minutes (often within 30 minutes) of exposure
It usually presents as well-demarcated wheals or erythema, sometimes with burning, stinging, or itching.
In severe cases (especially in immunological contact urticaria), systemic symptoms can occur: generalized urticaria, angioedema, bronchospasm, hypotension (risk of anaphylaxis).
Common triggers include:
Proteins: latex, raw meats, fish, fruits, vegetables.
Chemicals: preservatives, fragrances, disinfectants.
Plants: nettles, certain occupational exposures.
Diagnosis relies mainly on clinical history and exam, open application tests and prick tests. Specific IgE testing can be supportive
Management involves avoiding the trigger, anti-histamines for symptomatic control and epinephrine should be available if there’s a risk of anaphylaxis
Occupational contact urticaria to food proteins is important to be aware of in food handlers
FOOD-DEPENDENT EXERCISE-INDUCED ANAPHYLAXIS (FDEIA)
FDEIA is a distinct IgE-mediated allergy where both food ingestion and exercise are needed to trigger a reaction.
Eating the food alone or exercising on an empty stomach does not cause symptoms; the combination is necessary.
Symptoms typically develop during exercise, within 2–4 hours after eating the trigger food.
Clinical signs include flushing, urticaria, angioedema, and potentially full anaphylaxis (hypotension, bronchospasm).
The most common trigger is wheat, specifically the omega-5 gliadin protein (detectable via component-resolved IgE testing).
Other reported triggers include shellfish, celery, soy, and other foods.
Cofactors like NSAIDs and alcohol can lower the threshold, making reactions more likely.
Management involves avoiding exercise after eating trigger foods and avoiding cofactors like NSAIDs/alcohol around meals containing these foods.
Patients should be prescribed an epinephrine auto-injector and educated on anaphylaxis management.
Exercise challenge tests can confirm the diagnosis but are high-risk and should only be done in specialist centers.
FOOD PROTEIN INDUCED ENTEROCOLITIS SYNDROME
Considered a prototypical non-IgE mediated food allergy
Typically affects infants
Presents with characteristic delayed, repetitive, profuse vomiting occuring about 1-4 hours after ingesting the trigger food, this is quicker then the other delayed allergies
Can lead to lethargy, pallor and sometimes dehydration and even shock in severe cases
Diarrhoea can follow hours later
Does not cause hives or anaphylaxis
Common triggers- cow’s milk, soy, rice, oat
Diagnosis relies on history and an oral food challenge is the definitive test if history is unclear
FPIES usually outgrown by 3-5 years of age
FOOD PROTEIN-INDUCED ALLERGIC PROCTOCOLITIS
Benign, non-IgE allergy seen commonly in young infants (often breastfed), causing blood-streaked mucus in the stools due to inflammation in the colon. The main trigger is usually cow's milk protein
Infants are usually otherwise well.
It often resolves by 1 year of age
FOOD PROTEIN-INDUCED ENTEROPATHY
Rarer
Chronic ingestion of a food protein leads to malabsorption, chronic diarrhoea, vomiting and failure to thrive
It improves upon elimination of the offending protein
EOSINOPHILLIC OESOPHAGITIS
Chronic, immune mediated disease of the oesophagus
Often considered a mixed IgE and non-IgE mediated condition
Triggered by food allergens cuasing eosinophil-rich inflammation in the oesophageal lining
Symptoms depend on age but commonly include difficulty swallowing (dysphagia) and food impactions (food getting stuck) in older patients while younger children may have difficulty feeding or poor growth
Patients with EoE often have other atopic conditions like eczema or asthma
Common food triggers include milk, egg, wheat, soy, nuts, seafood
Diagnosis requires endoscopy with biopsies showing eosinophil coutns
EoE is a chronic conditions and typically not outgrown
Possible things for me to add or work on:
SPT to peanut:
5mm - sensitivity 92.9%, Specificity 94%
8mm - sensitivity 25.4%, specifficity 98.5%
Low level positive tests have a relatively low positive predictive value (50%) for food allergy. As a result ordering such tests should be done with caution and should only be tested for 2 or 3 suspected foods