Allergic rhinitis: A growing concern

Rhinitis refers to inflammation of the nasal passages which results in symptoms such as sneezing, nasal congestion, and airflow obstruction. Rhinitis which is caused by an allergic trigger is known as allergic rhinitis (AR). This accounts for about 75 per cent of total rhinitis cases, while the remaining 25 per cent are termed non-allergic rhinitis.

AR is frequently underdiagnosed and undertreated, largely because its symptoms are often perceived as mild. However, those affected may suffer a significant burden of disease, with disruptions to sleep quality and consequently cognitive and psychomotor function. In addition, AR increases the reactivity of the lower respiratory tract. This may worsen existing asthma or trigger asthmatic symptoms in non-asthmatics.

Living with AR can make it challenging to engage in social and physical activities, often leading to missed days at work. Children face additional difficulties as AR can interfere with education. School absences and reduced productivity are common, especially during hay fever season, which coincides with exam periods. A UK study¹ found that students with seasonal AR performed worse in exams during peak hay fever season. This is especially relevant for those undertaking major exams such as the Leaving Certificate.

AR is a condition with a significant global economic impact. The most recent estimates from the European Union² suggest that the indirect costs of untreated AR, particularly in terms of reduced workplace productivity, could range from €30-50 billion annually.

Globally, AR affects at least 400 million people, with European prevalence rates ranging between 17 and 29 per cent.³ The UK reports a prevalence of 26 per cent and Ireland is likely to have similar figures. Even more concerning is the rising incidence of AR worldwide. Research from the International Study of Asthma and Allergies in Childhood (ISAAC)⁴ revealed an increase in AR prevalence among 13-14 year-olds, rising from 13-19 per cent over an eight-year period. A smaller study in Cork⁵ observed a rise from 7.6-10.6 per cent among children aged six to nine years over a five-year period.

These trends highlight the urgent need for a more proactive approach in the management of this chronic condition. Addressing AR effectively can improve quality-of-life, enhance productivity, and reduce the broader economic burden of this common condition.

The rising prevalence of AR

The factors behind the increasing prevalence of AR remain uncertain. Environmental factors are believed to play a crucial role in the rising incidence of allergies.⁶ In the 1980s, the ‘hygiene hypothesis’ suggested that the modern Western lifestyle, characterised by reduced exposure to infections, leads to fewer type 1 immune responses, thereby increasing susceptibility to allergic conditions. However, recent research has also emphasised the importance of the development of the microbiome in early childhood in establishing allergen tolerance. Antibiotic use and other factors can impair this process.

Pollutants such as cigarette smoke and diesel exhaust fumes have been shown to potentiate AR symptoms. Climate change is also contributing to the problem, with milder temperatures resulting in a prolonged pollen season.

Genetic predisposition remains a significant factor. Atopy, or an inherited tendency to develop allergic diseases, accounts for at least 50 per cent of AR cases.⁷ Multiple susceptibility chromosomal loci linked to AR indicate a complex interplay between genetic and environmental factors.⁸

Pathophysiology of AR

The development of AR occurs in two distinct phases. The first phase, known as sensitisation, begins when an atopic individual is initially exposed to an allergen. Antigen-presenting cells, particularly dendritic cells (DCs), capture the allergen and process it into peptide fragments. These DCs then migrate through the lymphatic system to nearby lymph nodes, where they present the processed allergen to naïve T-cells.

The naïve T-cell becomes activated to express cytokines, which drives the differentiation of these cells to Th2 helper cells. This Th2-dominated environment, rich in interleukin (IL)-4 and IL-13, stimulates B-cells to produce immunoglobulin E (IgE).

At the same time, the activation of B-cells through T-cell-mediated interactions promotes cytokine secretion, particularly IL-4, leading to irreversible immunoglobulin class switching. This results in the production of allergen-specific IgE antibodies, which bind to mast cells and basophils – a process known as primary sensitisation. Alongside this, memory B- and T-cells are generated, allowing for a faster immune response upon future exposure.

The allergic reaction: Phase two

When the individual is re-exposed to the allergen it binds to the sensitised mast cells and triggers their degranulation. This leads to the rapid release of inflammatory mediators such as histamine, leukotrienes, and prostaglandins. These immunochemical mediators increase vascular permeability, eosinophil infiltration, and mucus production.

With repeated allergen exposure, a phenomenon known as nasal priming occurs. Effector cells accumulate within the nasal mucosa, which increases the sensitivity of the nasal passages and leads to a heightened response to even lower allergen concentrations. Additionally, a neural component has been implicated in this hyper-responsiveness, as structural changes in the sensory nerves of the nasal cavity have been observed in individuals with AR.

Understanding these mechanisms is crucial for developing targeted treatments that not only alleviate symptoms, but also modify the underlying immune response to reduce long-term disease progression.

Classification of AR

AR is traditionally categorised as either seasonal or perennial, depending on the nature of the allergen involved. Seasonal AR typically results from sensitisation to airborne allergens such as grass, tree, or weed pollen, as well as fungal spores. In contrast, perennial AR is primarily triggered by indoor allergens like house dust mite or animal dander. This classification is useful for identifying likely allergen triggers and appropriate avoidance strategies.

However, a more modern approach to classification has shifted the focus towards the impact on daily function, as well as the frequency and severity of symptoms. This updated system, introduced by the Allergic Rhinitis and its Impact on Asthma (ARIA)⁹ guidelines in collaboration with the World Health Organisation, provides a more effective framework for guiding treatment decisions (Figure 2). By focusing on how symptoms affect quality-of-life rather than just their seasonal occurrence, this system allows for a more personalised and clinically-relevant approach to managing AR.

Clinical presentation of AR

AR is an IgE-mediated inflammatory response that occurs upon exposure to a specific allergen. This immune reaction leads to inflammation of the nasal mucosa, and in some cases, the conjunctiva.

Typical symptoms include:

• Rhinorrhoea;

• Nasal congestion;

• Sneezing;

• Nasal itching.

In addition to these hallmark nasal symptoms, many individuals also experience:

• Itchy palate;

• Irritated, watery, and itchy eyes;

• Periocular oedema;

• Dark circles under the eyes (often referred to as allergic shiners) (Figure 3).

Beyond the classic nasal and ocular symptoms, AR can also lead to a range of secondary effects due to persistent inflammation and nasal obstruction. Patients may experience:

• Fatigue;

• Snoring and mouth breathing;

• Head heaviness or ‘fuzzy head’;

• Sinus pressure and headaches;

• Post-nasal drip;

• Altered sense of smell and taste.

These symptoms can significantly impact daily life, making effective management crucial for improving overall wellbeing.

Diagnosis of AR

The diagnosis of AR is primarily clinical, based on characteristic symptoms and patient history. However, allergy testing can be performed to identify specific triggers and confirm the diagnosis when required. Skin prick testing (SPT) is the primary method used to identify allergen sensitisation (Figure 4). However, where SPT is not feasible, serum-specific IgE blood testing can be performed to measure IgE antibodies to specific allergens.

In addition to taking a thorough history, a targeted clinical examination is crucial in differentiating AR from other nasal conditions, ensuring accurate diagnosis and effective management. The following features on nasal examination will likely be identified in patients with AR: 

• Enlarged, oedematous nasal turbinates. (Figure 5)

• Increased mucus production.

• Pale mucosal lining – a hallmark sign, particularly in persistent AR.

• Mucosal texture changes: Chronic allergic irritation can lead to a loss of smoothness, with ridging or pitting visible.

• Pre-polypoid tissue: In some cases, early polyp formation may be observed, suggesting prolonged allergic stimulation.

Non-pharmacological management of AR

While allergen avoidance is an essential aspect of managing AR, it is rarely sufficient as a standalone treatment. However, in cases where animal dander is the primary trigger, symptoms can significantly improve if the pet is removed from the home.

Smoking cessation should be advised as it is linked to chronic nasal symptoms and may contribute to the development of nasal polyps. Passive smoking and even exposure to vape aerosols appear to carry similar risks, worsening nasal inflammation.

Regular nasal saline irrigation is a simple yet effective way to manage AR by flushing out mucus, allergens, and inflammatory mediators from the nasal passages while also reducing bacterial burden. Furthermore, saline irrigation has been shown to improve mucociliary function which enhances the natural clearance of irritants.

While these non-pharmacological strategies can help alleviate symptoms, most patients will require additional medical treatment for optimal control of their condition.

Pharmacological management of AR

The choice of treatment for AR depends on the severity and frequency of symptoms, with therapy aimed at reducing inflammation and alleviating discomfort. A stepwise approach to treatment ensures that patients receive the most effective and least invasive therapy for their condition while minimising side-effects.

Mild intermittent symptoms

Second-generation antihistamines are the preferred option for this patient cohort due to their lower sedative and anticholinergic side-effects. Oral or nasal decongestants can be used for short-term relief, but should not be taken for more than five-to-seven days to prevent rebound congestion (rhinitis medicamentosa).

Moderate-to-severe or persistent symptoms

The ARIA¹⁰ guidelines recommend intranasal corticosteroids as the first-line treatment. Newer generation intranasal corticosteroids are preferred given their low bioavailability with reduced systemic absorption and thus minimisation of long-term side-effects. Where symptoms persist, combination intranasal therapy containing a topical steroid and antihistamine can be used to provide greater symptom relief. 

Ocular symptoms

Conservative measures using cold compresses and artificial tears can help relieve mild eye irritation. Additionally, topical antihistamines or topical mast cell stabilisers can be effective. Topical corticosteroids should only be used under the supervision of an ophthalmologist due to potential side-effects.

Additional therapies

Where there is evidence of lower airway involvement or concurrent asthma, leukotriene receptor antagonists can be considered. Short courses of oral corticosteroids are reserved for severe cases where other treatments have failed due to the risk of systemic side-effects.

The diagnosis of AR is primarily clinical, based on characteristic symptoms and patient history

Newer treatment options for AR

Immunotherapy is a highly effective treatment that reduces symptoms and medication dependence by gradually desensitising the immune system to allergens.

Immunotherapy works similarly to a vaccine, exposing the patient to small quantities of the allergen over time to build tolerance. Sublingual immunotherapy (SLIT) is commonly used in Ireland for grass pollen, house dust mites, and tree pollen. It requires daily administration over a three-to-five year period. It is generally well tolerated with minimal side-effects, although good compliance and regular follow-up are essential for success.

Both grass pollen and house dust mite immunotherapy are licenced for children and adults from age five years whereas tree pollen SLIT is currently licenced for adults only. 

Endonasal phototherapy: Phototherapy, commonly used for skin conditions such as psoriasis and eczema, is now being applied inside the nasal cavity to manage AR. This treatment utilises a combination of ultraviolet (UV)-A (25 per cent), UV-B (<5 per cent), and visible light (70 per cent). This induces local immunosuppression by inhibiting allergen-induced histamine release from mast cells while additionally triggering apoptosis of T-lymphocytes and eosinophils, reducing inflammation and desensitising the nasal mucosa.

Phototherapy is particularly beneficial for patients who do not respond to standard pharmacological treatment or those with contraindications to medication. As research continues, it is emerging as a promising adjunct therapy for more resistant cases of AR.

Author: Dr Simon Bull, MICGP, FRACGP, MB BAO, BCh, LRCP&SI, BA (Hons) Neuroscience, Allergy Ireland