This Update, the first in our Allergy and Immunology series, looks at the growing epidemic of allergic rhinitis. It is by Dr Karl Baumgart BSc (Med), MB, BS, PhD, FRACP, FRCPA.
Dr Karl Baumgart BSc (Med), MB, BS, PhD, FRACP, FRCPA
Immunologist in Allergy and Clinical Immunology; Director of Immunopathology at Douglass Hanly Moir Pathology, Sydney; Member of the Australasian Society of Clinical Immunology and Allergy.
ALLERGIC rhinitis is a major global public health issue. It affects up to 40% of the Australian population and its prevalence is increasing each year.1,2
The effects of allergic rhinitis are vastly underestimated and have a significant impact on quality of life and healthcare costs.
Although not life-threatening, for most patients allergic rhinitis is distinguished by its persistence, despite helpful symptomatic treatments.
The evidence of the sharp increase in allergic rhinitis is seen in general practice on a daily basis.
The rise in allergies is thought to be primarily due to changes in environmental factors interacting with an individual’s allergy genes.
Changes to our environment and lifestyle, growing urbanisation, pollution, active or passive smoking and changing dietary habits are all factors promoting the progression of allergy.
GLOBAL PREVALENCE AND CURRENT SITUATION IN AUSTRALIA
The WHO ranks allergy as the fourth most common global chronic disease,3 with a clinical burden of one in four people worldwide being affected by respiratory allergies.4
The incidence of this disease has risen in the past 50 years, particularly in areas where the prevalence was previously at low to medium levels. This is fast becoming a global health issue of major importance as the rates of allergic disease escalate in populous developing countries in Asia, Africa and South America.1
Consequences of allergic rhinitis include an increased risk of developing asthma. Conceptually, this has been described as united airway disease. Asthma is three times more common in those with allergic rhinitis than in the general population and more than 80% of allergic asthmatics have allergic rhinitis.4
Australia and New Zealand have among the highest prevalence of allergic disorders in the developed world. Our climate favours high dust mite populations in our bedrooms and our prolonged pollen seasons ensure more chronicity of airborne allergen exposure. The multicultural nature of our society ensures more diversity of food allergen exposures than in many other societies.
Allergic rhinitis is the most common form of allergic disease. Studies of Australian and New Zealand adults and children have shown an approximate doubling in the prevalence of allergic rhinitis and eczema in the past 10–15 years.
IMPACT ON QUALITY OF LIFE
Respiratory allergies are considered to be a major public health issue due to their prevalence, and the significant impact on the individual’s quality of life as well as school and work performance. For society, the impaired productivity constitutes a growing economic burden.2,5
Almost 70% of patients with allergic rhinitis feel that their condition limits their way of life.6
Characteristic symptoms of allergic rhinitis consequently impair the usual performance of daily activities; quality of sleep, leading to fatigue; cognitive function; work productivity; exam performance; and impaired psychosocial wellbeing.5
In 2008, a new classification system for allergic rhinitis was proposed by the Allergic Rhinitis and its Impact on Asthma (ARIA) guidelines.4
This was done in order to characterise rhinitis and its impact on quality of life according to its pattern (intermittent or persistent) and symptom severity. This led to standardised treatment recommendations:
- Persistent rhinitis (replaces ‘perennial rhinitis’) occurs more than four days a week and for more than four consecutive weeks in the year
- Intermittent rhinitis (replaces ‘seasonal rhinitis’) occurs less than four days a week or for less than four consecutive weeks a year
- Moderate to severe rhinitis: incapacitating symptoms accompanied by discomfort during day-to-day work or school activities, as well as disruption of sleep
- Mild rhinitis: minimal symptoms having little impact on sleep and day-to-day life.
Allergic rhinitis and asthma have a significant impact on patients based on the degree of the severity of their symptoms, and create an economic burden not only on the patient, but also their family and the community.
Economic burden results from direct costs (inpatient care, physician visits, drugs and devices, blood and diagnostic tests, research and education) and indirect costs (school days lost, travel, waiting time, lost productivity for carers, drop in work performance and absenteeism).2
The Australasian Society of Clinical Immunology and Allergy (ASCIA) report estimated that in 2007, the financial cost in Australia of all allergies per annum was $7.8 billion. When reduced quality of life is taken into consideration, the costs are estimated to be $21.5 billion per annum.2 To put this in perspective, it is about double the estimated costs for other common conditions such as arthritis.1
In per capita terms, this amounts to a financial cost of about $1912 per person with allergies per annum. Including the value of lost wellbeing, the cost is $7200 per person per annum.2
THE IMPORTANCE OF TREATING EARLY
Epidemiological studies have shown that while allergy symptoms can begin at any age, the tendency usually appears in early childhood.1
Atopic infants, at risk of developing multiple allergic sensitisations and allergic syndromes typically with familial predisposition, initially manifest eczema and food sensitisations.
These food allergies then tend to diminish and even disappear in most children.
Sensitisation to airborne allergens develops, resulting in allergic rhinitis, asthma and allergic conjunctivitis.
This natural progression from food-related allergies to respiratory allergies is known as the ‘allergic march’.
The practical implications mean that the results of allergy testing and drivers of allergic syndromes will evolve during development.
For example, transient sensitisations to food allergens are not uncommon in the first few years of life, while more sustained sensitisations to inhalant allergens progressively appear in later childhood.
Progression to respiratory allergy is greatest in children with more severe eczema and food allergies who experience the greatest diversity of allergic sensitisations (polysensiti-sation).
Figure 1: The allergic march
SEASONALITY AND AUSTRALIAN REGIONS
Symptoms of allergic rhinitis can be triggered by inhalation of airborne allergens, which include dust mite proteins; pollen from grasses, weeds or trees; moulds; and animal dander.
The ASCIA website and patient information resources (www.allergy.org.au) indicate that in our environment, pollen seasons can last for several months, while exposure is difficult to avoid.7
Plants such as pasture grasses and weeds rely on wind to disperse their pollen. These pollens are produced in vast quantities, are carried long distances by wind and cause allergies in people, even if they live a long way from the source.
Most of the troublesome pollen in Australia is produced by introduced Northern Hemisphere grass, tree and weed pollen. Improved pasture grasses are more allergenic than Australian native grasses.
Pollen from exotic trees is more allergenic than that from Australian trees. A number of weeds with highly allergenic pollen have also been introduced.7
A comprehensive pollen calendar summarising the distribution and seasonality of major pollen allergens is available on the ASCIA website.8
Pollen seasons can last for several months. Pollination times vary with the plant variety and its location. For example, trees pollinate in late winter and early spring. Grasses flower next, and the weed plantain flowers from August through to May. Pollen burdens are also higher in inland areas, where there are no natural barriers to wind dispersal.
Pollen numbers are lower on the east coast, where the prevailing winds come from the sea and where there is protection from westerly winds by the Great Dividing Range.
Pollen numbers are higher on the Victorian south coast because the prevailing winds are from the north, carrying pollen from the grasslands. In South Australia and Western Australia, the concentration of pollen can vary according to the prevailing winds.7
The principal grasses growing in the northern coastal areas are subtropical and mainly flower from January to March. Allergenic grasses in the southern part of Australia are mostly Northern Hemisphere grasses, with the main flowering period from October to December. The ASCIA pollen calendar provides a comprehensive list of allergenic grasses and their growing seasons.8
White cypress pine produces highly allergenic pollen. Its growth extends from the western slopes and plains of eastern Australia across to Western Australia, south of the Tropic of Capricorn, and it flowers from late July through to the end of August.
There are many species of casuarina or Australian oak trees that produce pollen throughout the year and may cause allergic rhinitis symptoms.7
Introduced urban tree pollens of allergenic concern include birch trees in Melbourne and Canberra, as well as sycamore trees in Sydney. Olive trees produce highly allergenic pollens that cross-react with privet as well as native oleaceae and are a dominant allergen in Adelaide.
TREATING MODERATE TO SEVERE ALLERGIC RHINITIS
Avoidance of the allergen is the first condition on which allergy treatment is based, but it may be difficult to put into practice, particularly in the case of allergic rhinitis triggered by pollens or dust mites.
The key elements for dust mite control include weekly hot washing (> 55°C) of bed linen and occlusive casings every four weeks, while drying bed linen indoors or in a dryer may reduce the importation of outdoor pollens to the bedroom.
Although many treatment options exist, many allergic rhinitis patients still suffer from inadequate treatment. Fewer than half (45%) seek medical advice or treatment for their condition.5
Intranasal corticosteroids are the first-line treatment in patients with moderate to severe allergic rhinitis. They work as a result of their potent and localised anti-inflammatory activity.
Most variants used in nasal sprays have minimal systemic absorption. They inhibit the inflammatory response irrespective of the triggering agent and can improve the biology of the disorder more than antihistamines. H1 antihistamines provide effective symptomatic treatment for persistent rhinitis and are available topically or orally with demonstrated efficacy and safety.
Leukotriene antagonists have been shown to be effective in seasonal rhinitis and asthma, especially in combination with antihistamines, although they are not commonly used.
These symptomatic treatments for allergic rhinitis are effective but do not solve the problem of allergic disease, particularly in severe forms, or its chronic nature. Symptoms of patients with moderate to severe allergic rhinitis may not be relieved by pharmacotherapy.
Although symptomatic treatments are the most common first-line treatment of allergic rhinitis, their efficacy remains questionable, especially in severe cases.
For example, a recent study indicated that 57.3% of patients with severe allergic rhinitis reported as poor, bad or very bad the control of their disease with symptomatic treatments.9
Allergen-specific immunotherapy is currently the only established method of altering the ‘natural history’ of allergic disease.1 The aim is to re-educate the immune system by administering increasing doses of allergens, thereby inducing specific long-term tolerance.10
Allergen immunotherapy is the only treatment option that can durably treat respiratory allergies by tackling the root cause of the disease. It works on both the humoral and cellular mechanisms of the immune system involved in allergic reactions.11 By durably modifying the immune system, it ultimately makes the body more tolerant to allergens. As a treatment, it has been used for more than 100 years in Europe.
Adults and children from the age of five years can be treated with allergen immunotherapy. There is good evidence that it is clinically effective to treat allergic rhinitis and asthma, and may prevent the progression of allergic disease.4
Allergen immunotherapy can be administered subcutaneously or sublingually. There are advantages and disadvantages of either system depending on a patient’s allergic sensitisations, their clinical syndromes and general circumstances. Recent developments in sublingual allergen immunotherapy treatments have greatly improved clinical efficacy to match that of subcutaneous immunotherapy and provide greater options for patients, particularly children.
Allergen immunotherapy is a long-term commitment for patients; it is recommended that it is continued for 3–5 years to decrease the chance that a patient’s allergies will return. It usually requires at least 4–5 months before symptoms improve.
A shared care model between the family physician and the allergy specialist can best support patients and improve their allergic journey.
Allergic rhinitis is a significant concern for many Australians and is growing in prevalence.
It can have a serious negative impact on quality of life for children and adults alike.
GPs will continue to see increasing numbers of patients presenting with allergic symptoms.
Accurate diagnosis of allergic rhinitis is critical to long-term outcomes and achieving a significant improvement in a patient’s quality of life.
Symptomatic treatments are effective, but may not solve the problem of allergic rhinitis in moderate to severe and chronic cases.
Allergen-specific immunotherapy currently represents the only causative treatment for allergic rhinitis.
It can durably reduce the symptoms of moderate to severe allergic rhinitis.
New developments in immunotherapy will assist in uptake and adherence to treatment.
A 10-year-old boy was referred for persistent rhinitis. He always seemed to have ‘colds’ more often than his older siblings. He went to sleep with difficulty, his bed was often a sea of tissues and he struggled to get up in the morning. His parents noticed he always breathed with his mouth open and that he would often snore. This did not change with seasons or holidays. Their dentist had recently referred him to an orthodontist.
As an infant there was a history of mild flexural eczema and an episode of angio-oedema to soft-boiled egg at age 10 months. Currently, he can eat all foods without difficulty, but dislikes prawns. Occasionally with chest infections he’d had asthma, with a hospital admission at age five. Grommets were required at age three, while tonsils and adenoids were removed at age four.
His father had seasonal allergic rhinitis, which had diminished in his fourth decade, only to be replaced by chronic sinus disease. He did not want his son to have the same ‘allergic journey’ that he’d had.
At home there were no pets, no mould issues and there were hard floors. Bedsheets were washed weekly in hot water in a front loader and dust mite casings had been fitted to the bed.
Examination revealed poor nasal airflow, a transverse nasal crease and white markings on the upper exposed front teeth. He was dark and puffy around the eyes, consistent with allergic shiners. The chest was clear and there was slightly dry skin without definite eczema. The turbinates were pale and congested.
Skin prick tests covering a wide range of inhalants and some food allergens (because of the history of eczema and dislike of prawns) were done. These were remarkable for significant sensitisation to dust mite, cockroach, paspalum, fescue grass, rye grass and couch grass pollen. There was definite low-level allergic sensitisation to crab, prawn and lobster.
The results demonstrate significant allergic sensitisation to dust mite, with some crustacean and cockroach cross-reactive sensitisation to dust mite-crustacean tropomyosin. There is also significant sensitisation to grasses, including paspalum.
Because of the significant obstructive symptoms, a lateral airway x-ray was performed and showed adenoid regrowth.
He was referred to an ENT surgeon for consideration of repeat adenoidectomy and surgical reduction of the inferior turbinates. Immunotherapy for dust mite and grasses was discussed, including the options of subcutaneous and sublingual immunotherapy (SLIT).
Four months after surgery and the commencement of SLIT for grasses and dust mite the patient was much improved, but immunotherapy continues, with a target treatment duration of five years.
- Respiratory allergies are a major public health issue due to their prevalence, the significant impact on quality of life and reduced productivity.
- Progression to respiratory allergy occurs in children with more severe eczema and food allergies who experience the greatest diversity of allergic sensitisations.
- The natural progression from food-related allergies to respiratory allergies is known as the ‘allergic march’.
- Avoidance of the allergen is the first condition on which allergy treatment is based, but it may be difficult to put into practice.
- Intranasal corticosteroids (ICS) are the first-line treatment in patients with moderate to severe allergic rhinitis.
- ICS inhibit the inflammatory response and can improve the biology of the disorder more than antihistamines.
- Allergen immunotherapy is the only treatment option that can durably treat respiratory allergies by tackling the root cause of the disease.
Australasian Society of Clinical Immunology and Allergy: www.allergy.org.au
1. Prescott S. The Allergy Epidemic: A Mystery of Modern Life. UWA Publishing, 2011.
2. Mullins RJ, et al. The economic impact of allergic disease in Australia: not to be sneezed at. ASCIA/Access Economics Report, November 2007. www.allergy.org.au/content/view/324/76/
3. International classification of diseases (ICD). http://www.who.int/classifications/icd/en/
4. Bousquet J, et al. Allergic Rhinitis and its Impact on Asthma (ARIA) 2008 update (in collaboration with the World Health Organization, GA(2)LEN and AllerGen). Allergy 2008;63 Suppl 86:8-160.
5. Canonica GW, Bousquet J, Mullol J, Scadding GK, Virchow JC. A survey of the burden of allergic rhinitis in Europe. Allergy 2007;62 Suppl 85:17-25.
6. Valovirta E, Myrseth SE, Palkonen S. The voice of the patients: allergic rhinitis is not a trivial disease. Curr Opin Allergy Clin Immunol 2008;8:1-9.
7. Australasian Society of Clinical Immunology and Allergy. www.allergy.org.au
9. Ibero M, et al. Diagnosis and treatment of allergic rhinitis in children: results of the PETRA study. Allergol Immunopathol (Madr) 2012; 40:138-43.
10. Moingeon P, et al. Immune mechanisms of allergen-specific sublingual immunotherapy. Allergy 2006;61:151-65.
11. Sub-lingual immunotherapy: World Allergy Organization Position Paper 2009. Allergy 2009;64 Suppl 91:1-59.
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