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 (urticaria + breathing difficulty/hypotension/GI symptoms, i.e., reactions affecting 2 or more organ systems) must leave the GP surgery with: two adrenaline auto-injectors (EpiPen 300 mcg for adults and children over 25-30 kg; 150 mcg for children under 25-30 kg), 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). The NICE guideline NG80 (Food Allergy) 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.

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. In population studies, approximately 30-40% of adults are sensitised to at least one common inhalant allergen (grass pollen, house dust mite) without having clinically significant allergic rhinitis. For food allergens, sensitisation rates considerably exceed clinical allergy prevalence — approximately 8% of children have a detectable peanut sIgE, while clinical peanut allergy affects only approximately 1-2%. 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.

The serum baseline tryptase is the most important investigation for excluding systemic mastocytosis in patients with recurrent unexplained anaphylaxis or very severe allergic reactions — tryptase is an enzyme stored in mast cell granules and released on mast cell activation. A persistently elevated baseline serum tryptase above 20 µg/L (or above 11.4 µg/L on three separate occasions) is a strong indicator of clonal mast cell disease (systemic mastocytosis). The clinical importance: patients with systemic mastocytosis have an abnormally high burden of mast cells throughout the body, meaning that when triggered (by venom, drugs, physical stimuli), the anaphylactic reaction is disproportionately severe and can be fatal. Any patient with recurrent severe anaphylaxis, particularly insect venom anaphylaxis, should have a baseline tryptase measured 24-48 hours after the acute reaction (when tryptase levels have returned to their baseline — peak tryptase measured within 1-2 hours of anaphylaxis itself confirms the diagnosis, but baseline tryptase between reactions identifies underlying mastocytosis).

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. OAS does NOT require adrenaline auto-injectors or dietary elimination — it requires explanation, reassurance, and advice that cooking food eliminates the reaction.

Venom immunotherapy (VIT) for bee or wasp allergy is one of the most effective and cost-effective interventions in allergy medicine — it reduces the risk of future anaphylaxis from a venom sting from approximately 60% (without VIT) to less than 5% (with VIT), with protection sustained long-term after a 3-5 year 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. GPs should ask about stinging insect allergy at every prescription of adrenaline auto-injectors and ensure allergy clinic referral is in place.

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 are reviewed within 4 weeks of starting for neuropsychiatric symptoms; (3) montelukast is stopped immediately if neuropsychiatric symptoms develop; and (4) children and adolescents are particularly closely monitored. The MHRA has also issued an alert that patients labelled with a mental health condition should generally not be prescribed montelukast 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.

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): approximately 50-55% of patients with severe atopic eczema achieve IGA 0-1 (clear or almost clear skin) at 16 weeks, compared to approximately 15-18% with placebo. The NICE approval covers adults and adolescents 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 (EASI >21, DLQI >10 despite adequate topical treatment, failed or contraindicated systemic immunosuppressant), monitoring for injection site reactions and conjunctivitis (approximately 10% — dupilumab-related conjunctivitis, often requiring ophthalmology co-management), and ensuring baseline and monitoring bloods are performed as per shared care agreement.

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.

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: the patient must carry glucagon 1 mg IM in addition to their AAI.