Rhinitis is defined as at least two symptoms from a list comprising of rhinorrhoea, blockage, sneezing and nasal itching. Rhinitis is divided into infectious and noninfectious and the latter further subdivided into allergic (AR) and non-allergic rhinitis (NAR).
Allergic rhinitis (AR) is an immunoglobulin E (IgE)-mediated, type 1 hypersensitivity reaction in the mucous membranes of the nasal airways to an allergen or allergens. AR significantly reduces quality of life and interferes with school and work attendance and performance. Although it is very common, it is underdiagnosed and often undertreated. It is therefore not possible to give a confident incidence or prevalence, but it has been estimated to affect 10 to 30% of the United Kingdom population. It can be either seasonal (e.g., hay fever) or perennial (sometimes with seasonal exacerbations). Such a clinical classification is useful in United Kingdom practice for diagnosis and treatment and can be used to complement the allergic rhinitis and its impact on asthma (ARIA) classification. Some patients are atopic. Atopic means that they have a genetic susceptibility to form an immune (allergic) response to a range of commonly found allergens. An allergen that causes AR may also cause allergic asthma, atopic eczema (allergic dermatitis) and allergic conjunctivitis. It is a risk factor for asthma and control of AR is associated with better asthma control. These associations are more likely in atopic individuals. Those with a family history of atopy and firstborn children have a higher risk of developing AR.
Sensitisation to an allergen occurs in genetically predisposed people who are, to a variable degree, atopic. Allergens are captured by dendritic allergen-presenting cells. This activates T-helper (Th) cells and these activated Th cells, called Th2 cells, release cytokines, the most important of which is interleukin 4 (IL-4). IL-4 drives B cells to produce allergen-specific IgE. This IgE binds through its high-affinity receptor, to effector cells such as mast cells and basophils. Subsequent contact of a nasal allergen with two molecules of allergen-specific IgE on the surface of a mast cell triggers the immediate release of inflammatory mediators such as histamine, tryptase and prostaglandin causing an immediate inflammatory response. Cytokines, most importantly IL-4 again, are also released which permit the migration of leucocytes, particularly eosinophils, to the sensitised mucosa. These leucocytes in turn release their own cytokines leading to a late-phase inflammatory response.
The 2008 ARIA guidelines recommend the following classification:
a. Intermittent. Symptoms are present fewer than 4 days a week or for fewer than 4 consecutive weeks.
b. Persistent. Symptoms present for 4 or more days a week or for 4 or more consecutive weeks.
Intermittent and persistent can each be subdivided into mild or severe.
a. Mild. Symptoms are not troublesome and in particular do not cause sleep disturbance, impair daily leisure, do not impair sport activities and do not impair school or work.
b. Moderate to severe. Symptoms are troublesome and in particular disturb sleep, impair daily activities and impair attendance/performance at school or work.
In the United Kingdom, AR may also be classified as seasonal and perennial and used alongside the ARIA classification. Some patients may therefore have intermittent, mild, seasonal allergic rhinitis, etc.
83.3 Clinical Features
Seasonal rhinitis occurs at a time when the patient is most exposed to the allergen. For example, the following:
Grass pollen—late spring to early summer.
Tree pollen—early spring to late spring.
House dust mite—perennial but usually more severe in autumn, winter and early spring.