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Managing allergic rhinitis

Key learning points:

- Understanding how to identify symptoms and triggers of allergic rhinitis

- Diagnose patients with the condition

- Managing and treating patients

Allergic rhinitis (AR) is a common condition characterised by inflammation of the nasal mucous membranes and in some individuals the eyes, leading to the use on occasions of the term rhino-conjuctivitis. It can in the more severe manifestations cause considerable morbidity.

This article discusses the aetiology, pathophysiology, diagnosis and the more common pharmacological management of AR, and the relationship between AR and allergic asthma.

For a broader and deeper approach readers are advised to read a summary of the British Society for Allergy and Clinical Immunology (BSCAI) guidelines on managing AR in primary care (1).

Background

AR is one of a number of conditions which are clinical manifestations of atopy; this is a predisposition to produce increased amounts of antibodies, notably immunoglobulin E (IgE) in response to molecules which are harmless.

Common examples of these molecules are animal dander, house dust mite faeces, and pollens from a wide variety of plants and trees. Other clinical manifestations of atopy include atopic dermatitis, asthma, and food allergy.

Atopy is known to have both environmental and genetic components. For manifestations of atopy such as asthma and AR, some evidence seems to show that genetic aspects play the larger part in development of these conditions (2).

Susceptible individuals may develop multiple allergies and this concept, termed 'the atopic march' has been examined in some depth by Bantz Zhu and Zheng (3).

AR is characterised by inflammation of the nasal mucous membranes. Many people have early and late phase responses. The early phase causes symptoms quickly, peaks in approximately 30 minutes, and has passed after approximately an hour. Approximately six to eight hours later the late phase response occurs. Classically this is driven by the oesinophil (as is the case in allergic asthma).

This is slower in onset, peaks in approximately six hours, and has passed after 12 hours, i.e from the time of encountering the allergen initially, passing through the early and late phase responses takes around 24 hours. In reality, differentiating these phases can be difficult due to ongoing encounters with allergens leading to overlapping early and late phases responses. The condition is common with approximately 25% of the UK population experiencing some form of it (4).

Diagnosis

This can be reached simply with a good history, one aim being to identify triggers of symptoms. Patients with seasonal AR (hay fever) can usually provide a good picture of their condition. Those with perennial AR (due for example to pet allergy, or allergies to different pollens at different times of the year) may not be able to be so clear. Other elements of the history can be useful, such as relief of symptoms on holiday can suggest a strong environmental influence.

There are a variety of tests available, but these are not always readily available, and should be used for the more difficult cases. Walker, Sheik, Angier and Willington (5) agree that for many patients an empirical trial of treatment may be sufficient, with clinical investigations reserved for the more difficult cases.

Other conditions can cause nasal symptoms which might lead to suspicion of AR, so care needs to be taken when considering these. In addition BSCAI provide important red flag features to be aware of, such as unilateral symptoms of pain and blockage, purulent blood stained discharge and, nasal deformity among others (1).

Management of AR

This section will discuss the major aspects of pharmacological management only. It should be noted that BSACI (6) outlines four interventions for AR, these being allergen/irritant avoidance, pharmacological treatments, immunotherapy, and surgery. Only the more common pharmacological interventions will be considered here. These are:

- Oral antihistamines (OAH).

- Intranasal antihistamines.

- Intranasal corticosteroids (INCS).

- Cromones.

Oral antihistamines: These are seen as first line treatment. They are effective against many symptoms such as nasal itching, rhinorrhoea, sneezing and conjunctivitis. One problem with them is their limited efficacy with reference to nasal congestion. They may also have limited impact on other AR symptoms in more severe cases.

ARIA (2010) (7) recommend the use of second generation OAHs such as ceterizine, loratadine or fexofenadine due to their reduced propensity to cause sedation.

Practical advice regarding the use includes:

- Advising patients to shop around if purchasing their own as generic molecules can be much cheaper than branded ones.

- For AR which manifests as hay fever in the summer months, try and start the OAH before the season starts. Opinions vary on this, but three to four days before seems reasonable although identifying the actual start of the season can be difficult.

- Anecdotally, it seems some patients seem to develop a tolerance to a molecule. There is no evidence of this in the literature, but swapping the molecule; changing from ceterizine to loratidine seems to work.

Intranasal antihistamines:These can be used for nasal features only. They do not seem to provide the same degree of benefits as OAH, and as might be expected have no impact on ocular symptoms. However, intraocular antihistamines are available for eye symptoms and can be used.

INCS:As in asthma, these are seen as the optimum treatment because in asthma the principle cell causing much of the problem is the eosinophil, and eosinophils are quite sensitive to corticosteroids, which decrease the recruitment of eosinophils to the nose, secretion of inflammatory mediators once there, and overall lifespan. Important issues in the use of ICNS include:

- Continued use is important - poor adherence reduces efficacy, so careful explanation is required.

- Like antihistamines, various preparations are available-some such as fluticasone proprionate can be purchased over the counter, while others such as mometasone (Nasonex) and fluticasone furoate (Avymis) are prescription only.

- As with the inhaler technique in asthma, correct device technique with INCS spray is essential. Basic advice is to clean the nose prior to use, to direct the spray towards the lateral wall of the nose, and importantly to avoid overzealous sniffing, which takes the drug into the nasal passages where it is less efficacious (and will be swallowed leading to complaints of unpleasant taste).

Cromones:Intranasally, their value lies in treating rhinorrhoea which does not respond to standard treatments, and vasomotor rhinitis, which results in continuous watery discharge form the nose. While effective, one issue with them is the treatment regimen, which involves four doses per day. They are however safe in pregnancy, and are an option here.

Cromones are also available as eye drops, and these can be useful in treating 'break through' symptoms. Again, their dosing schedule of four times a day may be a problem in terms of               adherence.

Generally, these treatments can be used as sole agents, or where disease is more severe, in combination, e.g. the patient who finds OAH help their eye symptoms and rhinorrhoea but is still troubled by marked nasal congestion will benefit from having an INCS added to their OAH. Patients who have more marked symptoms (and certainly those where congestion is a problem) should automatically be prescribed an INCS.

AR and asthma

Expert bodies have for some time advocated the notion of regarding the airways in their entirety as 'one airway', and as a consequence of this assessing patients with allergic inflammation at one end of the airway for allergic inflammation at the other end, so in practice assessing patients with AR for asthma symptoms and vice versa.

Evidence shows that individuals with allergic rhinitis are significantly more likely to develop asthma compared to those without AR(8). Angier et al state 78% of patients with asthma have AR (1).

Baser et al (9) et al screened 87 patients with AR for asthma, and following screening and treatment found approximately 25% of patients had undiagnosed asthma, so demonstrating the importance of this aspect of management. More recently Esteban et al found a similar picture in children with asthma in terms of a significant underdiagnosis of AR (10).

Other recent evidence (11) indicates that poorly controlled AR may impact negatively on asthma control, leading to suggestions that treating AR effectively may lead to better control of asthma. This view is debateable, but is not supported by British Thoracic Society and Scottish Intercollegiate Guidelines Network (BTS/SIGN) guidelines (12).

On this basis, various treatment options may be considered, taking into the account the options for AR described above. For example mild AR in a patient with concomitant asthma may be treated with an OAH; if the patient has more severe/persistent symptoms (and in particular nasal congestion), use of an INCS would be indicated.

Where there are worries about total corticosteroid dose if the patient is already taking these for asthma, prescribing fluticasone or mometasone is a useful option as systemic absorption of these molecules is negligible.

A further option is the use of a leukotriene receptor antagonist (LTRA). Leukotrienes are inflammatory molecules that drive the inflammation in both conditions and seem relatively more important in some individuals. Two molecules are available in the UK-Monteleukast and Zafirleukast. An advantage of these drugs is that they are oral formulations, so inhaler and/or nasal spray technique is not an issue.

Other issues

Where response is unsatisfactory, check adherence with treatment, and device technique if INCS have been prescribed. Some patients use decongestants.

While useful in providing rapid symptom relief, they should be used in the short term only (three to four days with an absolute maximum of 10 days) as they can produce rebound congestion which is more difficult to treat with INCS.

Some experts advocate the use of nasal douching (washouts) to help control symptoms. This might be worth considering where treatment response is sub optimal.

In the past, depot injections of corticosteroid have been used. These are not recommended as routine due to their adverse side effects. However for severe presentations of AR and in order to establish control, a short course of oral corticosteroid can be used; INCS should be commenced at the same time and used as maintenance thereafter.

Conclusion

AR is a common condition capable of causing marked morbidity. Most diagnoses can be reached with a satisfactory history. Investigations can be utilised in those cases where diagnosis is more difficult.

A number of treatments are available to manage most cases without referral to secondary/tertiary care. Careful selection of these with education regarding correct use of nasal sprays and continued use should also ensure control of the condition in the majority of cases.

AR commonly exists alongside asthma and patients with either of these conditions should be assessed for inflammation at the opposing end of the airway. Both conditions should be managed appropriately.

 

References

1. Angier E, Willington J, Scadding S, Holmes S, Walker S. Management of allergic and non allergic rhinitis: a primary care summary of the BSACI guideline. Primary Care Respiratory Journal 2010;19(3):271-222

2. Beijsterveldt C, Boomsa D. Genetics of parentally reported asthma, eczema and rhinitis in 5-yr-old twins. European Respiratory Journal 2007;29: 516-521

3. Bantz S, Zhu Z, Zheng T. The atopic march: Progression from Atopic Dermatitis to Allergic Rhinitis and Asthma. Journal of  Clinical and Cellular Immunology 2014;5(2)

4. National Institute for Health and Clinical Excellence (NICE) Allergic Rhinitis (2014) [Online] Available at: http://cks.nice.org.uk/allergic-rhinitis#!backgroundsub:3 (Accessed 2 February 2015)

5. Walker S, Morton C, Sheikh A. Diagnosing allergy in primary care: are the history and clinical examination sufficient? Primary Care Respiratory Journal 2006:15, 219-221

6. The British Socity for Allergy & Clinical Immunology (BSACI). Rhinitis (2014) [Online] Available at: http://www.bsaci.org/resources/rhinitis (Accessed 2 February 2015)

7. Allergic Rhinitis and its Impact on Asthma. Allergic Rhinitis and its Impact on Asthma Guidelines (2010) [Online] Available at: http://whiar.org/docs/ariareport_2010.pdf (Accessed 2 February 2015)

8. Settipane RJ, Hagy GW, Settipane GA. Long term risk factors for developing asthma and allergic rhinitis: a 23 year follow up of college students. Allergy Proceedings 1994:15(1), 21-25

9. Baser S, Ozkurt S, Topuz B, Kiter G, Karabulut H, Akdag B, Evyapan F. Peak expiratory flow monitoring to screen for asthma in patients with allergic rhinitis. Journal of Investigational Allergology and Clinical Immunology 2007:17(4): 211-215

10. Esteban C, Klein R,   Kopel S, McQuaid E, Fritz G, Seifer R, York D, Golova N, Jandasek B, Daphne Koinis-Mitchell D. Underdiagnosed and Undertreated Allergic Rhinitis in Urban School-Aged Children with Asthma Pediatric Allergy Immunology and Pulmonology 2014:27, 2, 75-81

11. Deliu M, Belgrave D, Simpson A, Murray C.S, Kerry G, Custovic A. Impact of rhinitis on asthma severity in school-age children.  Impact of rhinitis on asthma severity in school-age children 2014:69, 1515-1521

12. British Thoracic Society. Asthma Guidlelines (2014) [Online] Available at: https://www.brit-thoracic.org.uk/document-library/clinical-information/a... (Accessed 2 February 2015)