Allergy Treatment

Dr Jason Roth (MED0001185485) — Specialist Otolaryngologist & Head and Neck Surgeon, specialist registration in Otorhinolaryngology, Head & Neck Surgery.

Allergic rhinitis — commonly called hayfever — is one of the most prevalent chronic conditions in Australia, affecting approximately 18% of the population at some point in their lives. It is far more than a seasonal nuisance: persistent, inadequately managed allergic rhinitis drives chronic nasal obstruction, sleep disturbance, and reduced daytime function, and is the most common underlying condition in patients presenting to ENT with chronic sinus disease. Understanding the mechanisms, treatment hierarchy, and long-term management options for allergic rhinitis is central to managing many ENT patients effectively.

The Immunology of Allergic Rhinitis

Allergic rhinitis is an IgE-mediated hypersensitivity response to inhaled allergens. On initial exposure to an allergen — a protein from house dust mite, pollen, mould, or animal dander — sensitised individuals produce specific IgE antibodies that bind to mast cells in the nasal mucosa. On subsequent allergen exposure, the allergen cross-links these IgE molecules on the mast cell surface, triggering degranulation and the release of histamine, prostaglandins, leukotrienes, and other inflammatory mediators.

This produces the immediate phase reaction — sneezing, watery rhinorrhoea, nasal itch, and nasal congestion — that begins within minutes of allergen exposure. Several hours later, a late phase reaction driven by eosinophil recruitment causes prolonged nasal blockage and mucosal oedema. Chronic allergen exposure perpetuates ongoing eosinophilic inflammation that gradually remodels the nasal mucosa, progressively worsening obstruction over years.

Allergic rhinitis is classified as intermittent (symptoms fewer than 4 days per week or fewer than 4 consecutive weeks) or persistent (symptoms 4 or more days per week and more than 4 consecutive weeks), and as mild or moderate-severe depending on the impact on daily activities, sleep, and work or school performance.

Common Allergens in Australia

The allergen profile in Australia reflects the local climate and environment:

House dust mite (Dermatophagoides pteronyssinus and D. farinae): The dominant perennial allergen in coastal and humid regions, including Sydney. The allergenic proteins are contained in mite faecal pellets. Levels are highest in mattresses, bedding, carpets, and upholstered furniture.
Grass pollens: The primary cause of seasonal (spring/summer) allergic rhinitis in temperate Australia. Rye grass is particularly significant. The November–December pollen season in Sydney coincides with the peak of thunderstorm asthma risk.
Tree pollens: Contribute to spring rhinitis, particularly from plane trees, birch, and olive.
Mould spores (Alternaria, Cladosporium): Relevant in humid climates and following rain. Alternaria sensitisation is associated with a more severe asthma phenotype.
Cat and dog dander: Common triggers in pet-owning households. Cat allergen (Fel d 1) is particularly sticky and can remain detectable in homes for months after cat removal.
Cockroach: Increasingly recognised as a significant indoor allergen, particularly in urban environments.

The Impact of Untreated Allergic Rhinitis

Poorly controlled allergic rhinitis has consequences that extend well beyond the nose:

Turbinate Hypertrophy

The inferior turbinates are highly vascular structures on the lateral wall of the nasal cavity, covered by respiratory mucosa containing a rich submucosal venous plexus that responds to allergen exposure by engorgement. Chronic allergen-driven inflammation progressively enlarges the turbinate mucosa and, over years, causes irreversible submucosal fibrosis. The result is persistent nasal obstruction that persists even when allergen exposure ceases and medical treatment is optimised. Turbinate hypertrophy of this degree requires surgical reduction (turbinoplasty) to restore adequate airway, though medical treatment should continue to address the underlying allergic inflammation.

Chronic Rhinosinusitis

Allergic rhinitis promotes the development of chronic rhinosinusitis by impairing mucociliary clearance, promoting oedema at the sinus ostia, and sustaining eosinophilic inflammation that can extend into the paranasal sinuses. Patients with allergic rhinitis are significantly more likely to develop chronic rhinosinusitis with nasal polyps than the non-atopic population.

Sleep-Disordered Breathing

Nasal obstruction from allergic rhinitis impairs nasal breathing during sleep, promoting mouth breathing and increasing the likelihood of snoring and obstructive sleep apnoea. Nasal patency is an important determinant of upper airway stability during sleep, and improving nasal airflow in allergic rhinitis patients with sleep-disordered breathing can substantially reduce apnoea severity.

Asthma

Allergic rhinitis and asthma are closely linked: approximately 80% of patients with asthma have allergic rhinitis, and the presence of allergic rhinitis is a significant risk factor for asthma development. The concept of the “unified airway” — in which the upper and lower airways are understood as a single functional unit — means that controlling nasal inflammation has measurable downstream benefits for asthma control.

Investigation and Allergy Testing

Allergy testing allows identification of specific sensitisations to guide allergen avoidance and to determine suitability for allergen immunotherapy. The two principal methods are:

Skin Prick Testing

A small drop of standardised allergen extract is placed on the forearm and a lancet is used to introduce the allergen through the skin. A positive result — a wheal of at least 3mm — indicates specific IgE sensitisation to that allergen. Skin prick testing is the preferred first-line test: it is rapid, relatively inexpensive, and provides immediate results. It requires cessation of antihistamines for 5–7 days beforehand. Skin prick testing is not performed at Dr Roth’s practice — patients requiring allergy testing are referred to an allergist or clinical immunologist.

Specific IgE Blood Testing (RAST/ImmunoCAP)

Measurement of serum specific IgE to individual allergens can be performed in patients who cannot have skin prick testing — including those who cannot stop antihistamines, those with extensive skin disease, or those at risk of severe systemic reactions. The results are broadly concordant with skin prick testing though sensitivity is somewhat lower for some allergens.

Treatment

Management of allergic rhinitis follows a stepwise approach, escalating treatment based on symptom severity and the patient’s response.

Step 1 — Allergen avoidance

Where the triggering allergen can be identified, reducing exposure is the foundation of management. House dust mite avoidance measures — allergen-impermeable covers for mattress, pillows, and duvets; weekly washing of bedding in hot water (above 55°C); reducing carpet and soft furnishings; maintaining low indoor humidity — can reduce mite allergen loads meaningfully, though complete elimination is rarely achievable. For pollen-sensitive patients, keeping windows closed during high pollen periods and checking daily pollen counts before outdoor activity can reduce symptoms. For pet allergy, removing the pet is most effective, though allergen levels can persist for months after removal and most families choose not to remove pets — in this case, keeping pets out of the bedroom provides partial relief.

Step 2 — Intranasal corticosteroid sprays

Intranasal corticosteroids are the most effective treatment for allergic rhinitis, superior to antihistamines for nasal congestion and overall symptom control. They act locally to reduce mucosal eosinophilic inflammation and vascular engorgement. Available agents include mometasone (Nasonex), fluticasone furoate (Avamys), fluticasone propionate (Flixonase), budesonide (Rhinocort), and beclometasone. All are safe for long-term use in adults and children when used correctly. Systemic absorption is minimal. Onset of action is gradual — two to three weeks of consistent use are needed to reach peak effect. Correct technique is critical: the nozzle should be directed laterally (toward the ear) rather than toward the nasal septum to minimise contact with the septum and reduce the small risk of septal perforation with prolonged use. Regular use is more effective than as-needed use.

Step 3 — Oral antihistamines

Second-generation non-sedating antihistamines (cetirizine, loratadine, fexofenadine, desloratadine) are effective for sneezing, rhinorrhoea, nasal and ocular itch, and to a lesser extent watery eye symptoms. They are less effective than intranasal corticosteroids for nasal congestion. They can be used on an as-needed basis for intermittent symptoms or regularly for persistent allergic rhinitis, particularly when ocular symptoms are prominent. Combined intranasal corticosteroid / antihistamine sprays (Dymista — fluticasone/azelastine) are available for patients with persistent moderate-severe symptoms not controlled by intranasal corticosteroid alone.

Step 4 — Saline nasal irrigation

High-volume saline nasal rinse (NeilMed Sinus Rinse, Flo Saline Plus) washes allergens, inflammatory mediators, and mucus from the nasal lining, reducing direct allergen-mucosal contact and improving the effectiveness of topical nasal sprays. It is a low-risk, low-cost adjunct to medical management that provides meaningful symptom relief in many patients when used regularly. Correct technique involves a dedicated nasal rinse bottle with sterile or pre-boiled cooled water.

Step 5 — Allergen immunotherapy

Allergen immunotherapy — also called desensitisation — is the only treatment capable of modifying the underlying allergic response, rather than simply suppressing symptoms. It involves repeated controlled exposure to gradually increasing doses of the relevant allergen, inducing immunological tolerance characterised by a shift from a Th2 inflammatory response toward regulatory T-cell responses and increased allergen-specific IgG4. Both subcutaneous immunotherapy (SCIT — injection) and sublingual immunotherapy (SLIT — drops or tablets) are available and evidence-based for dust mite, grass pollen, and several other allergens. A treatment course typically lasts three years. Immunotherapy is most appropriate for patients with documented sensitisation who have not achieved adequate control with optimised pharmacotherapy. Please note that allergen immunotherapy is not administered at Dr Roth’s practice — referral to an allergist is arranged where indicated.

Surgical treatment — turbinoplasty

When turbinate hypertrophy has developed as a consequence of chronic allergic rhinitis and is causing persistent nasal obstruction despite optimised medical management, surgical reduction of the inferior turbinates (turbinoplasty) can restore adequate nasal airway with durable, well-tolerated results. Turbinoplasty addresses the structural consequence of chronic allergy — the enlarged turbinate — rather than the underlying immunological process. Medical treatment should therefore be continued postoperatively to prevent recurrence. The procedure is performed endoscopically through the nostril under general anaesthesia and does not leave external scars. Read more about turbinoplasty →

Dr Jason Roth | MBBS, FRACS (ORL-HNS) | MED0001185485
Specialist Otolaryngologist & Head and Neck Surgeon
Specialist registration — Otorhinolaryngology, Head & Neck Surgery
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