Lipid transfer protein. One of the allergen families. Cross reactions therefore seen with fruit (stoned fruit but also raspberry), nuts, seeds (eg linseed/flaxseed), pulses, even cereals, tomatoes, vegetables (lettuce! Cabbage!). You may also see reactions only to composite foods eg pizza, curry, due to multiple allergens being present, but only producing reaction due to co-factors.

A less common cause of Pollen food syndrome than PR10 allergy. Thought of as a Mediterranean thing but increasing reports from Northern and Western Europe. Plane tree and mugwort have LTP but not thought to be the usual cause for sensitisation (except maybe in China). In N/W Europe, often birch sensitised too but not to be confused with PR10 type PFS!

Important to identify because heat stable (so not affected by heat, processing, digestion etc in the way PR10 allergens are) and potential for severe reactions.

So do component testing if atypical (eg unusually severe) reactions to fruit.

LTP allergy also seems to be more likely to cause reactions of varying severity, compared with primary food allergy, with co-factors perhaps more important. Eating multiple different plant foods at the same time seems to be the most likely cause of co-factor associated severe reactions. Of course, co-factors can co-exist too (alcohol and dancing, for example). So some would advise:

• Avoid exercise for 2 hours before (more in same cases) and 4 hours after eating
• Avoid NSAIDs for 2 hours before and 2 hours after
• Avoid alcohol with food or after
• Eat cautiously if not had for many months
• (sleep deprivation, cannabis, stress, fasting, anti-reflux medication…)

Diagnosis

Danger that with LTP allergy you show sensitisation to multiple foods, and then you end up on a restricted diet without knowing whether there is allergy or not.

Peach allergen Pru p 3 is a good surrogate for LTP allergy, even if peach hasn’t been a problem! If not available, you could test with SPT reagent for peach that is rich in pru p 3 (but might be false positive due to other components being present. London plane and mugwort allergy would also support.

Wheat is a bit tricky – the wheat LTP Tri a 14 is only 45% homologous with Pru p 3 so may get missed. Given the co-factor issue, probably good to do Tri a 19 (omega 5 gliadin, as in exercise induced anaphylaxis) as well.

Where hay fever and atypical reactions to nuts, do the LTPs Ara h 9 (peanut), Cor a 8 (hazelnut), Jug r 3 (walnut). You would do the other components to exclude primary food allergy which can co-exist with LTP sensitisation.

Food challenges have limited use in this situation – if positive, unclear whether LTP is the cause, and if negative, perhaps because of co-factor issue! Exercise challenge?? May just need a bigger dose!

Management

Individualize, to balance risk of reaction against dietary restriction.

Safest fruit/veg appear to be potato, carrot/root vegetables, beans, peas, melon, cashew and pistachio. Avoid pips and skin. Banana is hit and miss.

Good results with Pru p 3 sublingual and oral peach juice immunotherapy in Spain and Portugal.

Julie McCabe died in 2011 as a result of anaphylaxis to Para-Phenylenediamine (PPD) in hair dye. Black henna is known to contain PPD, so may sensitise.

Getting it right is important because otherwise people (child but also the rest of the family) end up anxious and scared of foods, cut out different foods, spend out on expensive alternatives, and risk nutritional/growth problems as well as aversion in the child.

In young infants, avoiding foods unnecessarily makes it more likely that you will become allergic in the future (“iatrogenic food allergy”). This is especially true with atopy and sensitisation – one series of 11 patients sensitized to cow milk found that all developed true cow milk allergy after a median time of avoidance of 2.3 years (with no significant improvement in their atopic dermatitis, which was the initial reason for avoidance). Pronuts study confirmed that multiple nut/sesame allergies was a factor of age – “secondary spread”. Similarly, in the Learning Early About Peanut (LEAP) study, it was precisely the infants sensitized to peanuts who were more likely to benefit from early introduction.

Having unproven food allergies also causes huge problems for schools and nurseries, and may lead to the public becoming sceptical of true allergy, with potentially disastrous consequences.

Getting it right can identify other potential allergies; it can help estimate risk of anaphylaxis; it can help with predicting whether the allergy is going to go away or not.

Allergy focused history

EATERS method –

• Exposure – did they actually eat it!? Or was there clear skin contact? Perhaps from surface contamination?
• Allergen (suspected) – one of the common ones? Although you can be allergic to pretty much anything, it is really rare to have an isolated rare food allergy.
• Timing – type 1 is immediate (within 15 minutes, rarely up to 1hr after) and then settles even without treatment within 24 hours. Rare to fluctuate.
• Environment – home (usually during weaning)? Outside home? Co-factors (infection, medicines, exercise, sleep deprivation) come in here.
• Reproducible – consistent reactions with exposure? May have had before with type 1 allergy but often on trying for the first time, and won’t have had recently. Milk/egg different, of course…
• Symptoms – type 1 vs non type 1. Some overlap of course.

[Mich Erlewyn-Lajeunesse, ADC 2019]

Other issues are age (adolescents with hay fever more likely to develop secondary pollen food syndrome type allergies), alpha-gal allergy can be delayed up to 3 hours; raw vs cooked food sometimes makes a difference; usually you already have eczema and family history of atopy.

Testing

At the end of history taking, you should have be able to assess probability of type 1 allergy. If low, you may wish to proceed straight to challenge (unless reactions sound severe). Otherwise testing may help confirm or refute.

If negative/equivocal on initial skin prick or specific IgE testing, do another test! Skin prick if negative/equivocal IgE, and vice versa.

IgE Component testing may give added information, esp where potential pollen co-sensitisation – best evidence (mostly in US population, however) for Peanut, Hazelnut, Cashew (respectively Ara h 2, Cor a 14, Ana o 3 – other components may give extra information in some cases). Jug r 1 v specific (walnut) but not v sensitive.

Challenge

Challenge will be useful where results still equivocal – viz

• Results positive but never eaten or history inconsistent
• Results positive but possibly co-sensitivity without allergy
• Food in alternative form might be OK eg baked

Gold standard is double blind challenge, but who has time for that? And dangerous!

Mostly based on history – combination of characteristic features without other, more likely, explanation.

EAACI guidance 2023 says where type 1 allergy suspected (signs/symptoms but also timing and consistency of reaction):

• Do skin prick testing and/or specific IgE testing as first line
• After that, if still doubt then for peanut, hazelnut or cashew, if in doubt do component tests Ara h 2, Cor a 14, Ana o 3 respectively (if available) – otherwise do skin prick or IgE if not done already.
• Where peanut or sesame allergy still in doubt, do basophil activation test (BAT – if available – nowhere in Scotland, as far as I know)
• “Reassessment of food allergic children, at regular intervals, depending on age, food and patient’s history, is suggested for possible development of spontaneous tolerance”

Ara h 2 (cut off 0.44) has 82% sensitivity and 92% specificity cf 84 and 86% for SPT of 4mm, so equivalent. Cor a 14 (cut off 0.64) has 73 and 95%, so not great sensitivity. Ana o 3 (cut off 0.4) pretty good – 96 and 94%.

If random reactions, then consider hidden allergens: celery, mustard, cochineal, lupin, soy, fenugreek, other legumes such as pea/bean/lentil protein, insects/mealworm, pink peppercorns.

Panel tests

=multiple specific IgE tests done at the same time (the ultimate being the ALEX3 test, where 280+ different antigens are tested simultaneously) – likely reduced sensitivity, compared with individual test, but more importantly, potential for false positives, with attendant harms (including iatrogenic food allergy, if that food then avoided unnecessarily).

Advances of Alex3 over Alex2 include new molecular allergens including alpha-Gal, chicken (Gal d 7), celery (Api g 7, predicts anaphylaxis), wheat (Tri a 36, and Tri a 37), oak pollen, and honeybee venom; inclusion of lentil and pea.

Proteins responsible for a minority of allergic reactions to peanut, hazelnut, sesame among others – hydrophobic, so tend not to be well represented in skin prick and IgE test solutions. May explain false negatives.

Specific IgE tests have been developed, but otherwise you just have to challenge.

Dutch study however didn’t find that specific testing for oleosins helped much.

Once a child starts school/nursery, the risk of reactions (and anxiety about potential reactions) starts to ramp up. Obviously, this is because other people are responsible for sourcing and providing food, often to many different children at once.

In the UK, probably 1 pupil with a food allergy in every classroom.

“Schools are the most common setting for severe allergic reactions, with 18% of all food allergy reactions and 25% of first-time anaphylactic episodes occurring there. Fatal anaphylaxis in children occurs more often in schools than any other setting” [Benedict Blythe Foundation “Keeping the promise” document] – but this data appears to be from old US studies. From my data (19/8/26) I see 4 mentions of anaphylaxis related to school in the last 2 years (about 10% of all anaphylaxis reports) – but half of these were actually related to after school.

Miranda Crilley (CHI Dublin) reported on 521 food allergic children attending school/nursery, and found a 4.5/5% annual rate of reactions in schools. Half of nursery reactions due to milk.  6 of 7 nut reactions in schools with nut bans! 33% of children had not provided copies of their allergy action plans to the school. 22% or the reactions were judged as anaphylaxis, none received adrenaline from school staff. “Promoting milk/egg tolerance in infancy would prevent”.

Scottish government policy on healthcare needs in schools (2017): talks about “coordinated support plans” as well as individual health plans and child plans. Talks about local strategic joint arrangements between NHS boards and educational authority. Inhalers and defibrillators (!) specified.  “General awareness raising training of common conditions should be provided… for example, asthma, diabetes, epilepsy, eczema and allergic reactions (including anaphylaxis).”

Specific school arrangements may include:

• who in the school accepts responsibility, in principle, for supporting the healthcare needs of children and young people in the school;
• who is responsible in school for staff training in regard to supporting healthcare needs and administering medication;
• emergency procedures at the school including a main point of contact in the school health team [defined how?];
• details of any centrally held inhalers; anaphylaxis auto-injectors; the storage of and access to medication in the school;
• who is responsible for ensuring the safety of children and young people’s self-management of their medical conditions;
• the arrangements in place to ensure that staff are informed and kept up to date about children and young people’s healthcare needs at school.

First do no harm – parents tend to overestimate risk of anaphylaxis, whereas there are clear consequences to restricting the child’s ability to sit with other children at snack/meal times, or restricting the food choices of other children.

School Allergy Care

https://www.rightdecisions.scot.nhs.uk/school-allergy-care/ from George Raptis in Glasgow is a great resource.

Recommends that an Allergy management policy should be in place (even if incorporated into wider medical conditions policy) even if no currently diagnosed allergic children [quotes 25% undiagnosed reaction rate in school] – cites 2017 Government supporting CYP with healthcare needs document:

• Procedure for identifying pupils with allergy and high risk pupils.
• Details on developing Individual Healthcare Plans.
• Protocol for storage and access to emergency medication – emergency kits.*
• Arrangements for staff training.
• Policies and arrangements on Preventative Measures.
• Details on the administration of medications.
• Protocol for the emergency response to anaphylaxis.
• The rights, roles and responsibilities of staff, pupil(s) and parent/ carer(s).

Highlights breakfast clubs and after school as under the remit of schools (and school trips, too).

Refers to EAACI/DOH guidelines:

1. Allergy lessons as part of curriculum
2. Education for all school staff in preventing cross contamination of allergens during handling, preparation and serving of food.
3. Emergency medication stored in school for pupils with allergies.
4. Distribution of menus to parents/carers and pupils with the 14 allergens listed
5. (a full ingredients list should be made available upon request)
6. Supervision during meal times.
7. Allergen free areas, where there may be a high risk of allergen exposure, e.g. canteen or cooking classes.
8. Clear allergen labelling of all meals, drinks and snacks in the canteen.
9. Labelling individual cups/ bottles/ containers with children’s names.
10. No food sharing policy.
11. No eating utensil sharing policy.
12. Routine Cleaning (with warm soapy water and disinfectant) of tables, floors and food preparation areas, especially after meal times.
13. Encourage hand-washing after meals/ snacks.
14. Discuss with parents/carers and obtain their permission before giving food treats to pupils with allergies (e.g. birthday parties or special events).
15. Risk assessments completed for school trips, exchanges and excursions.
16. No eating policy on school buses.

“Things to consider:” specific food bans as not equitable; potential for stigma and restricted opportunities (“can’t guarantee”).

Discusses indemnity/insurance incl private schools. Getting insurance will usually require training and allergy plans as a condition!

Food also becomes an issue at special school events (festivals, shows, fundraisers), in art classes, as rewards/treats…

Nut bans

Probably better to increase allergy awareness (which varies widely) than rely on classroom or school-wide bans [Dave Stukus editorial]. Here is a podcast video I did with Anaphylaxis UK about nut bans in schools – https://youtu.be/1TcMqMe3Q_4?si=1rQ5AgA5QguO_F0I

And another about how schools can become more allergy aware – because it’s not just about nuts – https://youtu.be/JHnmcmUP6Cs?si=FgjhoxcOdMoEb7eS. George Raptis has shown how school allergy training (in NW England) can improve allergy awareness, not just confidence in managing an allergic emergency.

Benedict Blythe – School allergy code

https://theallergyteam.com/schools-allergy-code/ from the Allergy Team plus Benedict Blythe foundation.

Checklist, register, trust mark!

2 pages (plus separate checklist). 4 points – 

1. Whole school approach – not just catering/medical – skills (risk reduction, inclusion, first aid); allergy awareness in classroom activities [curriculum?]
2. Communicate clearly – Allergy and Anaphylaxis Policy (no template!) – (accessible), – and designated allergy lead.  IHPs (individual health plans)
3. Clear governance and risk management – designated lead, other roles/responsibilities. Allergies in every risk assessment
4. Readiness to respond – 2 in date AAIs for those prescribed them. Hold spare pens in obvious place. Annual risk reduction and ana training. “Ana emergency response plan” [in allergy policy, presumably?], rehearse

Schools allergy code backed by Dept of Education in England.

React report

Data from 2000 English schools, about 10%.

Assessed 4 allergy safe guards: a specific allergy policy, spare pens, allergy training for staff, incident reporting.

69% did not have all recommended safe guards in place. “Pot luck whether your local school has medication, communication and education relating to allergy made available to teachers”. But commented on how well schools are managing despite “seeming lack of guidance, training and funding from government”.

Training

“All schools that are OFSTED monitored AND provide early years education must have at least one member of staff paediatric first aid trained including anaphylaxis treatment”.

First aid training, and even anaphylaxis training, is not the same as allergy awareness, however. 25% of schools don’t train staff on identifying allergy symptoms and anaphylaxis, and what to do in an emergency. Mandatory in New York day care (Elijah’s law), Canadian schools (Sabrina’s law).

Various free and paid for training programmes available. KITT Medical includes training in its package, that includes emergency adrenaline autoinjectors. Natasha Allergy Research Foundation offers Allergy School – includes self assessment for primary schools (also for clubs). Free. Resources for age groups eg 5-7 including going to a party (Armadillo film), assembly plan, top 14 allergen poster.

School Allergy Policy

BSACI Model policy includes (last 9 pages actual template – mostly repetition of initial text): 

• reference to laws on supporting pupils with medical conditions; 
• how first aid falls under health and safety policy (designated first aiders)
• Anaphylaxis management
• SPare pens in schools
• Allergy action plans
• Staff allergy training (says “all staff”, annually) incl risk reduction (no detail), asthma
• Bullying
• Storage of medicines, expiry dates
• Catering – staff must be able to identify pupils with allergies; menus should be available (with ingredients); may contain; [cross contamination is a heading but nothing further]
• Ana UK safer schools programme and allergyWise training; 
• Working with parents – must keep school updated, provide medicines and allergy plans.
• Links to Wiltshire anaphylaxis risk assessment template
• Sports (in/out school)
• Insect stings (v brief)
• Checklist (11 points)

Individual Healthcare Plan

The need for an individual healthcare plan and the medical detail of such a plan should only be assessed by an appropriate designated health practitioner. May include:

• details of any diagnosed condition or symptoms;
• the impact that the condition or symptoms has to the individual;
• details of any medication, dosage, side effects and storage information;
• special requirements e.g. dietary needs, pre-activity precautions, access to facilities and other reasonable adjustments etc.;
• what to do, and who to contact, in an emergency;
• training needs for the support, how often these should be reviewed and who will deliver the training;
• consent;
• how often and when the plan should be reviewed;
• consideration of existing emergency plans, such as Anticipatory Care Plans.