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Allergic rhinitis

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Dave Burns, MSc, RGN, Cert Ed RNT

Senior lecturer, Edge Hill University, Ormskirk, and national training manager, Respiratory Education UK, Liverpool.

Dave Burns outlines the aetiology, pathophysiology and management of allergic rhinitis.

Dave Burns outlines the aetiology, pathophysiology and management of allergic rhinitis.

Allergic rhinitis (AR) has been defined as 'a symptomatic disorder of the nose induced by an immunoglobulin E (IgE)-mediated inflammation after allergen exposure of the membranes lining the nose' (Bousquet et al, 2001). It is part of the atopic triad of AR, asthma and atopic dermatitis that are most commonly caused by allergy. Atopy itself is not allergy, but rather a predisposition to make abnormal amounts of a particular antibody, IgE, in response to apparently harmless agents such as pollen. Although this can predispose people to allergy not all atopic individuals will develop the clinical features of allergy.

Allergic diseases occur in response to genetic and environmental factors. Genetic factors have been shown to play a major part in the development of atopy and there is an increased risk of developing it when first-degree relatives, especially parents, have atopy.

Continued exposure to a particular allergen produces increased amounts of IgE that binds to mast cells at the site of exposure, for example, in the lining of the nose. At some point, and for reasons that are unclear, the allergen driving the increased IgE production binds to the IgE on the mast cells and initiates the beginning of a complicated chain of reactions summarised as early and late phase responses.

Early-phase response

During this phase mast cells break down after the allergen binds to the IgE molecule and release a number of inflammatory mediators such as histamine, leukotrienes and various chemical messengers, collectively termed as cytokines and chemokines. The immediate response in terms of nasal tissue may include symptoms such as sneezing, itching, rhinorrhoea and a feeling of a blockage in the nose. These symptoms reach their worst after 30 minutes, and thereafter begin to settle. After one hour a complete recovery is usually made.

Late-phase response

This is driven by the cytokines and chemokines that migrate to the bone marrow and increase the production of white blood cells, notably eosinophils. These white blood cells arrive in the nose eight hours later to produce a later and longer-lasting response. Providing there is no further exposure to the allergen, the allergic responsewill settle within 24 hours. However, if re-exposure is frequent, for example, where the allergen is from an animal living in the house or pollen during the summer, early and late phase responses may overlap resulting in persistent symptoms. This leads to the nasal mucus membrane becoming hyper-responsive and patients may experience nasal symptoms such as rhinorrhoea.

Epidemiology of AR in theUK

Exact figures for AR are difficult to estimate. Many patients adjust to symptoms or learn to live with them, while others either rely on a pharmacist for advice or self treat. Bachau and Durham (2004) found that up to 45% of people with AR were undiagnosed.

An Allergy UK (2005) survey of 1,000 people found that over 90% had the condition for over 10 years, with most of these reporting poor control. Approximately half of these reported significant effects on work or school life. Howarth et al (2005) reviewed the impact of AR and reported that the condition impairs learning ability, school and work performance, and contributes to significant work/school absence, as well having financial implications for people who purchase remedies or pay prescription charges.

There is growing recognition that AR is closely related to asthma. Valovirta and Pawankar (2006) surveyed over 1,600 patients with asthma and found that 73% reported symptoms of AR before they were diagnosed with asthma. Patients with both conditions reported sleep disruption (79%), problems with leisure or sporting activities (75%), poor asthma control when AR was present (79%) and avoiding being outdoors in the pollen season as the asthma became poorly controlled (56%).

The current British Thoracic Society/Scottish Intercollegiate Guidelines Network guidelines (BTS/SIGN, 2005) do not emphasise the link between the two conditions, however other guidelines do (Price et al, 2006; Bousquet et al, 2001). These guidelinesadvocate assessing all patients with AR for asthma and vice versa, and suggest that poorly controlled AR may have a negative effect on asthma control.

Diagnosis of AR

A comprehensive history must include a family history of atopy/allergy and a full history of the present condition including the nature, severity and pattern of symptoms. Allergic Rhinitis and its Impact on Asthma (ARIA)defined AR as intermittent or persistent, which replaces previous terminology of seasonal and perennial. It also classifies AR as mild or moderate/severe (Bousquet et al, 2001), as shown in Figure 1.

Visual examination of the nose may reveal swollen turbinates, and other clues may be the presence of allergic shiners (dark circles under the eyes) or signs of the 'allergic salute' (habitual rubbing of the nose). Specific allergy testing may be carried out, but allergen avoidance can be difficult. The evidence supporting allergy avoidanceis questionable.

Treatment of AR

Most guidelines for AR adopt the same approach and education is identified as vitally important. Allergen avoidance may be of benefit in patients who have only one or two allergies, for example those who have a pet or dust mite allergy. Custovic and van Wijk (2005) acknowledge that the consensus is that avoidance/reduction of allergen exposure should lead to an improvement in the patient's clinical condition but they suggest the evidence supporting this is weak.

Immunotherapy (desensitisation) is recommended for patients with severe allergies but is only useful for those patients who have a limited number of allergies and it needs to be carried out at specialist centres.

Most front-line practitioners will use pharmacotherapy to manage their patient's condition. ARIA (Bousquet et al, 2001) and the International Primary Care Respiratory Group (IPCRG) (Price et al, 2006) recommend the treatments listed below. It should be noted that there is no preferred order, although conventionally the treatments are prescribed in the following sequence.

Oral antihistamines (OAH)

These have a good effect on most rhinitis symptoms such as sneezing, rhinorrhoea and itching but have little impact on nasal blockage. A further advantage of OAHs is that they have a systemic action and will therefore relieve eye symptoms if these are present.

The first generation of OAHs include chlorpheniramine, ketotifen and clemastine, which are highly effective but have a major side-effect of drowsiness. This has implications for people operating machinery or for performance at school/work.

Second-generation antihistamines such as cetirizine and loratadine are tolerated better as they have less side-effects. Ideally patients should start to take these a week or two before their AR commences but this may not happen if the patient forgets. In addition, changes in climate with spring commencing earlier than in previous years may also contribute to poor prophylaxis as it may be more difficult to anticipate when the hayfever season will start.

There may be times when a patient finds that a tried and tested OAH fails to provide relief from symptoms. Some experts advocate switching to another OAH, for example, from cetirizine to loratadine but there is no evidence to support this practice.

Topical antihistamines

Topical antihistamines are available in ocular and nasal preparations. They are quick-acting and are as effective as OAHs in reducing symptoms such as sneezing, rhinorrhoea and eye symptoms (Price et al, 2006). They need to be administered twice a day.

Intranasal corticosteroids (INCs)

INCs are available in a number of preparations including nasal drops and, more recently, nasal sprays. 'Older' INC preparations such as beclometasone come in drop form, while newer preparations such as mometasone come in a spray form. The advantage of the newer preparations is that they have very little bioavailabilty (<1%) and="" have="" a="" good="" safety="" profile.="" additionally,="" because="" they="" are="" in="" spray="" form="" they="" coat="" the="" nasal="" mucosa="" more="" evenly="" than="" drops.="" only="" a="" once-daily="" dose="" is="" required="" which="" is="" convenient="" and="" may="" improve="" concordance.="" patients="" do,="" however,="" need="" to="" be="" advised="" on="" how="" to="" use="" these="" medicines="" correctly="" (see="" box).="">

Box 1. Important points to consider when a nasal preparation is prescribed

  • Advise the patient to read the instruction leaflet supplied with the device.
  • The patient should clean their nose prior to use (blowing the nose is required, but manual cleaning with a tissue might also be essential/desirable).
  • The patient should lean forward slightly when the spray is used.
  • Manufacturer's literature recommends inhaling slightly as the device is actuated.
  • Patients should avoid spraying directly onto the nasal septum as the tissue here is thinner and more liable to damage resulting in epistaxis.
  • Once the spray has been delivered into the nose the patient should avoid sniffing. Overzealous sniffing will take the drug to the back of the throat and the patient will then taste it.
  • Patients who report a poor response, unpleasant taste or perhaps sore throat (where oropharyngeal thrush has developed because of steroid deposition in the throat) should have both their adherence and their technique assessed.

Other treatments

  • Saline washouts - these may reduce allergen levels in the nose and help clear the mucosa prior to use of INCs, particularly where patients produce large amounts of thick secretions (Price et al, 2006).
  • Nasal decongestants - these mimic the effects of the sympathetic nervous system, and cause vasoconstriction in the vessels of the nose and reduce obstruction. Examples include ephedrine and oxymetazoline. These drugs should not be used for more than 10 days, as a 'rebound' effect can occur in which they become gradually less effective and cause further obstruction that is then less responsive to other treatments. The advantage of decongestants is that as well as affording the patient some relief from symptoms they will open up the nasal passages and allow for better deposition of INCs.
  • Intranasal and intraocular cromones - these have very good safety profiles but have a short duration of action that may require repeated administration four times per day. This may cause problems with adherence. Examples include cromoglicate and nedocromil.

AR and concomitant asthma

There is growing evidence about the relationship between these two conditions. ARIA and IPCRG advocate assessing all patients with asthma for AR and vice versa as three out of every four patients with asthma will have some form of AR (Walker and Sheikh, 2005). Valovirta and Pawankar (2006) suggest that people with asthma will experience a worsening of their asthma symptoms when their AR is active and Corren et al (2004) found in a case control study that increasingly aggressive treatment of AR with OAHs, INCs or both combined reduces the chance of being admitted to hospital with an asthma exacerbation.

Another option is to use leukotriene receptor antagonists (LTRAs). Leukotrienes are known to be potent inflammatory mediators in many people with allergy and LTRAs block the receptor site for these molecules, so inhibiting their inflammatory effects. The advantages are that LTRAs can be taken orally as a tablet once a day and are licensed to treat seasonal AR and asthma. They can be used safely in children. One potential drawback is that they work moderately or very well for approximately two-thirds of patients but have negligible impact for the remaining third (Barnes et al, 2005).

Currie et al(2005) argue that LTRA may be a logical option for patients with poorly controlled asthma and AR who are at step two (using regular preventer therapy) of the BTS/SIGN (2005) asthma guidelines. However current advice is to automatically prescribe a long-acting beta-2 agonist (LABA).When control is poor, AR is absent and lung function is poor, the current recommendation of prescribing a LABA should be followed. Whether LTRAs or a LABA is used, the patient should be reviewed and control of both conditions reassessed.

Can treatments be combined?

Wilson et al (2000) administered either nasal budesonide plus inhaled budesonide, or OAH and LTRA plus inhaled budesonide to patients with AR and asthma. After two weeks treatment patients were switched to the alternative treatment.Both regimens were equally effective in improving symptoms.

The role of the nurse

The main issues for nurses in primary care are:

  • Routine assessment for AR of all people with asthma and vice versa;
  • Awareness of treatment options for AR;
  • Education of people with AR about the nature of treatments and the need to continue with treatment even when they are better;
  • Ensuring that patients prescribed ICNs are taught how to use devices correctly;
  • Following up patients to assess the effects of treatment and, where treatment appears to be unsuccessful, determining possible reasons for this and being aware of alternatives.


The numbers of people affected by allergic disease has risen considerably over the last four decades and two major manifestations of this are AR and asthma. AR can cause considerable morbidity on its own, and the evidence is accumulating that it impinges negatively on asthma control.

There are guidelines for managing AR on its own and in conjunction with asthma. Establishing a diagnosis following a detailed medical history is essential. A range of interventions is available and there are a number of similarities between the two conditions in that they are both inflammatory in nature, have similar aetiology and pathophysiology, and require anti-inflammatory medications.

Nurses need to provide adequate instruction about the duration of treatment and careful instruction in the use of devices as well as appropriate review and adjustment of treatment. This will help patients to manage their condition successfully.


AllergyUK (2005) Night and Day. London: Allergy UK.

Bachau, V.,Durham, S. (2004) Prevalence and rate of diagnosis of allergic rhinitis in Europe. European Respiratory Journal; 24: 5, 758-764.

Barnes, N. et al (2005) The national montelukast survey. Journal of Allergy and Clinical Immunology; 115: 1, 47-54.

Bousquet, J. et al (2001) Allergic rhinitis and its impact on asthma (ARIA guidelines. Journal of Allergy and Clinical Immunology; 108: 5 (Supplement), 147-334.

British Thoracic Society, Scottish Intercollegiate Guidelines Network (2005) Asthma Management Guidelines. London: BTS.

Corren, J. et al (2004) Rhinitis therapy and the prevention of hospital care for asthma: a case control study. Journal of Allergy and Clinical Immunology; 113: 3, 415-419.

Currie, G. et al (2005) Long-acting bronchodilator or leukotriene modifier as add-on therapy to inhaled corticosteroids in persistent asthma? Chest; 128: 4, 2954-2962.

Custovic, A., van Wijk, R.G. (2005) The effectiveness of measures to change the indoor environment in the treatment of allergic rhinitis and asthma: ARIA update (in collaboration with GA2LEN). Allergy; 60: 9, 1112-1115.

Howarth, P. et al (2005) Preface to outcome measures in allergic rhinitis. Journal of Allergy and Clinical Immunology; 15: 3 (Supplement 1), S387-389.

Price, D. et al (2006) International Primary Care Respiratory Group (IPCRG) guidelines: management of allergic rhinitis. Primary Care Respiratory Journal; 15: 58-70.

Valovirta, E., Pawankar, R. (2006) Survey of the impact of comorbid allergic rhinitis in patients with asthma. BMC Pulmonary Medicine; 6: Suppl 1, S3.

Walker, S., Sheikh, A. (2005) Self reported rhinitis is a significant problem for patients with asthma. Primary Care Respiratory Journal; 14; 2, 83-87.

Wilson, A. et al (2000) Antiasthmatic effects of mediator blockade versus topical corticosteroids in allergic rhinits and asthma. American Journal of Respiratory and Critical Medicine; 162: 4 (Part 1), 1297-1301.

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