Causes, treatments and consequences of asthma

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According to the World health organisation (WHO), asthma is considered to be one of the most prevalent and chronic conditions affecting the human race. Although the fatality rate is relatively low in comparison to other chronic diseases, it is reportedly responsible for approximately 250,000 premature deaths each year , and an estimated 300 million people worldwide have the disease . It is also the most common childhood illness, the prevalence of which has doubled in the last 20 years . In Australia, the economic burden of asthma is high; affecting 10-12% of the adult and 14-16% of the childhood population , with death rates three times that of Europe . On the financial side; $606 million, was spent on asthma in Australia in 2004/2005 .

Asthma is an incessant disease which disrupts normal breathing patterns through inflammation and narrowing of the bronchial tubes causing airway obstruction. At the onset of an asthma attack, the bronchial tubes become inflamed and produce thick mucus. The smooth muscles surrounding these airways then tighten limiting airflow and impairing gaseous exchange causing a shortness of breath . The obstructed air moving through the tightened passageways causes a whistling sound, otherwise known as wheezing. As the disease becomes more severe, however, the inflammation spreads to include the smaller airways and eventually adjacent alveoli . The impact of the condition varies in both frequency and severity amongst those affected.

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Whilst there are many traits relating to asthma, this paper will only consider three specific areas; causes, treatment and consequences. As previously indicated the prevalence of childhood asthma is of great concern and it is therefore fitting to discuss these traits in relation to this subset. The literature surrounding asthma is vast but there appears to be discrepancies, particularly related to causal factors, which the author will attempt to evaluate. The literature surrounding the treatment methods used in paediatric asthma are consistent, providing a clear and concise treatment regime which will be portrayed in the latter part of this paper. Similarly, the consequences of such a disease appear to be relatively homogenous however it is of the authors' opinion that these should be separated into short term consequences and long term consequences, the latter being that which will be discussed in more detail in this paper.

Of particular concern is the methodology that has been used in understanding causal influences of asthma. Some reports have considered shortcomings and confounding issues whilst others provide statements which seem plausible however omit to highlight confounding or bias. Confounding can be a source of error in all observational studies particularly when studying the relationship between a risk factor and disease occurrence . With the existence of an additional exposure or risk factor that it is associated with both the disease and the exposure of interest, in the study group, confounding will occur where there is an imbalance between each group. Although the primary aim of epidemiological research is to present a precise measure of disease occurrence, the quality or validity of this research is dependent on a number of different factors with many threats jeopardising the reliability of the results. Each study referred to in this paper has been analysed and unless otherwise stated, has been considered for both confounding and bias.

More than four decades ago, infection, allergy and emotion were believed to be the root causes of asthma with the degree of asthma varying at different points of time in a child's life . Today, although the actual causes of asthma are still not well understood, there is a common philosophy that the risk factors for asthma are based on genes, environment and lifestyle and the interrelationships between these . Some of the most commonly discussed (although inconsistent) environmental factors are indoor and outdoor allergens, tobacco smoke, exposures to aeroallergens related to pet dander, dust mites and cockroaches, chemicals and general air pollution. There are a number of other factors which have been associated with the cause of asthma, including maternal diet, duration of breast feeding and low birth weight however with no evidence, to this authors knowledge, linking these to the rising pervasiveness of asthma, will not be examined here. A number of different epidemiological studies will be considered in an attempt to understand the etiology of asthma, particularly concerned with lifestyle, passive smoking and genetics.

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Tattersfield, Knox, Britton & Hall suggest that asthma is particularly prevalent in affluent societies and less common in more destitute populations, indicating the importance of lifestyle factors and their relationship to asthma. Similarly, Bousquet, Bousquet, Godard and Daures state that asthma becomes more predominant with modern and urbanized lifestyles. This theory is supported by the Australian Institute of Health and Welfare who recognised that asthma prevalence was 5.5% more prevalent in non-remote areas as compared to remote areas. Within the Western Australian aboriginal population, the prevalence of asthma in children inclines substantially from 7% in extremely remote areas to 30% in the Perth metropolitan area . Added to this, children from low socioeconomic urban backgrounds have been shown to have a 30 to 35 percent higher risk of acquiring the disease . Furthermore, a substantial multicentre epidemiological survey conducted in China showed a three-fold higher prevalence of asthma in Hong Kong than in less affluent societies such as Guangzhou and Beijing . Although the higher prevalence rates indicate toward a more prosperous society, there are no specific or common causal factors that can be indentified across these studies other than an affluent and/or more urbanized lifestyle.

Well recognised and documented as a cause of asthma, is passive smoking , , . In support of this, Fleming concluded that 11% of Australian children live in homes where smoking occurs on a regular basis. Considering that 14-16% of the Australian childhood population as mentioned previously has asthma, it would be fair to agree with the conclusion that passive smoking may cause asthma. As Rose suggests however, the associations of these factors can only be confirmed where comparisons are concluded between populations instead of within them. It is therefore imperative that we consider similar studies in other countries. International studies reiterate these findings; severity of asthma or its precursor "wheeze", increases in children whose parents either smoke or where children are exposed to tobacco smoke on a regular basis . A longitudinal study conducted in Brisbane over a seventeen year period suggested that girls were at a higher risk of getting asthma where their mother had smoked during their childhood . In contrast, however to these findings, a large scale study conducted in China indicate that areas with the highest smoking rates, also have the lowest asthma prevalence rates . Less affluent societies also tend to have smaller houses with less ventilation which raises the question; how can a less affluent society, in a smaller home, exposed to more cigarette smoke have a lower incidence of asthma than their counterparts? Whilst there is an endless source of evidence linking passive smoking to asthma, any valid contradictory evidence to this cannot be ignored. None of the epidemiological studies that have been carried out, to this authors' knowledge, are able to answer this question.

With this question raised, it would be prudent to consider the philosophy that genetics plays a role in the cause of asthma. This author suggests that genetics may explain the low incidence rates of asthma experienced in some predominantly smoking environments. Family studies have demonstrated that genetics are linked to asthma, identifying more than 100 genes to be associated with or involved in the presence of the disease , in a variety of ethnically diverse populations . The level of involvement of these genes in the actual development of the disease however remains questioned by Wong et.al who showed varying asthma prevalence between regions where "similar genetic backgrounds" were evident. A limitation of this report however is the failure to demonstrate what genetic similarities could exist across a variety of regions. This may be as a result of environmental factors influencing asthma at contrasting periods during a child's life. Similarly, the child's genetic predisposition may also have an influence on both of these issues. In considering these points, this author would support the theory that the interrelationship between lifestyle, genetics and environmental factors are more likely to have a causal role in asthma than any one single factor alone.

The treatment of asthma may differ widely across the world dependant on a number of issues including national, economic, socioeconomic, cultural issues and differences in health care systems . As a result of better treatments and asthma management in developed countries, asthma related deaths have declined . Due to this and the limitations in the length of this paper, only the current mainstream treatments used in these countries will be considered here.

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Whilst there is no actual cure for the disease, the main purposes of asthma drug are for immediate relief of symptoms, for disease control (reducing symptoms and outbreaks of attacks) and to treat the attacks themselves. The most typically used drugs for relieving symptoms are metered doses of short acting beta2 agonists (salbutamol and terbutuline) via an inhaler and spacer . The addition of an anticholinergic drug such as ipratropium bromide to each dose of a beta2 agonist has been reported to be an even more effective treatment . The use of inhalers allow for smaller doses, a quicker reaction and lower chance of adverse effects than that of oral medication .

The uses of "inhaled corticosteroids (beclomethasone, budesonide and fluticasone)" have been found to be effective in controlling the disease, however combined formulations of long acting beta2 agonists together with the inhaled corticosteroids "(salmeterol+fluticasone and furomoterol+budesonide)" appears to provide considerably more benefit . Consistent use of inhaled corticosteroids has been shown to not only reduce asthma symptoms but reduce the likelihood of more severe episodes occurring and are recommended where more than one puff per day is required from a beta2 agonist inhaler . The dosage varies on the severity and frequency of the attacks and the drug in question, however generally, it will be between 400 (mu)g and 800 (mu)g of beclomethasone and half that of that for fluticasone.

Some treatments, although not very common, involve "long acting beta2 agonist drugs (formoterol) and short acting anticholinergic drugs (ipratropium)" and the use of intravenous theophylline. Theophylline, a methyl xanthine derivative, is occasionally used to treat severe attacks in children as it provides some improvement in lung function; however bronchodilator medication is still required. With potentially serious side effects theophylline cannot be used in long term therapy . Another group of drugs which have been used sporadically are leukotriene inhibitors, specifically oral montelukast. In emergency departments, supplemental oxygen is often used in conjunction with beta2 agonists administered via either a metered dose inhaler or nebuliser, for children suffering from an acute attack .

Whilst the most common therapies control and alleviate symptoms of asthma for most patients, there are instances where there is a lack of responsiveness to therapy. The Characterizing Response to Leukotriene Receptor Antagonist and Inhaled Corticosteroids (CLIC) study examined the treatment response in children of two specific drugs namely fluticasone and montelukast . The findings showed that treatment responses were highly variable with 55% of the 126 juvenile study participants not responding to either treatment. It was found that montelukast was associated with, but not exclusive to the younger patients and those who had experienced only a brief duration of disease. Those children with low pulmonary function responded better to fluticasone. A specific issue in asthma treatment is identifying the best possible drug and hence the use of pharmocogenetics could ensure drug efficacy and reduce side effects.

Asthma places a substantial burden not only on the patients themselves, but also their families and communities in a number of different ways. The consequences of such a disease need to be considered two fold; firstly the short-term effects and secondly the long-term consequences.

Some of the short-term consequences associated with asthma include shortness of breath, recurrent chest tightness, sputum production, dyspnoea and waking at night which interfere in restricting activity and disrupting sleep thereby causing absenteeism from work or school. The harshness of consequences being dependent on the frequency and severity of the attacks which affect quality of life, and cause hospitalisation . Supplementary to this are the cost factors associated with each of these consequences not only to the community, town or country but also to that of the individual and their family. Although the long-term consequences are no more critical than the short-term consequences, they do present an additional health risk to the patient and hence an increased burden on society. It is for this reason that the long-term consequences will be considered here in more detail.

Inadequately controlled asthma has potentially significant long term consequences which include physical, psychological and social areas. In physical terms, there is emerging literature which focuses on structural airway changes as a result of chronic and persistent inflammation commonly referred to as "airway remodelling" . These structural changes include increased smooth muscle mass, sub epithelial fibrosis, mucus gland hyperplasia, and mucus hyper secretion. This increased muscle mass results in a more acute response to bronchiole constriction as well as a reduction in diameter. In addition to this, the damage caused to the epithelium and subsequent loss of the protective barrier further jeopardises the deeper respiratory system which causes an excess production of several growth factors resulting in angiogenesis . Jarjour and Kelly also suggest that long term asthma may also be associated with elastic recoil loss which can have an effect on asthma control as it reinforces airway obstruction.

Other physical factors which have been associated with long terms consequences of childhood asthma include obesity and impoverished health. Fletcher, Green and Neidell , reported that childhood asthma correlated to a "14 percentage point decrease in the probability of being in excellent self-reported health" and "a 12 percentage point increase in being obese" in later life. Each of these mechanisms may have a reverse causality as they themselves can impact on the severity of the disease.

Under the psychological domain, major depression has not only been linked to severe asthma, but it can also effect treatment. It has been documented that depression affects cognitive mechanisms such as memory and decision making, each of which are integral factors required for effective treatment of asthma . In summary, it is the typical short term consequences that are likely to be what either gives rise to, or exacerbates the depression which in turn affects management of the disease, worsens the short term effects and thus creates a vicious cycle of events.

The Australian Institute of Health and Welfare demonstrated that people with asthma had missed work or school by 5.9 percent more than those without asthma and nearly double the amount of reduced activity. This data released is based on age standardised to the Australian population as at June 2001. As asthma typically develops in the early years of life , this clearly illustrates one of the long term consequences of childhood asthma.

Whilst it is necessary to consider all the research that has been undertaken in establishing the causal factors of asthma, it is important to recognise that as the identified risk factors and populations are so widespread in nature and location it is difficult to ascertain and pinpoint the causes of asthma. Whilst every attempt is made to discover the reasons for increased prevalence rates, we should not completely exclude the possibility that the increase in asthma prevalence may have some correlation with the increased awareness and subsequent increase in medical professionals' diagnosis. The use of short-acting beta2 agonists for short term relief and long acting beta2 agonists together with inhaled corticosteroids to control the disease have been proven to be effective however it would be poignant to add, that until the true causal factors are identified and better understood, treatment regimes will continue as a process of management and control, rather than attempting to cure the disease. The short term consequences may be curbed by treatment regimes but the long term consequences will continue to afflict the patient until such time as a cure is found.