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Managing allergic rhinitis

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The symptoms of allergic rhinitis can be disruptive and distressing. This article outlines their causes and triggers, and the main treatment options.

Abstract

An allergic reaction can occur at any age and present itself in many organs. Over the past five decades, the understanding of immunological mechanisms and pharmacological management of allergy has increased. This article outlines the mechanisms of allergy, its diagnosis and management in the context of the upper respiratory tract, and hay fever.

Citation: Pearce L (2012) Managing allergic rhinitis. Nursing Times [online]; 108: 17, 20-22.

Author: Linda Pearce is respiratory nurse consultant and clinical lead Suffolk COPD Services, West Suffolk Hospital, Bury St Edmunds.

Introduction

Allergic reactions can present at any age and in many forms. They can range from the mildly inconvenient to the potentially fatal anaphylactic reaction. An understanding of the mechanisms causing allergic reactions will enable nurses to help patients to manage allergic symptoms and to know when to refer them for specialist intervention.

Mechanics of allergic reactions

An allergic reaction (Greek “allo” = altered; “erg” = reaction) occurs when the body overreacts (that is, is hypersensitive) when defending itself against a perceived threat such as pollen, which would otherwise be harmless. Types of hypersensitivities and allergies are distinguished by the timing of their symptoms and whether antibodies or T cells are the principal immune element involved (Box 1).

Atopy is a predisposition to become sensitised and produce immunoglobulin E (IgE) antibodies in response to exposure to allergens that commonly occur in the environment. Atopic people can develop IgE-mediated allergic diseases including asthma, rhinoconjunctivitis or eczema (Johansson et al, 2001). Box 2 describes key terms used.

T helper 1 (Th1) immunity helps to fight viruses and bacteria, while Th2 immunity fights gut parasitic infections but makes us more vulnerable to developing allergies.

The uterine environment is powerfully Th2 allergy prone, which imprints Th2 dominance on neonates. Exposure to infections and dirty environments by the age of two years creates a balance between non-allergy prone Th1 and Th2. This mechanism is altered by less exposure to infections, improved hygiene and smaller families, which mean the body has longer to make and establish Th2 responses to environmental antigens (that is, allergens). Depending on family history (genetic predisposition) and environment during infancy, a child may show dominance of Th2 immunity, which promotes higher levels of allergy-related IgE in the bloodstream. An IgE-mediated reaction is recognised as an allergic reaction.

A atopic person can become IgE-sensitised on the first exposure or after several years of, for example, inhaling <1µg of grass pollen allergen per season. The first time allergy-prone individuals come into contact with allergens such as grass pollen, they produce a large amount of grass pollen IgE antibody.

These IgE molecules attach themselves to specific cells such as mast cells, which are capable of mediating inflammatory reactions. The mast cells then become “primed” to recognise grass pollens as an allergen. At a later time, which may be the next exposure or some time later, the primed IgE mast cells degranulate, releasing naturally occurring defence chemical mediators such as histamine, cytokines and leukotrienes, which cause the characteristic symptoms of allergy.

Between 1985 and 2003, Baatenburg de Jong et al (2009) assessed the prevalence of atopic sensitisation in 2,946 children aged 0-4 years who presented with allergic symptoms. Specific IgE tests were positive to aeroallergens in 505 (17%) of this group. Positive test results included 346 (12%) for house dust mite, 257 (9%) for dog dander, 240 (8%) for cat dander and 197 (7%) for grass pollen. These results suggest that sensitisation to aeroallergens is common in preschool children with symptoms of allergy. Although sensitisation to common allergens usually occurs in childhood and adolescence, some people develop IgE-mediated allergy in adulthood, often following a high level of exposure, as in occupational asthma (Quirce and Sastre, 1998).

Box 1. Terminology

  • Hypersensitivity causes objectively reproducible symptoms or signs, initiated by exposure to a defined stimulus at a dose tolerated by healthy people
  • Atopy is a personal or familial tendency to produce IgE antibodies in response to low doses of allergens, usually proteins, and to develop typical symptoms such as asthma, rhinoconjunctivitis or eczema/dermatitis
  • Allergy is a hypersensitivity reaction initiated by immunological mechanisms

Box 2. Types of hypersensitivity

Hypersensitivity IgE-mediated reaction (allergic reaction)

  • Binding of antigen to IgE on the surface of mast cells causes release of inflammatory mediators
  • Allergy can cause an immediate response such as urticaria, asthma, hay fever or angioedema
  • Anaphylaxis - rapid severe systemic reaction, as in sensitised nut allergy

IgM or IgG cytotoxic reaction

  • Antibody dependent
  • Binding of antibody to cell surface leads to a specific immune response and damage to host cell
  • For example, erythroblastosis foetalis, Goodpasture’s syndrome

IgG immune complex reaction

  • The formation of complexes between antigen and antibody leads to tissue damage as a result of deposition in blood vessels (vasculitis) and activation of inflammatory pathways, for example, in Arthus reactions (to vaccination), rheumatoid arthritis and subacute bacterial endocarditis

Cell-mediated reaction

  • Delayed-type hypersensitivity (DTH)
  • Activation of T cells around the site
    of the antigen leads to T-cell cytotoxicity and activation of macrophages, causing tissue damage, for example in Mantoux testing, contact dermatitis and coeliac disease

Rhinitis and causes

Rhinitis can be classified as allergic or non-allergic. Non-allergic symptoms are typically nasal blockage and rhinorrhoea. Allergic seasonal rhinitis, in the form of hay fever, has a symptom complex comprising of rhinorrhoea, sneezing, nasal congestion and nasal itching, which typically last for an hour or more on most days.

The UK prevalence of hay fever and asthma is among the highest in the world (Björkstén et al, 2008; Gupta et al, 2004). It is estimated that 20% of the UK population is at risk of developing hay fever, which rises to 50% if there is a family history of atopy (Punekar et al, 2009; Asher et al, 2006).

People may be allergic to more than one form of pollen, and to more than one allergen; such allergy may cause hay fever-type symptoms all year, which is known as perennial rhinitis. This type of rhinitis may be caused by allergy to, for example, animal dander or house dust mite. Those with multiple allergies may suffer from perennial rhinitis with seasonal exacerbations.

Wind-pollinated plants produce higher levels of pollen than insect-pollinated ones. In the UK, the main cause of hay fever is grass pollen, affecting 95% of people with the condition, followed by that from trees, particularly birch (20%), and weeds, particularly nettle. Ragweed, common in the US, Canada and some parts of Europe, produces millions of pollen grains and poses a significant hay fever problem (National Pollen and Aerobiology Research Unit, University of Worcester, undated).

Emberlin (2008) observed a decrease in the severity of the grass pollen seasons in London and Derby over the past 20 years, which appear to relate to changes in land use and the decline in grassland areas.

Alongside this, the effects of climate change mean warmer weather has encouraged grass growth, earlier pollen release, a change in the seasonal distribution of aeroallergens and an extended pollen season. The lengthening of the European pollen season has resulted in moderate pollen counts being recorded into August, where previously the season would have ended by late July. In addition, biological or air pollution stresses such as rising carbon dioxide levels are thought to result in trees producing pollen that is more allergenic (D’Amato, 2002).

History and diagnosis

When a patient presents with allergic symptoms, a history of symptoms and their relationship to exposure should be taken. Past or present personal and family history of allergy-related disorders such as eczema or asthma, which often coexists with rhinitis, should also be documented.

Outside the pollen season, when patients are asymptomatic, the diagnosis is primarily made on history; during the season, both history and examination support diagnosis.

There is usually a relationship between high pollen counts and IgE-mediated rhinitis; symptoms usually appear very shortly after allergen exposure and last for longer than four hours. They consist of itching, eye irritation and excessive discharge of watery fluid from the nose and eyes. On examination, nasal mucosa may appear normal or pale bluish, or swollen with watery secretions in symptomatic patients. The symptoms may be severe enough to cause difficulty in sleeping, working or studying (Walker et al, 2007; Malone et al, 1997).

To help plan treatment, it may be helpful to identify, where possible, the pollen (or pollens) or other aeroallergens to which the patient is sensitive. Skin prick testing (SPT) is easy to perform and rarely causes generalised reactions. SPT for a range of allergens should only be carried out following detailed history-taking. It is useful for:

  • Diagnosing allergy;
  • Confirmatory evidence (positive, negative) of IgE sensitisation in support of the clinical history (Fig 1);
  • Identifying the allergen against which IgE is directed, which is essential for allergen-avoidance measures;
  • Educational value - visual reinforcement strengthens concordance with verbal advice.

Patients may have positive SPT but no disease - a positive SPT indicates the presence of IgE antibodies against that allergen but does not indicate clinical sensitivity, so correlating the history with the SPT is essential. The results can be unreliable if patients take certain drugs, such as antihistamines.

Total IgE blood levels do not provide a sensitive enough measure for atopy; a test for allergen-specific IgE antibodies can be requested if SPT is not available or appropriate, for example in patients who:

  • Are taking antihistamines or other confounding medications for skin tests;
  • Have eczema;
  • Have experienced an anaphylactic event within the previous six weeks;
  • Are morbidly afraid of skin testing.

Screening is only beneficial if it will influence management by allergy avoidance, or in cases where immunotherapy is to be considered (Walker, 2011).

Differential diagnosis

Infective rhinitis may be caused by viruses or bacteria and is often seen in young children. Non-allergic rhinitis may be of unknown causes and, in rare cases, can be a symptom of underlying systemic disease such as Churg-Strauss disease or Wegener’s granulomatosis. Rhinitis may be a symptom of rhinosinusitis.

Management

It may be extremely difficult or impossible to completely avoid exposure to pollen. However, if a specific allergen or allergens can be identified, patients may be able to avoid or minimise exposure when pollen counts are high, for example by:

  • Avoiding passing a field or area where a specific allergen is prevalent;
  • Staying indoors with windows and doors closed when particular pollen counts are significantly raised;
  • Fitting pollen filters to air vents of cars;
  • Washing hair after journeys outside.

Treatment

Treatment consists of non-sedating antihistamines, nasal corticosteroids and anti-inflammatory eye drops (Angier et al, 2010). Other treatments are oral corticosteroids, leukotriene receptor antagonists, decongestant sprays and immunotherapy.

Corticosteroids: these are potent anti-inflammatory agents; for hay fever they are used once or twice daily as a nasal spray, depending on the formulation.

When applied nasally, corticosteroids may reduce the ocular effects of the allergy. The anti-inflammatory action may take some days to have a noticeable effect so, if possible, it should be started 5-7 days before symptoms are due to appear (with hay fever, the start of symptoms is often predictable from experience or from knowledge of when pollens are produced). To avoid nosebleeds, patients should be taught how to use their device (Box 3).

In severe cases, oral corticosteroids may be prescribed. This is most commonly done for short periods for patients whose activities are restricted at a critical time, for example when sitting exams.

Antihistamines: since histamine is the main cause of the allergic rhinitis response, it is not surprising that anti-histamines are an effective therapy for hay fever. However, while they may relieve many symptoms, nasal congestion may persist.

Antihistamines are often used where symptoms of allergic conjunctivitis are present. They normally begin acting within 20-30 minutes, and their action should last for several hours. Non-sedating antihistamines are preferred and may be used in conjunction with a nasal spray.

Mast-cell stabilisers: these may be added to the treatment regimen in the form of eye drops for uncontrollable eye symptoms; they should not be used with contact lenses.

Leukotriene receptor antagonists: these block one part of the inflammatory cascade that is initiated when a sensitised person is exposed to an allergen.

According to the British National Formulary (British Medical Association and Royal Pharmaceutical Society, 2012), they may be of benefit in exercise-induced asthma and in those with concomitant rhinitis. Prescribers should check the BNF for details on individual drugs.

Decongestant nasal sprays: these can be bought over the counter at pharmacies. They may provide short-term relief but should not be used for more than seven days as they will have a diminishing effect and may cause a rebound exacerbation of symptoms.

Grass pollen immunotherapy: these therapies are effective for those with mono sensitive IgE-mediated allergen (proven allergy to grass pollen). Desensitisation is sometimes used in patients who are severely affected and where other treatments have been unsuccessful.

Two types are available: subcutaneous injections; and sublingual immunotherapy tablets. Over a period of weeks, patients are given a series of subcutaneous injections containing an increasing concentration of the allergen, or sublingual immunotherapy tablets over three years to build up immunity. British Society for Allergy and Clinical immunology guidance (Walker et al, 2011) states that both subcutaneous and sublingual immunotherapy efficacy have been shown to be effective.

Box 3. How to use a nasal spray

  • Blow nose before spraying, if blocked
  • Prime the spray device according to the manufacturer’s instructions, including removing the cap
  • Tilt head slightly forward. Using the opposite hand to the nostril, gently insert the nozzle. This ensures the device is inserted at the correct angle, with the nozzle parallel to the roof of the mouth and tilted away from the septum
  • Apply one actuation at a time. Avoid sniffing hard during or after spraying. Sniffing could force the spray into the back of the throat instead of inside the nose where it needs to work
  • Repeat the process, remembering to use the opposite hand to the nostril
  • Wipe the tip of the spray device with a dry tissue, and replace the cap

Conclusion

The effects of hay fever may range from mildly inconvenient to severely disabling. The condition may impair patients, especially children and young adults, at critical times, for example, during and before school, college or university exams.

The potential effect of hay fever should not be underestimated. A careful history will elucidate the extent of the allergy’s effects, and will allow practitioners to advise and treat patients effectively.

Key points

  • Environmental changes influence pollen seasons
  • Rhinitis can be classified as allergic or non-allergic
  • Symptoms are debilitating and limit activity
  • Treatment should be started promptly
  • Rhinitis and asthma often coexist
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