2007 Annual Evidence Update on Rhinitis: Allergic Rhinitis

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Guideline summary - allergic rhinitis

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Contributing Authors: Glenis Scadding, Steven Durham

The prevalence of allergic rhinitis has increased since the 1950s[1] and continues to rise[2]. Recent surveys suggest that 26% of the UK population is affected [3;4].
Allergic rhinitis is the predominant form in children, and accounts for about a third of adult rhinitis cases. Atopic individuals, with a family history of rhinitis, first born children and immigrants are predisposed to develop allergic rhinitis [5-7]. 

In allergic rhinitis allergen induces IgE- formation and this allergy antibody then becomes attached to mast cells- this process is known as sensitization. Most, but not all, sensitized individuals react to subsequent allergen contact with mast cell degranulation and immediate release of mediators including histamine, prostaglandins and leukotrienes. Sneezing, itching, nasal running and blockage result. With prolonged allergen contact or high allergen exposure a late-phase inflammatory reaction ensues with infiltration of cells, predominantly eosinophils [8-10]. Symptoms are less obvious with chronic obstruction, poor sense of smell, post-nasal catarrh and nasal hyper-reactivity.

The World Health Organization workshop “Allergic Rhinitis and its impact on Asthma”(ARIA) [11] formed the first global, evidence – based rhinitis guidelines and suggested a new classification of allergic rhinitis based on frequency and severity of symptoms and applicable worldwide. Although subsequently validated and undoubtedly useful in determining therapy [12] it is useful in UK practice to continue to use the seasonal rhinitis classification in addition as it has diagnostic and therapeutic implications.
The ARIA document noted that there is a continuum from nose to alveoli and advocated a united approach to airways disease. It also advocated the concept of minimal persistent inflammation with the consequent recommendation for continuous treatment for many patients during allergen exposure, even if asymptomatic [11].

Diagnosis:
Allergic rhinitis is diagnosed by history and examination backed up by specific allergy tests, either skin prick or blood tests for specific IgE.

Treatment
 This involves:
• Allergen avoidance,
• Pharmacotherapy
• Immunotherapy
• Patient Education
• Surgery

Allergen avoidance
Complete avoidance is effective (hay fever does not trouble sufferers out of season) but very difficult to achieve for allergens such as house dust
mites. Studies of partial measures for house dust mites such as bedding covers alone have not shown therapeutic effects. Therefore most patients will need pharmacotherapy. Nasal air filters have shown benefit in grass pollen allergic patients but are not always tolerated.
Rhinitis may be induced by exposure to a respiratory sensitising agent in the workplace ('occupational rhinitis').This is approximately three times more frequent than occupational asthma but the two may co-exist [13;14]. The 300 plus agents that can cause occupational rhinitis are those that also cause occupational asthma. If diagnosed, occupational rhinitis necessitates avoidance of further occupational exposure – this reduces the risk of asthma development and can be curative [13;15].

Pharmacotherapy
Topical nasal corticosteroids are advocated for moderate to severe disease, based on two meta–analyses. Mild intermittent rhinitis responds well to antihistamines which are particularly effective against symptoms of running, itching and sneezing. Nasal obstruction is more effectively treated by corticosteroids. (Grades of recommendation=A).
The two can be combined if monotherapy is ineffective.
Other modalities include nasal douching with saline, anti-leukotrienes, sodium cromoglicate, ipratropium bromide, and oral corticosteroids. Details of their use can be found in the ARIA document and an updated version will be available shortly from the British Society for Allergy and Clinical Immunology.
Retrospective analysis from 3 large studies of rhinitis treatment in asthma suggests reduction of emergency visits and hospitalization for asthma. (Grade of recommendation=A)

Immunotherapy
Immunotherapy is the only treatment which alters the course of disease and is very effective for severely affected patients with one or two major allergens who are insufficiently responsive to pharmacotherapy. (Grade of recommendation=A)
Subcutaneous immunotherapy carries the potential for severe systemic side effects and so is only available in specialized centres with trained personnel and the availability of cardio-pulmonary resuscitation. Subjects must be observed for an hour post each injection. Three years treatment is associated with a good reduction in symptoms for several years thereafter.
Sublingual immunotherapy is probably less effective but considerably safer since the reaction is local rather than systemic. The recommendation is for the first dose to be administered under observation, with subsequent doses being taken daily at home. In the UK at present only one form is licensed – tablets for grass pollen allergy.
 
Patient Education
Standardised allergy education has been shown to improve disease specific quality of life [16]. Education about the nature of the disease and available treatments, including general information about the symptoms, causes and mechanisms of rhinitis, relevant allergens and possible avoidance should be given. Patients also need information on pharmacotherapy: including how, when and how long to use it; details about safety and potential side effects should be provided.
Patients should understand that complete cure is unlikely and that long term treatment may be needed.
Patients should be made aware of the potential negative impact of rhinitis on their quality of life, on possible co-morbidities and benefits of complying with therapeutic recommendations.
 
Surgery
Surgery is required only for a small minority of cases. Indications are inferior turbinate hypertrophy or septal deviation with symptoms persisting on adequate pharmacotherapy. Operative intervention may aid the delivery of topical nasal treatment. [17]
Surgical intervention may also be required in rhinosinusitis for anatomical variations of the bony pyramid with functional relevance,
chronic rhinosinusitis or acute severe sinusitis/periorbital cellulitis unresponsive to intravenous antibiotics, nasal polyposis and fungal sinus disease or other pathologies unrelated to allergy. European guidelines exist and an updated version will shortly be available [18].


References

1. Aberg N, Hesselmar B, Aberg B, Eriksson B. Increase of asthma, allergic rhinitis and eczema in Swedish schoolchildren between 1979 and 1991. Clin Exp Allergy 1995; 25:815-9. [Link to abstract]

2. Maziak W, Behrens T, Brasky TM, Duhme H, Rzehak P, Weiland SK, Keil U. Are asthma and allergies in children and adolescents increasing? Results from ISAAC phase I and phase III surveys in Munster, Germany. Allergy 2003; 58:572-9. [Link to abstract]

3. Bauchau V, Durham SR. Prevalence and rate of diagnosis of allergic rhinitis in Europe. Eur Respir J 2004; 24:758-64. [Link to abstract]

4. Bauchau V, Durham SR. Epidemiological characterization of the intermittent and persistent types of allergic rhinitis. Allergy 2005; 60:350-3. [Link to abstract]

5. Kaiser HB. Risk factors in allergy/asthma. Allergy Asthma Proc 2004; 25:7-10. [Link to abstract]

6. D'Amato G, Liccardi G, D'Amato M, Cazzola M. The role of outdoor air pollution and climatic changes on the rising trends in respiratory allergy. Respir Med 2001; 95:606-11.

7. Peden DB. Effect of pollutants in rhinitis. Curr Allergy Asthma Rep 2001; 1:242-6. [Link to abstract]

8. Park YJ, Baraniuk JN. Mechanisms of allergic rhinitis. Clin Allergy Immunol 2002; 16:275-93. No abstract available.

9. Smurthwaite L, Durham SR. Local IgE synthesis in allergic rhinitis and asthma. Curr Allergy Asthma Rep 2002; 2:231-8. [Link to abstract] 

10. Hansen I, Klimek L, Mosges R, Hormann K. Mediators of inflammation in the early and the late phase of allergic rhinitis. Curr Opin Allergy Clin Immunol 2004; 4:159-63. [Link to full text]

11. Bousquet J, Van CP, Khaltaev N. Allergic rhinitis and its impact on asthma. J Allergy Clin Immunol 2001; 108:S147-S334. No abstract available.

12. Demoly P, Allaert FA, Lecasble M, Bousquet J. Validation of the classification of ARIA (allergic rhinitis and its impact on asthma). Allergy 2003; 58:672-5. [Link to full text]

13. Karjalainen A, Martikainen R, Klaukka T, Saarinen K, Uitti J. Risk of asthma among Finnish patients with occupational rhinitis. Chest 2003; 123:283-8. [Link to abstract]

14. Siracusa A, Desrosiers M, Marabini A. Epidemiology of occupational rhinitis: prevalence, aetiology and determinants. Clin Exp Allergy 2000;30:1519-34. No abstract available.

15. Cortona G, Pisati G, Dellabianca A, Moscato G. Respiratory occupational allergies: the experience of the Hospital Operative Unit of Occupational Medicine in Lombardy from 1990 to 1998. G Ital Med Lav Ergon 2001; 23:64-70. [Link to abstract]

16. Walker S, Khan-Wasti S, Fletcher M, Harris J, Cuillinan P, Sheikh A. Hayfever has significant detrimental impact on national exam performance in UK teenagers: case control study. European Respiratory Journal 2005;26:134S. [Link to abstract]

17. Passali D, Passali FM, Damiani V, Passali GC, Bellussi L. Treatment of inferior turbinate hypertrophy: a randomized clinical trial. Ann Otol Rhinol Laryngol 2003; 112:683-8. [Link to abstract]

18. Fokkens W, Lund V, Bachert C, Clement P, Helllings P, Holmstrom M, Jones N, Kalogjera L, Kennedy D, Kowalski M, Malmberg H, Mullol J, Passali D, Stammberger H, Stierna P. EAACI position paper on rhinosinusitis and nasal polyps executive summary. Allergy 2005;60:583-601. [Link to ful text]