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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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