Allergic Rhinitis

A 35-year-old woman has a history of nasal congestion on most days of the year, dating back to her late teens. She has chronic nasal drainage, which is clear and thick. Her congestion is worst in the late summer and early fall and again in the early spring; at these times, she also has sneezing, nasal itching, and cough. Five years ago, she had an episode of shortness of breath with wheezing on a day when her nasal symptoms were severe, but this episode resolved spontaneously and has not recurred. Her eyes do not bother her. Over-the-counter oral antihistamines help her symptoms a little, as do nasal decongestants, which she uses occasionally. Her 6-year-old son has similar symptoms. How should this case be managed? THE CLINICAL PROBLEM Allergic rhinitis is defined as symptoms of sneezing, nasal pruritus, airflow obstruction, and mostly clear nasal discharge caused by IgE-mediated reactions against inhaled allergens and involving mucosal inflammation driven by type 2 helper T (Th2) cells.1 Allergens of importance include seasonal pollens and molds, as well as perennial indoor allergens, such as dust mites, pets, pests, and some molds. The pattern of dominant allergens depends on the geographic region and the degree of urbanization, but the overall prevalence of sensitization to allergens does not vary across census tracts in the United States.2 Sensitization to inhaled allergens begins during the first year of life; sensitization to indoor allergens precedes sensitization to pollens. Because viral respiratory infections occur frequently in young children and produce similar symptoms, it is very difficult to diagnose allergic rhinitis in the first 2 or 3 years of life. The prevalence of allergic rhinitis peaks in the second to fourth decades of life and then gradually diminishes.3,4 Copyright © 2015 Massachusetts Medical Society. Address reprint requests to Dr. Wheatley at the National Institutes of Health, 5601 Fishers Ln. , Rm. 6B56, Bethesda, MD 20892-9827, or at lisa.wheatley@nih.gov. An audio version of this article is available at NEJM.org No potential conflict of interest relevant to this article was reported. Disclosure forms provided by the authors are available with the full text of this article at NEJM.org. This Journal feature begins with a case vignette highlighting a common clinical problem. Evidence supporting various strategies is then presented, followed by a review of formal guidelines, when they exist. The article ends with the authors’ clinical recommendations. NIH Public Access Author Manuscript N Engl J Med. Author manuscript; available in PMC 2015 July 29. Published in final edited form as: N Engl J Med. 2015 January 29; 372(5): 456–463. doi:10.1056/NEJMcp1412282. N IH -P A A uhor M anscript N IH -P A A uhor M anscript N IH -P A A uhor M anscript The frequency of sensitization to inhalant allergens is increasing and is now more than 40% in many populations in the United States and Europe.2,5,6 The prevalence of allergic rhinitis in the United States is approximately 15% on the basis of physician diagnoses7 and as high as 30% on the basis of self-reported nasal symptoms.3 Allergic rhinitis contributes to missed or unproductive time at work and school, sleep problems, and among affected children, decreased involvement in outdoor activities.7 In addition, children with allergic rhinitis are more likely than unaffected children to have myringotomy tubes placed and to have their tonsils and adenoids removed.7 The ability to control asthma in people with both asthma and allergic rhinitis has been linked to the control of allergic rhinitis.8 Most people with asthma have rhinitis. The presence of allergic rhinitis (seasonal or perennial) significantly increases the probability of asthma: up to 40% of people with allergic rhinitis have or will have asthma.9,10 Atopic eczema frequently precedes allergic rhinitis.11 Patients with allergic rhinitis usually have allergic conjunctivitis as well.12 The factors determining which atopic disease will develop in an individual person and the reasons why some people have only rhinitis and others have rhinitis after eczema or with asthma remain unclear. Having a parent with allergic rhinitis more than doubles the risk.13 Having multiple older siblings and growing up in a farming environment are associated with a reduced risk of allergic rhinitis14,15; it is hypothesized that these apparently protective factors may reflect microbial exposures early in life that shift the immune system away from Th2 polarization and allergy.14,15 When persons are exposed to an allergen against which they are sensitized, cross-linking by the allergen of IgE bound to mucosal mast cells results in nasal symptoms within minutes (Fig. 1). This is due to the release of neuroactive and vasoactive substances such as histamine, prostaglandin D2, and cysteinyl leukotrienes.16 During the next hours, through a complex interaction of mast cells, epithelial cells, dendritic cells, T cells, innate lymphoid cells, eosinophils, and basophils, Th2 inflammation develops in the nasal mucosa with the participation of a wide array of chemokines and cytokines produced by these cells.16,17 As a consequence of mucosal inflammation, nasal symptoms can persist for hours after allergen exposure and the mucosa becomes more reactive to the precipitating allergen (priming) as well as to other allergens and to nonallergenic stimuli, such as strong odors and other irritants (nonspecific nasal hyperresponsiveness). 18,19 Allergic rhinitis should be viewed as a constellation of these mechanisms and not as a simple acute reaction to allergen exposure. STRATEGIES AND EVIDENCE