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Shellfish allergy guide









Food allergy · Shellfish

Shellfish Allergy Guide: Species, Allergen Components and Which Test to Choose

“Shellfish” covers two very different animal groups. Understanding which species you react to, and which protein is responsible, makes testing and day-to-day management far more precise.

Medical note: this guide is educational and is not a diagnosis. Blood tests measure IgE sensitisation; a positive result must be interpreted with your symptoms and history by an allergy specialist. If you have ever had breathing difficulty, throat swelling, collapse or dizziness after shellfish, seek urgent medical help and ask your GP for specialist referral.

1. Shellfish are two separate biological groups

In the UK food-labelling rules, crustaceans and molluscs are listed as two separate allergens among the 14 major allergens. Biologically they are only distantly related, but they share some muscle proteins, which is why cross-reactions happen and why some people react to both and others to only one.

Crustacea → Decapoda (10-legged crustaceans)

  • Pleocyemata
    • Brachyura & Anomura: edible crabs
    • Achelata: lobster (incl. spiny lobster)
    • Caridea: brown shrimp, North Atlantic prawn
  • Dendrobranchiata
    • Penaeoidea: tiger prawn, king prawn
Mollusca

  • Bivalvia: oyster, clams, mussels, scallops, cockles
  • Cephalopoda: squid, octopus, cuttlefish
  • Gastropoda: snails, limpets, whelks

Classification as presented in Stephen JN et al., Clin Exp Allergy 2017;47(3). Freshwater crayfish are also decapod crustaceans and are included below.

2. The allergen components: what you are actually reacting to

An allergy is triggered by specific proteins, not by the animal as a whole. Modern “component-resolved” testing looks at those proteins individually. The main ones in shellfish are:

  • Tropomyosin (e.g. Pen m 1 in tiger prawn, Lit v 1 in whiteleg shrimp, Cra c 1 in brown shrimp, Hom a 1 in lobster, Cra g 1 in oyster, Tod p 1 in squid). This is the major, heat-stable muscle protein and the main driver of cross-reactivity between crustaceans, between crustaceans and molluscs, and with house dust mite (Der p 10) and cockroach.
  • Arginine kinase (e.g. Pen m 2, Cra c 2). An energy-metabolism enzyme that is a second well-recognised crustacean allergen and is also found in mites and insects.
  • Myosin light chain (e.g. Pen m 3, Cra c 5, Hom a 3) and troponin C (e.g. Pen m 6, Cra c 6, Hom a 6). Additional muscle proteins that can be the only sensitisation in some patients.
  • Sarcoplasmic calcium-binding protein, SCP (e.g. Pen m 4, Lit v 4, Cra c 4). Often more species-specific than tropomyosin and relevant when tropomyosin results do not explain symptoms.
  • Triosephosphate isomerase (e.g. Cra c 8) and hemocyanin. Less common but documented crustacean allergens.

Names follow the WHO/IUIS allergen nomenclature (genus, species, number). Reaching for a whole-extract “shrimp” result alone cannot tell you whether the sensitisation is to a widely shared protein such as tropomyosin (higher cross-reactivity) or to a narrower one such as SCP.

3. Why component information matters

  • Cross-reactivity: strong tropomyosin sensitisation makes reactions to several crustaceans, and sometimes to molluscs, more likely. Sensitisation does not always equal clinical reaction, so tolerated species should only be reintroduced under specialist advice.
  • Dust-mite link: some people with mite allergy test positive to shellfish through tropomyosin without ever having had a reaction. Components help separate this from true food allergy.
  • Cooking and exposure: tropomyosin is heat-stable, so cooking does not make an allergenic shellfish safe. Steam and cooking vapours can trigger reactions in highly sensitised people.
  • Cross-contact: shared fryers, grills, woks and serving utensils are a real risk in restaurants.

4. Species-by-species testing

Each button opens the matching specific IgE test on FoodAllergyTest.co.uk (home finger-prick kit, analysed in a UK laboratory). Components listed are the principal allergens described for that species group.

Crustaceans (Crustacea, Decapoda)

Dendrobranchiata · Penaeoidea, and Caridea

Shrimp & prawns (incl. tiger prawn, king prawn, brown shrimp, North Atlantic prawn)

The most common cause of shellfish allergy and the most frequent cause of severe reactions. Tiger and king prawns belong to Penaeoidea; brown shrimp and North Atlantic prawn to Caridea. They share major allergens, so one test is a sensible starting point.

Components: tropomyosin (Pen m 1, Lit v 1, Cra c 1, Pan b 1), arginine kinase (Pen m 2, Cra c 2), myosin light chain (Pen m 3), SCP (Pen m 4, Cra c 4), troponin C (Pen m 6, Cra c 6).

Shrimp allergy test

Pleocyemata · Brachyura & Anomura

Crab (edible crab and relatives)

Crab allergy often co-exists with prawn allergy through shared tropomyosin, but some people react to crab alone, so testing individually can be informative. Brown crab meat and claw meat carry the same allergens.

Components: tropomyosin (e.g. Cha f 1, Por p 1), arginine kinase, myosin light chain, SCP.

Crab allergy test

Pleocyemata · Achelata

Lobster and spiny lobster (langoustine-type)

Lobster allergy is usually part of the wider crustacean picture. Spiny lobster (langust) has its own test because the tropomyosin differs slightly between species.

Components: tropomyosin (Hom a 1 lobster; Pan s 1 spiny lobster), myosin light chain (Hom a 3), troponin C (Hom a 6), arginine kinase.

Lobster allergy test
Spiny lobster test

Freshwater decapod

Crayfish

Common in salads, soups and Cajun dishes. Crayfish tropomyosin is closely related to that of other decapods.

Components: tropomyosin (Pro c 1), arginine kinase (Pro c 2).

Crayfish allergy test

Molluscs (Mollusca)

Bivalvia

Oyster

Raw and cooked oysters can both trigger reactions. Oyster allergy can occur without crustacean allergy.

Components: tropomyosin (Cra g 1) plus mollusc-specific proteins.

Oyster allergy test

Bivalvia

Clam, mussel and scallop (cockles tested through related bivalves)

Bivalves are filter feeders. Reaction patterns vary widely: some people tolerate scallop but not clam or mussel, so separate tests help build an accurate map. There is currently no dedicated cockle test on the site; discuss options with the team or consider ALEX³.

Components: tropomyosin (e.g. Mer l 1 clam, Chl n 1 scallop) and other heat-stable muscle proteins.

Clam
Blue mussel
Scallop

Cephalopoda

Squid and octopus (cuttlefish is related)

Calamari, octopus and cuttlefish ink dishes. Cephalopod tropomyosin is somewhat different from crustacean tropomyosin, so cross-reactivity with prawn is less predictable.

Components: tropomyosin (Tod p 1 squid, Oct v 1 octopus), SCP, arginine kinase and paramyosin in octopus.

Squid
Pacific squid
Octopus

Gastropoda

Snails, whelks, limpets and abalone

Escargot, whelks and abalone are gastropods. Snail tropomyosin cross-reacts with house dust mite, so mite-allergic patients sometimes react to snails. The snail test is currently out of stock; the abalone test is available.

Components: tropomyosin (Hel as 1 snail, Hal m 1 abalone).

Abalone allergy test
Snail test (details)

Browse every shellfish, mollusc and fish test: Fish, Shellfish & Molluscs tests. Individual tests are priced per allergen, with a laboratory handling fee per kit of up to three allergens. Check the site for current pricing and stock.

5. Single-species test or ALEX³ component test?

Individual specific IgE test ALEX³ molecular test
Best for Checking a specific species you have reacted to or eat regularly Unclear triggers, several suspected allergies, cross-reactivity questions
What it shows IgE to the whole species extract IgE to up to 300 allergens and components in one sample, food and airborne
Shellfish value Sensitisation to a named species Helps separate shared-protein sensitisation (e.g. tropomyosin, possible mite link) from narrower patterns
Collection Home finger-prick kit, up to 3 allergens per kit Home finger-prick kit or in clinic

ALEX³ allergy test
View full list of allergens tested

Antihistamines and diet do not affect blood IgE results and no fasting is required, so you do not need to stop medication before sampling.

6. Common questions

If I react to prawns, must I avoid all shellfish?

Not automatically. Many people with crustacean allergy tolerate some molluscs, but others react to both. Do not make or reverse dietary decisions based on a blood result alone; an allergy specialist can advise on whether supervised food challenge is appropriate.

Is shellfish allergy the same as fish allergy?

No. Fish allergy is typically driven by parvalbumin, a different protein, and requires separate testing.

Can a positive result be wrong?

A positive IgE result means sensitisation, which does not always cause symptoms, and a negative result does not completely exclude allergy. Interpretation with your clinical history is essential.

Can allergy start in adulthood?

Yes. Shellfish allergy is one of the most common food allergies to begin later in life, including in people who have eaten shellfish without problems for years.

Next steps

Choose the species tests that match your symptoms, or start with the broader ALEX³ test, then review results with a specialist at Allergy Clinic London.

Browse shellfish tests
How testing works



ALEX³ postal allergy test kit, yellow-capped blood sample tube and sublingual spray beside grass and birch, with London in the background.

Hay fever that keeps coming back: a patient guide to testing and sublingual immunotherapy

Hay fever and pollen allergy · Updated

If sneezing, itchy eyes and a blocked nose return every spring or summer despite treatment, a specialist assessment can help identify your triggers and review your options. This guide explains hay fever testing in London and sublingual immunotherapy (SLIT), with a focus on treatment administered as a spray under the tongue.

Postal allergy test kit, yellow-capped blood sample tube and sublingual spray beside grass and birch, with the London skyline behind.
Pollen allergy testing and sublingual immunotherapy for hay fever. This generated image is illustrative; kit contents and treatment packaging may differ.

In brief

  • Allergy results need to match your symptoms and exposure; a positive test alone is not a diagnosis.
  • Sublingual immunotherapy aims to reduce sensitivity to a relevant allergen over a course usually lasting at least three years.
  • Benefits depend on the individual preparation, dose, allergen and patient.
  • Asthma must be assessed and adequately controlled before treatment.

Why hay fever symptoms can return each year

Antihistamines, nasal corticosteroid sprays and eye drops can control symptoms, but they do not generally provide lasting changes to your sensitivity to pollen. Symptoms may therefore recur during a new pollen season.

Persistent symptoms can also reflect an unsuitable medicine, inconsistent use, nasal spray technique or an additional diagnosis. Tree pollen often causes symptoms in spring, grass pollen in late spring and summer, and some weed pollens later in the season. The exact timing varies with the plant, weather and location.

What hay fever testing in London involves

  1. A history of your symptoms
    We ask when symptoms begin and end, how they affect sleep and daily life, and whether you also have wheeze, cough or an itchy mouth after certain raw fruits.
  2. Skin prick or specific IgE blood testing
    The choice depends on your history, skin condition and medicines. Skin prick testing usually gives results during the appointment. Specific IgE blood testing may be useful when skin testing is unsuitable. Follow the clinic’s instructions about antihistamines; do not stop prescribed medicines without advice.
  3. Component testing when it can clarify the diagnosis
    Testing individual allergen proteins can help distinguish primary sensitisation from cross-reactivity. Broad tests such as ALEX³ are not necessary for every person with hay fever; your specialist should select testing that answers a clinical question.
  4. Breathing checks where appropriate
    Cough, wheeze or breathlessness may warrant an asthma assessment. An allergy test alone cannot diagnose asthma.
  5. A personalised management plan
    We explain which findings are relevant and discuss symptom control, possible immunotherapy and follow-up.

What does a positive allergy test mean?

A positive skin prick or specific IgE blood test indicates sensitisation. It becomes clinically relevant when it matches your symptoms and exposure. Test results need to be interpreted alongside your medical history.

Read more about
allergy tests available at the clinic.

Hay fever treatment options

Controlling symptoms

  • A nasal corticosteroid spray used consistently, with the correct technique
  • An appropriate antihistamine and, when needed, allergy eye drops
  • Reducing pollen exposure where practical and checking pollen forecasts

Considering immunotherapy

  • Specialist assessment when symptoms remain troublesome despite appropriate treatment
  • Allergen-specific treatment selected to match the clinical diagnosis
  • Continued symptom medicines and regular review where needed

Allergen immunotherapy may be considered when clinically relevant allergy is confirmed and symptoms remain significant despite appropriate treatment. It requires a discussion of expected benefits, risks and the commitment involved.
[1]
[8]

Sublingual immunotherapy: what to expect

Sublingual immunotherapy delivers a prescribed allergen preparation under the tongue. This page focuses on sprays. Drops, tablets and injection immunotherapy also exist, but preparations and routes are not interchangeable. Evidence for one product does not automatically establish the effectiveness of another.

Your clinic will arrange supervised initiation and explain the prescribed dose, administration method and monitoring. Follow the instructions for your own preparation, including how long to hold it under the tongue. Suitable patients then continue treatment at home with specialist follow-up.

A course usually lasts at least three years when the aim is sustained benefit. The schedule and total duration depend on the preparation and clinical response.
[1]

First months

Mouth itching or tingling can occur. Report troublesome reactions and follow the advice given at initiation. Continue your usual medicines unless your clinician advises otherwise.

First pollen season

Some people notice fewer symptoms or reduced medicine use, while others take longer to respond. Record symptoms, pollen exposure and medicine use to help assess progress.

Years two and three

Regular reviews assess benefit, side effects, adherence and asthma control. Your specialist will decide whether continuing treatment remains appropriate.

What research shows about immunotherapy

Research supports allergen immunotherapy for selected patients. The preparation, treatment route and study population matter when applying findings to an individual patient.

Benefits during a third year of grass pollen treatment

A small extension study of a high-dose six-grass sublingual preparation reported further improvement in symptom and medication scores during the third year, with more well days. No serious adverse events were reported in that study.
[4]

Study limitations:
This was a small study of one preparation; it does not establish the results of every grass pollen spray.

Evidence for specific liquid sublingual preparations

Two 2025 systematic reviews reported improvements in symptom and medication scores with the liquid preparations studied. One review assessed index-of-reactivity liquid products; the other examined a five-grass liquid formulation.
[2]
[3]
[9]

Study limitations:
These reviews are product-specific. Evidence for the preparations studied cannot be assumed to apply to all liquids or sprays. The first review also has a published correction.

Long-term follow-up in house dust mite allergy

A 2026 analysis of a 15-year follow-up study found less progression to the study-defined asthma outcome in patients who received three to five years of SLIT than in those receiving medicines alone.
[5]

Study limitations:
This was a post hoc analysis of an open-label study in mite-allergic patients with bronchial hyperreactivity. It is not direct evidence that pollen sprays prevent asthma.

Injection immunotherapy in local allergic rhinitis

A 2026 ten-year follow-up compared selected responders to subcutaneous immunotherapy with matched untreated patients. Asthma developed in 8.0% of treated patients versus 40.7% of untreated patients; new sensitisations occurred in 6.3% versus 38.2%.
[6]

Study limitations:
This involved injection immunotherapy, not SLIT, and a specific condition called local allergic rhinitis. Selection of responders and the non-randomised follow-up limit generalisation.

Immunotherapy and allergic asthma

A 2026 meta-analysis included 28 randomised controlled trials assessing allergen immunotherapy for allergic asthma. It reported improvements in symptoms and medication use, with greater average benefit for injection treatment. Systemic reactions were also increased.
[7]

Study limitations:
This does not establish the best route for every patient. Asthma treatment and monitoring must continue; immunotherapy does not replace prescribed inhalers.

Who needs extra care before immunotherapy?

Poorly controlled or severe asthma can make immunotherapy unsuitable. Your specialist will also review your medical history, current illness, mouth problems and medicines, including beta-blockers, because these can affect suitability or the management of a reaction.

Immunotherapy is generally not started during pregnancy. If you become pregnant during an established course, contact your specialist promptly for an individual review rather than changing treatment yourself.

Local mouth or throat symptoms are common with SLIT. Serious allergic reactions are uncommon but possible. Your team should provide instructions for reactions, missed doses, mouth ulcers and restarting after an interruption.

Questions to ask your allergy specialist

  • Which pollen is causing my symptoms, and how do the tests support this?
  • Could better nasal spray technique or a different medicine help?
  • What evidence supports the preparation you are considering?
  • What is the schedule, total duration and cost of the course?
  • How will we assess benefit, and what should I do about missed doses or reactions?

Common questions about hay fever tests and SLIT

Do I need an allergy test before starting immunotherapy?

Usually, yes. Your specialist needs evidence that a particular allergen is relevant to your symptoms. This generally involves skin prick testing or a specific IgE blood test. A positive test alone does not establish a clinical allergy.

When is the best time to start sublingual immunotherapy for hay fever?

The timing depends on the prescribed preparation and your pollen season. Many pollen regimens begin several months before the season, so autumn or winter can be a useful time to arrange an assessment.

Will I still need antihistamines?

You may still need antihistamines, nasal sprays or eye drops, particularly during the first pollen season. Your specialist will review your symptoms and advise on any changes to your medicines.

Is sublingual immunotherapy a cure for hay fever?

It can reduce symptoms and the need for medicines, and some preparations have evidence of benefits after treatment ends. It is not a guaranteed cure, and results vary between people and products.

Can children have sublingual immunotherapy?

Some children may be suitable. A specialist will consider the child’s age, symptoms, asthma control and the evidence and prescribing requirements for the proposed preparation.

Arrange a hay fever assessment in London

Discuss your symptoms, testing needs and treatment options with our specialist team.

This page provides general information and does not replace an individual clinical assessment. If an allergic reaction causes severe breathing difficulty, throat swelling or faintness, call 999. Use your prescribed adrenaline auto-injector if indicated by your emergency action plan.

Sources and further reading

  1. EAACI. Guidelines on allergen immunotherapy: allergic rhinoconjunctivitis. Allergy (2018).
  2. Di Bona et al. Efficacy of index of reactivity-liquid sublingual immunotherapy in allergic rhinoconjunctivitis: systematic review and meta-analysis. Frontiers in Allergy (2025).
  3. Di Bona et al. Efficacy of five-grass pollen liquid sublingual allergen immunotherapy: systematic review and meta-analysis. Journal of Investigational Allergology and Clinical Immunology (2025).
  4. Kuna et al. Sustained clinical efficacy of sublingual immunotherapy with a high-dose grass pollen extract. European Annals of Allergy and Clinical Immunology.
  5. Marogna et al. Long-term effects of SLIT in preventing the development of asthma in allergic rhinitis: revision of 15-year follow-up. World Allergy Organization Journal (2026).
  6. Testera-Montes et al. Long-term effect of allergen immunotherapy in responder local allergic rhinitis patients. Allergy (2026).
  7. Efficacy and safety of allergen-specific immunotherapy for allergic asthma: meta-analysis comparing sublingual and subcutaneous routes. Annals of Medicine (2026).
  8. British Society for Allergy and Clinical Immunology (BSACI). Immunotherapy.
  9. Correction to Di Bona et al., index-of-reactivity liquid SLIT review. Frontiers in Allergy (2025).

Autoimmune progesterone dermatitis (progestogen hypersensitivity) causing cyclical skin rash associated with the menstrual cycle.

Autoimmune Progesterone Dermatitis (Progesterone Hypersensitivity): Symptoms, Causes, Diagnosis and Treatment





Hormone allergy and skin reactions

Autoimmune Progesterone Dermatitis: Could Your Monthly Rash Be a Progesterone Allergy?

Autoimmune progesterone dermatitis (progestogen hypersensitivity) causing cyclical skin rash associated with the menstrual cycle.
Figure. Autoimmune progesterone dermatitis (progestogen hypersensitivity) is a rare hormone-related allergy that can cause cyclical rashes, hives, swelling and, occasionally, anaphylaxis.

Autoimmune progesterone dermatitis, now often described more broadly as
progestogen hypersensitivity, is a rare condition in which naturally produced
progesterone or a progesterone-containing medicine triggers recurrent allergic or inflammatory symptoms.

The most important clue is timing: symptoms often appear or become worse during the
second half of the menstrual cycle, commonly around 3–10 days before a period,
and improve when menstruation begins or shortly afterwards.

What is autoimmune progesterone dermatitis?

Progesterone rises after ovulation during the luteal phase of the menstrual cycle.
In people with progestogen hypersensitivity, this natural rise may trigger skin, mucosal or systemic
symptoms. Reactions may also follow exposure to synthetic progestogens in contraception,
fertility treatment, hormone replacement or other hormonal medicines.

The older term “autoimmune progesterone dermatitis” remains widely recognised, but it can
be misleading because not every reaction is proven to be autoimmune and not every patient has dermatitis.
The term progestogen hypersensitivity better reflects the range of possible reactions,
which includes urticaria, angioedema, breathing symptoms and anaphylaxis, as well as eczema-like rashes.

What did the 2026 research find?

A 2026 clinical study reviewed 13 patients diagnosed with autoimmune progesterone
dermatitis. The average age at which symptoms began was 24 years. Every patient reported
worsening around the menstrual period, and the most common skin presentation was
urticaria. Itching was reported by all patients.

Key findings from the 2026 case series

  • 69% had urticaria.
  • 38% experienced angioedema.
  • 38% had experienced anaphylaxis.
  • 100% reported a perimenstrual worsening pattern.
  • 61% had a positive intradermal progesterone test.
  • 62.5% of those tested had a positive autologous serum skin test.

The researchers emphasised that skin testing may support the diagnosis but is
not sufficiently reliable to be used alone. A negative progesterone skin test does not
exclude the condition, and false-positive results can occur. Diagnosis therefore depends heavily on a
detailed clinical history and the reproducible relationship between symptoms, the menstrual cycle and
exposure to hormonal medicines.

Other 2026 publications have reinforced the importance of recognising the severe end of the spectrum.
A literature review identified documented cases of both endogenous and medication-triggered
progesterone-induced anaphylaxis, including reactions associated with assisted
reproduction. The authors highlighted variation in testing methods and the need for individualised
management, particularly where progesterone is required for fertility treatment.

What does a progesterone-related rash look like?

There is no single characteristic rash. Symptoms may change from one cycle to another and may resemble
more common skin conditions. Reported presentations include:

  • Hives or urticaria — raised, itchy welts that may move around the body.
  • Angioedema — deeper swelling, often affecting the eyelids, lips, hands or feet.
  • Eczema-like dermatitis — red, dry, inflamed or intensely itchy patches.
  • Erythema multiforme-like lesions — round or target-shaped areas.
  • Mouth or genital symptoms — including soreness, ulcers or cyclical vulval eruptions.
  • Breathing or systemic symptoms — wheeze, throat tightness, dizziness, collapse or
    anaphylaxis.

Emergency warning: Call 999 immediately for difficulty breathing, throat or tongue
swelling, collapse, severe dizziness or rapidly progressing symptoms. Use an adrenaline auto-injector
without delay if one has been prescribed.

When do symptoms occur?

In endogenous progestogen hypersensitivity, symptoms typically begin after ovulation as progesterone rises.
A recurring flare in the days before menstruation, followed by improvement at or soon after the start of
the period, is highly suggestive.

However, timing is not always textbook. Symptoms can be influenced by irregular cycles, pregnancy,
the postnatal period, perimenopause, contraceptive use and fertility treatment. Some patients first develop
symptoms after exposure to a progesterone or progestin medicine, while others have never used one.

How is progestogen hypersensitivity diagnosed?

There is currently no single universally accepted gold-standard test. Assessment should be performed by a
clinician experienced in allergy, dermatology and, where appropriate, gynaecology. A careful history is
central to diagnosis.

1. A detailed symptom and menstrual-cycle history

Patients may be asked to record symptoms daily for at least two or three cycles, noting the first day of
menstruation, rash appearance, swelling, breathing symptoms, medicines, hormonal treatment and photographs
of visible reactions. A consistent monthly pattern is often more informative than a single laboratory result.

2. Review of hormonal exposure

The clinician will review contraceptive pills, hormonal coils, injections, implants, fertility medicines,
progesterone pessaries, hormone replacement therapy and previous pregnancies. It is important not to stop
a prescribed hormonal medicine without medical advice.

3. Allergy and skin testing

Intradermal or skin-prick testing with progesterone is sometimes used in specialist settings, but protocols
are not standardised. The test solution and its vehicle may irritate the skin, false-positive reactions are
possible, and a negative result cannot confidently rule out the diagnosis.

4. Supervised drug or hormone challenge

A carefully supervised challenge may occasionally help clarify whether a particular progestogen is tolerated.
This can provoke a significant reaction and should only be considered by an experienced specialist in an
appropriately equipped clinical setting.

5. Excluding other conditions

Other causes of recurrent rash or swelling may need to be considered, including chronic spontaneous
urticaria, contact dermatitis, drug allergy, urticarial vasculitis, mast-cell disorders, hereditary
angioedema and other cyclical hormonal conditions.

How is autoimmune progesterone dermatitis treated?

Treatment depends on the severity of symptoms, whether the trigger is endogenous or medication-related,
the need for contraception, plans for pregnancy and any requirement for progesterone during fertility
treatment. Management should be individualised and may involve an allergist, dermatologist, gynaecologist
and fertility specialist.

Symptom control

Non-sedating antihistamines may help urticaria and itching. Topical corticosteroids may be considered for
limited eczema-like inflammation, while short courses of systemic corticosteroids may occasionally be
required for significant flares. These measures may reduce symptoms but do not necessarily prevent the
underlying cyclical reaction.

Ovulation suppression

For patients reacting to their own progesterone, treatment may aim to suppress ovulation and reduce
progesterone fluctuations. Continuous combined hormonal contraception is one option, but it is not suitable
for everyone and may worsen symptoms in patients who react to the progestogen component. Specialist
supervision is essential.

Biological treatment

Omalizumab has been reported in selected patients, particularly where urticaria, angioedema or anaphylaxis
is prominent. Evidence remains limited because the condition is rare, so treatment decisions must be made
on an individual basis.

Progesterone desensitisation

Desensitisation may be considered when progesterone is medically necessary, particularly during in vitro
fertilisation. Protocols have used oral, intramuscular or intravaginal routes. Desensitisation is a high-risk
specialist procedure and continued regular exposure is usually required to maintain tolerance.

Other hormone-suppressing treatments or surgery

Gonadotrophin-releasing hormone medicines and other hormone-modulating treatments have been described in
severe cases. Surgery to remove the ovaries is irreversible and is reserved for exceptionally severe,
treatment-resistant disease when future fertility is not desired.

Pregnancy, IVF and progesterone hypersensitivity

Pregnancy does not affect every patient in the same way. Symptoms may improve, remain unchanged or worsen.
Reactions can also appear for the first time during fertility treatment or after pregnancy. Anyone with
suspected progesterone hypersensitivity who is planning pregnancy or IVF should seek specialist advice
before starting hormonal treatment.

Where progesterone support is essential, an allergy specialist and fertility team may be able to identify
a tolerated preparation or arrange desensitisation. Previous tolerance of pregnancy or progesterone does
not guarantee that future exposure will be reaction-free.

When should you see an allergy specialist?

Consider a specialist assessment if you experience recurrent hives, eczema, swelling or unexplained
allergic reactions that repeatedly occur before your period, or if symptoms began after hormonal
contraception, fertility medication or another progestogen-containing treatment.

Do your symptoms follow your menstrual cycle?

Our allergy specialists can review the timing of your symptoms, hormonal exposures and previous reactions
and advise whether further investigation is appropriate.


Book an allergy consultation

Frequently asked questions

Is autoimmune progesterone dermatitis a true allergy?

It is a hypersensitivity disorder. Some patients appear to have an immediate, potentially IgE-mediated
reaction, while others may have delayed immune mechanisms. The exact biology is not fully understood.

Can progesterone allergy cause anaphylaxis?

Yes, although it is rare. Progesterone-induced anaphylaxis has been reported after natural hormonal rises
and after progesterone medicines, including fertility treatment.

Can a progesterone skin test confirm the diagnosis?

A positive test can support the diagnosis, but it cannot confirm the condition on its own. False-positive
and false-negative results occur, and test methods vary between centres.

Can symptoms occur without previous use of hormonal contraception?

Yes. Some patients react to progesterone produced naturally after ovulation and have never knowingly used
an external progestogen.

Should I stop my contraceptive pill or fertility medication?

Do not stop prescribed hormonal treatment without speaking to the clinician responsible for your care.
Sudden changes may affect contraception, fertility treatment or other medical needs.

Clinical summary

Autoimmune progesterone dermatitis or progestogen hypersensitivity should be considered when
allergic or inflammatory symptoms recur in a predictable relationship with the menstrual cycle or
hormonal treatment.
Urticaria and itching are common, but presentations range from eczema and
mucosal lesions to angioedema and anaphylaxis. Diagnosis is primarily clinical because current testing is
imperfect. Treatment may include symptom control, ovulation suppression, biological therapy or specialist
desensitisation.

Medical disclaimer: This article is for general information and does not replace
individual medical advice. Seek urgent medical help for breathing difficulty, throat swelling, collapse
or suspected anaphylaxis.

References

  1. Bornsztein NT, Grabarz A, Rapozero AL, et al. Autoimmune progesterone dermatitis: diagnostic relevance
    and epidemiological analysis of 13 cases. Rev Bras Ginecol Obstet. 2026;48:e-rbgo30.
  2. Bumbăcea RS, Băloiu DA, Vintilă MR, et al. When Hormones Attack: A Literature Review of
    Progesterone-Induced Anaphylaxis. Current Allergy and Asthma Reports. 2026;26(1):24.
  3. Mittal S, Aghazadeh Mohandesi N, Divekar R, et al. Cyclical Rash Unveiled – Progestogen
    Hypersensitivity. Mayo Clinic Proceedings. 2026.
  4. Bui VK, Cao TT, Nguyen HN. Anaphylaxis due to progesterone hypersensitivity: a rare cause of recurrent
    anaphylaxis. Asia Pacific Allergy. 2026;16(2):138–140.
  5. AlSulami M, Alharbi JK, Alzahrani A, et al. Autoimmune Progesterone Dermatitis: A Case Report and Review
    of Literature. Cureus. 2026;18(4):e106760.
  6. Chiarella SE, Buchheit KM, Foer D. Progestogen hypersensitivity.
    J Allergy Clin Immunol Pract. 2023;11(12):3606–3613.e2.


Allergy Safety in Schools 2026: New DfE Guidance Explained













Allergy News & Guidance

New Statutory Guidance on Allergy Safety in Schools: What Parents and Schools Need to Know

Published 6 July 2026 by the Department for Education | Applies to England

New statutory allergy safety guidance for schools in England 2026, highlighting school allergy policies, staff training and Individual Healthcare Plans for pupils with allergies.

The Department for Education’s 2026 statutory guidance introduces new requirements for allergy safety in schools, including allergy policies, staff training and Individual Healthcare Plans (IHPs).

For the first time, schools in England now have statutory guidance on allergy safety, published by the Department for Education (DfE) on 6 July 2026. If your child lives with a food allergy or other allergic condition, this is a significant step towards safer classrooms, playgrounds and lunch halls. Here’s what the new guidance means, and how our allergy clinic can help your family and school meet it.

What Is the Allergy Safety in Schools Guidance?

The new guidance sets out what schools must do to support pupils with allergies. It applies to governing bodies of local-authority-maintained schools (including special schools), pupil referral units, and academies and free schools. Independent schools are not yet required to follow it, though the government has signalled it intends to bring allergy safety requirements into their regulatory standards too.

Key Requirements for Schools

Under the statutory guidance, schools must:

  • Create and publish an allergy safety policy — a clear, written approach to preventing and managing allergic reactions on site.
  • Provide allergy safety training for all staff — not just first-aiders, so that everyone knows how to recognise and respond to a reaction.
  • Identify pupils who need an Individual Healthcare Plan (IHP) — a personalised plan for managing a child’s allergy day to day.
  • Record and learn from serious incidents and near misses — so schools can continuously improve safety, not just react after an emergency.

The DfE has also released two supporting resources: an allergy safety policy template and an Individual Healthcare Plan template, along with guidance on record-keeping and training for the use of adrenaline auto-injectors (AAIs) in schools.

Why This Matters

Food allergies and anaphylaxis are a daily reality for many families, and school is often where a child spends the most time away from home. Clear policies, trained staff and a well-completed Individual Healthcare Plan can make the difference between a close call and a genuine emergency. This guidance gives schools a consistent, structured framework to work from rather than leaving allergy management to chance or to individual school policy alone.

How We Can Help

Our allergy clinic supports both families and schools in putting this guidance into practice. We can help with:

  • Completing an accurate, medically-informed Individual Healthcare Plan for your child
  • Confirming allergy diagnoses through proper testing, so IHPs are based on solid clinical evidence
  • Advising on adrenaline auto-injector prescriptions, technique and in-date supply for school
  • Providing letters and clinical summaries schools can use to inform their allergy safety policy
  • Guidance for school staff on recognising and responding to allergic reactions

Book an appointment: If your child has a suspected or diagnosed allergy and you’d like help preparing for the new school year under this guidance, get in touch with our clinic team today. We’ll work with you to make sure your child’s Individual Healthcare Plan is ready, current and school-approved.

Useful Resources

This article is for general information only and does not replace individual medical advice. Speak to our clinical team about your child’s specific allergy management needs.


Urticaria Allergic rhinitis Mental health

ACARE & UCARE Accredited Centre

Mind, Mucosa and Skin

How chronic urticaria, allergic rhinitis and psychological wellbeing can affect one another

At the London Allergy and Immunology Centre, we take a whole-person view of allergy care. New research highlights that chronic spontaneous urticaria, nasal allergy symptoms and emotional wellbeing are often closely connected. This matters because better understanding of this link can help patients access more complete and effective care.

The link between chronic urticaria hives, allergic rhinitis symptoms and psychological stress in allergy patients

The connection between chronic urticaria, allergic rhinitis and psychological stress affecting overall wellbeing.

Why this matters for patients with allergy and urticaria

Chronic spontaneous urticaria, often called CSU, is more than a skin rash. It can disrupt sleep, affect confidence, interfere with work and family life, and create constant uncertainty because symptoms may flare without warning. When allergic rhinitis is also present, the burden can become even greater. Nasal blockage, sneezing, poor sleep and persistent irritation may add to fatigue and emotional strain.

A 2026 study explored this triad of mind, mucosa and skin and showed that psychiatric comorbidities were very common among adults with antihistamine-refractory CSU receiving omalizumab. The findings support a more integrated model of care in which allergy, skin symptoms, sleep and mental wellbeing are considered together rather than separately.

What is chronic spontaneous urticaria?

Urticaria is characterised by itchy raised wheals, angioedema, or both. When symptoms persist for more than 6 weeks, the condition is defined as chronic urticaria. If the rash and swelling occur without a clear external trigger, it is called chronic spontaneous urticaria.

Many patients improve with antihistamines, but some continue to have frequent symptoms despite treatment. In these more difficult cases, specialist assessment is important to confirm the diagnosis, identify associated conditions, assess disease activity properly and consider advanced treatment options such as omalizumab where appropriate.

Common features of CSU
– Recurrent itchy wheals
– Swelling of the lips, eyelids, hands or other areas
– Symptoms lasting longer than 6 weeks
– Unpredictable flare-ups
– Sleep disturbance and reduced quality of life

What did the 2026 study find?

The study reviewed 72 adults with antihistamine-refractory CSU who received omalizumab and had a formal psychiatric evaluation at a tertiary allergy centre between 2015 and 2025. Most participants were female, with a median age of 45 years. Psychiatric diagnoses were identified in 90.3% of the cohort who underwent psychiatric assessment.

The most frequent psychiatric diagnostic group was anxiety disorders, followed by mood disorders and sleep-wake disorders. Generalised anxiety disorder was the single most common diagnosis. The authors also reported that allergic rhinitis was present in more than half of the cohort, suggesting an important upper-airway allergic burden in this patient group.

Study finding Result
Patients included 72 adults with antihistamine-refractory CSU treated with omalizumab
Female participants 70.8%
Median age 45 years
Any psychiatric comorbidity 90.3%
Most common psychiatric group Anxiety disorders
Allergic rhinitis in the cohort 51.4%

The stress-skin connection in chronic urticaria

Patients often tell us that stress seems to aggravate their hives. This fits with what clinicians and researchers have observed for many years. Chronic urticaria can itself be stressful because flare-ups are unpredictable and visible. At the same time, stress may influence inflammatory pathways, itch perception and symptom severity, which can then further increase anxiety and distress. This creates a self-perpetuating cycle.

The 2026 paper describes this as a close interaction between psyche and skin. Biological pathways thought to be involved include stress-related neuroimmune signalling and mast cell-mediated inflammation. For patients, the important message is simple: the symptoms are real, the burden is real, and both the physical and emotional impact deserve proper attention.

This does not mean urticaria is “just stress”. Rather, it means stress, sleep problems, allergy symptoms and inflammation may all affect one another. That is why good management often requires more than a prescription alone.

Response to treatment in the study

Under omalizumab treatment, disease control improved significantly in this cohort. Median UAS7 scores fell from 42 before treatment to 7 at 24 months, while UCT scores rose from 0 to 14. These results support the role of specialist treatment in patients whose symptoms remain poorly controlled on antihistamines alone.

The authors also noted that improving urticaria control may bring psychological benefits and better emotional wellbeing. In practice, this reinforces the importance of identifying uncontrolled disease early and ensuring that patients receive an expert review rather than simply repeating ineffective treatment.

What this means for care at our ACARE and UCARE accredited centre

As an ACARE and UCARE accredited centre, we believe patients with chronic urticaria deserve expert, evidence-based and compassionate care. This includes careful diagnosis, assessment of angioedema and inducible triggers, review of coexisting allergic diseases such as allergic rhinitis and asthma, and evaluation of how symptoms are affecting sleep, mood and daily functioning.

Where appropriate, management may involve optimisation of antihistamines, consideration of advanced treatment pathways, investigation of associated conditions and practical support around trigger awareness, sleep hygiene and stress reduction. In some cases, collaboration with other professionals may be helpful so that care is truly patient-centred and holistic.

For patients, the key message is that severe hives and swelling are not only skin symptoms. They can affect confidence, sleep, relationships and quality of life. Recognising that full burden is an important step towards better outcomes.

When to seek specialist urticaria assessment

– Your hives or swelling have lasted longer than 6 weeks
– Symptoms keep returning despite antihistamines
– You have troublesome angioedema
– Sleep is regularly disturbed by itch or nasal symptoms
– You feel that stress, anxiety or low mood are making symptoms harder to manage
– You may have both urticaria and allergic rhinitis

Book an expert review

If you are living with chronic hives, angioedema or allergic rhinitis, our specialist team can help assess the full picture and create a personalised plan. We offer consultant-led allergy care with a focus on accurate diagnosis, better symptom control and improved quality of life.

Book an appointment

Reference

This article is based on the 2026 paper by Zeynep Yegin Katran, İsmet Bulut, Andaç Salman, Ali Baz, Galip Muzaffer Kürşat Küçükali and Özge Argın, which examined the relationship between chronic spontaneous urticaria, allergic rhinitis and psychiatric comorbidities in omalizumab-treated adults.

Please note that this blog is for general education and does not replace personalised medical advice. Diagnosis and treatment should always be based on an individual clinical assessment.

Adrenaline nasal spray inserted into a person’s nostril, with a semi-transparent side view revealing the nasal cavity and fine particles dispersing inside

Intranasal Adrenaline: The Needle-Free Revolution in Anaphylaxis Treatment

A nasal spray that delivers the same life-saving medication as an injection — no needles, no fear, no complicated technique. Here is everything you need to know about intranasal adrenaline, backed by the latest medical evidence.

Updated February 2026  |  Evidence-based guide for patients & carers

Adrenaline nasal spray inserted into a person’s nostril, with a semi-transparent side view revealing the nasal cavity and fine particles dispersing inside

Adrenaline nasal spray being administered into the nasal passage, highlighting the internal structures and distribution of particles

Imagine being at a restaurant when a friend with a severe food allergy suddenly develops anaphylaxis — their throat tightening, skin erupting in hives, blood pressure plummeting. You reach for their emergency medication, but it is a needle-based auto-injector. If you or your friend have a fear of needles, hesitation in those crucial seconds could be fatal.

That scenario has driven decades of research into alternative ways to administer adrenaline, the only first-line medication proven to reverse a severe allergic reaction. In August 2024, the U.S. Food and Drug Administration (FDA) approved the first-ever nasal spray formulation of adrenaline for the emergency treatment of anaphylaxis — a milestone described by allergists worldwide as a potential game-changer for patient safety.

In Europe, the picture is evolving rapidly. The European Medicines Agency approved the first nasal spray formulation of adrenaline in August 2023, and the UK’s Medicines and Healthcare products Regulatory Agency (MHRA) followed with its own approval in July 2025 — making the UK the first country in the region to license a needle-free emergency treatment for anaphylaxis.

As in the US, allergists and patient advocates across Europe have welcomed the development as a significant step forward for people who struggle with auto-injectors due to needle phobia, dexterity issues, or the stress of an acute allergic reaction — though clinicians stress that decisions about which formulation is most appropriate should be made on an individual basis.

This article explains what intranasal adrenaline is, what the science says, who it is designed for, and what it means for people living with severe allergies.

~5%
of people in the US have experienced anaphylaxis at some point in their lives
225+
deaths per year in the US are attributed to anaphylaxis
~52%
of adults with severe food allergy have actually been prescribed an adrenaline auto-injector

What Is Anaphylaxis — And Why Does Timing Matter So Much?

Anaphylaxis is a severe, potentially life-threatening allergic reaction. It can be triggered by foods (such as peanuts, tree nuts, shellfish, or milk), insect stings, medications, latex, and sometimes exercise. The reaction is rapid — symptoms can escalate within minutes — and involves multiple organ systems simultaneously: the skin, airway, circulatory system, and gastrointestinal tract.

The World Allergy Organization estimates that anaphylaxis occurs globally at a rate of 50 to 112 episodes per 100,000 people per year, and among high-risk individuals, recurrence rates range from 26% to 54%. Despite how common it is, anaphylaxis is consistently under-treated, particularly in out-of-hospital settings. Delayed or absent adrenaline administration is the most common factor in anaphylaxis-related deaths.

“Delayed administration of adrenaline can lead to more severe outcomes such as prolonged reactions, hypotension, and increased mortality.”
— Emergency Medicine Research & Analysis, 2025

Adrenaline counters anaphylaxis by constricting blood vessels, relaxing the airways, reducing hives and swelling, and stimulating the heart. It works within minutes and remains the only medication endorsed as first-line treatment by every major international allergy guideline, including those from the World Allergy Organization, the European Academy of Allergy and Clinical Immunology (EAACI), and the American Academy of Allergy, Asthma & Immunology (AAAAI).

The Problem With Traditional Auto-Injectors

For decades, the standard method of emergency adrenaline delivery has been the auto-injector — a spring-loaded device that injects the medication intramuscularly (usually into the outer thigh). Auto-injectors are highly effective, but they come with real-world barriers that have always troubled clinicians and patients alike.

Common barriers to auto-injector use

  • Needle phobia — one of the most frequently cited reasons for hesitation
  • Fear of accidentally injuring someone (especially in bystander situations)
  • Needle length variability: in patients with obesity, the needle may not reach the muscle
  • Risk of incorrect technique under panic conditions
  • Relatively short shelf life; must be stored at specific temperatures
  • High cost and barriers to access in some countries
  • Inconvenient size and shape — many patients leave them at home

A 2022 US survey found that approximately 36% of adults with severe food allergy believed adrenaline auto-injectors could cause life-threatening side effects — a misconception that leads to dangerous hesitation. Meanwhile, researchers have long observed that needle phobia is widespread, and that parents in particular are reluctant to inject a child or a loved one.

These barriers have directly motivated the search for a needle-free alternative that can deliver adrenaline rapidly, reliably, and without any injection technique at all.

How Does Intranasal Adrenaline Work?

The nasal route has been used for decades to deliver medications — from decongestants to hormone therapies — because the nasal mucosa is richly supplied with blood vessels and can absorb drugs quickly into the systemic circulation.

Intranasal adrenaline is delivered as a fine spray directly into one nostril. The medication crosses the nasal lining into the bloodstream without any injection. Clinical research shows that when the correct formulation is used, the speed of absorption is comparable to — and in some formulations, faster than — intramuscular injection.

A 2025 systematic review presented at the European Emergency Medicine Congress (Vienna) analysed five clinical studies comparing intranasal and intramuscular adrenaline. The researchers found that intranasal adrenaline achieved its peak plasma concentration in 2.5 to 30 minutes, compared to 9 to 45 minutes for the intramuscular route — suggesting that, depending on the formulation and individual nasal characteristics, the nasal spray can reach the bloodstream at least as rapidly, and sometimes more rapidly.

“Nasal sprays could become a suitable and equally effective needle-free alternative to the EpiPen, which is the current treatment for anaphylaxis.”
— Dr. Danielle Furness, University of Buckingham, European Emergency Medicine Congress 2025

What the Clinical Evidence Shows

The FDA’s 2024 approval of the first intranasal adrenaline product was supported by rigorous pharmacokinetic and clinical trial data. Here is what current medical research tells us:

Comparable effectiveness to injection

A landmark Phase 3 prospective trial showed that all 15 participants who received intranasal adrenaline during an oral food challenge responded successfully to a single dose, with no requirement for a second dose to control the reaction. Separate real-world data collected from over 500 patients treated by clinicians in the United States showed an approximately 89% success rate with a single dose — a figure that closely matches the historic success rates of intramuscular injection and autoinjectors across published meta-analyses.

Faster or comparable absorption

Pharmacokinetic studies have consistently shown that well-formulated intranasal adrenaline achieves plasma levels similar to or higher than intramuscular adrenaline. The 2025 dose-optimisation study published in the Journal of Allergy and Clinical Immunology: Global confirmed that nasal powder formulations in particular enable fast, high absorption within the short therapeutic window critical for anaphylaxis treatment.

Interestingly, nasal congestion does not appear to be a barrier

One concern researchers initially raised was whether nasal congestion — common during an allergic reaction — might reduce absorption. However, clinical studies have actually observed that nasal congestion can enhance adrenaline absorption through the nasal mucosa, likely due to increased local blood flow, addressing a key theoretical concern about the nasal route.

Well-tolerated safety profile

Published research in peer-reviewed journals has consistently described intranasal adrenaline as well tolerated. The side effect profile mirrors that of injected adrenaline (such as transient increase in heart rate and mild anxiety) but avoids injection-site pain, bruising, and the risk of inadvertent intravenous injection. A 2024 review in the Journal of Allergy and Clinical Immunology found no evidence of severe adverse reactions specific to the nasal route.

Effective for children and adults

A 2025 review published in Current Opinion in Allergy and Clinical Immunology specifically examined the evidence for intranasal adrenaline in the paediatric setting. The authors concluded that it represents a “promising, well-tolerated option that could significantly improve the accessibility and effectiveness of anaphylaxis management” in children — a population where needle fear is particularly acute and accurate injection technique especially difficult to achieve under stress.

Intranasal Adrenaline vs. Auto-Injector: A Quick Comparison

Feature Intranasal Spray Auto-Injector (Injection)
Delivery method Nasal spray — no needles Intramuscular injection (thigh)
Needle required No Yes
Speed of absorption 2.5–30 min (comparable or faster) 9–45 min
Ease of use under stress High — single-step nose spray Moderate — requires correct technique
Needle phobia barrier Eliminated Significant for many patients
Body weight variability Not affected by adipose tissue Needle may not reach muscle in obese patients
FDA-approved for anaphylaxis Yes (2024, adults & children ≥30 kg) Yes (long-established)
Suitable as first-line treatment Yes — per 2024 GA²LEN consensus Yes — longstanding first-line standard

Who Can Use Intranasal Adrenaline?

Following FDA approval in August 2024, intranasal adrenaline is indicated for the emergency treatment of Type 1 allergic reactions, including anaphylaxis, in adults and children weighing at least 30 kilograms (approximately 66 pounds). It is intended for use as an emergency rescue treatment — not a preventive or routine medication.

The approved dosing protocol (per the 2024 GA²LEN anaphylaxis consensus tool) is one spray (2 mg adrenaline) into one nostril. If symptoms do not improve or worsen after 5 minutes, a second dose may be administered in the same nostril using a new spray device.

⚠ Important: Call emergency services immediately

Intranasal adrenaline — like all forms of emergency adrenaline — is a bridge to definitive medical care, not a substitute for it. Anyone who receives adrenaline for anaphylaxis must be taken to an emergency department immediately, even if they feel better. Biphasic reactions (a second wave of symptoms hours later) can occur without warning. Always call emergency services as soon as possible.

What Do Current Allergy Guidelines Say?

The 2024 GA²LEN Anaphylaxis Consensus Report — a major international agreement involving multiple allergy organisations — formally incorporated intranasal adrenaline into its anaphylaxis clinical support tool alongside intramuscular auto-injectors. This reflects a significant shift in global medical thinking.

The Resuscitation Council UK’s updated anaphylaxis evidence review (2025) continues to establish adrenaline as the unambiguous first-line treatment for anaphylaxis, and notes the evolving evidence base for needle-free delivery methods. Researchers in the UK have called for intranasal adrenaline to be incorporated into national guidelines “once strong, real-world evidence supports its safety and effectiveness” — with initial rollout to include close monitoring and systematic outcome reporting.

The EAACI (European Academy of Allergy and Clinical Immunology), which last updated its major anaphylaxis guidelines in 2021, is expected to incorporate needle-free alternatives in forthcoming revisions as real-world evidence continues to accumulate.

Why This Matters for Everyday People With Allergies

For patients and their families, the practical implications of a nasal spray option are significant. Consider the following scenarios where intranasal delivery could be transformational:

Children at school: Teachers and school staff are sometimes reluctant to use an auto-injector on a child experiencing anaphylaxis, even with training, due to fear of the needle. A nasal spray could be easier to administer confidently by non-medical personnel in an emergency.

Adolescents managing their own allergy: Teenagers are a high-risk group for anaphylaxis fatalities precisely because they often fail to carry or use their adrenaline auto-injector. A spray that fits in a pocket and involves no needle may meaningfully improve adherence.

Bystanders at public events: In out-of-hospital settings — restaurants, airports, sporting venues — the likelihood of a willing bystander using an auto-injector on a stranger is low. The nasal route dramatically lowers the psychological barrier to intervention.

Patients with obesity: Studies have shown that standard auto-injector needle lengths may fail to reach the muscle in patients with greater adipose tissue, resulting in subcutaneous rather than intramuscular delivery. The nasal route is unaffected by body composition.

Are There Any Limitations or Concerns?

While the evidence is encouraging, researchers and clinicians urge balanced perspective. Intranasal adrenaline is a powerful advance, but several areas warrant ongoing attention:

Weight restriction: The current approval covers patients weighing at least 30 kilograms. Smaller children — including infants and toddlers, who are a particularly high-risk group — cannot yet use the approved product, and different dosing considerations apply.

Real-world evidence is still maturing: Although the real-world data collected in 2025 from over 500 patients is highly encouraging, the clinical trials supporting approval included relatively small populations. Larger post-market studies will be important to confirm long-term safety and effectiveness across diverse patient groups.

Not a replacement for medical education: Patients and carers still need clear instruction on when and how to use any adrenaline device, whether injection or nasal spray. Training and anaphylaxis action plans remain essential.

Access and cost: As a recently approved product in the United States, insurance coverage and affordability may vary. International regulatory approvals are still pending in many countries.

What Should You Do If You or Someone You Know Has Severe Allergies?

Whether you opt for an auto-injector, an intranasal spray, or carry both, the single most important principle remains unchanged: adrenaline must be accessible, and you must know how to use it. Here are steps every person with a serious allergy — or anyone who cares for one — should take:

Practical steps for people at risk of anaphylaxis

  • Discuss all available adrenaline options with your allergist or GP, including intranasal sprays
  • Always carry your prescribed emergency adrenaline — and ensure it has not expired
  • Have a written anaphylaxis action plan and share it with family, school, and workplace
  • Know the early signs of anaphylaxis: hives, throat tightening, dizziness, vomiting, difficulty breathing
  • Use adrenaline at the first sign of anaphylaxis — do not wait to see if antihistamines work
  • Call emergency services (999 / 112 / 911) immediately after giving adrenaline
  • Go to hospital even if symptoms improve — biphasic reactions can occur hours later
  • Review and practise your adrenaline technique or spray technique regularly

The Bottom Line

Intranasal adrenaline represents one of the most meaningful advances in allergy emergency medicine in a generation. For the first time, patients and bystanders have access to an FDA-approved, needle-free option to treat a life-threatening allergic reaction — one that the latest clinical evidence shows to be at least as effective as traditional injection for adults and most children.

It will not replace conventional auto-injectors overnight, and the global medical community rightly calls for further real-world evidence and guideline integration. But for the millions of people who carry adrenaline every day — and the many more who do not carry it at all — this innovation has the potential to save lives that might otherwise be lost to hesitation, needle phobia, or simply not having the device at hand.

Speak to your doctor or allergist to find out whether intranasal adrenaline is the right option for you or your child. The most important thing is that when anaphylaxis strikes, you are prepared — and ready to act.


Sources & Further Reading

  1. Crescioli G, et al. “Adrenaline nasal spray for the treatment of anaphylaxis: perspectives in paediatrics.” Current Opinion in Allergy and Clinical Immunology. 2025;25(6):511–517.
  2. Ebisawa M, Muraro A, Worm M, et al. “Optimizing Adrenaline Administration in Anaphylaxis: Clinical Practice Considerations and Safety Insights.” Clinical and Translational Allergy. 2025;15(8):e70085.
  3. Furness D, et al. Systematic literature review on intranasal vs intramuscular adrenaline for anaphylaxis. Presented at: European Emergency Medicine Congress; September 2025; Vienna, Austria.
  4. Lapidot T, Tal Y, Megiddo D, et al. “First-in-class intranasal adrenaline spray for anaphylaxis: Dose finding clinical study.” Journal of Allergy and Clinical Immunology: Global. 2025;4(3):100487.
  5. Campbell RL, et al. “Anaphylaxis definition, overview, and clinical support tool: 2024 consensus report — a GA²LEN project.” Journal of Allergy and Clinical Immunology. 2025. doi:10.1016/j.jaci.2025.00072.
  6. U.S. Food and Drug Administration. “FDA approves first nasal spray for treatment of anaphylaxis.” August 2024. fda.gov
  7. Cardona V, Ansotegui IJ, Ebisawa M, et al. “World Allergy Organization Anaphylaxis Guidance 2020.” World Allergy Organization Journal. 2020;13(10):100472.
  8. Dodd A, et al. “Evidence update for the treatment of anaphylaxis.” Resuscitation. Resuscitation Council UK, 2025.

Medical disclaimer: This article is written for general information purposes only and does not constitute medical advice. The information presented reflects peer-reviewed literature and publicly available guidelines available as of early 2026. Always consult a qualified healthcare professional — such as your GP, allergist, or emergency physician — before making decisions about your treatment or your child’s treatment. In an emergency, always call your local emergency services.

 

© 2026 · Evidence-based health content for the general public · Always consult a qualified medical professional for personal health advice.

 

New Gut Mast Cells Mediator for Severe Food Allergic Reactions

Scientists Discover a New Gut Mast Cell Mediator for Severe Food Allergic Reactions

A groundbreaking study published in Science has identified a previously underappreciated biological pathway behind severe food allergy reactions and anaphylaxis.

Gut mast cells linked to severe food allergy and anaphylaxis through leukotriene release

Gut mast cells and leukotriene release in severe food allergy and anaphylaxis.

Researchers discovered that specialised mast cells in the gut lining can trigger life-threatening allergic reactions through powerful inflammatory chemicals – even before allergens enter the bloodstream.

The research, available via PubMed Central, helps explain why swallowing even a tiny amount of a food allergen can rapidly cause whole-body symptoms.


Why This Discovery Matters for Severe Food Allergy

Food allergies affect millions of people in the UK and worldwide. In susceptible individuals, exposure to even trace amounts of allergenic food can trigger anaphylaxis — a medical emergency characterised by:

  • Difficulty breathing
  • Swelling of the throat or tongue
  • A sudden drop in blood pressure
  • Dizziness or fainting
  • Skin reactions such as urticaria (hives)

Although the mechanisms behind injected or inhaled allergen reactions are well described, the biological pathways driving gut-initiated anaphylaxis have remained poorly understood.

Key scientific question: What initiates systemic anaphylaxis when an allergen is eaten?


The Role of Gut Mast Cells in Food-Induced Anaphylaxis

Mast cells are tissue-resident immune cells central to IgE-mediated allergic reactions. Upon allergen exposure, IgE antibodies cross-link on the mast cell surface, triggering rapid mediator release.

The study demonstrates that intestinal mast cells differ significantly from mast cells found in the skin or lungs.

Distinct Characteristics of Intestinal Mast Cells

  • Reside directly within the intestinal epithelial layer
  • Are shaped by signals from surrounding gut epithelial cells
  • Produce comparatively lower levels of histamine
  • Generate substantially higher levels of leukotrienes

This unique gut mast cell phenotype suggests that food-triggered allergic reactions follow a distinct biological pathway compared with parenteral allergen exposure.


Leukotrienes – A Major Driver of Severe Food Allergy Reactions

Leukotrienes are lipid-derived inflammatory mediators synthesised via the 5-lipoxygenase pathway. They are well recognised in asthma for promoting airway narrowing, vascular permeability, and tissue inflammation.

The study found that during food-induced anaphylaxis:

  • Leukotrienes are dominant mediators of systemic reaction severity
  • Pharmacological blockade of leukotriene synthesis significantly reduced severe reactions in experimental models
  • Antihistamines alone were less effective in preventing systemic symptoms

By contrast, allergic reactions triggered by injected allergens relied more heavily on histamine release.

This may explain why antihistamines are often insufficient in preventing severe food allergy reactions.


How Food-Induced Anaphylaxis May Begin in the Gut

Based on the experimental findings, researchers propose the following mechanism:

  1. A food allergen is ingested
  2. The allergen crosses the intestinal epithelial barrier
  3. IgE antibodies activate mast cells within the gut lining
  4. Gut mast cells release large quantities of leukotrienes
  5. Systemic inflammation develops, leading to anaphylaxis

This model reframes severe food allergy as a gut-initiated immune event rather than purely a circulating allergic response.


Why Some Food Allergy Reactions Are More Severe

The research suggests that severity of food-induced anaphylaxis may depend on:

  • Mast cell density within the intestinal mucosa
  • Magnitude of leukotriene production
  • Integrity of the intestinal barrier
  • Local immune and epithelial signalling pathways

These biological variables may explain why some individuals experience mild oral symptoms while others develop life-threatening systemic reactions.


Implications for Future Food Allergy Treatment

An important clinical implication is that leukotriene-targeting medications already exist and are widely used in asthma management.

In experimental models:

  • Blocking leukotriene pathways significantly reduced reaction severity
  • Combined targeting of histamine and leukotrienes may offer enhanced protection

However:

  • Current evidence is largely based on animal models
  • Human clinical trials are required
  • Standard management guidelines remain unchanged

Patients with diagnosed severe food allergy must continue to:

  • Avoid known trigger foods
  • Carry adrenaline auto-injectors at all times
  • Seek urgent medical attention if symptoms occur

The Gut as a Central Immune Organ in Allergy

This discovery reinforces the concept that the intestine functions as a major immune organ. Constant exposure to dietary proteins and microbes requires careful immune regulation. When tolerance mechanisms fail, severe food allergic reactions may result.

Understanding the role of gut mast cells and leukotrienes in food-induced anaphylaxis may transform future approaches to risk prediction, prevention, and targeted therapy.


Key Take-Home Messages

  • Gut mast cells play a central role in severe food allergy
  • Leukotrienes — not just histamine — drive food-induced anaphylaxis
  • Targeting leukotriene pathways represents a promising therapeutic strategy
  • Current emergency management recommendations remain essential

This research provides a major step forward in understanding the biological mechanisms underlying life-threatening food allergic reactions.

baked-milk-oral-immunotherapy-cows-milk-allergy

Baked Milk Oral Immunotherapy: A New Advance in Cow’s Milk Allergy Treatment

Cow’s milk allergy (CMA) is one of the most common food allergies in children and can have a significant impact on daily life, nutrition, and family wellbeing. Strict milk avoidance is challenging, as milk proteins are present in many everyday foods, particularly baked products.A randomised clinical trial published in January 2025 has provided encouraging evidence that baked milk oral immunotherapy (BMOIT) may offer a safer and effective treatment option for selected patients with cow’s milk allergy.

At London Allergy and Immunology Centre, we closely monitor emerging research to ensure our patients benefit from the most up-to-date, evidence-based allergy care.

What Is Baked Milk Oral Immunotherapy (BMOIT)?

Oral immunotherapy (OIT) is a treatment approach designed to desensitise the immune system by exposing patients to very small, gradually increasing amounts of an allergen under specialist supervision.

Baked milk oral immunotherapy for cow’s milk allergy: a UK doctor consulting a mother and child, child drinking baked milk, immune system changes with IgE and IgG4 antibodies, desensitisation from baked milk to fresh milk, London landmarks in the background, and icons for safety, improved quality of life, and research insights

Baked milk oral immunotherapy (BMOIT) helps children with cow’s milk allergy build tolerance safely, guided by a UK allergy consultant, with immune system changes and improved quality of life

Baked milk OIT differs from traditional milk OIT because it uses milk that has been extensively heated, such as milk baked into muffins or cakes. Heating changes the structure of milk proteins, making them less allergenic while still capable of training the immune system to tolerate milk.

Many children with cow’s milk allergy can already tolerate baked milk, even if they react to fresh milk. This makes baked milk an attractive starting point for immunotherapy.

Key Findings From the January 2025 Study

The study, titled “Clinical and immunological outcomes after randomized trial of baked milk oral immunotherapy for milk allergy”, followed children aged 3 to 18 years with confirmed cow’s milk allergy.

  • Baked milk OIT was well tolerated, with most reactions being mild
  • 70% of participants achieved desensitisation to baked milk
  • 37% also developed tolerance to unheated (fresh) milk
  • No severe allergic reactions were reported during treatment

These findings suggest that baked milk oral immunotherapy may safely increase milk tolerance while reducing the risks often associated with traditional milk OIT.

How Does Baked Milk OIT Affect the Immune System?

In addition to clinical outcomes, researchers analysed immune markers to understand how tolerance develops during baked milk OIT.

  • Reduction in milk-specific IgE antibodies, which trigger allergic reactions
  • Increase in IgG4 antibodies, associated with immune tolerance
  • Favourable changes in immune cells involved in regulating allergic inflammation

These immunological changes confirm that baked milk OIT actively modifies the allergic immune response rather than simply masking symptoms.

Why This Research Matters for Families

Living with cow’s milk allergy can lead to anxiety about accidental exposure, nutritional concerns, and social challenges at school, childcare, and family events.

Baked milk oral immunotherapy may help by:

  • Increasing safety margins against accidental milk exposure
  • Expanding dietary options
  • Improving quality of life for children and their families

While not every patient is suitable for oral immunotherapy, this approach offers new hope for carefully selected individuals.

Is Baked Milk Oral Immunotherapy Available?

Baked milk oral immunotherapy should only be performed under specialist medical supervision. It is not suitable for all patients with cow’s milk allergy and requires careful assessment, monitoring, and long-term follow-up.

At London Allergy and Immunology Centre, we assess each patient individually to determine whether oral immunotherapy, including baked milk protocols, is appropriate and safe.

Expert Care at London Allergy and Immunology Centre

We specialise in the diagnosis and management of food allergies, including cow’s milk allergy, using the latest diagnostic tools and evidence-based treatments.

  • Comprehensive allergy assessments
  • Supervised food challenges
  • Personalised allergy management plans
  • Expert advice on emerging treatments such as oral immunotherapy

If your child has a cow’s milk allergy and you would like to explore current or future treatment options, our specialist team is here to help.

To book a consultation, please contact London Allergy and Immunology Centre.


This article is for educational purposes only and does not replace individual medical advice.

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Eczema and multiple food allergies

Early Eczema and Food Allergy Risk in Children: 2026 Medical Insights for Parents and Clinicians

The relationship between eczema (atopic dermatitis) and food allergies in children is one of the most important areas in modern allergy prevention. New research published in 2025, supported by emerging 2026 data, shows that the age at which eczema begins plays a critical role in determining whether a child develops food allergies or respiratory allergic diseases.

Key takeaway: Eczema starting in early infancy significantly increases the risk of multiple food allergies, while later onset is more closely linked to asthma and hay fever.

Key Findings from Recent Research

A large study involving 1,309 children under 12 years with diagnosed food allergies provides strong evidence linking eczema timing to allergic outcomes:

  • 77% of children with food allergies had eczema
  • Over 80% developed eczema within the first year of life
  • Earlier onset strongly increases the likelihood of multiple food allergies
  • Eczema starting after 12 months reduces risk of multiple food allergies by 43%
  • Early-onset eczema is particularly associated with milk and egg allergy
Relationship between eczema onset and food allergy risk in children

Why Early-Onset Eczema Increases Food Allergy Risk

Recent advances in allergy science support the skin barrier hypothesis, which explains how eczema contributes to food allergy development. In infants, the skin acts as a critical protective barrier. When this barrier is disrupted, allergens can enter the body through the skin rather than through the digestive system.

Clinical insight: Allergen exposure through inflamed skin may lead to immune sensitisation, while early oral exposure may promote tolerance.

  • Impaired skin barrier allows allergens (e.g. milk, egg) to penetrate
  • Triggers IgE-mediated immune responses
  • Leads to higher risk of multiple food allergies
  • Strongly associated with filaggrin (FLG) gene mutations

Role of the Skin Microbiome (2026 Update)

Emerging 2026 research highlights the importance of the skin microbiome in eczema and allergy development. Children with eczema often show increased colonisation with Staphylococcus aureus, which can worsen inflammation and further damage the skin barrier.

  • Microbial imbalance increases skin inflammation
  • Promotes allergic sensitisation
  • May influence long-term immune development

Late-Onset Eczema and Respiratory Allergies

In contrast to early eczema, children who develop eczema after 12 months show a different allergic pattern:

  • Higher likelihood of developing asthma
  • Increased risk of allergic rhinitis (hay fever)
  • Less association with multiple food allergies

Interpretation: This suggests distinct allergic pathways, refining the traditional concept of the “atopic march”.

What This Means for Prevention (2026 Guidance)

Modern allergy guidelines emphasise early intervention for infants at high risk. Identifying eczema early provides an opportunity to reduce the likelihood of developing food allergies.

Recommended Strategies

  • Introduce allergenic foods early under medical supervision
  • Maintain consistent skin hydration using emollients
  • Treat eczema proactively to reduce inflammation
  • Seek specialist allergy assessment in moderate-to-severe cases
  • Monitor for early signs of food reactions

Important: Early identification of high-risk infants allows for targeted prevention strategies and improved long-term outcomes.

Summary

The timing of eczema onset is a powerful predictor of allergic disease patterns:

  • Early eczema (≤3 months): High risk of multiple food allergies
  • Later eczema (>12 months): Higher risk of asthma and hay fever

Recognising these patterns enables clinicians and parents to take proactive steps in preventing allergic disease progression.

Reference: Hussien H, Moore DL, Nimri S, et al. The age of eczema onset and multiple food allergies. Ann Allergy Asthma Immunol. Published online December 3, 2025.

 

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