Allergic Rhinitis — Hay Fever Causes, Symptoms & Treatment Guide — Symptoms, Causes & Treatment | MyMedicPlus

Allergic rhinitis is an IgE-mediated allergic inflammation of the nasal mucosal lining triggered by inhaled allergens, characterised by mast cell degranulation and type 2 T-helper (Th2) immune response causing nasal inflammation, mucus secretion, and vascular leak. It is classified into seasonal allergic rhinitis (hay fever, triggered by tree, grass, and weed pollens during specific seasons) and perennial allergic rhinitis (year-round symptoms triggered by indoor allergens — house dust mites, pet dander, cockroach allergen, and mould spores). The ARIA (Allergic Rhinitis and its Impact on Asthma) classification further grades severity as intermittent (symptoms fewer than 4 days/week or fewer than 4 weeks/year) or persistent, and as mild or moderate-severe based on impact on sleep, daily activities, work/school, and symptom severity. Allergic rhinitis affects 10-30% of adults and up to 40% of children worldwide, making it the most prevalent allergic condition globally and the fifth most common chronic disease overall. Despite being often perceived as trivial, allergic rhinitis causes substantial morbidity — sleep disruption, impaired concentration and academic performance, increased workplace absenteeism and presenteeism, and a significant economic burden. It is also strongly associated with asthma (30-40% comorbidity), chronic rhinosinusitis, otitis media with effusion, and atopic dermatitis — collectively representing the 'atopic march.'

Allergic rhinitis results from IgE-mediated sensitisation to inhaled allergens. On initial allergen exposure, dendritic cells present allergen peptides to naive T-cells, driving Th2 differentiation and IgE production by B-cells. On re-exposure, allergen cross-links mast-cell-bound IgE, triggering degranulation and release of histamine (causing sneezing, itch, rhinorrhoea), leukotrienes (causing nasal congestion), prostaglandins, and cytokines (IL-4, IL-5, IL-13 — sustaining eosinophilic inflammation). Seasonal allergens: tree pollens (birch, hazel — early spring), grass pollens (ryegrass, timothy — May-July), and weed pollens (mugwort, ragweed — late summer/autumn) vary by geography and season. Perennial indoor allergens: house dust mites (Dermatophagoides pteronyssinus and farinae — the most common perennial allergen globally, thriving in warm humid bedding and carpets), cat and dog dander (albumin proteins in saliva, skin, and urine — among the most potent allergens), cockroach allergen, and Alternaria and Cladosporium moulds. Risk factors: strong family history of atopy (if both parents are atopic, risk in child approaches 70-80%); early sensitisation; Western lifestyle (hygiene hypothesis — reduced microbial exposure shifting immune balance toward Th2 responses); urban living; air pollution (nitrogen dioxide, ozone, diesel particles — all enhance allergen sensitisation); tobacco smoke; and occupational allergen exposures (flour, latex, animal proteins — occupational rhinitis).

The hallmark symptoms of allergic rhinitis form the classic early-phase response (within minutes of allergen exposure): repetitive explosive sneezing (often in runs of 5-10+), profuse watery rhinorrhoea (clear mucus), bilateral nasal obstruction/congestion (often worse at night — contributing to snoring, sleep apnoea, and poor sleep quality), intense nasal itch (often extending to soft palate, throat, and ears — 'the allergic salute'), and postnasal drip causing throat clearing and sore throat. Late-phase response (4-8 hours after exposure): persistent nasal congestion from eosinophilic mucosal oedema. Ocular symptoms (allergic conjunctivitis) — itchy, watery, red, and gritty eyes — occur in 50-70% of allergic rhinitis patients and cause significant impairment. Constitutional effects: persistent nasal congestion causes sleep disruption and non-restorative sleep, leading to daytime somnolence, impaired concentration, fatigue, and cognitive slowing — with a measurable negative impact on exam performance in students during pollen season (studies show up to 40% reduction in exam scores during high-pollen days). Loss of smell (hyposmia or anosmia) occurs in chronic persistent disease. The 'allergic salute' — rubbing the nose upward with the palm — may leave a characteristic 'allergic crease' across the nose. Physical signs: pale, boggy nasal mucosa; dark circles under the eyes ('allergic shiners'); Dennie-Morgan lines (infraorbital skin folds) — particularly in children.

Diagnosis is primarily clinical — based on a characteristic history of IgE-mediated nasal and ocular symptoms temporally related to known allergen exposures, confirmed by allergen testing. Skin prick testing (SPT) is the gold standard for allergen identification: a positive result (wheal diameter 3 mm or more than the negative control at 15 minutes) demonstrates sensitisation; a positive SPT interpreted in the context of clinical symptoms confirms clinically relevant allergy. Specific serum IgE (sIgE) testing using ImmunoCAP is preferred when SPT is not feasible — due to antihistamine use, severe eczema, dermatographism, or risk of anaphylaxis — and provides objective allergen-specific antibody levels; it has slightly lower sensitivity than SPT but good specificity. Nasal endoscopy: performed if structural nasal pathology (nasal polyps, septal deviation, adenoidal hypertrophy) or sinusitis is suspected, or if symptoms do not respond as expected to treatment. The Total Nasal Symptom Score (TNSS) or Rhinoconjunctivitis Total Symptom Score (RTSS) provides objective symptom quantification for monitoring treatment response. ARIA classification (severity and chronicity) guides treatment choices. Spirometry or peak flow measurement and asthma assessment should be performed in any patient with allergic rhinitis, given the high comorbidity. Component-resolved diagnosis (CRD) — testing specific allergen molecular components — is increasingly used in specialist settings to distinguish true primary sensitisation from cross-reactive proteins and to guide allergen immunotherapy selection.

Treatment is step-based according to ARIA classification and symptom severity. Allergen avoidance is foundational — reduce exposure to identified allergens (impermeable dust-mite mattress and pillow covers, regular hot washing of bedding, air purifiers with HEPA filters for pet and mould allergy, pollen avoidance strategies including monitoring pollen counts, keeping windows closed, showering after outdoor activities). Saline nasal irrigation (isotonic or hypertonic — using nasal douche or neti pot) washes allergens and inflammatory mediators from nasal passages and reduces symptom load as an adjunct to medication. Intranasal corticosteroids (INCSs) are the most effective pharmacological treatment for persistent or moderate-severe allergic rhinitis: fluticasone furoate (Avamys), mometasone furoate (Nasonex), fluticasone propionate (Flixonase), or budesonide — used once or twice daily; takes 2-4 weeks for full anti-inflammatory effect; minimal systemic absorption at therapeutic doses; proven to reduce all nasal symptoms including congestion (which antihistamines do not adequately address). Antihistamines: second-generation non-sedating oral antihistamines (cetirizine 10 mg, loratadine 10 mg, fexofenadine 120-180 mg, bilastine 20 mg, levocetirizine 5 mg) provide rapid relief of sneezing, rhinorrhoea, and ocular itching within 30-60 minutes; suitable for mild or intermittent disease; daily use is preferred over 'as-needed' for persistent rhinitis. Combined intranasal antihistamine and corticosteroid (MP-AzeFlu — azelastine plus fluticasone) provides faster and superior relief than either alone. Leukotriene receptor antagonists (montelukast) can be added particularly if asthma coexists. Decongestants (oxymetazoline nasal spray, pseudoephedrine tablets): short-term use only (maximum 3-5 days) — rebound rhinitis (rhinitis medicamentosa) occurs with prolonged topical use. Allergen immunotherapy (AIT) — subcutaneous immunotherapy (SCIT, allergy injections) or sublingual immunotherapy (SLIT, drops or tablets — e.g., grass SLIT-tablet Grazax, HDM SLIT-tablet Acarizax) — is the only disease-modifying treatment: a 3-year course reduces allergen-specific sensitivity, symptom scores by 30-40%, medication requirements, risk of asthma development, and may induce lasting immunological tolerance after stopping. Dupilumab (anti-IL-4/IL-13 biologic) is approved for severe chronic rhinosinusitis with nasal polyps and may benefit severe refractory allergic rhinitis.

Poorly controlled or untreated allergic rhinitis leads to multiple complications. Chronic rhinosinusitis — persistent mucosal oedema from allergic inflammation obstructs sinus ostia, leading to recurrent sinusitis; nasal polyps develop in approximately 20-40% of patients with longstanding perennial rhinitis, causing severe nasal obstruction, anosmia, and requiring endoscopic sinus surgery in refractory cases. Asthma development: 30-40% of allergic rhinitis patients develop asthma ('united airway disease' concept — the same IgE-mediated Th2 process involves both upper and lower airways), and uncontrolled rhinitis makes asthma harder to control; conversely, effective rhinitis treatment reduces asthma exacerbation risk by approximately 50%. Otitis media with effusion (glue ear) — eustachian tube dysfunction from allergic nasal inflammation causes middle ear fluid accumulation, particularly in children — contributing to conductive hearing loss and delayed language development. Sleep-disordered breathing: severe nasal congestion causes mouth breathing, snoring, and obstructive sleep apnoea, particularly in children — leading to growth delay, behavioural problems, and learning difficulties. Dental malocclusion (high-arched palate, open bite) from chronic mouth breathing in children. Quality of life equivalent to chronic diseases like diabetes — validated RQLQ (Rhinoconjunctivitis Quality of Life Questionnaire) scores confirm impairment comparable to moderate-severe medical conditions.

Allergen avoidance is the primary preventive strategy and reduces allergen load even if not eliminating symptoms entirely. For house dust mite allergy: use impermeable allergen-barrier mattress and pillow encasings, wash bedding weekly in water above 60°C (kills mites), reduce indoor humidity below 50%, avoid carpets and heavy upholstered furniture in bedrooms, use HEPA vacuum filters. For pet allergy: keep pets out of bedrooms, use HEPA air purifiers, wash hands after contact. For pollen allergy: monitor daily pollen forecasts and avoid outdoor activities on high-count days, keep windows closed, shower and change clothes after outdoor activities, use sunglasses outdoors, avoid drying clothing outdoors during high pollen. Daily saline nasal irrigation (isotonic or hypertonic) removes allergens and inflammatory secretions from nasal passages, reducing symptom burden. For seasonal allergic rhinitis: begin intranasal corticosteroid spray 1-2 weeks before the anticipated pollen season to establish pre-emptive anti-inflammatory protection before symptoms start. Allergen immunotherapy (subcutaneous or sublingual) is the only treatment that provides genuine long-term prevention by modifying the underlying immune response — should be considered in patients with moderate-severe persistent symptoms or those wishing to avoid long-term medication. Annual review with an allergist ensures optimal management and monitors for developing asthma.

See your GP or an allergist if: nasal symptoms persist for more than 2 weeks despite over-the-counter antihistamines and nasal sprays; symptoms are severe enough to impair sleep, concentration at work or school, or daily activities; you develop new or worsening asthma symptoms (wheeze, chest tightness, cough) alongside rhinitis — both conditions need coordinated management. Seek urgent care for: severe facial pain or swelling with fever (suggesting acute sinusitis with complications); sudden onset of hives, throat swelling, or difficulty breathing after allergen exposure (anaphylaxis — emergency). Refer for allergy testing (skin prick test or specific IgE) if you want to know your specific triggers to guide environmental control or consider allergen immunotherapy. Children with persistent rhinitis causing sleep disruption, behaviour change, or educational difficulties should be referred to an allergist or ENT specialist.