Therefore, allergic rhinitis is now classified according to symptom duration (intermittent or persistent) and severity (mild, moderate or severe) (see Fig. For example, some allergic triggers, such as pollen, may be seasonal in cooler climates, but perennial in warmer climates, and patients with multiple “seasonal” allergies may have symptoms throughout most of the year. However, not all patients fit into this classification scheme. Traditionally, allergic rhinitis has been categorized as seasonal (occurs during a specific season) or perennial (occurs throughout the year). The mediators and cytokines released during the early phase of an immune response to an inciting allergen trigger a further cellular inflammatory response over the next 4–8 h (late-phase inflammatory response) which results in recurrent symptoms (usually nasal congestion) that often persist. Crosslinking of IgE bound to mast cells by allergens, in turn, triggers the release of mediators, such as histamine and leukotrienes, that are responsible for arteriolar dilation, increased vascular permeability, itching, rhinorrhea, mucous secretion, and smooth muscle contraction in the lung. In allergic individuals, the T cells infiltrating the nasal mucosa are predominantly T helper 2 (Th2) in nature and release cytokines (e.g., interleukin -3, IL-4, IL-5, and IL-13) that promote immunoglobulin E (IgE) production by plasma cells. In allergic rhinitis, numerous inflammatory cells, including mast cells, CD4-positive T cells, B cells, macrophages, and eosinophils, infiltrate the nasal lining upon exposure to an inciting allergen (most commonly airborne dust mite fecal particles, cockroach residues, animal dander, moulds, and pollens). This article provides an overview and update of the recommendations provided in these guidelines as well as a review of current literature related to the pathophysiology, diagnosis, and appropriate management of allergic rhinitis. Ĭomprehensive and widely-accepted Canadian guidelines for the diagnosis and treatment of allergic rhinitis were published in 2007. Therefore, allergic rhinitis and asthma appear to represent a combined airway inflammatory disease, and this needs to be considered to ensure the optimal assessment and management of patients with allergic rhinitis. Evidence has shown that allergen provocation of the upper airways not only leads to a local inflammatory response, but may also lead to inflammatory processes in the lower airways, and this is supported by the fact that rhinitis and asthma frequently coexist. Furthermore, the submucosa of both the upper and lower airways includes a collection of blood vessels, mucous glands, supporting cells, nerves and inflammatory cells. For example, both tracts contain a ciliated epithelium consisting of goblet cells that secrete mucous, which serves to filter the incoming air and protect structures within the airways. ![]() There are a number of physiological, functional and immunological relationships between the upper (nose, nasal cavity, paranasal sinuses, Eustachian tube, pharynx and larynx) and lower (trachea, bronchial tubes, bronchioles and lungs) respiratory tracts. In the past, allergic rhinitis was considered to be a disorder localized to the nose and nasal passages, but current evidence indicates that it may represent a component of a systemic airway disease involving the entire respiratory tract. Severe allergic rhinitis has been associated with significant impairments in quality of life, sleep and work performance. Allergic rhinitis is the most common type of chronic rhinitis, affecting 10–20% of the population, and evidence suggests that the prevalence of the disorder is increasing. ![]() It is a common disorder that affects up to 40% of the population. Rhinitis is broadly defined as inflammation of the nasal mucosa.
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