PATHOPHYSIOLOGY

Over 90% of adults and 80% of children with asthma are diagnosed as atopic and therefore management of this condition requires knowledge of the factors that trigger an allergic response. In the patient with chronic or persistent asthma, the key physiological feature underlying this condition is airways hyperresponsiveness (AHR), which in the context of allergic asthma manifests as a heightened or exaggerated bronchoconstrictor response to aeroallergens. The underlying basis for this condition is a persistent inflammatory response into the airways that ultimately results in airway remodelling, narrowing of the airways and heightened responsiveness to allergic and non-allergic triggers. How this condition develops over the life of a patient is still poorly understood. However, it seems likely that genetically susceptible individuals are primed at birth (or even in utero) to develop an atopic response to one or more environmental allergens. An understanding of the nature of the inflammatory response is important in order to guide correct diagnosis of the disease and choice of treatment approaches (Holgate & Polosa, 2006).

It is interesting to note that the incidence of atopy and allergy in Australia, and other western and developing nations, is increasing. Again, the reason for this is not fully understood, but its basis is likely to be in the early years of life and may perhaps relate to the increasing ‘cleanliness’ of urban home environments in these regions: the so called ‘hygiene hypothesis’. For example, there is evidence to suggest that early exposure to the high bacterial loads in some farm environments can prevent the development of atopy and asthma (Holt, 2004). Other environmental factors may also be at play, including increased levels of pollution in metropolitan regions and likely increasing effect of global warming: increased atmospheric CO₂ levels are known to stimulate pollinosis, which can increase the levels of allergens in the atmosphere, while changing climates will alter the geographic spread of allergens and the types of allergens to which people are exposed. It is therefore important to identify allergen triggers where possible, so that avoidance strategies for the patient can be put in place. However, it may also be important to establish whether the environmental conditions of the patient have also changed. In the case of Kade in Case study 17.1, moving into a dusty environment with high levels of passive smoke exposure represented a high-risk environment. The environment which the patient is moving into should be taken into account when considering discharge from hospital of the stabilised patient, and all other potential trigger factors should be considered (see below).

However, it should also be noted that a lack of diagnosis for atopy does not preclude a diagnosis of asthma—this is particularly the case for children—and asthma can develop in response to a variety of non-allergenic triggers. These include cold air, exercise, stress, oesophageal reflux and responses to medications such as aspirin and non-steroidal antiinflammatory drugs (NSAIDs). However, as Kade has been diagnosed as atopic, it is likely that his exacerbation was triggered by an allergic response and we will therefore focus this discussion on the allergic triggers of asthma.

ALLERGEN TRIGGERS

For patients with allergic asthma, it is well established that exposure to allergens can trigger an asthmatic response. In Australia and other developed countries, one of the most common indoor allergic triggers are allergens of the house dust mite (HDM) Dermatophagoides pteronyssinus and Dermatophagoides farinae. HDM allergens usually take the form of small protein molecules that are part of the mite or are excreted as waste products (Holt & Thomas, 2005). However, in addition to HDM, other common indoor allergens include animal dander from cats and dogs, cockroach allergens and occasionally moulds. Food allergens such as peanuts and seafood are also reported by some patients to induce asthma exacerbations, although this often occurs in conjunction with other more generalised food allergy reactions such as skin rashes and gut symptoms that occur as part of a systemic anaphylactic response (DoHA, 2004). Cat allergens are a particularly potent form of allergen: they are secreted by the sebaceous glands, salivary glands and uterus, stick to the hair and become airborne when hair is shed. About 50% of patients who are allergic to cats make IgE that binds to the cat allergen Fel d 1—a uteroglobin (blastokinin) secreted by the uteruses of many mammals, the cat version of which is especially allergenic (Holt & Thomas, 2005). The most important outdoor allergens are the pollens of grasses, weeds (especially ragweed), olive, birch and conifers: patients may react to one or several of these allergens, but sensitisation will depend on geographical location.

ALLERGEN AVOIDANCE

The case for allergen avoidance in the prevention of asthma is complex. However, in some cases, allergen avoidance or reduced allergen exposure can be effective in reducing asthma symptoms and requirement for medications. For example, patients with a proven allergy to HDM can take measures to kill mites or restrict their breeding and remove the allergens they produce. However, in some individuals there may not be a direct relationship between allergen exposure and development of asthma symptoms. This may be the case because the individual is sensitised to more than one allergen or that allergen exposure is exacerbated by exposure to other triggers, such as influenza virus infection, cigarette smoke or medications. This is likely to be the case for Kade, as several factors may be involved in triggering his exacerbation and contribute to the severity of symptoms: moving into a dusty environment, exposure to passive cigarette smoke and a recent influenza infection. Care should be taken to reduce allergen exposure and triggers in the home environment when the patient is stabilised and to identify and minimise exposures in the workplace.