Epidemiology & Pathophysiology
Epidemiology Pathophysiology Epidemiology Allergic rhinitis affects between 10% and 40% of children and adults worldwide, 1,2,3,4,5,6,7,8 approximately 80% developing before the age of 20 years, with a peak at 20–40 years and then a gradual decline. 6,8 The burden in low- and middle income countries is similarly substantial and has been increasing since the 1990s. 1,2,6 In the International Study
Epidemiology
Allergic rhinitis affects between 10% and 40% of children and adults worldwide,1,2,3,4,5,6,7,8 approximately 80% developing before the age of 20 years, with a peak at 20–40 years and then a gradual decline.6,8 The burden in low- and middle income countries is similarly substantial and has been increasing since the 1990s.1,2,6 In the International Study of Asthma and Allergies in Childhood (ISAAC), the SA cohort of 13- to 14-year olds showed substantial and increasing prevalence from 30.4% in 1995 to 38.5% in 2002.2 Urbanisation and increasing levels of pollutants, as well as changes in pollen concentrations, allergenic potential and composition because of climate change, have been implicated in the increase in the prevalence of AR.23,24
Pathophysiology
Allergic rhinitis is a result of a Type 1 hypersensitivity reaction of the nasal mucosa. Allergens deposited onto the nasal mucosa of sensitised individuals bind to allergen specific
immunoglobulin E (IgE) on the surface of mast cells, resulting in the release of preformed mediators such as histamine. This causes the early phase of the allergic response and leads to acute symptoms such as itching, sneezing and rhinorrhoea.6,7,25 The late phase of the allergic response, which precipitates a cycle of chronic allergic symptoms, manifests 4 h – 6 h after allergen exposure, with nasal mucosal inflammation from activation and influx of inflammatory cells, including T-cells, eosinophils, basophils and neutrophils.6,25
Priming (increased nasal responsiveness to an allergen with repeated allergen exposure) occurs as a result of increased numbers of mast cells in the epithelium, increased permeability of the epithelium and easier allergen penetration to IgE-bearing cells and exaggerated responses of the nasal end organs.6,8 Air pollutants can also contribute to priming. Treatment with intranasal corticosteroids (INCS) can suppress the priming response.6,8,25
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Richards GA, McDonald M, Gray CL, et al. Allergic rhinitis: Review of the diagnosis and management: South African Allergic Rhinitis Working Group. S Afr Fam Pract. 2023;65(1), a5806. https://doi.org/10.4102/safp.v65i1.5806