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Epidemiology IN the 2007 / 2008 Australian Bureau of Statistics’ National Health Survey, 3.1 million Australians( 15.1 %) self-reported“ Hayfever and allergic rhinitis” as a long-term medical condition. 2 Females were slightly more affected( 16 %) compared with males( 14.1 %).

Much of the prevalence of this condition is realised by the late teens to early 20s. For reasons that aren’ t clear, the prevalence in Australia has a significant geographic variation with prevalence as high as 21 % in Tasmania compared with only 13.3 % and 11.3 % in NSW and Queensland respectively. Despite this wide variation by state, rurality seems to have no bearing on prevalence. 3

It is likely, however, that these figures underestimate the true prevalence. Patients with milder forms of the disease and less troublesome symptoms are less likely to seek medical advice or to report it as a“ long-term medical condition”. The specific financial cost of allergic rhinitis in Australia is not clear. However in 2005, the total direct and indirect cost of allergic disease was estimated at $ 30 billion. 4

Classification The 2001 article‘ Allergic Rhinitis and its Impact on Asthma’( ARIA

AUSTRALIA HAS A SIGNIFICANT GEOGRAPHIC VARIATION WITH PREVALENCE AS HIGH AS 21 % IN TASMANIA COMPARED WITH ONLY 13.3 % AND 11.3 % IN NSW AND QUEENSLAND RESPECTIVELY.

2001) defined the current classification for allergic rhinitis according to the persistence and duration of symptoms, and their severity( see table 1). 5

Prior to this, the condition was classified according to time of exposure into perennial, seasonal and occupational. Perennial was generally considered to be the result of indoor allergens( house dust mites, moulds, insects, animal dander) while seasonal resulted from sensitisation and exposure to a wide variety of outdoor allergens( pollens, grasses, moulds). The ARIA 2001 classification reflects the fact that many patients are sensitised to more than one allergen and that many‘ outdoor allergens’ are perennial.

Table 1. Classification of allergic rhinitis Class Presence of symptoms Features

Number per 100,000 population 24,000

20,000

16,000

12,000

8,000

4,000

0

0-14 15-24 25-34 35-44 45-54 55-64 65-74 75 + Age group( years)

Notes 1. Directly age standardised to the 2001 Australian population. 2. The thin vertical bars attached to the top of each column are 95 % confidence intervals. We can be 95 % confident that the true value is within the interval depicted. Source: ABS National Health Survey, 2007 – 08.

Male Female

Figure 1. Prevalence of allergic rhinitis in Australia by age and sex.

Source: Australian Institute of Health and Welfare.

ALLERGIC rhinitis is a type I hypersensitivity reaction, closely related in its pathogenesis to asthma and atopic dermatitis.

Cellular pathogenesis As in other atopic conditions, the development of allergic rhinitis begins with initial sensitisation followed by a subsequent allergen challenge that produces the typical symptoms of hay fever.

Sensitisation Turbulent airflow during nasal inspiration promotes deposition of particulate matter( including aeroallergens) in the nasal mucosa, where it is imbibed by antigen-presenting cells( such as macrophages, CD1 + dendritic cells and B lymphocytes). Antigens are processed and their fragments are presented with class II major histocompatibility matrix( MHC II) proteins to T-helper 2( TH2) cells. 6 Secretion of interleukins and cell surface protein interactions promote isotypic transformation of B lymphocytes and results in the production of large quantities of allergen-specific IgE( see figure 2). This abundant IgE binds highaffinity receptors on mast cells and basophils that are concentrated in the nasal lamina propria.

Antigen challenge Subsequent exposure to an allergen to which an atopic individual is sensitised invokes a two-phase immune response in allergic rhinitis. In the early phase reaction, processed allergen peptides presented by dendritic cells to

Dermatophagoides pteronyssinus, a species of house dust mite. Source: http:// bit. ly / 2qYO2ci

‘ primed’ mast cells causes release of preformed mediators: vasoactive amines( histamine), enzymes and proteoglycans. Histamine is the mediator of most relevance in the development of symptoms and in the treatment, causing smooth muscle contraction, increasing vascular permeability and promoting mucous secretion. The late phase response is induced by synthesised chemokines, some of which amplify the early phase response and others that attract and promote migration of leukocytes( eosinophils in particular) without further antigen exposure. 7

Genetics This is a multifactorial disease with a clear genetic role in its aetiology. Allergic rhinitis, asthma and other atopic diseases show strong familial and intra-individual clustering. 8

Numerous loci of the HLA gene within chromosome 6 have been implicated in the pathogenesis of atopic diseases, particularly in the propensity toward TH2 compared with TH1 immune responses.

Allergens Inhaled aeroallergens are the principal environmental factor in the pathogenesis of allergic rhinitis. Allergens are classically divided into indoor( house dust mites, animal dander, insects and plant matter), outdoor( pollens and moulds) and occupational( chemicals, bakery allergens, laboratory animals). Outdoor allergens typically result in seasonal variation of symptoms and indoor allergens are more likely to cause persistent rhinitis. However, up to 50 % of patients sensitive to pollens have Figure 2. IgE-mediated type I hypersensitivity reaction in allergic rhinitis. cont’ d page 22 Image: Robbins and Cotran Pathologic Basis of Disease. 7th edn. Elsevier.

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