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Asthma, triggers and treatments

The incidence and mortality rate of asthma has increased over the past thirty years, especially in developed countries. In the UK alone over 5.2 million people suffer from asthma and over 71 thousand people die from the disease each year (Asthma UK, 2004).

There are many reasons for this including misdiagnosis and poor patient compliance to drug therapy. This essay will discuss the causes and triggers of asthma, and the public health strategies for prevention, control and treatment of this disease.

What is asthma?

Asthma is a disease in which the bronchi of the lungs narrow due to inflammation of the bronchial mucosa, bronchoconstriction in the surrounding smooth muscle and/or the presence of mucus. The lining of the airways is permanently sensitive to irritants and the presence of a trigger can lead to breathing difficulties, coughing, wheezing and breathlessness (Global Initiative for Asthma, n.d.). Asthma was traditionally defined as reversible airway obstruction but in many asthmatics a decline in lung function occurs because of bronchial wall thickening (Djukanovic, 2000).

It is not known whether asthma is a single disease or a collection of several disorders, and this makes it difficult to find a cure for asthma. Treatments are based on easing the symptoms of asthma to ensure patients have good quality of life.

Lung anatomy and physiology

The bronchi are the two tubes leading from the trachea which supply the lungs with inhaled air. The bronchi divide into many smaller tubes, known as bronchioles at the end of which are alveoli, where gas exchange takes place. The thin lining of the bronchi (bronchial mucosa) is coated with mucus which catches inhaled dust particles and cilia which sweeps particulates towards the trachea (Lane, 1996).

The smooth muscle surrounding the bronchi are under the control of the autonomic nervous system and will contract upon chemical or mechanical stimulation. The narrowing of the airway that follows is normally asymptomatic, but in patients with asthma an exaggerated response (hyperresponsiveness) to exogenous stimuli is seen.

Expiration is a passive process and is due to the elastic recoil of the bronchial walls. During normal expiration the elastic recoil pressure and flow are reduced, but an asthmatic patient needs to force expiration using the expiratory muscles. This increases pleural pressure surrounding the lung which compresses and further narrows the airways, limiting airflow (Clark et al, 1992).

In the clinic, a spirometer is used to measure forced expiratory volume (FEV1) and forced vital capacity (FVC), which measures the amount of air exhaled in the first second and the maximum amount of air forcibly exhaled from the lungs until the residual volume is reached. A low FEV1 reading reflects narrowing of the medium to large airways and gives the physician an idea of the severity of airflow obstruction (Young, 2002). An improvement in FEV1 of greater than 15% after administration of a bronchodilator is a test used to diagnose the disease.

What causes asthma?

Genetics

Some individuals are genetically predisposed to asthma but the disease may not be manifest until it is triggered by some environmental factor. The mechanism of how the disease is inherited is not known but asthma is more likely to be inherited from the mother than the father, possibly due to interactions between the mother and the foetus (Moffat & Cookson, 1998). Asthma is more common in families where other atopic diseases such as hayfever and eczema are present (Duffy, 2002).

There is no single "asthma gene", and the inheritability of the disease is thought to be due to the moderate effects of a few genes rather than the small effects of many. Scientists have identified some of the genes potentially involved in the disease by using genome screening and positional cloning (Caroll, 2005).

Gene studies are useful because knowledge of the genes involved in the disease process may eventually lead to disease prevention or improvement in patient care (Tattersfield et al., 2002). For example, treatment responses could be predicted in cases where asthma drugs show genetic variability. More recently, studies have shown that the use of antioxidant supplements improve lung function in patients exposed to environmental pollutants (Caroll, 2005).

Environment

Studies have shown that the development of asthma in affluent areas has increased much more than in less affluent ones. Living in insulated and centrally heated houses is thought to maximise exposure to dust mites and other allergens (Peat, 2002).

Lower rates of asthma are seen in children that are exposed to animals from an early age. It has been suggested that limited contact with infections leaves children more likely to develop allergic diseases (Tattersfield et al., 2000).

Air pollution was thought to be a major factor in the increase of asthma but generally levels of sulphur dioxide, nitrogen dioxide, ozone and other pollutants have decreased in developed countries so this theory is unlikely to be true. However, high levels of pollution are known to exacerbate symptoms in asthmatics and on days when levels of air pollution do exceed the recommended levels, susceptible people are warned to stay indoors (Marks, 2000).

The increasing prevalence of asthma over the past thirty years has been attributed to changes in diet. Studies have shown that people who eat fish more than once a week are less likely to have the disease. It is possible that the omega-3 fatty acids found in fish oils protect against airway inflammation, but there has not been any reduction seen in disease severity in people that are already asthmatic (Peat, 2000). Other studies have found a link between increased rates of asthma and diets which are low in magnesium, and vitamins C and E (Tattersfield et al., 2002).

Evidence from epidemiological studies show that breastfeeding within the first six months after birth can protect a child from developing asthma. Possible explanations are that breastfeeding reduces the exposure to proteins in cow's milk or that the long chain fatty acids in found in breast milk have a protective effect against inflammation (Peat, 2000).

Other factors that have been suggested to cause an increase in the prevalence of asthma are smoking, prematurity and low birth weights, but these have not been shown to have a significant impact. The major environmental causes are still to be determined (Tattersfield et al., 2000).

Asthma symptoms can be triggered by a number of stimuli which include allergens, changes in temperature, perfumes, chemical irritants and exercise (Ringsberg et al, 2002). In addition, non steroidal anti-inflammatory drugs, food additives and menstruation in females can provoke symptoms to a lesser extent.

Occupational asthma is responsible for 10 % of new asthma cases in European adults and is due to chemical irritants found in the workplace such as isocyanates, in the paint spraying industry, or ammonium persulphate in hairdressers. It is characterised by a reduction in symptoms during holidays and weekends and the consequences can be severe if the patient is not removed from the agent that is causing the allergic response (Currie & Ayres, 2004).

The effect of asthma on the body

The two major effects of asthma on the body are persistent inflammation of the bronchial mucosa and a thickening of the bronchial walls known as airway remodelling. Increased levels of eosiniphils, mast cells and T lymphocytes are all found in the sputum of asthmatic patients and are implicated in the inflammation process. T lymphocytes (of the Th2 phenotype) stimulate the production of IgE whereas eosinophils damage the airway mucosa and epithelial cells by releasing eosinophil major basic protein. Activated mast cells are involved in the acute airway response to allergens (Tattersfield et al., 2002).

Airway remodelling occurs as a result of excessive repair processes after repeated airway injury. Over time this is seen as an increase in the thickness of the smooth muscle, an increase in the mass of the mucous glands, a thickening of the basement membrane and the development of new blood vessels (angiogenesis). Airway remodelling leads to a reduction in the diameter of the bronchi and increases the resistance to airflow, which is the cause of breathing difficulties in asthmatic patients (Vignola et al., 1998).

Prevention, treatment and control of asthma

Prevention

There are four levels of prevention strategies that have been identified, primordial, primary, secondary and tertiary (Crane & Fitzharris, 2000). The aims for each strategy are:

Primordial To recognise environmental factors that are likely to have an effect on future disease patterns. It is recognised that the prevalence of asthma has increased and is related to a more affluent lifestyle, but at present the risk factors are not fully understood and it is therefore difficult to make recommendations.

Primary To limit the acquisition of the disease. Recommendations include the reduction of exposure to tobacco, diesel particulates, dust mites and dietary modifications.

Secondary To reduce morbidity by early detection/intervention. Anti-inflammatory treatment using inhaled corticosteroids is the main treatment used to manage the disease. Strategies include avoidance of dust mites, occupational and cat allergens and other known triggers.

Tertiary To reduce the impact of the established disease. The symptoms of asthma must be well controlled by the use of anti-inflammatory drugs to prevent airway remodelling and decline in lung function.

Treatment

Bronchodilators work quickly to relieve bronchoconstriction. There are three types of bronchodilator available including beta-2 agonists, anticholinergics and theophylline. The beta-2 agonists are most widely used and they work by binding to receptors found in airway smooth muscle resulting in relaxation and bronchodilation. They are generally inhaled meaning a lower dose can be used and fewer side effects are seen compared to when given by oral administration.

There are both short and long term beta-2 agonists. The short term drugs such as salbutamol are used in acute asthma attacks and may cause deterioration when used excessively. The introduction of long acting beta-2 agonists such as salmeterol is a recent development in the management of the disease. These drugs produce bronchodilation over 12 hours, can be used on a regular basis and the symptoms are better controlled compared to the short term agonists (Seale, 2000).

Theophylline is a bronchodilator which is usually given as a tablet. It has a narrow therapeutic window and is more likely to interact with other drugs, so it is not used as a front line treatment. Theophylline is a phosphodiesterase inhibitor and as it has a different mode of action to the 2 agonists it is used in cases where the corticosteroids and 2 agonists are not as effective as expected (Seale, 2000).

Acetylcholine acts on the muscarinic receptors of airway smooth muscle to cause bronchoconstriction. Ipratropium bromide acts as an acetylcholine antagonist and is mainly used during asthmatic attacks rather than for regular symptom relief as it is less effective than the 2 agonists.

Corticosteroids are the most effective anti-inflammatory drugs used in the long term treatment of asthma. They are best used in patients with mild to moderate asthma as low doses can be used to control the symptoms with fewer side effects. High doses of corticosteroids taken over a long period of time can cause a reduction in bone density, although pharmaceutical companies are developing new treatments aimed to minimise adverse effects. Studies also show that corticosteroids reduce levels of eosinophils, mast cells and T lymphocytes and are effective in the limitation of airway remodelling (Tavakkoli & Rees, 1999).

Leukotriene receptor antagonists (LTRA) are a newer class of drugs that are effective in the treatment of mild to moderate asthma. These drugs are taken orally and block the production of leukotrienes, which are released from mast cells and eosinophils, and cause bronchoconstriction and increased mucous production. LTRA's have been shown to improve lung function and reduce symptoms and asthma attacks in long term studies (Tattersfield et al., 2002).

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Conclusion

Asthma is a disease which is not yet fully understood. Much research is being done to identify the genes involved in asthma in the hope of finding better treatments. The interaction between genes and environment is complex and the major environmental causes of the disease are still being determined. It is known however, that asthma is a serious disease with potentially fatal consequences if left untreated. The use of disease management programs with the emphasis on better patient education is the best way to overcome this.

References

Asthma UK (2004) Retrieved 26th March 2005 from the World Wide Web:www.asthma.org.uk

Caroll, W. (2005).Asthma genetics: pitfalls and triumphs. Paediatric Respiratory Reviews, 6, 68 - 74

Clark, T.J.H, Godfrey, S. & Lee, T.H. (eds.) (1992) Asthma (Third edition). Chapman and Hall Medical.

Crane, J., Fitzharris, P. (2002) Prevention a clinical reality. In: Walls, R.S, Jenkins, C.R (eds.) (2002) Understanding Asthma: A management companion. MacLennon & Petty Pty Ltd.

Currie, G.P. Ayres, J.G. (2005) Occupational asthmagens. Primary Care Respiratory Journal,14, 72-77

Djukanovic, R. (2000) Asthma: A disease of inflammation and repair. Journal of Allergy and Clinical Immunology, 105, S522-S526

Duffy, D.L. (2002) Genetics of asthma. In: Walls, R.S, Jenkins, C.R (eds.) (2002) Understanding Asthma: A management companion. MacLennon & Petty Pty Ltd.

Global Initiative for Asthma (date unknown) Q & A: What is asthma. Retrieved 24th March 2005 from the World Wide Web: www.ginasthma.com/QAndA.asp?topicId=1&l1=3&l2=3

Lane, D.J. (1996) Asthma: The facts 3rd Edition. Oxford University Press.

Marks, G.B (2002) Air pollution and asthma. In: Walls, R.S, Jenkins, C.R (eds.) (2002) Understanding Asthma: A management companion. MacLennon & Petty Pty Ltd.

Moffat M. and Cookson W. (1998). The genetics of asthma. Maternal effects in atopic disease. Clinical and Experimental Allergy 28, 56-61.

Peat, J.K. (2002) Epidemiology and the changing prevalence of asthma. In: Walls, R.S, Jenkins, C.R (eds.) (2002) Understanding Asthma: A management companion. MacLennon & Petty Pty Ltd.

Ringsberg, K. C. Bjarneman, P., Lowhagen, O., Oden, A. and Toren, K. (2002). Differences in trigger factors and symptoms between patients with asthma-like symptoms and patients with asthma: development of a basis for a questionnaire. Respiratory Medicine. 96, 305-311

Seale, P. (2002) Use of bronchodilators. In: Walls, R.S, Jenkins, C.R (eds.) (2002) Understanding Asthma: A management companion. MacLennon & Petty Pty Ltd.

Tattersfield A.E, Knox, A.J. Hall, I.P. and Britton, J.R. (2002) Asthma. The Lancet, 360, 1313-1322

Tavakkoli, A, Rees, P. (1999) Achievements and new strategies in asthma treatment. In: Mallarkey, G. (ed.) (1999) Asthma management for the new millenium. Adis International Ltd.

Vignola, P. Chanez, L. Siena, G. Chiappara, G. Bonsignore, J. Bousquet (1998). Airways Remodelling in Asthma. Pulmonary Pharmacology & Therapeutics 11, 359-367

Young, I. (2002) Physiology. In: Walls, R.S, Jenkins, C.R (eds.) (2002) Understanding Asthma: A management companion. MacLennon & Petty Pty Ltd.

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