Allergy Treatments Prescribed by UK Doctors

Allergic disease represents a hypersensitivity response in which the immune system mounts an IgE-mediated reaction against normally harmless environmental proteins (allergens).

In the UK, allergic conditions have tripled in prevalence over the past 30 years, with allergic rhinitis (hay fever) now affecting 26% of adults and 10-15% of children.

Allergic rhinitis is classified as intermittent (symptoms fewer than 4 days/week or fewer than 4 consecutive weeks) or persistent (exceeding those thresholds), and as mild or moderate-severe based on impact on sleep, daily activities, and work or school performance.

This ARIA classification guides treatment intensity.

Pathophysiology involves two phases.

The early phase (minutes after allergen exposure) is driven by mast cell degranulation releasing histamine, leukotrienes, and prostaglandins, causing sneezing, rhinorrhoea, and itch.

The late phase (4-8 hours) involves eosinophilic infiltration producing nasal congestion, mucosal oedema, and sustained inflammation.

Common allergen triggers in the UK:

• Tree pollen (birch, oak, ash): February to May
• Grass pollen (timothy, rye): May to July, peak mid-June
• Weed pollen (nettle, dock): June to September
• House dust mite: perennial, worse in autumn and winter
• Animal dander (cat, dog): perennial
• Mould spores (Alternaria, Cladosporium): summer and autumn peaks

Comorbidities are frequent.

Approximately 40% of allergic rhinitis patients have coexistent asthma (the "unified airway" concept), and uncontrolled rhinitis increases asthma exacerbation risk by 2-3 fold.

Allergic conjunctivitis accompanies rhinitis in 60-70% of cases. Chronic rhinosinusitis, nasal polyposis, and otitis media with effusion are additional associated conditions.

Severe allergy (anaphylaxis) affects approximately 1 in 1,333 UK people. Adrenaline auto-injectors and allergen identification through specialist immunology services are essential for this population.

Pharmacotherapy for allergic rhinitis follows a stepwise approach guided by the ARIA classification and NICE Clinical Knowledge Summaries.

Second-generation (non-sedating) antihistamines are first-line oral therapy.

They block H1 receptors peripherally with minimal blood-brain barrier penetration, avoiding the sedation and cognitive impairment of first-generation agents.

Fexofenadine 180 mg once daily is the most potent non-sedating antihistamine and is now the preferred choice for moderate-severe seasonal rhinitis.

It has true non-sedating pharmacology (no CNS penetration at any dose), no cardiac QT prolongation, and no interaction with grapefruit juice (unlike some alternatives).

Duration of action is 24 hours.

Cetirizine 10 mg once daily is effective and widely used. It does cause mild sedation in 5-10% of patients, making it a reasonable choice when allergy-related insomnia is a problem.

Loratadine 10 mg is the least potent of the three but is safe in pregnancy (Category B).

Intranasal corticosteroids (INS) are the single most effective drug class for allergic rhinitis, reducing all four cardinal symptoms: sneezing, itch, rhinorrhoea, and congestion.

Oral antihistamines do not effectively address nasal congestion.

Fluticasone furoate (Avamys) one spray per nostril once daily provides 24-hour efficacy with low systemic bioavailability (0.5%).

Mometasone and fluticasone propionate are alternatives with similar profiles. Onset of benefit occurs within 12 hours, but maximal efficacy requires 1-2 weeks of consistent daily use.

Prescribing strategy:

• Mild intermittent: oral antihistamine PRN
• Moderate-severe or persistent: intranasal corticosteroid daily plus oral antihistamine
• Refractory: add intranasal antihistamine (azelastine) or consider short course of oral prednisolone (10-20 mg for 5-7 days) for severe seasonal exacerbations
• Eye symptoms: add topical ocular antihistamine (olopatadine, azelastine) or chromone (sodium cromoglicate)

Combination intranasal sprays containing fluticasone plus azelastine (Dymista) provide superior relief to either component alone and are an effective step-up option for patients failing monotherapy.

A proportion of allergy sufferers experience inadequate symptom control despite optimised pharmacotherapy.

These patients require additional investigation and consideration of specialist interventions.

Allergen immunotherapy (desensitisation) is the only treatment that modifies the underlying allergic disease process rather than merely suppressing symptoms.

It involves administering gradually increasing doses of the relevant allergen over 3-5 years, inducing immunological tolerance through regulatory T-cell generation and IgG4 blocking antibody production.

Two delivery routes are available in the UK:

• Subcutaneous immunotherapy (SCIT): injections administered in a specialist clinic, typically monthly after an initial updosing phase
• Sublingual immunotherapy (SLIT): daily tablets or drops self-administered at home after the first dose is supervised (e.g., Grazax for grass pollen)

NICE recommends immunotherapy for patients with moderate-severe allergic rhinitis unresponsive to 2 years of optimised pharmacotherapy.

Efficacy data shows 30-40% reduction in symptom scores and 40-50% reduction in rescue medication use, with benefits persisting 7-12 years after completion.

Anaphylaxis management is a critical component of allergy care. Patients at risk must carry two adrenaline auto-injectors at all times. Key elements:

• Adrenaline (epinephrine) 0.3 mg IM is first-line treatment, administered into the anterolateral thigh
• 999 ambulance should be called immediately after adrenaline administration
• Common triggers: peanuts, tree nuts, shellfish, insect venom (wasp/bee), medications (penicillin, NSAIDs), latex
• All patients with anaphylaxis history should be referred to an NHS allergy clinic for trigger identification and management plan

Drug allergy affects 10% of the population by history, though confirmed allergy on testing is far lower (1-2%).

Penicillin allergy is over-reported — 90% of patients labelled as penicillin-allergic tolerate it on formal challenge.

De-labelling through specialist assessment improves antibiotic stewardship and patient outcomes.

Chronic spontaneous urticaria (hives lasting 6+ weeks without identifiable trigger) may require updosing of antihistamines to 4x standard dose under specialist guidance, or addition of omalizumab (anti-IgE monoclonal antibody) per NICE TA339.

Environmental control measures reduce allergen exposure and complement pharmacotherapy. While complete avoidance is rarely achievable, targeted interventions can meaningfully reduce symptom burden.

Pollen exposure reduction during the grass pollen season (May-July):

• Monitor Met Office pollen forecasts and limit outdoor activity when counts exceed 50 grains/m3 (high)
• Pollen peaks in early morning (7-9 am) and evening (5-7 pm); midday outdoor activity may be better tolerated
• Shower and change clothes after outdoor exposure to remove pollen from skin and hair
• Keep windows closed during high-count days; use air conditioning with HEPA filters where available
• Wrap-around sunglasses reduce ocular pollen exposure by 30-50%
• Nasal saline irrigation (NeilMed sinus rinse or similar) physically removes allergen and mucus, reducing symptom scores by 20-30%

House dust mite measures for perennial rhinitis:

• Encase mattress, pillows, and duvets in allergen-proof covers (reduces mite antigen exposure by 90%)
• Wash bedding at 60 degrees Celsius weekly (kills mites; lower temperatures do not)
• Maintain indoor humidity below 50% using dehumidifiers (mites require 70%+ humidity to thrive)
• Remove bedroom carpets where practical; hard flooring reduces dust mite colonisation significantly
• HEPA-filter vacuum cleaners reduce airborne allergen compared with standard vacuums

Pet allergen management when removing the pet is not feasible:

• Keep pets out of bedrooms entirely
• HEPA air purifiers in main living areas reduce airborne Fel d 1 (cat allergen) by 50-60%
• Wash pets weekly (reduces allergen shedding by 85% for 2-3 days)
• Leather or wood furniture collects less allergen than fabric upholstery

Dietary considerations: a Mediterranean diet rich in antioxidants, omega-3 fatty acids, and flavonoids has been associated with reduced allergic rhinitis severity in epidemiological studies.

Vitamin D deficiency (below 50 nmol/L) correlates with more severe allergic disease; supplementation to maintain adequate levels is reasonable.