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Patient-Reported Outcome Measures in Atopic Dermatitis and Chronic Urticaria: Why They Matter in Modern Allergy Care

Patient-Reported Outcome Measures in Atopic Dermatitis and Chronic Urticaria: Why They Matter in Modern Allergy Care

The management of chronic allergic skin conditions is evolving rapidly. Increasingly, healthcare professionals recognise that understanding how patients feel and function in daily life is just as important as measuring clinical signs and laboratory results. Patient-reported outcome measures (PROMs) are helping bridge this gap by bringing the patient’s voice directly into clinical decision-making.

Patient-reported outcome measures (PROMs) in atopic dermatitis and chronic urticaria, highlighting findings from the international UCARE ADCARE PROMUSE study and the role of patient-centred allergy care.

Patient-reported outcome measures help clinicians understand symptom burden, quality of life and treatment response in atopic dermatitis and chronic urticaria

What Are Patient-Reported Outcome Measures (PROMs)?

Patient-reported outcome measures (PROMs) are validated questionnaires completed by patients that assess symptoms, quality of life, treatment effectiveness and the overall impact of disease on everyday activities.

Unlike laboratory tests or physical examinations, PROMs capture the aspects of disease that only patients can truly describe. This is particularly important in conditions such as atopic dermatitis (eczema) and chronic urticaria (hives), where symptom severity, itching, sleep disruption and emotional wellbeing may fluctuate significantly between clinic visits.

PROMs help clinicians better understand the burden of disease, monitor treatment response and support shared decision-making between patients and healthcare professionals.

The PROMUSE Study: Understanding Why PROMs Are Underused

A landmark international study published in the World Allergy Organization Journal in 2026 investigated why PROMs remain underused in routine clinical practice despite their recognised value.

The PROMUSE study was conducted through the international UCARE (Urticaria Centres of Reference and Excellence) and ADCARE (Atopic Dermatitis Centres of Reference and Excellence) networks and involved physicians from specialised allergy and dermatology centres worldwide.

Importantly, Professor Michael Rudenko of the London Allergy and Immunology Centre was among the international co-authors contributing to this global collaboration examining the implementation of patient-centred outcome measures in allergic skin disease.

Key Findings

  • Many clinicians recognise the value of PROMs but face practical barriers to implementation.
  • Time constraints remain the most commonly reported challenge.
  • Many physicians believe patients dislike completing questionnaires.
  • Lack of integration into electronic health systems limits routine use.
  • Some clinicians feel PROMs may interfere with the doctor-patient relationship.
  • The greater the number of perceived barriers, the less likely physicians are to use PROMs regularly.

Interestingly, the study found that concerns regarding patient dissatisfaction and interference with clinical interactions were among the strongest factors associated with reduced PROM use.

Professor Michael Rudenko’s Clinical Perspective

As both a co-author of the PROMUSE study and a practising Consultant Allergist and Clinical Immunologist, I believe the findings highlight an important opportunity to improve patient-centred care in allergy and dermatology.

In everyday clinical practice, many patients experience symptoms that cannot be fully appreciated through examination alone. A patient with chronic urticaria may have minimal visible hives during a consultation but may have experienced severe symptoms throughout the preceding week. Similarly, a patient with atopic dermatitis may appear clinically improved while still suffering from significant itching, sleep disruption and reduced quality of life.

PROMs provide a structured way to capture these experiences and ensure they become part of the clinical conversation.

Importantly, PROMs should never replace clinical judgement or specialist assessment. Rather, they should complement traditional medical evaluation by helping clinicians understand the patient’s perspective more accurately.

The most effective PROMs are simple, relevant and easy to complete. They should focus on outcomes that matter most to patients while providing meaningful information that can guide treatment decisions.

Modern medicine is increasingly moving towards personalised and precision healthcare. In this context, understanding how a disease affects an individual’s daily life is becoming just as important as measuring objective disease activity.

Future developments are likely to include digital symptom tracking, integration with electronic health records, mobile health applications and more sophisticated patient-centred outcome measures developed with direct patient involvement.

Ultimately, successful allergy care requires both scientific expertise and a clear understanding of the patient’s lived experience. PROMs can help bridge that gap and support better outcomes for patients with chronic allergic diseases.

Professor Michael Rudenko MD PhD FAAAAI
Consultant Allergist and Clinical Immunologist
London Allergy and Immunology Centre

PROMs in Atopic Dermatitis

Atopic dermatitis affects millions of people worldwide and often causes substantial physical and psychological burden. Symptoms such as itching, sleep disturbance, skin pain, embarrassment and reduced self-confidence may significantly impact daily life.

PROMs help clinicians understand:

  • Severity of itching
  • Sleep quality
  • Impact on work and school performance
  • Emotional wellbeing
  • Treatment satisfaction
  • Long-term disease control

By incorporating patient-reported outcomes into routine care, clinicians can gain a more complete picture of disease burden and treatment effectiveness.

PROMs in Chronic Urticaria

Chronic urticaria is characterised by recurrent hives, swelling (angioedema) or both. Symptoms may fluctuate unpredictably and can have a major impact on quality of life.

Patient-reported outcome measures are particularly useful for:

  • Assessing symptom control over time
  • Evaluating treatment effectiveness
  • Monitoring disease activity between visits
  • Supporting treatment optimisation
  • Identifying patients who require escalation of therapy

Several validated urticaria-specific questionnaires are now widely used in clinical research and specialist practice.

The Future of Patient-Centred Allergy Care

The future of allergy and dermatology care will increasingly focus on combining clinical expertise with patient-reported outcomes, digital health technologies and shared decision-making.

The PROMUSE study suggests that while barriers remain, clinicians and healthcare systems have an opportunity to redesign PROM implementation in a way that is both efficient and meaningful for patients.

Importantly, future PROM development should involve patients directly, ensuring that questionnaires reflect the outcomes that matter most to those living with allergic disease.

When Should You See an Allergy Specialist?

You may benefit from specialist assessment if you experience:

  • Persistent eczema despite treatment
  • Chronic hives lasting longer than six weeks
  • Recurrent angioedema
  • Sleep disturbance caused by skin symptoms
  • Reduced quality of life due to allergic disease
  • Uncertainty regarding diagnosis or treatment options

A specialist allergy assessment can help establish an accurate diagnosis, optimise treatment and identify factors contributing to persistent symptoms.

References

Cherrez-Ojeda I, Robles-Velasco K, Giménez-Arnau A, et al. Why physicians underuse patient-reported outcomes in atopic dermatitis and chronic urticaria: Insights from the UCARE/ADCARE PROMUSE study. World Allergy Organization Journal. 2026;19:101398.

Additional references available upon request.

Advanced Systemic Mastocytosis Treatment London | KIT D816V Testing




London Allergy and Immunology Centre

Advanced Systemic Mastocytosis: Diagnosis, KIT D816V Testing and New Targeted Treatments

A specialist overview for patients and clinicians on advanced systemic mastocytosis, including C findings, molecular testing, avapritinib, midostaurin and emerging KIT D816V inhibitors such as bezuclastinib.

Important: This article is for education only and does not replace specialist medical advice. Advanced systemic mastocytosis is rare and should be assessed by clinicians experienced in mast cell disorders, haematology, allergy and clinical immunology.

What is advanced systemic mastocytosis?

Systemic mastocytosis is a clonal mast cell disease in which abnormal mast cells accumulate in organs such as the bone marrow, liver, spleen, gastrointestinal tract and bones. Most patients have non-advanced disease, but a smaller group develop advanced systemic mastocytosis, where mast cell infiltration causes measurable organ damage.

Aggressive SM

Systemic mastocytosis with organ damage caused by mast cell infiltration.

SM-AHN

Systemic mastocytosis with an associated haematological neoplasm; this is the most common advanced subtype.

Mast cell leukaemia

A rare and aggressive form with a high mast cell burden and usually rapid clinical progression.

advanced systemic mastocytosis showing abnormal mast cells, KIT D816V mutation, bone marrow involvement, gastrointestinal organs, blood testing and targeted treatment for mast cell disease.

Advanced systemic mastocytosis is defined by organ damage directly caused by mast cell infiltration. These are known as C findings. Examples include low blood counts, liver dysfunction with portal hypertension or ascites, enlarged spleen with hypersplenism, malabsorption with weight loss, and significant bone disease such as large osteolytic lesions or pathological fractures.

The key diagnostic concept: C findings

Advanced systemic mastocytosis is defined by organ damage directly caused by mast cell infiltration. These are known as C findings. Examples include low blood counts, liver dysfunction with portal hypertension or ascites, enlarged spleen with hypersplenism, malabsorption with weight loss, and significant bone disease such as large osteolytic lesions or pathological fractures.

Symptoms alone are not enough

Flushing, abdominal discomfort, brain fog, bone pain, fatigue and anaphylaxis can occur in mast cell disorders, but advanced disease is diagnosed by objective organ damage, not by symptom severity alone.

KIT D816V: why molecular testing matters

Most adults with systemic mastocytosis carry the KIT D816V mutation, which drives abnormal mast cell growth and survival. Testing for KIT D816V helps confirm the diagnosis, assess disease burden and guide targeted treatment choices.

A standard next-generation sequencing panel may miss KIT D816V when the variant allele frequency is low. If clinical suspicion remains high, more sensitive techniques such as digital droplet PCR or allele-specific PCR may be needed, especially in patients with indolent or low-burden disease.

Current treatment options

Treatment Main role Important safety points
Midostaurin Multi-kinase inhibitor used in advanced systemic mastocytosis. Nausea, vomiting, diarrhoea and blood count suppression may occur.
Avapritinib Potent targeted KIT D816V inhibitor with deep and durable responses in advanced SM. May cause oedema, cognitive effects and risk of intracranial bleeding. It is not recommended with very low platelet counts.
Cladribine Sometimes used when rapid cytoreduction is needed. Can suppress immunity and blood counts; requires specialist monitoring.
Imatinib Only useful in selected rare cases without KIT D816V or with imatinib-sensitive mutations. Not effective for typical KIT D816V-positive systemic mastocytosis.

Bezuclastinib: an emerging KIT D816V inhibitor

Bezuclastinib is an investigational, next-generation KIT D816V inhibitor being studied in systemic mastocytosis. Its key mechanistic distinction is potent activity against mutant KIT D816V while aiming to spare wild-type KIT and related kinases.

Unlike avapritinib, bezuclastinib has been described in clinical development as having minimal brain penetration. This is clinically important because it may reduce concerns about cognitive adverse effects and intracranial bleeding risk. However, all targeted therapies can still have side effects and require careful specialist monitoring.

Corrected safety summary

Bezuclastinib should not be described as having a greater CNS risk than avapritinib. Current clinical development highlights its selectivity and minimal brain penetration as potential advantages. Its final place in treatment will depend on full peer-reviewed trial data, regulatory review and real-world safety experience.

Supportive care remains essential

Even when targeted treatment is used, patients with systemic mastocytosis usually need a personalised supportive care plan. This may include trigger avoidance, emergency medication, assessment of anaphylaxis risk, bone density monitoring, vitamin D optimisation, osteoporosis treatment when indicated, and review of gastrointestinal symptoms, nutrition and weight loss.

When to seek specialist review

Unexplained anaphylaxis, persistently high tryptase, abnormal blood counts, enlarged liver or spleen, unexplained weight loss, fractures, osteoporosis or suspected KIT D816V-positive disease should prompt specialist assessment.

What a specialist clinic may arrange

Assessment may include serum tryptase, blood tests, KIT D816V testing, bone density scan, allergy and anaphylaxis review, haematology input, bone marrow assessment and personalised treatment planning.

Practical action points for patients

  • Ask whether your disease is non-advanced or advanced systemic mastocytosis.
  • Confirm whether KIT D816V has been tested using a sufficiently sensitive method.
  • Carry adrenaline auto-injectors if prescribed and ensure you know when and how to use them.
  • Discuss bone density monitoring, calcium and vitamin D status, and osteoporosis prevention.
  • Before avapritinib, platelet count and bleeding risk must be carefully reviewed by the treating specialist.
  • Consider review in a centre with experience in mast cell disorders when the diagnosis or treatment plan is uncertain.

Specialist allergy and immunology assessment in London

London Allergy and Immunology Centre provides specialist assessment for mast cell activation symptoms, recurrent anaphylaxis, raised tryptase and suspected mast cell disorders. Patients with suspected advanced systemic mastocytosis may require coordinated care with haematology and specialist mastocytosis services.

Appointments: Please contact the clinic to arrange a specialist consultation and review of previous test results.

References and further reading

  1. World Health Organization and international consensus classifications of systemic mastocytosis and advanced systemic mastocytosis.
  2. Valent P, Akin C, Hartmann K, et al. Updated diagnostic criteria and classification of mast cell disorders.
  3. DeAngelo DJ, Radia DH, George TI, et al. Avapritinib in advanced systemic mastocytosis: EXPLORER and PATHFINDER clinical trial data.
  4. Gotlib J, Kluin-Nelemans HC, George TI, et al. Midostaurin in advanced systemic mastocytosis.
  5. Cogent Biosciences. Bezuclastinib APEX study updates in advanced systemic mastocytosis.
  6. American Academy of Allergy, Asthma and Immunology. Mastocytosis patient information and clinical resources.

FcRn Blockade and IgG Autoantibodies | Immunology Treatment Explained

Patient Immunology Information

FcRn Blockade and IgG Autoantibodies

A medical explanation of how the neonatal Fc receptor helps IgG antibodies survive in the body, and how FcRn blockade may reduce disease-causing IgG autoantibodies in selected antibody-mediated autoimmune conditions.

Key message

FcRn blockade is a targeted immunological treatment strategy designed to lower immunoglobulin G, known as IgG. It interrupts the recycling system that normally protects IgG from breakdown. In conditions where IgG autoantibodies contribute to inflammation, receptor dysfunction or tissue injury, reducing circulating IgG may help reduce disease activity without broadly suppressing the whole immune system.

Immunology of FcRn-mediated IgG recycling and FcRn blockade, showing antibody recycling under normal conditions and accelerated degradation of pathogenic IgG autoantibodies after FcRn inhibition.

Immunology illustration demonstrating the role of the neonatal Fc receptor (FcRn) in IgG recycling and how FcRn blockade promotes degradation of pathogenic IgG autoantibodies in antibody-mediated autoimmune disease.

What is FcRn?

FcRn stands for neonatal Fc receptor. Despite the word neonatal, FcRn is not only important in newborn babies. It remains active throughout life and is found in several tissues, including vascular endothelial cells, immune cells and epithelial surfaces. Its main role is to regulate the survival of IgG antibodies and albumin in the circulation.

IgG is the most abundant antibody class in the blood. It plays an essential role in protection against infection, long-term immune memory and the response to vaccination. However, in some autoimmune diseases, the immune system produces IgG autoantibodies. These are antibodies that bind to the body’s own proteins. If these IgG autoantibodies are pathogenic, they may activate inflammatory pathways, interfere with normal receptor function, recruit complement, promote tissue injury or disturb normal cell signalling.

How FcRn protects IgG from breakdown

Cells constantly take up small amounts of fluid and proteins from the bloodstream. Many internalised proteins are sent to lysosomes, where they are broken down. IgG is different because FcRn binds to IgG inside acidic endosomes and diverts it away from lysosomal degradation. The IgG is then recycled back to the cell surface and released into the bloodstream.

This recycling process gives IgG a long biological half-life compared with many other circulating proteins. In healthy immunity, this is useful because protective antibodies remain available for longer. In antibody-mediated autoimmunity, the same protective recycling pathway may also prolong the survival of harmful IgG autoantibodies.

The FcRn recycling pathway in simple terms

1. IgG enters cells from the bloodstream.

2. FcRn binds IgG inside acidic endosomes.

3. Bound IgG is protected from lysosomal breakdown.

4. IgG is returned to the bloodstream.

5. This prolongs IgG survival, including the survival of pathogenic IgG autoantibodies.

What is FcRn blockade?

FcRn blockade means using a medicine that prevents FcRn from rescuing IgG. When IgG can no longer bind effectively to FcRn, more IgG is directed towards lysosomal degradation. This leads to a reduction in total circulating IgG, including pathogenic IgG autoantibodies.

This approach is different from many traditional immunosuppressive treatments. FcRn blockade does not aim to shut down broad immune-cell activity. It does not directly deplete B cells, T cells or plasma cells. Instead, it reduces the circulating level of IgG antibodies that have already been produced. This is why the effect can be relatively rapid and reversible.

Why IgG autoantibodies matter in autoimmune disease

Autoimmune diseases are not all the same. Some are mainly driven by T-cell inflammation, some by cytokines, some by immune-complex formation, and some by disease-causing autoantibodies. FcRn blockade is most relevant where IgG autoantibodies have a clear pathogenic role.

In IgG-mediated autoimmune disease, autoantibodies may bind to cell-surface receptors, structural proteins, platelets, red blood cells, skin adhesion proteins or other self-antigens. The clinical effect depends on the target. In some conditions the antibody blocks normal receptor function. In others it activates complement, marks cells for clearance, or causes inflammation at a tissue surface.

The important principle is that lowering pathogenic IgG may reduce the autoimmune signal while leaving other immune mechanisms more intact than with broad immunosuppression. Immunoglobulin A, immunoglobulin M and many cellular immune functions are not directly targeted by FcRn blockade, although clinical monitoring remains essential because IgG is an important part of infection defence.

Examples of FcRn-targeting medicines

Several FcRn-targeting treatments have been developed or are under clinical investigation. These include efgartigimod alfa, rozanolixizumab, nipocalimab and batoclimab. They differ in molecular structure, route of administration, dosing schedule, regulatory status and clinical development programme.

Efgartigimod alfa is an engineered human IgG1 Fc fragment designed to bind FcRn and reduce IgG recycling. Rozanolixizumab is a humanised monoclonal antibody directed against FcRn. Nipocalimab and batoclimab are FcRn-blocking monoclonal antibodies being studied across several IgG-mediated autoimmune conditions. Availability in the UK and Europe depends on the licensed indication, local commissioning, specialist assessment and individual patient suitability.

Important clinical point

FcRn blockade is not a general treatment for all autoimmune symptoms. It is a specialist treatment strategy considered when the disease mechanism, antibody profile, clinical severity, previous treatment response and safety profile support an IgG-lowering approach.

How quickly does FcRn blockade work?

Because FcRn blockade increases the breakdown of circulating IgG, it may reduce IgG levels more quickly than treatments that depend on slowly altering antibody production. The timing of clinical improvement varies between conditions and between patients. A fall in antibody level does not always translate immediately into symptom improvement because tissue inflammation, complement activation, organ damage or downstream immune pathways may take longer to settle.

The effect is also reversible. When treatment is stopped, FcRn function gradually resumes and IgG levels may recover over time. This reversibility can be clinically useful, but it also means that repeated or maintenance treatment may be required in some chronic relapsing conditions.

Is FcRn blockade immunosuppression?

FcRn blockade is best understood as targeted immunomodulation rather than broad immune suppression. It lowers IgG by increasing IgG catabolism. It does not directly suppress bone marrow function, does not directly deplete lymphocytes and does not act like high-dose corticosteroids or conventional cytotoxic immunosuppressants.

However, IgG is important for immune protection. Patients being considered for FcRn blockade require specialist assessment of infection history, vaccination status, current medicines, immunoglobulin levels, pregnancy status where relevant, co-existing medical conditions and the need for monitoring during treatment.

Safety considerations and monitoring

The safety profile depends on the specific medicine, the dose, the route of administration and the patient’s underlying condition. Reported adverse effects vary between products but may include headache, injection-site reactions, upper respiratory tract infections, nausea, diarrhoea, fever, rash or infusion-related symptoms. Because FcRn also participates in albumin homeostasis, some FcRn-targeting approaches may require attention to serum albumin, although the extent of albumin change differs between molecules.

Before treatment, clinicians may check full blood count, liver and kidney function, immunoglobulin levels, infection risk, vaccination history and disease-specific autoantibody markers. During treatment, monitoring may include symptom scores, clinical examination, infection surveillance, IgG levels where appropriate, treatment tolerance and review of concomitant medicines.

Patients should inform their clinician if they develop recurrent infections, persistent fever, new unexplained symptoms, severe headache, allergic-type symptoms, pregnancy, planned surgery, or if they are due to receive vaccines. Live vaccines and timing of vaccination should be discussed with the treating specialist.

How FcRn blockade differs from other antibody-lowering treatments

Plasma exchange can remove antibodies rapidly from the circulation, but it is a procedure-based treatment and may require vascular access. Intravenous immunoglobulin can modulate immune function through several mechanisms, including Fc receptor effects, complement modulation and anti-inflammatory signalling. B-cell targeted treatments reduce the formation of new antibody-producing immune responses but may take longer to affect established antibody levels and may have broader immune effects.

FcRn blockade occupies a different position. It is pharmacological rather than procedure-based, reduces IgG by accelerating its natural breakdown, and can be repeated according to the licensed product schedule and specialist treatment plan. It may be considered when the aim is to lower pathogenic IgG without using broad immune suppression, although it is not suitable for every patient or every autoimmune condition.

Who may benefit from specialist assessment?

A specialist immunology or relevant organ-specific specialist assessment may be appropriate for patients with suspected antibody-mediated autoimmune disease, especially where standard treatments have not provided adequate disease control, where corticosteroid exposure is problematic, or where there is a documented pathogenic IgG autoantibody associated with active disease.

Assessment should include confirmation of diagnosis, review of previous investigations, antibody testing, disease activity measurement, treatment history, infection history and discussion of the balance between potential benefit and risk. FcRn blockade should not be started purely because an autoantibody is present; the antibody must be interpreted in the full clinical context.

Patient information

This page is for general medical education. FcRn-blocking medicines are prescription-only specialist treatments. They should only be considered after diagnosis, antibody testing and clinical review by an appropriately experienced clinician.

Summary

FcRn is a natural recycling receptor that protects IgG antibodies from degradation. This mechanism is useful for normal immune protection but may also prolong the survival of pathogenic IgG autoantibodies in antibody-mediated autoimmune disease. FcRn blockade interrupts this recycling pathway, increases IgG breakdown and can reduce circulating pathogenic IgG without directly suppressing the whole immune system.

This is an important development in modern immunology because it offers a targeted way to address IgG-driven disease mechanisms. Its role depends on the specific condition, the antibody involved, the licensed indication, treatment availability and the patient’s overall clinical situation.

References

  1. Gjølberg TT, Andersen JT, Sandlie I. Targeting the neonatal Fc receptor in autoimmune diseases: pipeline and progress. BioDrugs. 2025.
  2. Zhu L, et al. FcRn inhibitors: transformative advances and significant potential in autoimmune diseases. Front Immunol. 2025.
  3. Yang CW, et al. Evaluating the clinical impact of FcRn inhibition in IgG-mediated autoimmune disease. Autoimmun Rev. 2025.
  4. Seth NP, et al. Nipocalimab, an immunoselective FcRn blocker that lowers IgG, including pathogenic autoantibodies. Clin Pharmacol Ther. 2025.
  5. Nilforoushzadeh MA, et al. FcRn inhibitors in immune thrombocytopenia: a comprehensive review of therapeutic advances and clinical outcomes. Transfus Apher Sci. 2025.
  6. Yasuda M, et al. Opposing effects of efgartigimod and rozanolixizumab on serum albumin levels. Naunyn Schmiedebergs Arch Pharmacol. 2026.
  7. European Medicines Agency. Vyvgart: efgartigimod alfa. European public assessment report.
  8. European Medicines Agency. Rystiggo: rozanolixizumab. European public assessment report.

Early SLIT Immunotherapy for Hay Fever and Asthma Prevention London

SLIT Immunotherapy London

Early SLIT Immunotherapy: Could Treating Hay Fever Earlier Help Protect Against Asthma?

New medical evidence suggests that sublingual allergen immunotherapy (SLIT) may be more than symptom control. For carefully selected patients, it may help change the long-term course of allergic rhinitis and allergic asthma.

Key message

SLIT immunotherapy is increasingly being viewed as a disease-modifying treatment for allergic rhinitis and allergic asthma, rather than only a final option when antihistamines and nasal sprays are not enough.

What is SLIT immunotherapy?

Sublingual allergen immunotherapy (SLIT) is a specialist allergy treatment designed to gradually train the immune system to tolerate a specific allergen. It may be used for selected patients with allergic rhinitis, allergic conjunctivitis and allergic asthma caused by triggers such as grass pollen, tree pollen, house dust mite or animal dander.

Unlike standard medicines, which mainly reduce symptoms while they are being taken, SLIT aims to reduce the body’s allergic response over time. Treatment is usually administered as liquid allergen drops under the tongue according to the prescribed treatment plan.

How SLIT works

Small amounts of allergen are introduced regularly under the tongue to encourage immune tolerance over time. The treatment plan is individualised according to the allergen profile, symptoms and medical history.

Why is earlier treatment being discussed?

A 2026 expert review in Current Opinion in Allergy and Clinical Immunology highlights a shift in thinking. Traditionally, allergen immunotherapy was often considered only after symptoms remained troublesome despite medication. However, newer real-world evidence suggests that starting immunotherapy earlier in suitable patients may offer a “window of opportunity” to influence the natural history of allergic airway disease.

This is particularly relevant for patients with persistent allergic rhinitis, with or without mild to moderate allergic asthma. Allergic rhinitis and asthma are closely linked, and untreated or poorly controlled nasal allergy may contribute to lower airway symptoms in some patients.

Potential benefits of earlier SLIT immunotherapy

  • Reduced need for long-term allergy medication
  • Improved control of allergic rhinitis symptoms
  • Fewer severe asthma exacerbations in some patient groups
  • Possible reduction in the risk of developing asthma
  • Possible reduction in the development of new allergen sensitisation
  • Long-lasting benefit after completion of treatment in selected patients

What does recent evidence show?

Large real-world studies, including the REACT programme and the EfficAPSI study, suggest that adding allergen immunotherapy to standard care may reduce medication use, severe asthma exacerbations and healthcare use over long-term follow-up.

The 2026 review also highlights that younger patients may gain particular benefit when treatment is started before allergic airway disease becomes more established. This supports the idea that allergic rhinitis should not always be viewed as a minor condition, especially when symptoms are persistent, seasonal year after year, or associated with wheeze, cough or exercise-related breathing symptoms.

Who may be suitable for SLIT immunotherapy?

SLIT is not suitable for everyone. It should only be considered after specialist allergy assessment, including a careful clinical history and confirmation that symptoms match relevant IgE sensitisation on skin prick testing or blood testing.

You may be considered if you have:

  • Moderate to severe hay fever
  • Persistent house dust mite allergy
  • Allergic rhinitis with confirmed pollen, mite or animal allergy
  • Symptoms despite regular antihistamines or nasal sprays
  • Allergic asthma that is mild to moderate and controlled enough for treatment

A specialist review is essential if you have:

  • Uncontrolled asthma
  • A history of severe allergic reactions
  • Multiple allergies requiring prioritisation
  • Other medical conditions or regular medication
  • Uncertainty about the main allergen causing symptoms

Why accurate diagnosis matters

The success of SLIT depends on selecting the correct allergen. For example, a patient with spring symptoms may be reacting to birch pollen, grass pollen, plane tree pollen, or more than one pollen. A patient with year-round symptoms may have house dust mite allergy, animal dander allergy, mould allergy, non-allergic rhinitis, or a combination of causes.

At a consultant-led allergy clinic, testing may include skin prick testing, specific IgE blood testing and, where appropriate, molecular allergy testing. This helps confirm whether immunotherapy is likely to be clinically relevant and which allergen should be prioritised.

Early treatment does not mean rushed treatment

Earlier SLIT means considering disease-modifying treatment before allergic disease progresses further. It does not mean starting treatment without proper assessment. The allergen profile, safety considerations and asthma control must all be reviewed carefully.

How long does treatment take?

SLIT immunotherapy is usually a long-term commitment. Many treatment courses continue for around three years, depending on the allergen and clinical response. The aim is to achieve sustained immune tolerance and longer-lasting benefit, rather than short-term symptom relief only.

Can SLIT replace antihistamines and nasal sprays?

Not immediately. Symptomatic treatment remains important, especially during the early stages of immunotherapy and during high pollen exposure. Many patients continue to use nasal sprays, antihistamines or eye drops as needed. Over time, some patients may need less medication, but this should be reviewed individually.

Why choose a specialist allergy clinic?

SLIT should be prescribed and monitored by clinicians experienced in allergy diagnosis, asthma assessment and immunotherapy safety. A specialist clinic can help identify the most relevant allergen, assess asthma risk and monitor response throughout the course.

Considering SLIT immunotherapy for hay fever, dust mite allergy or allergic asthma?

A consultant-led allergy assessment can help determine whether SLIT immunotherapy is appropriate for you or your child.

Book an Allergy Consultation

Summary

SLIT immunotherapy is increasingly recognised as a treatment that may modify the course of allergic respiratory disease. For suitable patients with confirmed allergic rhinitis, and especially those at risk of asthma progression, earlier discussion of immunotherapy may be clinically valuable.

The decision should always be personalised. The most important first step is accurate diagnosis, followed by careful selection of the correct allergen treatment plan.

Medical disclaimer: This article is for general information only and does not replace medical advice. Immunotherapy should only be started after assessment by an appropriately qualified allergy specialist.

References include: Lombardi C. et al. Allergen-specific immunotherapy at earlier stages of allergic respiratory diseases. Current Opinion in Allergy and Clinical Immunology. 2026; ARIA-EAACI allergic rhinitis guidance; AAAAI, London Allergy and Immunology Centre’s patient information on allergy immunotherapy.

Why Some “Mild” Food Allergies Aren’t Always Mild

Why Some “Mild” Food Allergies Aren’t Always Mild

Oral Allergy Syndrome, PR-10 and LTP Explained

If you’ve ever eaten an apple, peach, hazelnut or peanut and felt itching, tingling or swelling in your mouth or throat, you may have been told: “Don’t worry, it’s just oral allergy syndrome.”

For many people, that is true.
For others, it is an oversimplification that misses important risks.

Modern allergy medicine has shown that not all food allergies behave the same way, even when symptoms start in the mouth. The key difference lies in which specific allergen proteins your immune system reacts to – something that only component-resolved allergy testing can reveal.


What Is Oral Allergy Syndrome?

Oral Allergy Syndrome (OAS), also called pollen-food allergy syndrome, occurs when the immune system mistakes certain food proteins for pollen allergens.

Oral allergy syndrome,  pollen–food cross-reactivity, PR-10 versus LTP proteins, and component-resolved allergy testing.

Understanding oral allergy syndrome and the difference between PR-10 and lipid transfer protein (LTP) sensitisation using component-resolved allergy testing.

This happens because some foods contain proteins that closely resemble pollen allergens, particularly from birch, grass, or mugwort pollen. When these proteins are eaten raw, the immune system reacts locally.

Typical symptoms include:
– Itching or tingling of the lips, tongue or throat
– Mild swelling inside the mouth
– Symptoms appearing within minutes of eating raw fruit, vegetables or nuts
– Symptoms often disappearing when the food is cooked

For years, OAS was considered harmless. However, research published between 2024 and 2026 has clearly shown that OAS is not one single condition, but a spectrum – and this distinction matters.


The Two Key Protein Families Behind OAS

PR-10 vs LTP

PR-10 Proteins – Usually Mild and Heat-Sensitive

PR-10 proteins are most commonly linked to birch pollen allergy. The best-known example is Bet v 1, the main birch pollen allergen.

Foods that commonly contain PR-10 proteins include:
– Apple
– Pear
– Hazelnut
– Peach
– Carrot
– Soy

PR-10 proteins:
– Are heat- and digestion-sensitive
– Usually cause local mouth symptoms only
– Are often tolerated when foods are cooked or baked
– Rarely cause systemic reactions

For many patients, identifying PR-10 sensitisation is reassuring. It explains symptoms and helps avoid unnecessary food avoidance.


LTP Proteins – More Stable and Potentially High Risk

Lipid Transfer Proteins (LTPs) are very different.

LTPs are:
Heat-stable
Resistant to digestion
– Able to trigger reactions beyond the mouth

Foods commonly linked to LTP sensitisation include:
– Peach (especially the peel)
– Nuts
– Peanut
– Wheat
– Tomato
– Grape

Medical literature from Southern and Central Europe initially highlighted LTP allergy, but recent UK and Northern European studies show that LTP sensitisation is increasingly recognised in the UK, often mislabelled as “mild OAS”.

LTP allergy may cause:
– Urticaria (hives)
– Abdominal pain or vomiting
– Breathing difficulties
– Exercise- or alcohol-associated reactions
– Anaphylaxis in some cases

This is why distinguishing PR-10 from LTP sensitisation is clinically crucial.


 
Current understanding of oral allergy syndrome and its underlying mechanisms is guided by robust international medical evidence. Guidance from the British Society for Allergy & Clinical Immunology (BSACI) recognises pollen–food syndrome as a common cause of oral symptoms linked to cross-reactivity between pollens and plant foods, while emphasising the importance of accurate diagnosis and risk stratification. At a European level, the European Academy of Allergy and Clinical Immunology (EAACI) has published detailed position papers highlighting the clinical value of molecular, component-resolved allergy diagnostics, particularly in distinguishing PR-10 sensitisation from lipid transfer protein (LTP) allergy, which may carry a higher risk of systemic reactions. For patients, UKAllergy provides clear, accessible explanations of oral allergy syndrome and reinforces why symptoms and risks can vary between individuals. In parallel, peer-reviewed literature indexed on PubMed, including reviews published between 2024 and 2026, consistently shows that component-resolved testing improves diagnostic accuracy, supports personalised risk assessment, and helps avoid both unnecessary dietary restriction and false reassurance.
 

Why Standard Allergy Tests Are Often Not Enough

Traditional allergy tests measure sensitisation to whole foods such as “apple”, “peanut” or “hazelnut”.

The problem is simple:
– A positive result does not tell you which protein is responsible
– Risk can vary dramatically depending on the protein involved
– Patients may be falsely reassured or unnecessarily restricted

For example:
– A positive peanut test could reflect PR-10 cross-reactivity (low risk)
– Or LTP sensitisation (higher risk)
– Or storage proteins (high risk)

Without component testing, these differences remain hidden.


What Is Component-Resolved Allergy Testing?

Component-resolved diagnostics (CRD) identify specific allergenic proteins rather than whole allergen sources.

This approach allows clinicians to:
– Differentiate PR-10-driven OAS from LTP-mediated allergy
– Assess the true risk of systemic reactions
– Provide tailored dietary advice
– Avoid unnecessary food avoidance
– Improve patient confidence and safety

Large-scale studies published between 2024 and 2026 confirm that CRD:
– Improves diagnostic accuracy
– Reduces misclassification of food allergy severity
– Supports personalised allergy management plans


Why This Matters for You

If you:
– Have mouth symptoms with raw fruit or nuts
– Were told you have “just oral allergy syndrome”
– Experience symptoms that feel unpredictable
– React differently depending on exercise, alcohol or stress
– Avoid many foods without clear answers

Then component allergy testing can provide clarity.

Understanding whether your symptoms are driven by PR-10 proteins or LTP proteins changes how your allergy is managed – and how safe you truly are.


The Future of Allergy Diagnosis Is Personalised

Modern allergy care is no longer about simple yes-or-no answers.

It is about:
– Knowing which proteins trigger your immune system
– Understanding your personal risk profile
– Making informed, evidence-based decisions

Component-resolved allergy testing represents a major shift in allergy medicine – one that empowers patients rather than restricting them.

If you have been living with uncertainty around food reactions, the answer may not be more avoidance, but better information.

 

Drug allergy in the UK

Drug allergy in the UK

Drug allergy represents a significant challenge to clinical practice within the United Kingdom, carrying substantial implications for patient safety, antimicrobial stewardship, and optimisation of therapeutic outcomes.

Drug allergy presents an enduring and significant clinical challenge within the United Kingdom, reflecting worldwide trends but influenced by specific regional factors in sensitisation, diagnosis, and management.

The recognition and management of drug hypersensitivity reactions remain a priority in UK healthcare, given their direct impact on patient safety, morbidity, and cost of care within the NHS.

Nevertheless, sensitisation to food and drug allergens among patients with atopic backgrounds is recognised, and the discordance between sensitisation (as evidenced by IgE or skin testing) and true clinical allergy persists as a diagnostic complexity within UK practice.

Alpha-gal syndrome, a distinct form of IgE-mediated hypersensitivity to galactose-α-1,3-galactose, remains rare in the UK population, with only sporadic cases reported and limited evidence of widespread sensitisation. In contrast, international studies highlight greater prevalence in areas where tick exposure is endemic, but in the UK, clinical cases are exceptional and do not represent a significant portion of allergy consultations.

Anaphylaxis management in the UK is guided by standards established by national bodies, including the Resuscitation Council UK and NICE guidelines.

Following the widespread public health response to SARS-CoV-2 vaccination programmes, there has been a substantial improvement in the availability and use of adrenaline autoinjectors across both community and perioperative settings.

NHS clinical pathways now emphasise rapid access to autoinjectors, particularly for individuals with identified anaphylaxis risk. However, challenges persist regarding equitable access, patient self-management education, and NHS prescription policies governing the supply and renewal of autoinjectors. The stakes are especially acute in non-hospital environments, where reliance on ampoule-based adrenaline administration may lead to critical delays.

In the perioperative environment, peri-anaesthetic anaphylaxis remains a rare but life-threatening emergency. Tertiary centres in the UK, including specialist Allergy and Anaesthetic services, report a moderate to high rate of trigger identification when systematic skin testing and in vitro immunoassays are performed promptly post-reaction.

Neuromuscular blocking agents (including rocuronium and suxamethonium) and antibiotics (notably beta-lactams) are consistent with those most frequently implicated in UK cases. When investigations fail to identify a specific culprit drug, safe clinical management relies on thorough risk assessment, careful documentation, and—where unavoidable—supervised test dosing under anaesthetic care. National audits have highlighted the need for standardisation of protocols and improved perioperative documentation to further reduce risk.

The stratification of drug allergy risk in the UK is subject to ongoing debate and iterative refinement. NICE has supported the movement away from indiscriminate allergy labelling and now recommends that only high-risk patients—such as those with histories of severe cutaneous adverse reactions (e.g., Stevens–Johnson syndrome, toxic epidermal necrolysis)—are categorically excluded from direct drug provocation testing.

Recent guidance advocates for algorithms, such as the Beta Lactam Allergy Stratification Tool (BLAST) and emerging adaptations validated in both UK and European cohorts, to be incorporated into local allergy management pathways.

Meta-analyses confirm that supervised direct oral drug provocation in rigorously selected low-risk patients confers a minimal risk of serious adverse events, supporting NHS efforts at “de-labelling” incorrect drug allergy status. De-labelling is increasingly recognised as essential to optimise antimicrobial stewardship and patient safety.

Barriers to wider adoption of safe risk stratification and de-labelling within UK practice include persistent concerns among GPs, non-specialist prescribers, and secondary care teams regarding the complexity of algorithmic guidance, combined with variable local access to confirmatory testing (skin, in vitro, and challenge).

There is also lingering overuse of pre-emptive skin testing for antibiotics, despite evidence reviewed in recent UK consensus statements discouraging the practice due to potential for iatrogenic sensitisation and poor predictive value.

National recommendations now emphasise simple, practical protocols, educational initiatives, and the necessity of improved interprofessional communication, particularly between primary and specialist care settings.

Securing universal access to adrenaline autoinjectors and investing in sustained professional education are priorities in UK allergy service provision.

The trend towards simplified and reproducible risk stratification criteria, together with national targets for antibiotic allergy de-labelling, hold the promise of reducing inappropriate allergy records, supporting antimicrobial stewardship, and improving wider clinical outcomes across the NHS.

Ongoing audit, implementation of digital decision-support tools, and alignment with international evidence remain central to optimising UK practice in this field.

Internationally recognised guidelines and evidence-based standards, including those published by the British Society for Allergy and Clinical Immunology (BSACI), the National Institute for Health and Care Excellence (NICE), and the European Academy of Allergy and Clinical Immunology (EAACI), provide a foundation for best practice.

However, context-specific considerations within the UK, such as healthcare infrastructure, population epidemiology, and clinical traditions, shape the approach to drug hypersensitivity.

Recent nationwide cohort analyses have demonstrated that approximately 6–10% of the UK population carries a drug allergy label in their health record, with beta-lactam antibiotics, particularly penicillins, representing the most common cause.

Notably, up to 90% of penicillin allergy labels are found to be inaccurate upon systematic evaluation, resulting in widespread unnecessary avoidance, suboptimal antibiotic selection, and increased risk of adverse patient outcomes, including surgical site infections, extended hospital admissions, antimicrobial resistance, and Clostridioides difficile infection.

The mislabelling of penicillin allergy is a key barrier to effective antimicrobial stewardship. Routine use of broader-spectrum agents—such as vancomycin, macrolides, or carbapenems—in patients with inappropriate penicillin allergy labels contributes to selection pressure, intensifies the risk of multidrug-resistant organism emergence, and is associated with inferior clinical outcomes.

Furthermore, the impact on perioperative management is profound, as inaccurate allergy labels restrict optimal surgical prophylaxis, often necessitating less effective or more toxic alternatives.

Central to current UK strategy is the implementation of robust, multidisciplinary penicillin allergy delabelling pathways.

Multiple randomised controlled trials and large observational studies have confirmed the safety and efficacy of protocol-driven direct oral amoxicillin challenge in low-risk adults and children, without prior skin testing.

Allied health professional-led services, particularly pharmacist- and nurse-led clinics, have demonstrated equivalence—or in some measures, superiority—to traditional physician-led models regarding patient satisfaction, education, and waiting times.
These initiatives have been successfully integrated into wider NHS practice and supported by national toolkits such as those developed by NHS England and the BSACI.

The role of skin testing in penicillin allergy diagnosis continues to evolve. UK guidance recommends selective use in patients with histories suggestive of higher risk IgE-mediated or delayed hypersensitivity reactions, while cautioning against indiscriminate pre-emptive use, which risks false positives and unnecessary antibiotic avoidance.

Protocols for drug provocation testing, tailored to identified risk strata, remain the reference standard for definitive allergy exclusion.

Documentation and investigation of perioperative anaphylaxis remain priorities for patient safety in UK hospitals.

Prompt measurement of acute and baseline serum tryptase, comprehensive clinical documentation, and review of all administered medicinal products, including neuromuscular blocking agents, antibiotics, latex, chlorhexidine, and intravenous colloids, are fundamental to accurate diagnosis and prevention of future episodes.

Future priorities for UK practice include systematic identification and delabelling of inaccurate drug allergy records, universal adoption of evidence-based risk stratification and testing, expanded role for specialist-trained allied health professionals, and robust education of patients and clinicians.

These approaches collectively underpin the reduction of antimicrobial resistance and improvement of safe, effective patient care.

References:

  1. Khan DA, Solensky R. Drug allergy. J Allergy Clin Immunol. 2024;153(4):929-941. doi:10.1016/j.jaci.2023.11.024
    Verhoeven E, Vercammen A, Sabato V, Bridts CH, Ebo DG. Perioperative anaphylaxis: Diagnostic challenges. Curr Opin Allergy Clin Immunol. 2022;22(3):228-234. doi:10.1097/ACI.0000000000000836
  2. Trubiano JA, Phillips EJ. Antibiotic allergy de-labelling and diagnostic pathways: International best practices. J Antimicrob Chemother. 2023;78(7):1579-1588. doi:10.1093/jac/dkad071
  3. Lang DM, Castells MC, Khan DA. Practical guidance for the evaluation and management of drug hypersensitivity. Ann Allergy Asthma Immunol. 2022;129(2):169-179. doi:10.1016/j.anai.2022.03.019
  4. National Institute for Health and Care Excellence (NICE). Drug allergy: Diagnosis and management. NICE guideline [CG183]. Updated 2023.
  5. Krishna MT, Ewan PW, Diwakar L, et al. Prescription and administration of adrenaline auto-injectors in the United Kingdom: Survey of healthcare professionals. Clin Exp Allergy. 2020;50(4):514-524. doi:10.1111/cea.13557
  6. National Audit Project 6 (NAP6): Major perioperative anaphylaxis (Royal College of Anaesthetists, UK). 2018.
  7. Blumenthal KG, Parker RA, Shenoy ES, et al. Delabeling Penicillin Allergy in the UK: A Multicentre Prospective Analysis. J Antimicrob Chemother. 2022;77(5):1309–1317.
  8. Satta G, Hill V, Lanzman M, Balakrishnan I. ‘Allergy’ labels in hospital: Appropriateness and implications. J Infect. 2021;83(2):144–151.
  9. Elvy J, Lim R, Loke YK, Simmons R, Lyratzopoulos G. Impact of inaccurate penicillin allergy labels on antimicrobial prescribing and hospital outcomes: a systematic review and meta-analysis. BMJ Open. 2023;13(1):e067901.
  10. Avery AJ, Carter YH, Powell SC, Sheikh A. Investigating the Prevalence and Validity of Penicillin Allergy Documentation in UK Primary Care: A Cohort Study. Br J Gen Pract. 2023;73(730):e418-e426.
  11. Trubi and, Vogrin S, Chua KYL, et al. Misdiagnosed drug allergy labels in antimicrobial stewardship: clinical consequences and approaches to rectification. Clin Infect Dis. 2021;72(6):1036–1044.
  12. Powell N, Taylor J, Hewitt J, et al. Consequences of wrongly labelled penicillin allergy in hospitalised adults: a prospective cohort study. J Hosp Infect. 2022;119:1–7.
  13. Macleod, Stone SF, Phillips E. Perioperative anaphylaxis: current UK recommendations for investigation and prevention. Anaesthesia. 2022;77(3):351–358.
  14. Bourke T, Pavlos R, James I, Phillips E. Improving the management of antibiotic allergy: a UK perspective. Br J Clin Pharmacol. 2022;88(1):30-39.
  15. Koo G, Desai S, Berry A, et al. Direct oral amoxicillin challenge in penicillin allergy delabelling: a UK multicentre study. Allergy. 2023;78(7):2053–2056.
  16. Hanson E, Nunn D, Bingham J, et al. Pharmacist-led penicillin allergy de-labelling in secondary care: Results from a UK pilot programme. Int J Clin Pharm. 2022;44(4):927–934.
  17. British Society for Allergy and Clinical Immunology. BSACI guideline: penicillin allergy delabelling. Clin Exp Allergy. 2023;53(2):139–157.
  18. National Institute for Health and Care Excellence. Drug allergy: diagnosis and management. NICE guideline (CG183). Published September 3, 2014. Updated March 4, 2022.
  19. Stone CA Jr, Trubiano JA, Phillips EJ, Hipo A. The role of skin testing and oral challenges in antibiotic allergy diagnosis. Clin Exp Allergy. 2022;52(4):462–473.
  20. Harper NJN, Cook TM, Garcez T, et al. Anaesthesia, surgery, and life-threatening allergic reactions: epidemiology and clinical features of perioperative anaphylaxis in the UK. Br J Anaesth. 2021;127(1):77–88.
  21. Patel V, Pareek A, Gaddipati V, et al. Artificial intelligence in drug allergy education and training: a new horizon for NHS practice. Clin Med (Lond). 2023;23(6):573–579. 

Biological treatments and biomarkers in asthma and nasal polyps

Biological treatments and biomarkers in asthma and nasal polyps.

Recent developments in the management of asthma and related airway diseases have underscored the growing importance of early biologic therapy, particularly for patients with Global Initiative for Asthma (GINA) step 4 disease. While the application of biologics in GINA step 3 remains under evaluation, emerging registry data may broaden future indications. The rationale for early use is reinforced by the frequent occurrence of chronic rhinosinusitis with nasal polyps (CRSwNP) as a precursor to severe asthma, both conditions sharing type 2 (T2) inflammatory pathways that biologics effectively target.

Management strategies for non-steroidal anti-inflammatory drug (NSAID)-exacerbated respiratory disease (N-ERD) increasingly incorporate biologic therapies alongside traditional approaches. Initial treatment often combines inhaled corticosteroids, long-acting beta agonists, and leukotriene receptor antagonists. Escalation to T2 biologics, including anti–interleukin-5 and anti–interleukin-4 receptor antibodies such as dupilumab, is guided by peripheral eosinophil counts and the severity of concurrent rhinosinusitis.

A central theme in therapeutic evaluation is the distinction between clinical remission and cure remission. Clinical remission reflects disease control achieved while treatment is ongoing, whereas cure remission implies durable control after treatment discontinuation. True cure remission remains rare with biologic agents, with relapses frequently occurring within two to three months of cessation, as demonstrated in post-marketing studies of mepolizumab. In contrast, allergen immunotherapy—whether subcutaneous or sublingual—offers a greater likelihood of long-term remission beyond the treatment period, a distinction that highlights the limitations of biologics in achieving lasting disease modification.

Biomarker research is expanding the precision of treatment selection, particularly in allergen immunotherapy. Studies of Timothy grass immunotherapy have shown that variability in sensitisation profiles and IgG responses strongly influences clinical outcomes. Artificial intelligence–based tools are being developed to analyse complex biomarker datasets with the aim of predicting which patients are likely to respond to therapy. However, these approaches require further validation in large, prospective cohorts to overcome the heterogeneity of disease mechanisms and clinical endpoints.

The terminology surrounding remission remains unsettled, as biologic-induced remission differs fundamentally from that achieved after immunotherapy. Greater standardisation of definitions is needed to support consistent interpretation in both research and clinical practice. There is also growing interest in combining biologics with allergen immunotherapy, particularly for severe, mite-sensitised asthma, with the goal of achieving deeper and more durable disease modification. Current evidence, however, is preliminary.

Safety considerations remain an integral part of biologic therapy. Transient peripheral eosinophilia is a recognised effect of treatments such as dupilumab and is usually self-limited, though rare cases of eosinophilic granulomatosis with polyangiitis (EGPA) have been reported. Regional variation exists in thresholds for concern and intervention, underscoring the need for tailored monitoring protocols.

Looking forward, research is beginning to explore cell-based immunomodulatory therapies, including regulatory T lymphocyte–based strategies, though the systemic and polygenic nature of airway disease presents challenges not encountered in oncology. Insights from food allergy research, particularly studies of combined biologic therapy and immunotherapy in children, may provide valuable models for advancing asthma care.

Future priorities include strengthening collaboration between respiratory and ear, nose, and throat specialists to clarify the temporal links between CRSwNP and asthma, as well as designing adequately powered studies to test combination therapies. Efforts should also focus on refining eosinophil monitoring, standardising remission terminology, and validating biomarker algorithms in large, well-phenotyped cohorts to improve patient stratification and treatment outcomes.

References:

  • Holguin F, et al. Management of severe asthma: a European Respiratory Society/American Thoracic Society guideline. Eur Respir J. 2020;55(1):1900588. doi:10.1183/13993003.00588-2019.
  • Bachert C, et al. Biologics in chronic rhinosinusitis with nasal polyps. J Allergy Clin Immunol. 2022;149(5):1443-1451. doi:10.1016/j.jaci.2022.02.017.
  • Wechsler ME, et al. Mepolizumab or placebo for eosinophilic granulomatosis with polyangiitis. N Engl J Med. 2017;376(20):1921-1932. doi:10.1056/NEJMoa1702079.
  • Shamji MH, et al. Biomarkers for immunotherapy in allergic disease. J Allergy Clin Immunol. 2017;140(6):1489-1498. doi:10.1016/j.jaci.2017.10.009.
  • Agache I, et al. Artificial intelligence and biologicals for allergy. Allergy. 2023;78(2):471-478. doi:10.1111/all.15412.

Lentil allergy

Lentil Allergy: Clinical Relevance of Len c 1 and Len c 3

Lentil allergy
Lentil allergy is an important food allergy concern due to its prevalence in diets across Mediterranean, Middle Eastern, Asian, and North American regions. Key lentil allergens, Len c 1 (7/8S globulin) and Len c 3 (nsLTP), are implicated in IgE-mediated hypersensitivity reactions ranging from mild oral allergy syndrome to severe anaphylaxis. Their identification is critical for accurate diagnosis and management of legume allergies.

Overview of Lentil Allergens

Lentils (Lens culinaris) contain two major protein allergens:

  • Len c 1 – A 7/8S globulin (gamma-vicilin seed storage protein)
  • Len c 3 – A non-specific lipid transfer protein (nsLTP)

Biochemical Properties

Len c 1 is the major vicilin-type allergen in lentils, commonly linked to legume-induced allergic responses. Len c 3 is a potent nsLTP, structurally stable and capable of provoking systemic reactions in sensitised individuals. Understanding these properties aids in predicting severity and cross-reactivity.

Exposure and Geographic Prevalence

Allergic reactions primarily occur via ingestion, though inhalational exposure during cooking has been reported. High prevalence areas include:

  • Southern Europe (Spain, Italy)
  • Middle East
  • South Asia
  • North America

Cross-Reactivity with Other Legumes

Len c 1 shares IgE-binding epitopes with other vicilin allergens:

  • Ara h 1 (peanut)
  • Pis s 1 (pea)
  • Cic a 1 (chickpea)

Len c 3 cross-reacts with Pru p 3 (peach nsLTP), relevant in LTP syndrome prevalent in southern Europe. These cross-reactivities explain overlapping allergic responses among legumes and certain fruits.

Thermal Stability and Allergenicity

  • Some IgE-binding proteins are heat-labile and lose allergenicity when cooked
  • Len c 1 and Len c 3 remain heat-stable and can provoke reactions even after boiling

Diagnostic Value of Component-Resolved Testing (CRD)

Recombinant Len c 1 and Len c 3 allow for component-resolved diagnostics:

  • Higher sensitivity in detecting lentil allergy
  • Improved risk stratification
  • Differentiation between true allergy and cross-reactive sensitisation

This molecular approach is particularly useful in cases involving multiple legumes.

Conclusion

Len c 1 and Len c 3 are central to lentil allergy diagnosis and management. Their structural stability and cross-reactive potential make them key targets in personalised allergy testing and risk assessment. Accurate identification improves clinical decision-making and patient outcomes.

References

  1. Vieths S, et al. Component-resolved diagnostics for legume allergy. Allergy. 2023.
  2. Garcia-Blanco A, et al. Thermal stability of legume vicilin allergens. Clin Exp Allergy. 2024.
  3. Sénéchal H, et al. Cross-reactivity among edible legumes: molecular insights. Mol Immunol. 2023.

Individual allergy test for Lentil (whole allergen) is available at www.FoodAllergyTest.co.uk

Breastfeeding and Cow’s Milk Allergy in Babies: What Parents Need to Know<

 

Breastfeeding and Cow’s Milk Allergy in Babies: What Parents Need to Know

Cow’s milk allergy in babies is one of the most common food allergies in infancy, affecting up to 7% of babies under one year of age. It occurs when a baby’s immune system reacts abnormally to proteins found in cow’s milk, triggering a range of symptoms from digestive issues to skin rashes and breathing difficulties.Breastfeeding plays a crucial role in managing cow’s milk allergy, and for many infants, continued breastfeeding is the safest and most beneficial form of nutrition — even after a diagnosis is confirmed by an allergy test.
Milk Allergy Test

Milk Allergy Test

What Is Cow’s Milk Allergy?

Cow’s milk allergy (CMA) is an immune-mediated reaction to one or more proteins in cow’s milk, such as casein or whey. There are two main types:

  • IgE-mediated CMA – immediate allergic reactions, often within minutes to 2 hours of ingestion.
  • Non-IgE-mediated CMA – delayed reactions, which can appear several hours or even days later and are typically gastrointestinal or skin-related.

A confirmed diagnosis via a reliable milk allergy test is key to managing the condition effectively.

The Role of Breastfeeding in Babies with Milk Allergy

Breastfeeding offers unmatched health benefits, including immune protection, gut development, and reduced risk of infection. For babies with CMA, breast milk remains the gold standard — but with one important consideration:

If a baby reacts to cow’s milk proteins while being breastfed, it means these proteins are passing through the mother’s diet into her milk.

This doesn’t mean you should stop breastfeeding. In fact, prolonging breastfeeding is strongly recommended. Instead, mothers are advised to eliminate cow’s milk and dairy products from their own diet under the guidance of a healthcare professional or dietitian.

Excluding Cow’s Milk from the Maternal Diet

When CMA is diagnosed in a breastfed baby, the first step is often maternal dietary adjustment:

  • Remove all cow’s milk and dairy-containing products from your diet (e.g., milk, cheese, yoghurt, butter).
  • Check food labels carefully for hidden sources of milk proteins such as whey, casein, lactose (in some cases), and milk solids.
  • Ensure you’re still getting enough calcium and other essential nutrients — often through supplements or dairy-free alternatives.

Dietary changes should always be supervised to avoid nutritional deficiencies, especially in breastfeeding mothers.

Why Prolonged Breastfeeding Matters in Cow’s Milk Allergy

Breastfeeding for at least 6 months — and ideally up to 12 months or beyond — is linked with better outcomes for babies with food allergies:

  • Supports immune system regulation, helping reduce future allergy risk.
  • Protects the gut lining, which can be compromised in allergic conditions.
  • Lowers the risk of infections that may otherwise trigger or worsen allergic responses.

In cases of non-IgE-mediated CMA, where symptoms may be subtle or delayed, breast milk provides gentle nutrition without triggering inflammation or gut upset (assuming maternal diet is dairy-free).

Combining Breastfeeding with Allergy Testing

If you suspect your baby has a milk allergy, the first step is accurate diagnosis. Our cow’s milk allergy test offers a reliable, easy-to-use, at-home option to identify milk-specific IgE antibodies. Once the allergy is confirmed, your care plan can include:

  • Maternal dietary adjustments
  • Referral to a paediatric dietitian
  • Ongoing breastfeeding support

When to Seek Medical Advice

Always consult your GP, health visitor, or allergy specialist if your baby shows signs of cow’s milk allergy, such as:

  • Eczema or hives (skin rashes)
  • Vomiting or diarrhoea
  • Blood or mucus in stools
  • Colic or excessive crying
  • Breathing difficulties or wheezing
  • Poor weight gain

Early identification and proper management can significantly improve quality of life for both baby and parent.

Important Thoughts

Breastfeeding remains the best choice for babies with cow’s milk allergy, provided that cow’s milk is removed from the mother’s diet. It delivers essential nutrients and immune protection, while helping manage allergy symptoms in a natural, nurturing way.

If you’re concerned about a possible milk allergy in your baby, consider taking our cow’s milk allergy test and consult with a healthcare professional for tailored advice.

References

  1. Host A. Frequency of cow’s milk allergy in childhood. Ann Allergy Asthma Immunol. 2002;89(6 Suppl 1):33-37. doi:10.1016/S1081-1206(10)62105-3
  2. Vandenplas Y, Koletzko S, Isolauri E, et al. Guidelines for the diagnosis and management of cow’s milk protein allergy in infants. Arch Dis Child. 2007;92(10):902-908. doi:10.1136/adc.2006.110999
  3. Fiocchi A, Brozek J, Schünemann H, et al. World Allergy Organization (WAO) Diagnosis and Rationale for Action against Cow’s Milk Allergy (DRACMA) guidelines. World Allergy Organ J. 2010;3(4):57-161. doi:10.1097/WOX.0b013e3181defeb9
  4. Muraro A, Werfel T, Hoffmann-Sommergruber K, et al. EAACI food allergy and anaphylaxis guidelines: diagnosis and management of food allergy. Allergy. 2014;69(8):1008-1025. doi:10.1111/all.12429
  5. Allen KJ, Campbell DE, Assa’ad AH, et al. The role of breastfeeding in the prevention and management of cow’s milk allergy. Curr Opin Allergy Clin Immunol. 2020;20(3):234-240. doi:10.1097/ACI.0000000000000634
  6. Fleischer DM, Sicherer S, Greenhawt M, et al. Consensus communication on early peanut introduction and the prevention of peanut allergy in high-risk infants. Pediatrics. 2015;136(3):600-604. doi:10.1542/peds.2014-4022
  7. Lozinsky AC, Meyer R, Anagnostou K, et al. Cow’s milk protein allergy from diagnosis to management: a very different journey for general practitioners and parents. Children (Basel). 2015;2(3):317-329. doi:10.3390/children2030317
  8. Greer FR, Sicherer SH, Burks AW; American Academy of Pediatrics Committee on Nutrition; American Academy of Pediatrics Section on Allergy and Immunology. Effects of early nutritional interventions on the development of atopic disease in infants and children: the role of maternal dietary restriction, breastfeeding, timing of introduction of complementary foods, and hydrolyzed formulas. Pediatrics. 2008;121(1):183-191. doi:10.1542/peds.2007-3022

Related Searches:

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  • Food allergy test for babies UK

 

University Risk for Students with Asthma

The history of hay fever
Every parent of a first-year student can relate to the nagging concern that their child isn’t taking care of their own health. It explains the food parcels, the multi vitamins posted special delivery and the strict instructions not to drink too much, sleep plenty and phone home when stressed. For most parents, there’s little need for concern. Their adult child gets along just fine and at the end of the first term returns home for Christmas looking exactly like they did in September.

For parents of children with asthma it’s often a very different story. According to Asthma UK, young people with the condition are more likely to have uncontrolled asthma and least likely to get life-saving basic care. 18-34 were the least likely to have a personalised asthma action plan, with only 26% saying they used one. They were also the age group least likely to attend their annual asthma review, with only 64% doing so.

A new environment, exposure to allergic asthma triggers such as house dust mites and mould spores and the change in season, means that students with allergic asthma are at high risk of hospital admission if their asthma isn’t managed properly.

Of the 5.4 million asthma sufferers in the UK, 50% of adults and 90% of children have allergic triggers. This makes allergic asthma the commonest form of the condition, responsible for roughly 1 in 3 asthma attacks. Yet despite the fact that allergy testing could help asthmatics manage their triggers and potentially save lives, new research has shown that over three million with the condition have never been tested.
Specific IgE testing to identify allergens are recommend by NICE guidelines as soon as a formal asthma diagnosis has been made. Over 50% of people who took part in the research said they did not know what triggered their asthma, however 97% believed that understanding their asthma triggers would help them to manage their condition. 90% of those who had been tested believed this was the case.
For asthma sufferers, taking steps to manage their exposure to allergic triggers can be as simple as washing sheets at a higher temperature to kill dust mites and vacuuming regularly. Choosing accommodation with limited carpeting, keeping living areas well ventilated and wiping surfaces to prevent a build-up of mould is also key. Mould spores flourish in warm, damp environments and house dust mites are commonly found in common living areas like sitting rooms and bedrooms.
A better knowledge of asthma triggers could save lives. Dr Shuaib Nasser, Consultant in the Department of Allergy, Cambridge University Hospitals NHS Foundation Trust, states, “We know that triggers can be identified for many people with asthma – the attacks don’t come out of the blue.” Known triggers include grass pollen, pet dander, food allergy, dust mites, fungal spores. Dr Nasser emphasises that “allergen testing is widely available and should be offered to everyone where allergy is likely to trigger asthma attacks.
Asthma is a serious condition. Every ten seconds, someone in the UK has an asthma attack and around three people every day die as a result. Studies earlier this year have shown that over 1 million asthma sufferers could be using their inhalers incorrectly due to poor information and a horrifying 1 in 11 people don’t believe asthma can kill. Allergy testing, attending an annual review and making use of a personalised asthma action plan is vital, particularly as new students move away from home for the first time and are particularly vulnerable.

A group of 5,003 people (4,000 adults and 1,000 children) nationwide were surveyed between 10th – 31st October 2018. This real-world evidence study was based on a questionnaire produced by a Delphi-style group made up of the BSACI, Allergy UK and individual GPs.
Asthma: diagnosis, monitoring and chronic asthma management. November 2017. https://www.nice.org.uk/guidance/ng80
Asthma & Allergy, Making the Connection; A Real-World Study by Dr Shuaib Nasser, 2019.
The Reality of Asthma Care in the UK, p 21. By Lottie Renwick, Asthma UK, 2018. https://www.asthma.org.uk/578f5bcf/globalassets/get-involved/external-affairs-campaigns/publications/annual-asthma-care-survey/annual-asthma-survey-2018/asthmauk-annual-asthma-survey-2018-v7.pdf
Majority Are Clueless About Asthma Attacks. Asthma UK. April 2016. https://www.asthma.org.uk/about/media/news/press-release-majority-are-clueless-about-asthma-attacks/
The Reality of Asthma Care in the UK. Asthma UK. 2018. https://www.asthma.org.uk/578f5bcf/globalassets/get-involved/external-affairs-campaigns/publications/annual-asthma-care-survey/annual-asthma-survey-2018/asthmauk-annual-asthma-survey-2018-v7.pdf
Your Quick Guide to… House Dust Mite. Allergy UK. August 2018.
Your Quick Guide to… Mould Allergy Advice. Allergy UK. June 2018.

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