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EDITORIAL |
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| Year : 2010 | Volume
: 5
| Issue : 2 | Page : 63-64 |
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| Asthma and allergic rhinitis: Linked in treatment and outcomes |
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David Price
General Practice Airways Group, Department of General Practice and Primary Care, University of Aberdeen, Foresterhill Health Centre, Westburn Road, Aberdeen, United Kingdom
| Date of Submission | 06-Mar-2010 |
| Date of Acceptance | 10-Mar-2010 |
| Date of Web Publication | 13-Apr-2010 |
Correspondence Address:
David Price
General Practice Airways Group, Department of General Practice and Primary Care, University of Aberdeen, Foresterhill Health Centre, Westburn Road, Aberdeen AB25 2AY
United Kingdom
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/1817-1737.62467
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How to cite this article:
Price D. Asthma and allergic rhinitis: Linked in treatment and outcomes. Ann Thorac Med 2010;5:63-4 |
Asthma and allergic rhinitis (AR) frequently coexist, with epidemiological data suggesting that most asthma patients also suffer from AR. [1] We also find similar trends in asthma and AR prevalence around the world using objective epidemiological instruments. [2] Both diseases share similar triggers and similar pathophysiology characterized by similar inflammatory cell infiltrates. [3] It has also been found that the degree of inflammation in asthma correlates highly with the level of inflammation in the nose, [4] and that allergen challenge of the nose leads to hyperresponsiveness in the lungs [5] and allergen challenge in the lung with inflammation in the nose. [6] This and other evidence suggests a central mechanism behind the link with eosinophil precursors emanating from the bone marrow in response to triggers migrating not only to the site of stimulation, such as the nasal mucosa, but also to other sites within the one airway, including the lower respiratory tract.
Three areas of research suggest there is a real importance clinically in the 'one-airway' concept. The first of these relates to the possibility of interference in the development of asthma in patients with rhinitis; the second is that the severity of rhinitis appears to be a risk factor for poor asthma control and thirdly that common anti-inflammatory therapy may improve outcomes for both.
Examining the first of these, one study from the United States showed that those students with rhinitis in college were up to three times more likely to develop asthma by the age of 40 than those without rhinitis. [7] Intriguingly, Johnstone and Möller observed that young patients with rhinitis receiving subcutaneous immunotherapy for their rhinitis were less likely to develop subsequent asthma suggesting that intervention in patients with rhinitis might reduce the likelihood of developing asthma. [8]
Regarding the second of these, it has been found that clinically diagnosed AR is associated with significantly worse asthma control in adults and children. A recent analysis of patients in a General Practice database in the UK found that children with physician-diagnosed AR were more than twice as likely to be hospitalized for asthma as those without and 50% more likely in adults. [9],[10] Studies on children hospitalized for asthma in Norway showed that those children with clinically recognized rhinitis had a greater risk of rehospitalization for asthma. [11] In addition, a recent evaluation of asthma control in general practice suggested that those with asthma and moderate-to-severe rhinitis were four times more likely to have poor asthma control than those with no rhinitis symptoms. [12]
Considering the third one, treatment guidelines have recognized that asthma and AR are linked conditions of 'One Airway' and recommend that patients with asthma be evaluated for AR and vice versa. These guidelines support a combined approach to treating both conditions. [3] Such strategies with our current range of therapeutic options include:
Upper airway treatment options
Nasal steroids
Antihistamines
Lower airway treatment options
Inhaled steroids
Upper and lower airway treatment options
Leukotriene receptor antagonists
Anti-IgE
Immunotherapy
What evidence beyond a common-sense approach do we have to support this approach? Many of the studies that have supposedly set out to test this hypothesis have unfortunately been flawed, in that they have often only looked at using treatment for one part of the airway. For example, we have many studies of nasal steroids in patients with rhinitis and asthma but not used in conjunction with inhaled steroids to treat the asthma - these studies in seasonally triggered rhinitis and asthma have been examined in a recent meta-analysis and showed minimal impact on asthma outcomes - which is unsurprising and neither refute nor support the one-airway approach. [13] Because of this lack of appropriate, randomized, controlled trials we have until recently had to rely on data from observational studies relating to the use of antihistamines and nasal steroids. One of these studies used the MarketScan database in Washington, USA, that examined patients with asthma and rhinitis treated for concomitant rhinitis compared to those only treated for their asthma and found asthma-related events were reduced by 49% in those treated for both conditions. [14] Whilst certainly supporting the one-airway approach, randomized trials are needed to confirm these findings.
The advent of treatments that both treat the upper and lower airways provides an opportunity to examine this in a different way. These include drugs that block IgE, cysteinyl leukotrienes and the use of immunotherapy as all three approaches have evidence to support their usage in patients with asthma and AR. [15],[16],[17],[18],[19] The ideal study design would compare the benefits of a sole lower airway approach with a combined approach in patients with asthma alone and asthma with rhinitis. The only analysis that has set out to do this to date is that of the COMPACT study. The COMPACT study was a randomized, double-blind trial of 889 adults with asthma, whose asthma symptoms persisted despite being prescribed inhaled steroids with groups randomized to an increase in inhaled steroids or addition of a leukotriene receptor antagonist. [20] Further analysis examined the response in patients with and without a physician and patient report of rhinitis. This showed that those patients with asthma and no rhinitis had similar improved outcomes irrespective of the type of treatment increase; however, those with rhinitis showed a greater benefit with a one-airway approach of using upper and lower airways treatment with inhaled steroids and a leukotriene antagonist. This benefit was predominantly produced because of a reduced efficacy from increasing inhaled steroids in this subgroup. [21]
In conclusion, AR and asthma are inflammatory disorders that have been linked epidemiologically, pathophysiologically and clinically. Allergic rhinitis increases morbidity, therapeutic needs and use of healthcare resources in patients with asthma. It is, therefore, important to recognize co-morbidity in patients with asthma and consider management strategies from this perspective; failure to do so appears to result in adequate asthma control.
 References | |  |
| 1. | Leynaert B, Bousquet J, Neukirch C, Liard R, Neukirch F. Perennial rhinitis: An independent risk factor for asthma in nonatopic subjects: Results from the European Community Respiratory Health Survey. J Allergy Clin Immunol 1999;104:301-4.  |
| 2. | Worldwide variation in prevalence of symptoms of asthma, allergic rhinoconjunctivitis, and atopic eczema: ISAAC. The International Study of Asthma and Allergies in Childhood (ISAAC) Steering Committee. Lancet 1998;351:1225-32. |
| 3. | Bousquet J, Van Cauwenberge P, Khaltaev N; Aria Workshop Group; World Health Organization. Allergic rhinitis and its impact on asthma. J Allergy Clin Immunol 2001;108:S147-334. |
| 4. | Gaga M, Lambrou P, Papageorgiou N, Koulouris NG, Kosmas E, Fragakis S, et al. Eosinophils are a feature of upper and lower airway pathology in non-atopic asthma, irrespective of the presence of rhinitis. Clin Exp Allergy 2000;20:663-9. |
| 5. | Corren J, Adinoff AD, Irvin CG. Changes in bronchial responsiveness following nasal provocation with allergen. J Allergy Clin Immunol 1992;89:611-8. |
| 6. | Braunstahl GJ, Kleinjan A, Overbeek SE, Prins JB, Hoogsteden HC, Fokkens WJ. Segmental bronchial provocation induces nasal inflammation in allergic rhinitis patients. Am J Respir Crit Care Med 2000;161:2051-7. |
| 7. | Settipane RJ, Hagy GW, Settipane GA. Long-term risk factors for developing asthma and allergic rhinitis: a 23-year follow-up study of college students. Allergy Proc 1994;15:21-5. |
| 8. | Möller C, Dreborg S, Ferdousi HA, Halken S, Høst A, Jacobsen L, et al. Pollen immunotherapy reduces the development of asthma in children with seasonal rhinoconjunctivitis (the PAT-study). J Allergy Clin Immunol 2002;109:251-6. |
| 9. | Thomas M, Kocevar VS, Zhang Q, Yin DD, Price D. Asthma-related health care resource use among asthmatic children with and without concomitant allergic rhinitis. Pediatrics 2005;115:129-34. |
| 10. | Price D, Zhang Q, Kocevar VS, Yin DD, Thomas M. Effect of a concomitant diagnosis of allergic rhinitis on asthma-related health care use by adults. Clin Exp Allergy 2005;35:282-7. |
| 11. | Sazonov Kocevar V, Thomas J 3rd, Jonsson L, Valovirta E, Kristensen F, Yin DD, et al. Association between allergic rhinitis and hospital resource use among asthmatic children in Norway Allergy. Allergy 2005;60:338-42. |
| 12. | Clatworthy J, Price D, Ryan D, Haughney J, Horne R. The value of self-report assessment of adherence, rhinitis and smoking in relation to asthma control. Prim Care Respir J 2009;18:300-5. |
| 13. | Taramarcaz P, Gibson PG. Intranasal corticosteroids for asthma control in people with coexisting asthma and rhinitis. Cochrane Database Syst Rev 2003;(4):CD003570. |
| 14. | Crystal-Peters J, Neslusan C, Crown WH, Torres A. Treating allergic rhinitis in patients with comorbid asthma: The risk of asthma-related hospitalizations and emergency department visits. J Allergy Clin Immunol 2002;109:57-62. |
| 15. | Vignola AM, Humbert M, Bousquet J, Boulet LP, Hedgecock S, Blogg M, et al. Efficacy and tolerability of anti-immunoglobulin E therapy with omalizumab in patients with concomitant allergic asthma and persistent allergic rhinitis: SOLAR. Allergy 2004;59:709-17. |
| 16. | Marogna M, Spadolini I, Massolo A, Canonica GW, Passalacqua G. Clinical, functional, and immunologic effects of sublingual immunotherapy in birch pollinosis: a 3-year randomized controlled study. J Allergy Clin Immunol 2005;115:1184-8. |
| 17. | Rouadi P, Naclerio R. Leukotrienes as mediators in the nose. SRS-A to Leukotrienes: The Dawning of a New Treatment. In: Dahlen S, editor. Oxford, England: Blackwell Science; 1997. p. 301-18. |
| 18. | Howarth PH. Leukotrienes in rhinitis. Am J Respir Crit Care Med 2000;161:S133-6. |
| 19. | Philip G, Nayak AS, Berger WE, Leynadier F, Vrijens F, Dass SB, et al. The effect of montelukast on rhinitis symptoms in patients with asthma and seasonal allergic rhinitis. Curr Med Res Opin 2004;20:1549-58. |
| 20. | Price DB, Hernandez D, Magyar P, Fiterman J, Beeh KM, James IG, et al. Randomised controlled trial of montelukast plus inhaled budesonide versus double dose inhaled budesonide in adult patients with asthma. Thorax 2003;58:211-6. |
| 21. | Price DB, Swern A, Tozzi CA, Philip G, Polos P. Effect of montelukast on lung function in asthma patients with allergic rhinitis: analysis from the COMPACT trial. Allergy 2006:61:737-42. |
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