🧬 Allergy Test Abnormalities — Assessment & Management

RCGP SCA Algorithm — UK Primary Care

RCGP SCA10-min consult
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Allergy Test Abnormalities — Assessment & ManagementSensitisation is not clinical allergy — interpret with the history · no AAI for a positive test alone · anaphylaxis: IM adrenaline + 999, two in-date AAIs prescribed by brand + allergy referral (NICE NG258) · timed acute tryptase; raised baseline tryptase → specialist · pollen-food syndrome usually mild, systemic reactions possible · drug allergy: no primary-care sIgE testing, governed de-labelling · venom systemic reaction → VIT assessment · beta-blocker adrenaline interaction
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⚡ Snapshot. The whole pathway on one page: act now, triage, classify, treat today and safety-net. The Steps tab holds the detail.

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Safety

Red Flags — Anaphylaxis Risk, Mast Cell Disease & Dangerous Sensitisations

Previous reaction clinically compatible with anaphylaxis (throat tightening, hypotension, collapse, laryngeal oedema) to a food, venom, latex or idiopathic trigger that remains a realistic future risk High risk of anaphylaxis on re-exposure. A positive sIgE or SPT demonstrates sensitisation — it does not diagnose clinical allergy or predict the severity of a future reaction; never prescribe an AAI for a positive test alone. → Two in-date AAIs prescribed by brand (dose checked against weight, age, product authorisation and specialist advice) as an interim measure — not needed where the reaction was to an easily avoidable drug. Brand-specific training and a written action plan. Refer to a specialist allergy service (NICE NG258). Risk assessment (BSACI): severity and features of the previous reaction, likelihood of re-exposure, whether the allergen can be reliably avoided, asthma control, mast-cell disease or raised baseline tryptase, age, occupation, geography and access to emergency care, and ability to recognise anaphylaxis and give adrenaline.
Child or adult + cow milk / peanut / tree nut specific IgE positive + airway symptoms (wheeze, stridor, hoarse voice) on accidental exposure Anaphylaxis to food allergen — life-threatening on next exposure without adrenaline. → Two in-date AAIs prescribed by brand + written action plan. Urgent allergy clinic referral (oral immunotherapy is specialist-led).
Persistently raised baseline serum tryptase + recurrent unexplained or severe anaphylaxis (especially to venom) ± skin lesions with a positive Darier sign, bone pain or splenomegaly Possible mast-cell disease — systemic mastocytosis, hereditary alpha-tryptasaemia or other causes. A baseline tryptase persistently above 20 µg/L is a minor diagnostic criterion for systemic mastocytosis, not a diagnosis by itself; reference ranges are assay- and laboratory-dependent. A positive Darier sign supports cutaneous mastocytosis but is not proof of systemic disease. → Acute anaphylaxis: 999. Otherwise allergy/haematology referral for specialist interpretation; bone-marrow assessment and KIT D816V testing are specialist decisions, not a primary-care response. Risk of severe anaphylaxis.
Previous systemic reaction or anaphylaxis to a bee or wasp sting (± positive venom sIgE) + carries no adrenaline auto-injector Risk of a severe reaction to the next sting. → Two in-date AAIs prescribed by brand. Urgent allergy clinic referral for venom immunotherapy (VIT) assessment — VIT is highly effective and substantially reduces the risk and severity of systemic reactions to future stings; baseline tryptase should be considered (specialist pathway). Large local reactions alone generally do not need VIT or routine sIgE testing.
Drug allergy label (e.g. penicillin) in notes + significant clinical consequence of avoidance Unverified drug allergy label causing suboptimal prescribing. → Take and document a structured drug-reaction history (drug, formulation, route, dose, timing, symptoms, treatment, severity) and separate drug allergy from non-allergic adverse reactions. Do not use serum-specific IgE to diagnose drug allergy in a non-specialist setting (NICE CG183). High-risk reactions (severe immediate reaction, DRESS, SJS/TEN, AGEP, organ involvement or other severe delayed reaction) → avoid and refer to specialist allergy services. Clearly low-risk histories → approved local de-labelling pathway where one exists. Most penicillin allergy labels are not confirmed when formally assessed; published estimates are commonly around 90–95%, depending on the population and testing pathway.
Child + severe eczema + multiple food sensitisations + poor growth Severe atopic disease with risk of eosinophilic oesophagitis, growth failure, or nutritional deficiency from elimination diets. → Paediatric allergy clinic urgently. Dietitian. Supervised food challenges for accurate diagnosis.
Anaphylaxis is the only clinical scenario in allergy testing where the primary care action before any specialist review is immediate prescription of adrenaline auto-injectors — any patient who has had a severe allergic reaction with systemic features (sudden airway, breathing or circulation problems, usually with skin or mucosal changes — skin features may be absent) must leave the GP surgery with: two in-date adrenaline auto-injectors prescribed by brand (dose checked against current weight, age, product authorisation and specialist advice), a written personalised anaphylaxis action plan, and a verbal briefing on when to use the auto-injector (inject into outer thigh at first signs of anaphylaxis — do not wait for symptoms to worsen before injecting). NICE NG258 (Anaphylaxis: assessment and referral) and the BSACI anaphylaxis guidelines both emphasise: prescription of adrenaline auto-injectors should not be deferred pending allergy clinic review in any patient with a history meeting the criteria for anaphylaxis — except where the reaction was to an easily avoidable drug. A positive test without a compatible history is never an indication for an AAI.
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Diagnose

Allergy Testing — Types, Indications & Limitations

Allergy testing modalities
Skin prick test (SPT): small volume of allergen extract applied to skin and pricked through — positive when the allergen weal is sufficiently larger than the negative control according to the local laboratory protocol (commonly at least 3 mm). A positive result indicates sensitisation, not necessarily clinical allergy; diagnostic performance varies by allergen, extract, population and technique, and results must be interpreted with the clinical history. SPT is not intrinsically superior to sIgE — either may be appropriate depending on the allergen, patient and local expertise. SPT only by trained staff with appropriate resuscitation facilities. Intradermal testing: specialist use only — not a routine food-allergy test, and it can cause systemic reactions. Serum specific IgE (sIgE, formerly RAST): measures allergen-specific IgE antibodies in blood — safe in any setting. Total IgE: non-specific — elevated in atopy, parasitic infection, IgE myeloma. Basophil activation test (BAT): specialist — measures CD63/CD203c on basophils in vitro. Oral food challenge: the reference diagnostic procedure in equivocal cases — specialist, appropriately equipped setting only, not primary care. Do not request broad food panels in patients without a compatible history: they generate false-positive sensitisation results and can lead to unnecessary exclusion diets. Serum-specific IgG, Vega testing, applied kinesiology and hair analysis have no role in diagnosing food allergy (NICE CG116).
Component-resolved diagnosis (CRD)
CRD identifies which specific protein within an allergen the patient is sensitised to — this distinguishes: true primary sensitisation (sensitisation to the food allergen itself — higher clinical risk) from cross-reactive sensitisation (sensitisation to pollen proteins that share structural homology with food proteins — often causes mild oral allergy syndrome rather than systemic anaphylaxis). Examples: peanut — Ara h 2 (storage protein) suggests primary peanut sensitisation; Ara h 8 (PR-10 protein) suggests pollen cross-reactivity, usually limited to the mouth — but systemic reactions can occur, particularly with other components such as lipid-transfer proteins or with cofactors. Hazelnut — Cor a 9/14 suggests primary nut sensitisation; Cor a 1 suggests birch-pollen cross-reactivity. Component testing may refine diagnostic probability and distinguish primary from cross-reactive sensitisation, but it should be requested or interpreted with specialist advice and must not be used alone to predict reaction severity or decide whether a patient needs an AAI. NICE (HTG413, formerly DG24) regards multiplex/component testing as potentially useful in complex cases, not a routine replacement for history and conventional testing.
Patch testing (contact allergens)
Patch test: for type IV delayed hypersensitivity (contact dermatitis) — NOT IgE-mediated. Standardised allergens applied to back under occlusive patches for 48h, read at 48h and 96h. Common allergens: nickel (most common contact allergen — costume jewellery), fragrances, preservatives (methylisothiazolinone — wet wipes, cosmetics), rubber accelerators (latex — gloves), cobalt, chromate (cement). Performed in dermatology or allergy clinics — not primary care. Indication: chronic or recurrent contact dermatitis not responding to topical treatment.
The distinction between sensitisation and clinical allergy is the most important conceptual framework in allergy testing — sensitisation means the immune system has produced IgE antibodies against an allergen (detectable by sIgE blood test or SPT), but this does not automatically mean the person will have clinical symptoms on exposure. Many people are sensitised to common inhalant allergens (grass pollen, house dust mite) without clinically significant allergic rhinitis, and for food allergens sensitisation is considerably more common than clinical allergy. The interpretation principle: a positive allergy test result is clinically meaningful ONLY in the context of a consistent clinical history. A positive sIgE to a food that the patient has eaten multiple times without any symptoms represents sensitisation without clinical allergy — it does not require dietary elimination or auto-injector prescription.
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Diagnose

Assessment — History, Examination & Investigations

Allergy-focused history
Reaction characterisation: what happened (urticaria, angioedema, vomiting, wheezing, rhinorrhoea, anaphylaxis), onset (minutes = IgE-mediated; hours-days = non-IgE, contact allergy), duration, severity (mild/moderate/severe — did it require epinephrine/hospital?). Triggers: food (exactly which food, raw vs cooked — cooked often tolerated in oral allergy syndrome), timing after ingestion. Drug (reaction during course or after — amoxicillin rash often appears after stopping — may be viral). Venom (bee vs wasp — different allergens; clinical features with sting). Occupational (latex, flour, animal dander). Inhalant (seasonal = pollen; perennial = HDM, pet). Cofactors: exercise, alcohol, NSAIDs, infections (all can lower the threshold for anaphylaxis — "augmentation factors"). Reproducibility, route and quantity of exposure, treatment required, and whether the suspected allergen has since been tolerated. Family history (atopic disease).
Examination
Skin: eczema severity (EASI score — eczema area severity index), urticaria (chronic spontaneous vs inducible), dermographism (factitious urticaria — pressure-induced weal). Angioedema: episodes of non-pitting swelling (face, lips, tongue, larynx, genitalia) — distinguish from hereditary angioedema (HAE — C1 inhibitor deficiency, no urticaria, no itch, family history). Rhinitis: turbinate appearance, nasal polyps. Chest: wheeze (asthma). Mastocytosis: Darier sign (rubbing a skin lesion causes urticaria/weal) supports cutaneous mastocytosis but is not proof of systemic disease.
Investigations
Specific IgE (sIgE) to suspected allergens (targeted to allergens suggested by the history only — no broad screening panels; components only with specialist advice; not to diagnose drug allergy in primary care) · Total IgE (context — a very high value suggests severe atopy or parasites) · Serum baseline tryptase (adults after suspected anaphylaxis: acute sample as soon as possible after emergency treatment and a second ideally within 1–2 hours, no later than 4 hours from symptom onset; baseline after recovery via the specialist pathway — reference ranges are assay-dependent and a raised value needs specialist interpretation) · FBC + eosinophil count (eosinophilia >0.5 × 10⁹/L = atopy, parasites, eosinophilic disorders, drug reaction) · C4 + C1 inhibitor level + function (recurrent angioedema without urticaria → hereditary angioedema screen) · Skin prick test (trained staff with resuscitation facilities only; oral food challenge for equivocal cases in a specialist setting)
Tryptase is stored in mast-cell granules and released on mast-cell activation. After suspected anaphylaxis in adults, take an acute tryptase sample as soon as possible after emergency treatment and a second sample ideally within 1–2 hours, no later than 4 hours from symptom onset; a baseline sample is obtained after recovery through the specialist pathway (NICE NG258). A normal tryptase does not exclude anaphylaxis, particularly in food-triggered or predominantly respiratory reactions. Reference ranges are assay- and laboratory-dependent. A persistently raised baseline tryptase warrants specialist interpretation — consider systemic mastocytosis, hereditary alpha-tryptasaemia and other causes. A baseline above 20 µg/L is a minor diagnostic criterion for systemic mastocytosis; it does not diagnose it, and many people with a raised tryptase do not have mastocytosis. Mast-cell disease matters because reactions (especially to venom) can be disproportionately severe, so recurrent severe or venom anaphylaxis needs specialist assessment.
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Diagnose

Interpreting Common sIgE Results

Inhalant allergen sIgE interpretation
House dust mite (HDM — Dermatophagoides pteronyssinus/farinae): perennial symptoms (year-round rhinitis, worsening in bed/morning), asthma worse at home. A positive sIgE with a compatible history supports HDM allergy. Treatment: pharmacotherapy (antihistamine + intranasal corticosteroid) first; environmental measures have variable clinical benefit and should not replace pharmacotherapy; sublingual immunotherapy (Acarizax) only via the specialist/local commissioning pathway (NICE TA1045). Grass pollen (Timothy — Phleum pratense): seasonal rhinitis, mainly May–July. A positive sIgE with seasonal symptoms supports hay fever. Subcutaneous (SCIT) or sublingual (SLIT) immunotherapy is specialist-led/locally commissioned for symptoms uncontrolled despite pharmacotherapy. Cat/dog dander (Fel d 1, Can f 1): pet allergy. Fel d 1 sensitisation indicates primary cat sensitisation; cat allergen can persist in the home for a prolonged period after the cat is removed.
Food allergen sIgE — clinical risk stratification
Higher-risk components (associated with systemic reactions — interpret with specialist advice; components alone do not predict severity): Ara h 2 (peanut), Cor a 9/14 (hazelnut), Tri a 14 (wheat), Ses i 1 (sesame), milk casein (Bos d 8), egg ovomucoid (Gal d 1) — heat-stable, so baked forms may not be tolerated. Moderate risk — dose-dependent reactions, heat-labile proteins, baked forms often tolerated: milk whey Bos d 5, egg ovalbumin Gal d 2. Lower risk — oral allergy syndrome (usually mild and limited to the mouth, but systemic reactions can occur — especially with lipid-transfer-protein sensitisation or cofactors): Ara h 8 (peanut PR-10), Cor a 1 (hazelnut PR-10), apple Mal d 1 — all sensitised via birch pollen cross-reactivity. Symptoms: immediate tingling/itching of mouth/lips/throat; rarely systemic.
Drug allergy — penicillin de-labelling
Most penicillin allergy labels are not confirmed when formally assessed; published estimates are commonly around 90–95%, depending on the population and testing pathway. Most common reason for label: childhood rash during amoxicillin course (often viral exanthem or amoxicillin-associated rash from viral illness, not true IgE allergy). Risk of true penicillin allergy: original severe reaction (anaphylaxis, urticaria ± angioedema within 1h). Low risk: delayed maculopapular rash without systemic features, rash >72h after starting. Direct oral penicillin/amoxicillin challenge may be appropriate for carefully selected low-risk patients, but only within a governed service with trained staff, resuscitation facilities and specialist-network support; skin testing and challenge after higher-risk histories are specialist procedures. Do not perform drug provocation or skin testing, or de-label after a severe immediate reaction or a severe delayed reaction (DRESS, SJS/TEN, AGEP, organ involvement), in routine general practice.
The oral allergy syndrome (OAS) — also called pollen-food allergy syndrome (PFAS) — is one of the most frequently misunderstood and over-investigated food reactions in primary care, resulting in unnecessary elimination diets and unjustified allergen avoidance. OAS occurs when raw plant proteins (particularly PR-10 proteins in fruits, vegetables, and tree nuts) cross-react with aeroallergen-specific IgE developed from pollen sensitisation. The classic pattern: a birch-pollen-allergic adult develops tingling/itching of the lips, mouth, and throat within minutes of eating raw apple, pear, stone fruits, hazelnuts, or celery — but has no reaction to cooked forms of the same foods (PR-10 proteins are heat-labile). The clinical features that distinguish OAS from true food allergy: strictly limited to the oropharynx (no urticaria, no angioedema beyond the lips, no vomiting, no anaphylaxis), immediate onset (within seconds to minutes), resolves within minutes without treatment, and cooked forms are tolerated. Typical pollen-food syndrome is usually mild, but systemic reactions are possible. Do not automatically prescribe an AAI for uncomplicated, specialist-confirmed pollen-food syndrome; reconsider — with specialist assessment — if there are systemic symptoms, reactions to nuts or peanut, lipid-transfer-protein sensitisation, reactions involving exercise or NSAIDs, respiratory disease or previous anaphylaxis. Explain the mechanism and that cooked forms are often tolerated; elimination of tolerated foods is not needed.
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Refer

Referral Pathways

Same-day / 999
Acute anaphylaxis (IM adrenaline, call 999) · Tongue or laryngeal angioedema · Recurrent or biphasic symptoms after a reaction (IM adrenaline; antihistamines and steroids never delay adrenaline) · Known mast-cell disease with acute anaphylaxis
Allergy clinic (urgent)
Any history of anaphylaxis (food, venom, drug, idiopathic) — NICE NG258 · Systemic reaction to bee/wasp venom for VIT assessment · Significant food reactions (not a positive test alone) · Suspected mast-cell disease or persistently raised baseline tryptase · Suspected hereditary angioedema (recurrent angioedema without urticaria, C4 low; urgent if airway involvement) · Clinically important drug-allergy labels (high-risk histories; low-risk penicillin labels via an approved local de-labelling pathway)
Paediatric allergy clinic (urgent)
Child with confirmed food anaphylaxis · Severe eczema + multiple food allergies + growth failure · Suspected eosinophilic oesophagitis (EoE) · Cow milk protein allergy (CMPA) requiring formula guidance
Immunology/haematology
Suspected immunodeficiency (recurrent severe infections + low Ig + low specific antibody responses) · Suspected systemic mastocytosis (bone-marrow assessment and KIT D816V testing are specialist decisions)
GP management
Hay fever (grass/tree pollen sIgE positive): intranasal corticosteroid (beclometasone 50 micrograms per spray, 2 sprays into each nostril BD, or fluticasone propionate 2 sprays into each nostril OD) + non-sedating antihistamine (cetirizine 10 mg OD). HDM allergy: pharmacotherapy + allergen avoidance education ; Acarizax only after initiation by a physician experienced in allergic disease and per local commissioning (see Step 7). Uncomplicated, specialist-confirmed pollen-food syndrome: explain the mechanism and reassure — usually mild, but systemic reactions are possible; reconsider an AAI if systemic symptoms, relevant cofactors or a different phenotype. Avoid unnecessary elimination diets (dietitian where multiple or nutritionally important foods are excluded). Optimise asthma control.
Venom immunotherapy (VIT) for bee or wasp allergy is one of the most effective and cost-effective interventions in allergy medicine — it is highly effective and substantially reduces the risk and severity of systemic reactions to future stings, with protection sustained after a full course. The eligibility criteria for NHS VIT: confirmed venom allergy (venom sIgE positive OR SPT positive) AND history of systemic allergic reaction grade II or above (urticaria + at least one of: hypotension, laryngeal oedema, bronchospasm). VIT is performed by subcutaneous injection at an allergy clinic, starting with a very low dose and incrementing over 3-6 months (build-up phase) to maintenance. BSACI guideline: any patient with venom anaphylaxis should be referred to an allergy clinic for VIT consideration — it is not optional safety management. Large local reactions alone generally do not require VIT or routine sIgE testing, and baseline tryptase should be considered in patients with systemic reactions to Hymenoptera venom (BSACI). GPs should ask about stinging insect allergy at every prescription of adrenaline auto-injectors and ensure allergy clinic referral is in place.
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Treat

Anaphylaxis Management, Antihistamines & AAI Prescription

Adrenaline auto-injector (AAI) — prescribing and counselling
Prescribe two in-date AAIs by brand (devices differ in activation method and needle characteristics) as an interim measure after suspected anaphylaxis — except where the reaction was to an easily avoidable drug (NICE NG258). Check the dose against current weight, age, product authorisation and local specialist advice: EpiPen and Jext come as 150 and 300 microgram devices; Emerade has a 500 microgram device (check current UK availability) — device choice follows the product information and specialist/local guidance, so do not assume every adult needs a 300 microgram device. Review the dose at each repeat prescription in children and adolescents. Use the AAI immediately when anaphylaxis is suspected (outer mid-thigh, through clothing if needed); call 999 and say "anaphylaxis"; lie flat with legs raised — or sit up cautiously only if breathing is difficult — and do not stand or walk; use the second device after 5 minutes if symptoms have not improved or recur (MHRA). Brand-specific training for patient and family/carers, repeated whenever the brand changes and at repeat prescribing; written brand-specific action plan (BSACI template — bsaci.org). Check that the patient physically carries two in-date devices, not merely that they are prescribed. MedicAlert bracelet.
Anaphylaxis — acute treatment in primary care
Resuscitation Council UK algorithm: (1) Recognise sudden airway, breathing or circulation problems, usually with skin/mucosal changes — skin features may be absent. (2) Call for help and dial 999. (3) Remove the trigger if possible. (4) Lie the patient flat with legs raised — do not allow them to stand or walk; if breathing is difficult, allow them to sit up cautiously and avoid sudden postural change. (5) Give IM adrenaline 1:1000 into the anterolateral thigh without delay: adult and child over 12 years 500 mcg (0.5 mL); child 6–12 years 300 mcg (0.3 mL); child 6 months–6 years 150 mcg (0.15 mL); child under 6 months 100–150 mcg (0.1–0.15 mL). (6) Repeat IM adrenaline after 5 minutes if airway, breathing or circulation problems persist. (7) Give high-flow oxygen and IV crystalloid if trained and indicated. (8) Do not delay adrenaline for antihistamines, steroids, venous access or tryptase sampling. (9) Transfer to hospital after treatment (observation per NICE NG258). Antihistamines do not treat airway obstruction, bronchospasm or shock and must never delay adrenaline (a non-sedating oral antihistamine may be given for skin symptoms once stable); corticosteroids are not routine first-line treatment for anaphylaxis (Resuscitation Council UK 2021). All practices must have injectable adrenaline 1:1000 + 1 mL syringes available.
Antihistamines and intranasal steroids for allergic rhinitis
Non-sedating antihistamines (first-line): cetirizine 10 mg OD, loratadine 10 mg OD, fexofenadine 120 mg OD. Sedating (avoid driving): chlorphenamine 4 mg TDS (useful for acute urticaria or nighttime use only). Intranasal corticosteroid (most effective for rhinitis): fluticasone propionate 50 mcg 2 sprays per nostril OD (superior to antihistamine alone for nasal symptoms). Combination: INCS + antihistamine (additive effect for combined nasal + ocular symptoms). Montelukast (leukotriene receptor antagonist): MHRA 2019 warning — neuropsychiatric adverse effects (depression, suicidal ideation) — only use if rhinitis + asthma; counsel patient and caregivers to seek advice promptly if neuropsychiatric symptoms occur (MHRA Drug Safety Update 2019, boxed-warning reminder April 2024); use with caution if there is a history of psychiatric illness.
The montelukast neuropsychiatric warning issued by the MHRA in 2019 significantly changed the prescribing position of this drug in allergic rhinitis and asthma — based on accumulating post-marketing evidence, the MHRA now requires that: (1) prescribers explain potential neuropsychiatric effects (sleep disturbance, nightmares, depression, suicidal ideation, anxiety, aggression, hallucinations) to patients before prescribing; (2) patients and caregivers are told to speak to their prescriber or seek urgent help if neuropsychiatric symptoms occur (reinforced with a boxed warning in April 2024); (3) montelukast is stopped immediately if neuropsychiatric symptoms develop; and (4) children and adolescents are particularly closely monitored. In the UK montelukast is licensed for seasonal allergic rhinitis only in people who also have asthma, so it is not used for rhinitis alone. The drug retains a role in combined asthma + rhinitis (where it treats both simultaneously) and in exercise-induced bronchospasm, but should not be used as routine first-line rhinitis therapy given the safety profile and the availability of equally effective intranasal corticosteroids.
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Treat

Allergen Immunotherapy, Biologics & Food Allergy

Allergen immunotherapy (SLIT/SCIT) — specialist-initiated, local commissioning
Requires a compatible clinical history with confirmed relevant sensitisation, and moderate to severe symptoms despite appropriate pharmacotherapy and adherence. Assess and control asthma before initiation; do not start during an unstable asthma exacerbation. HDM SLIT (Acarizax 12 SQ-HDM, NICE TA1045): initiated by a physician experienced in allergic disease, with the first dose and initiation pathway per the product information and local specialist protocol, following local commissioning arrangements — not a general GP treatment for any positive HDM test. Grass/tree-pollen SLIT (e.g. Grazax) and venom immunotherapy: specialist/local commissioning arrangements. SCIT must be given in specialist facilities with immediate resuscitation capability. Contraindications include uncontrolled asthma, eosinophilic oesophagitis, autoimmune disease and immunosuppression (see product information).
Biologics for severe allergic disease
Omalizumab (Xolair) (anti-IgE): for severe allergic asthma (uncontrolled on high-dose ICS + LABA). Also approved under NICE TA339 (2015) for severe chronic spontaneous urticaria (CSU; UAS7 28 or more) not responding to H1-antihistamines and leukotriene receptor antagonists, age 12 and over — initiated and managed by secondary-care specialists, with objective assessment such as UAS7. Dose (SPC): asthma — 75–600 mg SC every 2–4 weeks by baseline IgE and weight; CSU — 300 mg SC every 4 weeks (not IgE-based). Dupilumab (Dupixent) (anti-IL-4Rα): for moderate-severe atopic eczema + severe allergic asthma + eosinophilic oesophagitis + chronic rhinosinusitis with nasal polyps. SC injection, usually every 2 weeks. Mepolizumab/benralizumab (anti-IL-5/IL-5Rα): severe eosinophilic asthma. All specialist-initiated — GP monitoring of injection sites, infections, safety bloods.
Food allergy management and OIT
Peanut oral immunotherapy (OIT): PALFORZIA (was licensed in the UK for peanut allergy age 4-17; discontinued by the manufacturer, NICE TA769 withdrawn) — gradually increasing peanut doses over months to achieve desensitisation. Specialist-led oral immunotherapy — not a routine GP treatment. NICE TA769 (2022) recommended it for ages 4–17 in specialist paediatric allergy centres, but NICE has withdrawn TA769 because Stallergenes Greer discontinued the Palforzia initial dose escalation pack: no new patients start it in the UK, and anyone already on it needs a specialist plan. Milk and egg OIT: evidence-based, performed in specialist paediatric allergy centres. Elimination diet guidance: managed by specialist dietitian (BSACI food allergy pathway) — nutritional deficiency risk from elimination diets without dietitian guidance (particularly milk in children — calcium + vitamin D).

Next steps: see Anaphylaxis · Urticaria · Angioedema · Allergic rhinitis · Asthma · Atopic eczema

Dupilumab for atopic eczema represents one of the most significant treatment advances in dermatology in decades — it targets the shared IL-4/IL-13 receptor chain (IL-4Rα), blocking both IL-4 and IL-13 signalling, the central cytokines driving type 2 (Th2) inflammatory responses in atopic disease. Clinical trial data (SOLO 1 and 2, CHRONOS): substantially more patients with severe atopic eczema achieve IGA 0-1 (clear or almost clear skin) at 16 weeks than with placebo. NICE TA534 (2018) approval covers adults with moderate-to-severe atopic eczema inadequately controlled by topical treatments and at least one systemic treatment (ciclosporin, azathioprine, or methotrexate). The key GP roles: referring appropriate patients (moderate-to-severe atopic eczema despite adequate topical treatment, failed or contraindicated systemic immunosuppressant), monitoring for injection site reactions and conjunctivitis (dupilumab-related conjunctivitis, often requiring ophthalmology co-management), and ensuring baseline and monitoring bloods are performed as per shared care agreement.
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Lifestyle

Allergen Avoidance, Patient Education & Anaphylaxis Preparedness

Adrenaline auto-injector — carrying and training The key principle is immediate access: carry two in-date AAIs at all times. Additional devices (e.g. a spare at school) may be needed for practical safeguarding arrangements, particularly in children, but this is individualised. Train patient + parents/carers + school staff (Anaphylaxis Campaign) on the specific brand prescribed; retrain whenever the brand changes and at repeat prescribing. Check expiry: replace when expired even if unused. Keep the AAIs with the written brand-specific action plan in a clearly labelled case.
Food allergy — label reading and "may contain" warnings The 14 major allergens must be declared on pre-packaged food in the UK (EU Food Information for Consumers Regulation 2014). Learn the technical names: milk (lactalbumin, casein, whey), egg (albumin, ovalbumin), peanut, tree nuts (listed individually), wheat (gluten, flour), sesame, celery, mustard, sulphites. "May contain" warnings: precautionary allergen labels (PAL) — voluntary, inconsistently used. UK allergy consensus: advise high-risk patients (previous anaphylaxis) to avoid "may contain" for their relevant allergen. Natasha's Law (2021): all pre-packaged for direct sale food must label all 14 allergens.
House dust mite reduction measures Environmental interventions have variable clinical benefit and should not replace pharmacotherapy — offer only as optional, low-certainty practical advice: allergen-impermeable mattress and pillow covers, washing bedding at ≥60°C, reducing bedroom carpets and soft toys, and lowering indoor humidity. Immunotherapy for moderate-severe HDM allergy not controlled by pharmacotherapy via the specialist/local pathway.
Pet allergy management Cat allergen can persist in the home for a prolonged period after a cat is removed, so improvement after rehoming may be slow. Optional, low-certainty measures if not rehoming: HEPA air purifiers and keeping the cat out of the bedroom. Washing the cat and commercial anti-Fel d 1 cat food have uncertain clinical benefit and should not be presented as proven interventions. Allergen immunotherapy for animal allergy is specialist-led.
Hay fever seasonal management Start treatment 2-4 weeks BEFORE pollen season (March for tree pollen, May for grass pollen). Pollen calendar: use the Met Office pollen forecast for daily counts. Optional, low-certainty practical measures on high pollen days: keep windows closed, change clothes and shower after being outdoors, wrap-around sunglasses; a barrier balm in the nostrils is optional rather than a standard recommendation. Monitor pollen forecast via MetOffice app.
Occupational allergy awareness Occupational asthma: bakers (flour dust), healthcare workers (latex), hairdressers (persulfate bleaches), painters (isocyanates in spray paint), animal handlers. Refer to occupational physician if work-related allergen identified. If occupational asthma confirmed: removal from exposure is usually required — medicolegal implications (COSHH Regulations, industrial injury benefit). RAST/SPT for occupational allergens (specialist).
Chronic urticaria management Chronic spontaneous urticaria (CSU): recurrent wheals for more than 6 weeks without an identifiable trigger. Confirm wheals last less than 24 hours and leave no bruising or pigmentation; ask about inducible triggers, infection, NSAIDs and ACE inhibitors. Routine ANA, thyroid peroxidase antibodies or extensive testing are not indicated in uncomplicated CSU — consider a limited FBC and other tests only when clinically indicated. Investigate urticarial vasculitis if lesions are painful, last more than 24–48 hours, bruise or leave residual pigmentation, or come with systemic symptoms; C4/C1-inhibitor testing for recurrent angioedema without urticaria. Treatment: a regular second-generation H1 antihistamine; if inadequate, consider off-label up-dosing to a maximum of four times the usual dose after checking renal/hepatic function, age, pregnancy and sedation risk. Do not routinely combine different H1 antihistamines; H2 blockers have insufficient evidence for routine use; montelukast may be considered selectively but is not mandatory. Omalizumab (NICE TA339) is initiated and managed in secondary care with objective assessment such as UAS7. Do not use long-term systemic corticosteroids.
Psychological impact of allergy and anaphylaxis Food allergy anxiety is a significant and underrecognised cause of health-related anxiety in children and adults. Anxiety can impair social eating and school participation, and some patients develop post-traumatic symptoms after severe anaphylaxis (avoidance, hypervigilance, intrusive memories). NHS Talking Therapies referral for allergy-specific anxiety. Allergy UK and Anaphylaxis Campaign (anaphylaxis.org.uk): peer support, social eating advice, restaurant communication cards.
The Natasha's Law (UK Food Information (Amendment) (England) Regulations 2021) changed the labelling requirements for pre-packaged for direct sale (PPDS) food following the death of Natasha Ednan-Laperouse from anaphylaxis to sesame in a Pret a Manger baguette in 2016 — before this law, PPDS food (food packaged on site before sale — sandwiches, salads, bakery items) was exempt from full allergen labelling. Now all PPDS food must display a full ingredients list with all 14 major allergens highlighted. GPs managing food-allergic patients should advise: (1) always read the label on PPDS food; (2) ask staff about allergens in loose or freshly prepared food (legal duty of food businesses to provide allergen information on request); (3) allergy cards (translated into multiple languages) are available from Allergy UK for communicating allergy needs in restaurants. Despite legislative improvements, accidental exposure remains the leading cause of fatal anaphylaxis in young adults with food allergy.
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Safety

Follow-Up, Review & Patient-Held Safety Plans

Annual allergy review (GP — food/venom allergy)
Record: current weight and device dose; expiry dates; possession of two devices (physically carried); brand-specific technique demonstration; written plan (update for new allergens, weight change or new co-prescriptions — beta-blockers reduce adrenaline efficacy); asthma control (poor asthma control is a major risk factor for fatal food anaphylaxis); new reactions and cofactors; referral status and need for specialist reassessment.
Allergen immunotherapy monitoring
SLIT (grass, HDM): after specialist initiation and per local commissioning, GP may continue prescribing and monitor — check compliance, local reactions (sublingual tingling/swelling — expected, not anaphylaxis), systemic reactions (rare with SLIT, common with SCIT). Any systemic reaction to SCIT: stop and refer back to allergy clinic. Annual symptom reassessment (VAS or TNSS — total nasal symptom score) to confirm benefit.
Drug allergy de-labelling follow-up
After successful assessment and challenge in a governed de-labelling service: document "allergy label removed" clearly in GP record (allergy section, code as resolved/incorrect). Inform patient in writing. This reduces antibiotic restrictions and improves future antimicrobial prescribing options.
Biologics shared care
Omalizumab: inject every 2-4 weeks (patient self-administers or practice nurse). Check IgE + weight-adjusted dose annually. Dupilumab: self-injection, usually every 2 weeks. Monitor: EASI score, DLQI, conjunctivitis symptoms, injection site reactions. Annual FBC (eosinophil rebound on stopping dupilumab — specialist decision).
999
Anaphylaxis — sudden airway, breathing or circulation problems, usually with skin/mucosal changes (skin features may be absent) · Angioedema of the tongue or larynx
Urgent allergy clinic (within 2-4 weeks)
Any history of anaphylaxis not yet referred · Systemic reaction to venom (VIT assessment) · Significant food reaction (not a positive test alone) · Suspected mast-cell disease or persistently raised baseline tryptase (specialist interpretation) · Recurrent angioedema without urticaria (C4/C1-inhibitor; urgent if airway involvement)
Do not routinely
Broad food or IgE screening panels · serum IgG, Vega testing, hair analysis or applied kinesiology · drug-specific IgE to diagnose drug allergy in primary care · AAI for a positive test alone · component testing without specialist advice · bone-marrow work-up for raised tryptase from primary care
The beta-blocker interaction with adrenaline auto-injectors is a critical drug interaction in allergy management — beta-blockers (both selective beta-1 blockers like bisoprolol/atenolol and non-selective like propranolol/carvedilol) significantly impair the cardiovascular response to adrenaline during anaphylaxis. The mechanisms: beta-blockers block the beta-2 receptor-mediated bronchodilation (worsening the bronchospasm of anaphylaxis), block the heart rate and contractility response to adrenaline (reducing the pressor effect), and can cause paradoxical hypertension from unopposed alpha-1 vasoconstriction with adrenaline. The clinical consequence: patients on beta-blockers who have anaphylaxis may require higher doses of adrenaline, require IV glucagon (to bypass beta-blockade via adenylate cyclase), and have a significantly higher risk of fatal anaphylaxis. GPs prescribing beta-blockers to patients with known anaphylaxis risk should document this interaction, consider whether the beta-blocker indication can be met by an alternative drug class (calcium channel blockers, ACE inhibitors for hypertension), and ensure the allergy team is aware. If beta-blocker is unavoidable: record the interaction and make sure the allergy team is aware; glucagon may be needed in hospital for anaphylaxis refractory to adrenaline in a beta-blocked patient.
Educational use only. Based on NICE NG258 (2026, replaced CG134) Anaphylaxis: assessment and referral, Resuscitation Council UK Emergency treatment of anaphylaxis (2021), MHRA Drug Safety Update: adrenaline auto-injectors — safe-use advice, BSACI guidance (anaphylaxis, AAI prescribing in primary care), NICE CG116 Food allergy in under-19s, NICE CG183 Drug allergy, NICE HTG413 (formerly DG24) Multiplex allergen testing, BSACI penicillin allergy de-labelling by non-allergists (2022), BSACI Hymenoptera venom allergy guideline (2011), NICE TA339 Omalizumab for chronic spontaneous urticaria, NICE TA1045 12 SQ-HDM SLIT (Acarizax), NICE TA769 Peanut oral immunotherapy (2022, withdrawn), NICE TA534 Dupilumab (2018), BSACI rhinitis guideline (sublingual immunotherapy), MHRA Montelukast 2019, your local formulary / APC website, adrenaline and antihistamine SPCs.