Allergy Treatments A–Z page: common allergy triggers, modern treatments and specialist-led allergy care.
Allergy Treatments A–Z
A comprehensive guide to allergy treatments — from allergen avoidance and antihistamines to the latest biologics and immunotherapies — based on current clinical evidence and international guidelines.
Allergy care has undergone a remarkable transformation. The goal of modern treatment is no longer simply suppressing symptoms, but modifying the underlying immune response for long-term control. From targeted biologic medicines to next-generation immunotherapy, patients today have more evidence-based options than ever. This A–Z guide explains each condition and its current evidence-based management, updated with the latest 2025–2026 clinical data.
A Anaphylaxis
Anaphylaxis is a severe, rapid-onset systemic allergic reaction that is potentially life-threatening. It is triggered when a sensitised individual is exposed to an allergen — most commonly foods (peanut, tree nuts, fish, shellfish, milk, egg), insect stings, latex, or medications.
Immediate Treatment
The cornerstone of anaphylaxis management remains intramuscular adrenaline (epinephrine), administered into the outer mid-thigh. It must be given without delay. All patients at risk should carry at least two adrenaline auto-injectors (AAI) — such as EpiPen, Jext, or Emerade — at all times and know how and when to use them.
Long-Term Management & Allergen Identification
Referral to a specialist allergy clinic is essential following any episode of anaphylaxis. Investigation includes skin-prick testing, specific IgE blood tests, and — where appropriate — supervised oral food challenges to identify the responsible allergen(s). A personalised written Anaphylaxis Action Plan should be provided to every patient.
Emerging Therapies (2025–2026)
As Asthma
Asthma is a chronic inflammatory airway disease affecting over 300 million people worldwide. There are two main phenotypes: allergic asthma, where a specific allergic trigger is identified (e.g. seasonal grass or birch pollen, perennial house dust mite, mould, or occupational allergens), and non-allergic asthma, where no identifiable allergic sensitisation is present. Many patients have features of both.
GINA Guidelines & Stepwise Treatment
Asthma is managed according to the GINA (Global Initiative for Asthma) guidelines, updated annually. Treatment follows a stepwise approach: from short-acting reliever inhalers, through low-dose inhaled corticosteroids (ICS), ICS/long-acting beta-agonist (LABA) combinations, to add-on therapies for difficult-to-control disease. The ultimate goal is the lowest effective level of medication that achieves good symptom control and reduces future risk.
Allergen Avoidance
Identifying and reducing exposure to specific triggers is a fundamental component of allergic asthma management. For house dust mite sensitisation this includes mattress and pillow encasings, reducing soft furnishings, and maintaining low indoor humidity. A novel environmental control technology called Airsonett uses temperature-controlled laminar airflow to displace almost all allergens from the breathing zone during sleep, with clinical evidence showing meaningful improvements in asthma control, particularly in patients sensitised to airborne allergens.
Biologic Therapies for Severe Asthma 2025–2026
For patients with severe, uncontrolled asthma despite optimised inhaler therapy, a range of targeted biologic agents are now available, each addressing a different inflammatory pathway:
Omalizumab (anti-IgE)
For severe allergic asthma with elevated IgE. Reduces exacerbations and steroid use. Also being investigated in combination with allergen immunotherapy.
Mepolizumab & Benralizumab (anti-IL-5)
Target eosinophilic inflammation. Significantly reduce severe exacerbations in eosinophilic asthma phenotypes.
Dupilumab (anti-IL-4Rα)
Blocks IL-4 and IL-13 signalling. Approved for type-2 moderate-to-severe asthma; also effective for co-existing eczema and nasal polyps.
Tezepelumab (anti-TSLP)
The broadest-acting biologic for severe asthma — active across all inflammatory phenotypes including non-eosinophilic. Shown to reduce exacerbations by ~70% in trials.
Depemokimab (Exdensur) (anti-IL-5)
A next-generation, ultra–long-acting monoclonal antibody, designed to suppress eosinophilic inflammation with extended dosing intervals. Unlike earlier anti-IL-5 therapies, depemokimab has been developed for 6-monthly administration, offering a significant improvement in treatment convenience and adherence for patients with severe eosinophilic asthma and related type 2 inflammatory diseases. Phase 3 clinical trial data (2024–2026) demonstrate substantial reductions in exacerbation rates and sustained eosinophil suppression with a favourable safety profile. This therapy represents an important advancement in biologic treatment — particularly for patients seeking effective long-term disease control with minimal treatment burden.
Allergen Immunotherapy (Desensitisation)
In selected patients with allergic asthma, allergen immunotherapy (AIT) — delivered as sublingual drops/spray (SLIT) — can induce long-term immune tolerance. This is the only treatment that modifies the underlying disease rather than just controlling symptoms, and it can prevent further sensitisation to new allergens.
B Bee & Wasp Venom Allergy
Venom allergy affects up to 3% of the population and can be life-threatening. Most people experience only normal local pain and swelling after a sting, but sensitised individuals can develop severe systemic or anaphylactic reactions. Large local reactions (significant swelling extending beyond the sting site) are common and often alarming but are not in themselves an indication for venom immunotherapy.
Who Needs Specialist Assessment?
Any person who experiences a systemic reaction following an insect sting should be referred to an allergy clinic. Systemic reactions can include:
- Generalised urticaria (hives) or angioedema away from the sting site
- Drop in blood pressure (dizziness, fainting, collapse)
- Swelling of the throat or tongue, difficulty swallowing or breathing
- Cardiovascular collapse (anaphylactic shock)
Diagnosis
Diagnosis involves a thorough allergy history, skin-prick testing with bee and/or wasp venom extracts, and measurement of specific IgE in the blood. Baseline serum tryptase levels should be checked in all patients who react to stings, as elevated baseline tryptase can indicate mastocytosis — a condition that significantly increases anaphylaxis risk and influences management decisions.
Venom Immunotherapy (VIT) — The Definitive Treatment
Venom immunotherapy (VIT) is a highly effective, potentially life-saving treatment that desensitises the immune system to bee or wasp venom through a programme of gradually increasing injections. It is the only treatment that addresses the underlying immune mechanism of venom allergy. Key facts:
- Recommended for all patients with severe systemic reactions (anaphylaxis) and for those with moderate systemic reactions who have significant occupational or lifestyle exposure to stings
- Treatment typically involves a build-up phase (weekly injections over several months) followed by a maintenance phase (monthly injections for 3–5 years)
- Protection rates exceed 90–95% for wasp venom and around 75–85% for bee venom after a full course
- Protection can persist for many years after completing the course, particularly with wasp VIT
- Ultra-rush and rush protocols (completing build-up in 1–3 days) are available in specialist centres for patients needing faster protection
C Contact Dermatitis
Contact dermatitis is a skin reaction caused by direct contact with a substance. There are two main types: irritant contact dermatitis (the most common — caused by direct chemical damage to skin, e.g. from detergents or solvents) and allergic contact dermatitis (ACD), a delayed-type (Type IV) hypersensitivity reaction to a specific allergen.
Common Allergens
Frequent causes of ACD include nickel and other metals (in jewellery, belt buckles, watches), fragrance compounds, preservatives, hair dyes (particularly paraphenylenediamine/PPD), rubber chemicals in latex gloves, and resins used in construction and adhesives. Occupational exposure is an important consideration.
Diagnosis: Patch Testing
The gold standard investigation for allergic contact dermatitis is patch testing, performed by an allergy or dermatology specialist. A standardised series of suspected allergens is applied to the back under adhesive patches for 48 hours, with readings at 48 and 96 hours. This identifies the responsible allergen(s) and guides avoidance advice.
Treatment
The primary treatment is allergen identification and strict avoidance. Topical corticosteroids are used to settle active flares. For chronic hand eczema from occupational contact dermatitis, newer targeted topical agents including delgocitinib cream (topical Janus kinase (JAK) inhibitor) have demonstrated early reductions in itch and pain in 2025–2026 clinical trial data. Unlike Type I (IgE-mediated) allergies, there is currently no causal immunotherapy available for Type IV contact allergy — avoidance remains the cornerstone of long-term management.
D Drug Allergy
Adverse reactions to medications are common, but true drug allergy (immunologically mediated) accounts for only a minority of these. The most frequent culprits are antibiotics (especially penicillins and cephalosporins), aspirin and NSAIDs, anaesthetic agents, and contrast media. Accurate diagnosis is crucial: unnecessary avoidance of antibiotics leads to use of broader-spectrum agents, contributing to antimicrobial resistance.
Assessment & De-labelling
Many patients carry an incorrect label of “penicillin allergy” — often based on a distant childhood reaction or a family report. Specialist assessment involving detailed history, skin-prick and intradermal testing, and supervised graded drug challenges can safely de-label the majority of these patients, restoring access to first-line antibiotics. Drug allergy de-labelling programmes are a clinical priority in healthcare systems worldwide.
Treatment
Acute mild-to-moderate drug reactions are managed with antihistamines and, where needed, corticosteroids. Severe reactions (anaphylaxis) require emergency adrenaline. Where a medication is essential and no alternative exists, drug desensitisation — a carefully supervised protocol of escalating doses — can be performed by specialist teams in hospital settings, particularly for platinum chemotherapy agents, aspirin, and antibiotics.
E Eczema (Atopic Dermatitis)
Atopic dermatitis (AD) is a chronic, relapsing inflammatory skin disorder affecting approximately 11% of children and adolescents and 6% of adults worldwide. It is characterised by intensely itchy, dry, inflamed skin and is strongly associated with other atopic conditions — asthma, allergic rhinitis, and food allergy — collectively known as the “atopic march.” The face, neck, and hands are among the most commonly and most severely affected areas, and involvement in these visible regions has a particularly significant impact on quality of life.
Skin Care & Emollients
The foundation of eczema management is a consistent, daily emollient (moisturiser) regimen — applied liberally and frequently — to restore and maintain the skin barrier. Regular, gentle bathing followed by immediate emollient application is recommended. Avoiding irritant soaps, detergents, and known contact allergens is equally important.
Topical Treatments
Topical corticosteroids (TCS) remain first-line treatment for eczema flares and should be used at the lowest effective potency for the shortest necessary duration. Topical calcineurin inhibitors (tacrolimus, pimecrolimus) are steroid-sparing alternatives, particularly suitable for the face and skin folds. Newer non-steroidal topical agents approved in recent years now expand the armamentarium considerably:
- Tapinarof cream (aryl hydrocarbon receptor agonist)
- Ruxolitinib cream (JAK1/2 inhibitor)
- Roflumilast cream (PDE4 inhibitor)
- Delgocitinib cream (Topical Janus kinase (JAK) inhibitor) — particularly showing promise for chronic hand eczema (2025–2026 data)
Systemic & Biologic Therapies 2025–2026
For moderate-to-severe eczema that does not respond adequately to topical treatments, a rapidly expanding range of targeted systemic therapies is now available:
Dupilumab (Dupixent) (IL-4Rα blocker)
The landmark biologic for moderate-to-severe AD. Approved from age 6 months. Blocks both IL-4 and IL-13 signalling. Up to 85% of patients achieve significant skin clearance. Also approved for asthma, nasal polyps, and EoE.
Tralokinumab (Adtralza) (IL-13 blocker)
Selectively targets IL-13. Approved for adults and adolescents. ECZTEND long-term data (up to 6 years, 2025) confirm durable disease control. Flexible maintenance dosing (every 4 weeks possible). Valuable alternative for those who switch from dupilumab.
Lebrikizumab (Ebglyss) (IL-13 blocker)
High binding affinity to IL-13. Associated with lower rates of dupilumab-associated conjunctivitis and facial redness when switching, making it useful for patients with these specific side effects.
Nemolizumab (Nemluvio) (IL-31Rα blocker)
Targets the “itch pathway” directly. Particularly effective for prurigo nodularis. Offers a complementary mechanism to IL-13 targeted agents.
Abrocitinib (Cibinqo) & Upadacitinib (Rinvoq) (JAK inhibitors)
Oral targeted agents. Real-world 52-week data (2025) show upadacitinib demonstrates the highest effectiveness across multiple eczema outcomes compared with dupilumab and tralokinumab.
Cyclosporine & Methotrexate
Traditional immunosuppressants. Still used in settings where biologics are not available or funded, with regular safety monitoring required.
F Food Allergy
Food allergy affects an estimated 8% of children and 3–4% of adults in Western countries — a prevalence that has increased by approximately 50% since the 1990s. The most common food allergens are peanut, tree nuts, cow’s milk, egg, fish, shellfish, wheat, and sesame. IgE-mediated reactions range from mild oral allergy syndrome to severe anaphylaxis; non-IgE-mediated food allergy (e.g. food protein-induced enterocolitis syndrome) can also occur, particularly in infants.
Allergen Avoidance & Emergency Preparedness
Strict avoidance of the responsible allergen(s) and carrying two adrenaline auto-injectors at all times remain the first-line management for IgE-mediated food allergy. Detailed dietetic advice, label-reading guidance, and school/workplace action plans are essential.
Early Introduction & Prevention
Landmark evidence — including the LEAP trial — has established that early introduction of peanut in high-risk infants (from around 4–6 months, following allergy assessment where needed) substantially reduces the risk of peanut allergy developing. This has changed international guidance, and early dietary diversification is now recommended rather than avoidance.
Oral Immunotherapy (OIT) 2025–2026
Oral immunotherapy involves the supervised, daily ingestion of increasing amounts of the food allergen to raise the threshold for a reaction. The only FDA-approved pharmaceutical-grade food OIT product is Palforzia (peanut allergen powder) for children aged 1–17 years. Research in 2025 has highlighted growing interest in multi-allergen OIT, including the investigational agent ADP101, as well as sublingual immunotherapy (SLIT) for foods. A systematic review (2025) confirms OIT significantly improves food allergy-related quality of life.
Omalizumab for Multiple Food Allergies
For patients with multiple simultaneous food allergies who are poor candidates for individual OIT programmes, omalizumab (anti-IgE) has received FDA approval to reduce the risk of allergic reactions during accidental exposure. It raises the threshold for reaction but does not cure food allergy. Dupilumab has also been studied as an adjunct to OIT in paediatric patients, with 2025 data supporting its use in reducing adverse events during peanut OIT.
H Hereditary Angioedema (HAE)
Hereditary angioedema (HAE) is a rare but potentially life-threatening genetic disorder characterised by recurrent episodes of swelling (angioedema) affecting the skin, gastrointestinal tract, and upper airway. It is caused by a deficiency or dysfunction of C1-inhibitor and is distinct from allergic (histamine-mediated) angioedema — antihistamines and corticosteroids are ineffective.
On-Demand Treatment (Acute Attacks)
Acute HAE attacks should be treated early with specific agents: C1-inhibitor concentrate, icatibant (bradykinin B2-receptor antagonist), or lanadelumab. In the December 2025 phase 3 RAPIDe-3 trial, deucrictibant — an oral bradykinin B2-receptor antagonist — demonstrated significantly faster onset of symptom relief compared with placebo, with over 93% of attacks controlled by a single 20 mg dose. An FDA New Drug Application submission is planned for 2026.
Prophylactic Treatment
Long-term prophylaxis reduces attack frequency and severity. Options include: lanadelumab (subcutaneous injection every 2–4 weeks), C1-inhibitor (IV or subcutaneous), tranexamic acid, or attenuated androgens. The FDA approval of berotralstat oral granules for children aged 2–11 years (December 2025) is a significant advance, providing the first oral prophylactic option specifically designed for this paediatric population.
R Rhinitis & Hay Fever (Allergic Rhinitis)
Allergic rhinitis (AR) is one of the most prevalent chronic conditions globally, affecting up to 30% of the population. It causes nasal congestion, sneezing, watery discharge, and nasal itch, and is frequently associated with conjunctivitis (hay fever). There are two main patterns:
- Seasonal allergic rhinitis (SAR/hay fever): Caused by pollen allergens — tree pollens (birch, hazel, alder) in early spring; grass pollens in early summer; weed pollens in late summer and autumn.
- Perennial allergic rhinitis: Year-round symptoms driven by indoor allergens — house dust mite, pet dander (cat, dog), cockroach, and moulds.
The number of allergens to which a patient is sensitised, and whether meaningful avoidance is achievable, significantly influences the treatment approach.
Allergen Avoidance
For house dust mite allergy: allergen-impermeable mattress and pillow covers, weekly hot washing of bedding, reducing soft furnishings, and maintaining humidity below 50%. For pollen allergy: monitoring pollen forecasts, keeping windows closed on high-count days, and wearing sunglasses outdoors.
Pharmacological Treatment
Following ARIA (Allergic Rhinitis and its Impact on Asthma) guidelines, treatment is stepped according to symptom severity:
- Second-generation oral antihistamines (e.g. cetirizine, loratadine, fexofenadine) — first-line for mild intermittent symptoms; non-sedating and well tolerated
- Intranasal antihistamines — fast-acting, useful for breakthrough symptoms
- Intranasal corticosteroid sprays (e.g. fluticasone, mometasone, budesonide) — the most effective pharmacological treatment for persistent moderate-to-severe rhinitis; work best when used regularly and started before the pollen season
- Oral leukotriene receptor antagonists (montelukast) — second-line, particularly useful when rhinitis and asthma coexist
- Combination intranasal corticosteroid/antihistamine sprays — for more rapid and comprehensive relief in moderate-to-severe disease
Allergen Immunotherapy (AIT) — Disease-Modifying Treatment
For patients inadequately controlled by pharmacotherapy, or who wish to reduce long-term medication use, allergen-specific immunotherapy is the only treatment that modifies the underlying cause of allergic rhinitis. It can prevent the progression of rhinitis to asthma and halt sensitisation to additional allergens.
- Subcutaneous immunotherapy (SCIT, “allergy injections”): Escalating injections given in a specialist setting, with a 3–5 year maintenance course are less commonly used in recent years.
- Sublingual immunotherapy (SLIT, allergy drops or tablets): Taken daily at home after a supervised initial dose. Grass and birch pollen sublingual treatment (Grazax, Itulazax and combination sprays) as well as house dust mite SLIT have excellent evidence and regulatory approval in many countries.
Biologics for Severe Allergic Rhinitis 2025–2026
For patients with severe rhinitis unresponsive to standard pharmacotherapy — particularly those with co-existing nasal polyps (chronic rhinosinusitis with nasal polyps/CRSwNP) — targeted biologic therapies are now available or in development:
- Dupilumab: Approved for CRSwNP with strong evidence for improving nasal symptom scores and reducing polyp size.
- Omalizumab: Meta-analysis (2025) confirms benefit in AR patients with uncontrolled sinusitis.
- CM310 (IL-4Rα antagonist): Approved by China’s NMPA in February 2025 — the first IL-4Rα antagonist approved specifically for seasonal allergic rhinitis. Demonstrated sustained improvement in nasal and ocular symptoms on a twice-monthly subcutaneous regimen.
U Urticaria (Hives) & Angioedema
Urticaria (hives) presents as intensely itchy, raised wheals (weals) on the skin that typically resolve within 24 hours. Angioedema is deeper swelling of the skin or mucous membranes, often affecting the lips, face, eyelids, hands, or genitalia. The two conditions frequently occur together.
- Acute urticaria (under 6 weeks) is often triggered by infections, medications, or foods, and usually resolves spontaneously.
- Chronic urticaria (over 6 weeks) — most commonly chronic spontaneous urticaria (CSU) — frequently has no identifiable trigger and can persist for years.
Treatment
Treatment follows international EAACI/GA²LEN/EDF/WAO guidelines:
- Step 1: Licensed dose of a second-generation antihistamine (cetirizine, loratadine, bilastine, rupatadine)
- Step 2: Increased dose (up to fourfold) of the antihistamine
- Step 3: Addition of omalizumab — strongly recommended for antihistamine-refractory CSU. Clinical trial data consistently show >50% complete response rates, with many patients becoming symptom-free.
- Step 4: Addition of cyclosporine for omalizumab non-responders
Physical Urticarias
A subset of urticaria is triggered by physical stimuli — including cold (cold urticaria), heat, pressure, vibration, sunlight (solar urticaria), and water (aquagenic urticaria). These are diagnosed by specialist provocation tests and managed with antihistamines, trigger avoidance, and, in selected cases, omalizumab.
★ Emerging & Future Allergy Treatments
The field of allergy is advancing rapidly. The following approaches are at various stages of clinical development and are shaping the future of allergy care:
Intralymphatic Immunotherapy (ILIT)
Delivers small allergen doses directly into lymph nodes via injection. Requires as few as 3 injections. Early studies suggest faster desensitisation with fewer clinic visits than traditional SCIT. Long-term safety and scalability under evaluation.
mRNA Allergy Vaccines
Building on COVID-19 vaccine technology, mRNA platforms are being explored to train the immune system to tolerate allergens safely without the risk of triggering reactions seen with traditional protein-based extracts.
Microbiome-Based Therapies
Growing evidence links gut microbiome diversity with protection against allergic disease. Research into targeted probiotics and microbiome modulation to reduce immune reactivity is ongoing.
B-Cell Peptide Immunotherapy
Next-generation immunotherapy using allergen-derived peptides fused to carrier proteins to build protective IgG antibodies while minimising IgE stimulation and reaction risk during treatment.
Biosimilars
Interchangeable biosimilar versions of established biologics (e.g. OMLYCLO, an omalizumab biosimilar) offer equivalent efficacy at lower cost, expanding access to targeted biologic treatments.
Combination Biologic + AIT
Combining biologics (especially omalizumab or tezepelumab) with allergen immunotherapy to accelerate desensitisation, improve safety, and enhance long-term immune tolerance outcomes.
