Cause Of Asthema

sthma is caused by environmental and genetic factors,[11] which can influence how severe asthma is and how well it responds to medication.[12] Some environmental and genetic factors have been confirmed by further research, while others have not been.

[edit] Environmental

Many environmental risk factors have been associated with asthma development and morbidity in children, but a few stand out as well-replicated or that have a meta-analysis of several studies to support their direct association.

Environmental tobacco smoke, especially maternal cigarette smoking, is associated with high risk of asthma prevalence and asthma morbidity, wheeze, and respiratory infections.[13] Poor air quality, from traffic pollution or high ozone levels, has been repeatedly associated with increased asthma morbidity and has a suggested association with asthma development that needs further research.[13][14]

Recent studies show a relationship between exposure to air pollutants (e.g. from traffic) and childhood asthma [15]. This research finds that both the occurrence of the disease and exacerbation of childhood asthma are affected by outdoor air pollutants.

Caesarean sections have been associated with asthma when compared with vaginal birth; a meta-analysis found a 20% increase in asthma prevalence in children delivered by Caesarean section compared to those who were not. It was proposed that this is due to modified bacterial exposure during Caesarean section compared with vaginal birth, which modifies the immune system (as described by the hygiene hypothesis).[16]

Psychological stress has long been suspected of being an asthma trigger, but only in recent decades has convincing scientific evidence substantiated this hypothesis. Rather than stress directly causing the asthma symptoms, it is thought that stress modulates the immune system to increase the magnitude of the airway inflammatory response to allergens and irritants.[13][17]

Viral respiratory infections at an early age, along with siblings and day care exposure, may be protective against asthma, although there have been controversial results, and this protection may depend on genetic context.[13][18][19]

Antibiotic use early in life has been linked to development of asthma in several examples; it is thought that antibiotics make one susceptible to development of asthma because they modify gut flora, and thus the immune system (as described by the hygiene hypothesis).[20] The hygiene hypothesis is a hypothesis about the cause of asthma and other allergic disease, and is supported by epidemiologic data for asthma. For example, asthma prevalence has been increasing in developed countries along with increased use of antibiotics, c-sections, and cleaning products.[16][20][21] All of these things may negatively affect exposure to beneficial bacteria and other immune system modulators that are important during development, and thus may cause increased risk for asthma and allergy.

Recently scientists connected the rise in prevalence of asthma, to the rise in use of paracetamol, suggesting the possibility that paracetamol can cause asthma.[22]

[edit] Genetic

Over 100 genes have been associated with asthma in at least one genetic association study.[23] However, such studies must be repeated to ensure the findings are not due to chance. Through the end of 2005, 25 genes had been associated with asthma in six or more separate populations:[23]

* GSTM1
* IL10
* CTLA-4
* SPINK5
* LTC4S



* LTA
* GRPA
* NOD1
* CC16
* GSTP1



* STAT6
* NOS1
* CCL5
* TBXA2R
* TGFB1



* IL4
* IL13
* CD14
* ADRB2 (β-2 adrenergic receptor)
* HLA-DRB1



* HLA-DQB1
* TNF
* FCER1B
* IL4R
* ADAM33

Many of these genes are related to the immune system or to modulating inflammation. However, even among this list of highly replicated genes associated with asthma, the results have not been consistent among all of the populations that have been tested.[23] This indicates that these genes are not associated with asthma under every condition, and that researchers need to do further investigation to figure out the complex interactions that cause asthma. One theory is that asthma is a collection of several diseases, and that genes might have a role in only subsets of asthma. For example, one group of genetic differences (single nucleotide polymorphisms in 17q21) was associated with asthma that develops in childhood.[24]

[edit] Gene–environment interactions

Research suggests that some genetic variants may only cause asthma when they are combined with specific environmental exposures, and otherwise may not be risk factors for asthma.[11]

The genetic trait, CD14 single nucleotide polymorphism (SNP) C-159T and exposure to endotoxin (a bacterial product) are a well-replicated example of a gene-environment interaction that is associated with asthma. Endotoxin exposure varies from person to person and can come from several environmental sources, including environmental tobacco smoke, dogs, and farms. Researchers have found that risk for asthma changes based on a person’s genotype at CD14 C-159T and level of endotoxin exposure.[25]
CD14-endotoxin interaction based on CD14 SNP C-159T[25] Endotoxin levels CC genotype TT genotype
High exposure Low risk High risk
Low exposure High risk Low risk

[edit] Risk factors

Studying the prevalence of asthma and related diseases such as eczema and hay fever have yielded important clues about some key risk factors. The strongest risk factor for developing asthma is a family history of atopic disease; [26] this increases one's risk of hay fever by up to 5x and the risk of asthma by 3-4x. [27] In children between the ages of 3-14, a positive skin test for allergies and an increase in immunoglobulin E increases the chance of having asthma. [28] In adults, the more allergens one reacts positively to in a skin test, the higher the odds of having asthma.[29]

Because much allergic asthma is associated with sensitivity to indoor allergens and because Western styles of housing favor greater exposure to indoor allergens, much attention has focused on increased exposure to these allergens in infancy and early childhood as a primary cause of the rise in asthma. [30][31] Primary prevention studies aimed at the aggressive reduction of airborne allergens in a home with infants have shown mixed findings. Strict reduction of dust mite allergens, for example, reduces the risk of allergic sensitization to dust mites, and modestly reduces the risk of developing asthma up until the age of 8 years old. [32][33][34][35] However, studies also showed that the effects of exposure to cat and dog allergens worked in the converse fashion; exposure during the first year of life was found to reduce the risk of allergic sensitization and of developing asthma later in life.[36][37][38]

The inconsistency of this data has inspired research into other facets of Western society and their impact upon the prevalence of asthma. One subject that appears to show a strong correlation is the development of asthma and obesity. In the United Kingdom and United States, the rise in asthma prevalence has echoed an almost epidemic rise in the prevalence of obesity. [39][40] In Taiwan, symptoms of allergies and airway hyperreactivity increased in correlation with each 20% increase in body-mass index.[41]

[edit] Hygiene hypothesis
Main article: Hygiene hypothesis

One theory for the cause of the increase in asthma prevalence worldwide is the so-called "hygiene hypothesis" — that the rise in the prevalence of allergies and asthma is a direct and unintended result of the success of modern hygienic practices in preventing childhood infections. Studies have shown repeatedly that children coming from environments one would expect to be less hygienic (East Germany vs. West Germany,[42] families with many children,[43][44][45] day care environments,[46][47]) tended to result in lower incidences of asthma and allergic diseases. This seems to run counter to the logic that viruses are often causative agents in exacerbation of asthma [48][49][50] Additionally, other studies have shown that viral infections of the lower airway may in some cases induce asthma, as a history of bronchiolitis or croup in early childhood is a predictor of asthma risk in later life. [51] Studies which show that upper respiratory tract infections are protective against asthma risk also tend to show that lower respiratory tract infections conversely tend to increase the risk of asthma. [52]

[edit] Population disparities

Asthma prevalence in the US is higher than in most other countries in the world, but varies drastically between diverse US populations.[13] In the US, asthma prevalence is highest in Puerto Ricans, African Americans, Filipinos and Native Hawaiians, and lowest in Mexicans and Koreans.[53][54][55] Mortality rates follow similar trends, and response to Ventolin is lower in Puerto Ricans than in African Americans or Mexicans.[56][57] As with worldwide asthma disparities, differences in asthma prevalence, mortality, and drug response in the US may be explained by differences in genetic, social and environmental risk factors.

Asthma prevalence also differs between populations of the same ethnicity who are born and live in different places.[58] US-born Mexican populations, for example, have higher asthma rates than non-US born Mexican populations that are living in the US.[59] This probably reflects differences in social and environmental risk factors associated with acculturation to the US.[citation needed]

Asthma prevalence and asthma deaths also differ by gender. Males are more likely to be diagnosed with asthma as children, but asthma is more likely to persist into adulthood in females.[60] Sixty five percent more adult women than men will die from asthma.[citation needed] This difference may be attributable to hormonal differences, among other things. In support of this, girls who reach puberty before age 12 were found to have a later diagnosis of asthma more than twice as much as girls who reach puberty after age 12.[citation needed] Asthma is also the number one cause of missed days from school.[citation needed]

[edit] Socioeconomic factors

The incidence of asthma is highest among low-income populations (asthma deaths are most common in low to middle income countries [2]), which in the western world are disproportionately ethnic minorities[61] and are more likely to live near industrial areas. Additionally, asthma has been strongly associated with the presence of cockroaches in living quarters, which is more likely in such neighborhoods.

Asthma incidence and quality of treatment varies among different racial groups, though this may be due to correlations with income (and thus affordability of health care) and geography. For example, African Americans are less likely to receive outpatient treatment for asthma despite having a higher prevalence of the disease. They are much more likely to have emergency room visits or hospitalization for asthma, and are three times as likely to die from an asthma attack compared to whites. The prevalence of "severe persistent" asthma is also greater in low-income communities compared with communities with better access to treatment.[62][63]

[edit] Asthma and athletics
See also: Exercise-induced asthma

Asthma appears to be more prevalent in athletes than in the general population. One survey of participants in the 1996 Summer Olympic Games, in Atlanta, Georgia, U.S., showed that 15% had been diagnosed with asthma, and that 10% were on asthma medication.[64]

There appears to be a relatively high incidence of asthma in sports such as cycling, mountain biking, and long-distance running, and a relatively lower incidence in weightlifting and diving. It is unclear how much of these disparities are from the effects of training in the sport.[64][65]

[edit] Occupational asthma
Main article: Occupational asthma

Asthma as a result of (or worsened by) workplace exposures is the world's most commonly reported occupational respiratory disease. Still most cases of occupational asthma are not reported or are not recognized as such. Estimates by the American Thoracic Society (2004) suggest that 15–23% of new-onset asthma cases in adults are work related.[66] In one study monitoring workplace asthma by occupation, the highest percentage of cases occurred among operators, fabricators, and laborers (32.9%), followed by managerial and professional specialists (20.2%), and in technical, sales, and administrative support jobs (19.2%). Most cases were associated with the manufacturing (41.4%) and services (34.2%) industries.[66] Animal proteins, enzymes, flour, natural rubber latex, and certain reactive chemicals are commonly associated with work-related asthma. When recognized, these hazards can be mitigated, dropping the risk of disease.[67]

[edit] Pathophysiology

Asthma is an airway disease that can be classified physiologically as a variable and partially reversible obstruction to air flow, and pathologically with overdeveloped mucus glands, airway thickening due to scarring and inflammation, and bronchoconstriction, the narrowing of the airways in the lungs due to the tightening of surrounding smooth muscle. Bronchial inflammation also causes narrowing due to edema and swelling caused by an immune response to allergens.

[edit] Bronchoconstriction
Inflamed airways and bronchoconstriction in asthma. Airways narrowed as a result of the inflammatory response cause wheezing.

During an asthma episode, inflamed airways react to environmental triggers such as smoke, dust, or pollen. The airways narrow and produce excess mucus, making it difficult to breathe. In essence, asthma is the result of an immune response in the bronchial airways.[68]

The airways of asthmatics are "hypersensitive" to certain triggers, also known as stimuli (see below). (It is usually classified as type I hypersensitivity.)[69][70] In response to exposure to these triggers, the bronchi (large airways) contract into spasm (an "asthma attack"). Inflammation soon follows, leading to a further narrowing of the airways and excessive mucus production, which leads to coughing and other breathing difficulties. Bronchospasm may resolve spontaneously in 1–2 hours, or in about 50% of subjects, may become part of a 'late' response, where this initial insult is followed 3–12 hours later with further bronchoconstriction and inflammation.[71]

The normal caliber of the bronchus is maintained by a balanced functioning of these systems, which both operate reflexively. The parasympathetic reflex loop consists of afferent nerve endings which originate under the inner lining of the bronchus. Whenever these afferent nerve endings are stimulated (for example, by dust, cold air or fumes) impulses travel to the brain-stem vagal center, then down the vagal efferent pathway to again reach the bronchial small airways. Acetylcholine is released from the efferent nerve endings. This acetylcholine results in the excessive formation of inositol 1,4,5-trisphosphate (IP3) in bronchial smooth muscle cells which leads to muscle shortening and this initiates bronchoconstriction.

[edit] Bronchial inflammation

The mechanisms behind allergic asthma—i.e., asthma resulting from an immune response to inhaled allergens—are the best understood of the causal factors. In both asthmatics and non-asthmatics, inhaled allergens that find their way to the inner airways are ingested by a type of cell known as antigen-presenting cells, or APCs. APCs then "present" pieces of the allergen to other immune system cells. In most people, these other immune cells (TH0 cells) "check" and usually ignore the allergen molecules. In asthmatics, however, these cells transform into a different type of cell (TH2), for reasons that are not well understood.

The resultant TH2 cells activate an important arm of the immune system, known as the humoral immune system. The humoral immune system produces antibodies against the inhaled allergen. Later, when an asthmatic inhales the same allergen, these antibodies "recognize" it and activate a humoral response. Inflammation results: chemicals are produced that cause the wall of the airway to thicken, cells which produce scarring to proliferate and contribute to further 'airway remodeling', causes mucus producing cells to grow larger and produce more and thicker mucus, and the cell-mediated arm of the immune system is activated. Inflamed airways are more hyper-reactive, and will be more prone to bronchospasm.

The "hygiene hypothesis" postulates that an imbalance in the regulation of these TH cell types in early life leads to a long-term domination of the cells involved in allergic responses over those involved in fighting infection. The suggestion is that for a child being exposed to microbes early in life, taking fewer antibiotics, living in a large family, and growing up in the country stimulate the TH1 response and reduce the odds of developing asthma. [72]

[edit] Stimuli

* Allergens from nature, typically inhaled, which include waste from common household pests, the house dust mite and cockroach, as well as grass pollen, mold spores, and pet epithelial cells;[73]
* Indoor air pollution from volatile organic compounds, including perfumes and perfumed products. Examples include soap, dishwashing liquid, laundry detergent, fabric softener, paper tissues, paper towels, toilet paper, shampoo, hairspray, hair gel, cosmetics, facial cream, sun cream, deodorant, cologne, shaving cream, aftershave lotion, air freshener and candles, and products such as oil-based paint. [7][73]
* Medications, including aspirin,[74] β-adrenergic antagonists (beta blockers),[75] and penicillin.[76]
* Food allergies such as milk, peanuts, and eggs. However, asthma is rarely the only symptom, and not all people with food or other allergies have asthma.[77]
* Use of fossil fuel related allergenic air pollution, such as ozone, smog, summer smog, nitrogen dioxide, and sulfur dioxide, which is thought to be one of the major reasons for the high prevalence of asthma in urban areas.[7]
* Various industrial compounds and other chemicals, notably sulfites; chlorinated swimming pools generate chloramines—monochloramine (NH2Cl), dichloramine (NHCl2) and trichloramine (NCl3)—in the air around them, which are known to induce asthma.[78]
* Early childhood infections, especially viral upper respiratory tract infections. Children who suffer from frequent respiratory infections prior to the age of six are at higher [79] risk of developing asthma, particularly if they have a parent with the condition. However, persons of any age can have asthma triggered by colds and other respiratory infections even though their normal stimuli might be from another category (e.g. pollen) and absent at the time of infection. In many cases, significant asthma may not even occur until the respiratory infection is in its waning stage, and the person is seemingly improving. [7] In children, the most common triggers are viral illnesses such as those that cause the common cold.[80]
* Exercise or intense use of respiratory system. The effects of which differ somewhat from those of the other triggers, since they are brief. They are thought to be primarily in response to the exposure of the airway epithelium to cold, dry air.
* Hormonal changes in adolescent girls and adult women associated with their menstrual cycle can lead to a worsening of asthma. Some women also experience a worsening of their asthma during pregnancy whereas others find no significant changes, and in other women their asthma improves during their pregnancy.[7]
* Psychological stress. There is growing evidence that psychological stress is a trigger. It can modulate the immune system, causing an increased inflammatory response to allergens and pollutants.[17]
* Cold weather can make it harder for asthmatics to breathe.[81] Whether high altitude helps or worsens asthma is debatable and may vary from person to person.[82]

[edit] Pathogenesis

The fundamental problem in asthma appears to be immunological: young children in the early stages of asthma show signs of excessive inflammation in their airways. Epidemiological findings give clues as to the pathogenesis: the incidence of asthma seems to be increasing worldwide, and asthma is now very much more common in affluent countries.

In 1968 Andor Szentivanyi first described The Beta Adrenergic Theory of Asthma; in which blockage of the Beta-2 receptors of pulmonary smooth muscle cells causes asthma.[83] Szentivanyi's Beta Adrenergic Theory is a citation classic[84] using the Science Citation Index and has been cited more times than any other article in the history of the Journal of Allergy and Clinical Immunology.

In 1995 Szentivanyi and colleagues demonstrated that IgE blocks beta-2 receptors.[85] Since overproduction of IgE is central to all atopic diseases, this was a watershed moment in the world of allergy.[86]

[edit] Asthma and sleep apnea

It is recognized with increasing frequency that patients who have both obstructive sleep apnea and asthma often improve tremendously when the sleep apnea is diagnosed and treated.[87] CPAP is not effective in patients with nocturnal asthma only.[88]

[edit] Asthma and gastro-esophageal reflux disease

If gastro-esophageal reflux disease (GERD) is present, the patient may have repetitive episodes of acid aspiration. GERD may be common in difficult-to-control asthma, but according to one study, treating it does not seem to affect the asthma.[89]

[edit] Diagnosis

Asthma is defined simply as reversible airway obstruction. Reversibility occurs either spontaneously or with treatment. The basic measurement is peak flow rates and the following diagnostic criteria are used by the British Thoracic Society:[90]

* ≥20% difference on at least three days in a week for at least two weeks;
* ≥20% improvement of peak flow following treatment, for example:
o 10 minutes of inhaled β-agonist (e.g., salbutamol);
o six weeks of inhaled corticosteroid (e.g., beclometasone);
o 14 days of 30 mg prednisolone.
* ≥20% decrease in peak flow following exposure to a trigger (e.g., exercise).

In many cases, a physician can diagnose asthma on the basis of typical findings in a patient's clinical history and examination. Asthma is strongly suspected if a patient suffers from eczema or other allergic conditions—suggesting a general atopic constitution—or has a family history of asthma. While measurement of airway function is possible for adults, most new cases are diagnosed in children who are unable to perform such tests.

In children, the key to asthma diagnosis is the sound of wheezing or a high-pitched sound upon exhalation. Other clues are recurrent wheezing, breathing difficulty, or chest tightness, or a history of coughing that is worse at night. The doctor should also know if the child's symptoms are worse with exercise, colds,or exposure to certain irritants such as smoke, emotional stress, or changes in the weather. [72]

Other information important to diagnosis is the age at which symptoms began and how they progressed, the timing and pattern of wheezing, when and how often a child had to visit a clinic or hospital emergency department because of symptoms, whether the child ever took bronchodilator medication for the symptoms and the nature of the response to medication. [72]

Although pediatricians may tend to ask parents for information about their children's symptoms, studies suggest that children themselves are reliable sources as early as age 7 and perhaps even as early as age 6.[91]

In adults and older children, diagnosis can be made with spirometry or a peak flow meter (which tests airway restriction), looking at both the diurnal variation and any reversibility following inhaled bronchodilator medication. The latest guidelines from the U.S. National Asthma Education and Prevention Program (NAEPP) recommend spirometry at the time of initial diagnosis, after treatment is initiated and symptoms are stabilized, whenever control of symptoms deteriorates, and every 1 or 2 years on a regular basis.[92]

The NAEPP guidelines do not recommend testing peak expiratory flow as a regular screening method, because it is more variable than spirometry. However, testing peak flow at rest (or baseline) and after exercise can be helpful, especially in young asthmatics who may experience only exercise-induced asthma. It may also be useful for daily self-monitoring and for checking the effects of new medications.[92] Peak flow readings can be charted on graph paper charts together with a record of symptoms or use peak flow charting software. This allows patients to track their peak flow readings and pass information back to their doctor or nurse.[93]

In the Emergency Department doctors may use a capnography which measures the amount of exhaled carbon dioxide,[94] along with pulse oximetry which shows the percentage of hemoglobin that is carrying oxygen, to determine the severity of an asthma attack as well as the response to treatment.

More recently, exhaled nitric oxide has been studied as a breath test indicative of airway inflammation in asthma.

[edit] Differential diagnosis
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Before diagnosing someone as asthmatic, alternative possibilities should be considered. A clinician taking a history should check whether the patient is using any known bronchoconstrictors (substances that cause narrowing of the airways, e.g. certain anti-inflammatory agents or beta-blockers). Among elderly patients, the presenting symptom may be fatigue, cough, or difficulty breathing, all of which may be erroneously attributed to COPD, congestive heart failure, or simple aging.[95]

After a pulmonary function test has been carried out, radiological tests, such as a chest X-ray or CT scan, may be required to exclude the possibility of other lung diseases. Occasionally, a bronchial challenge test may be performed using methacholine or histamine to assess bronchial hyperresponsiveness.

Chronic obstructive pulmonary disease, which closely resembles asthma, is correlated with more exposure to cigarette smoke, an older patient, less symptom reversibility after bronchodilator administration (as measured by spirometry), and decreased likelihood of family history of atopy.[96]

Pulmonary aspiration, whether direct due to dysphagia (swallowing disorder) or indirect (due to acid reflux), can show similar symptoms to asthma. However, with aspiration, fevers might also indicate aspiration pneumonia. Direct aspiration (dysphagia) can be diagnosed by performing a Modified Barium Swallow test and treated with feeding therapy by a qualified speech therapist. If the aspiration is indirect (from acid reflux) then treatment directed at this is indicated.

In some people, asthma-like symptoms may be triggered by gastroesophageal reflux disease, which can be treated with suitable antacids.

A majority of children who are asthma sufferers have an identifiable allergy trigger. Specifically, in a 2004 study, 71% had positive test results for more than 1 allergen, and 42% had positive test results for more than 3 allergens.[97]

The majority of these triggers can often be identified from the history; for instance, asthmatics with hay fever or pollen allergy will have seasonal symptoms, those with allergies to pets may experience an abatement of symptoms when away from home, and those with occupational asthma may improve during leave from work. Allergy tests can help identify avoidable symptom triggers.

Asthma is categorized by the United States National Heart, Lung, and Blood Institute as falling into one of four categories: intermittent, mild persistent, moderate persistent and severe persistent. The diagnosis of "severe persistent asthma" occurs when symptoms are continual with frequent exacerbations and frequent night-time symptoms, result in limited physical activity and when lung function as measured by PEV or FEV1 tests is less than 60% predicted with PEF variability greater than 30%.

[edit] Prevention and Control

Prevention of the development of asthma is different from prevention of asthma episodes. Aggressive treatment of mild allergy with immunotherapy has been shown to reduce the likelihood of asthma development. In controlling symptoms, the crucial first step in treatment is for patient and doctor to collaborate in establishing a specific plan of action to prevent episodes of asthma by avoiding triggers and allergens, regularly testing for lung function, and using preventive medications (see especially "Control of Environmental Factors" @ http://www.nhlbi.nih.gov/guidelines/asthma/asthgdln.htm.)

Current treatment protocols recommend controller medications such as an inhaled corticosteroid, which helps to suppress inflammation and reduces the swelling of the lining of the airways, in anyone who has frequent (greater than twice a week) need of relievers or who has severe symptoms. If symptoms persist, additional controller drugs are added until almost all asthma symptoms are prevented. With the proper use of control drugs, asthmatics can avoid the complications that result from overuse of rescue medications.

Asthmatics sometimes stop taking their controller medication when they feel fine and have no problems breathing. This often results in further attacks after a time, and no long-term improvement.

The only preventive agent known is allergen immunotherapy. Controller medications include the following:

* Inhaled glucocorticoids are the most widely used prevention medications and normally come as inhaler devices (ciclesonide, beclomethasone, budesonide, flunisolide, fluticasone, mometasone, and triamcinolone). Long-term use of corticosteroids can have many side effects including a redistribution of fat, increased appetite, blood glucose problems and weight gain. High doses of steroids may cause osteoporosis. These side effects are generally not seen with the inhaled steroids when used in conventional doses for control of asthma due to the smaller dose which is targeted to the lungs, unlike the higher doses of oral or injected preparations. Patients on the highest doses of inhaled steroids should take prophylactic treatment (usually Calcium and exercise, but sometimes Fosamax or similar) to prevent osteoporosis. Deposition of steroids in the mouth may result in oral thrush. Deposition near the vocal cords can cause hoarse voice. These may be minimised by rinsing the mouth with water after inhaler use, as well as by using a spacer. Spacers also generally increase the amount of drug that reaches the lungs. A new agent, ciclesonide, is inactive until activated in the lung. For this reason changing to ciclesonide can relieve dysphonia in some patients.
* Leukotriene modifiers (montelukast, zafirlukast, pranlukast, and zileuton) provide both anti-spasm and anti-inflammatory effects. In general they are weaker than inhaled corticosteroids, but the do not have any steroid side-effects and the benefit is additive with inhaled steroid.
* Mast cell stabilizers (cromoglicate (cromolyn), and nedocromil). These medications are believed to prevent the initiation of the allergy reaction, by stabilizing the mast cell. They are not effective once the reaction has already begun, and typically must be used 4 times a day for maximal effect. But they do truly prevent asthma symptoms and are nearly free of side-effects.
* Antimuscarinics/anticholinergics (ipratropium, oxitropium, and tiotropium). These agents both relieve spasm and reduce formation of mucous. They are more effective in patients with empysema or 'smokers lung.' They are rarely effective in asthma and are not true asthma controller medications.
* Methylxanthines (theophylline and aminophylline). These agents are bronchodilators with minimal anti-inflammatory effect. At one time they were the only effective asthma medications available. They are sometimes considered if sufficient control cannot be achieved with inhaled glucocorticoid, leukotriene modifier, and long-acting β-agonist combintaions.
* Antihistamines are often used to treat the nasal allergies which can accompany asthma. Older agents are too drying and can result in thick mucous so should be avoided. Newer antihistamines which do not have this effect can safely be used by asthmatics.
* Allergy Desensitization, also known as allergy immunotherapy, may be recommended in some cases where allergy is the suspected cause or trigger of asthma. Allergy shots are dangerous in severe asthma and in uncontrolled asthma. However if allergy immunotherapy is started early in the disease there is a good chance that a remission of asthma can be induced (aka "asthma cure"). Typically the need for medication is reduced by about half with injection allergy immunotherapy, when done correctly. If a patient is only allergic to one or two items, oral allergy immunotherapy can be used. This is safe, much easier in young children, and is about half as effective. Unfortunately if a patient is allergic to more than 2 or 3 items then oral therapy cannot be given in a dose which is proven safe and effective.
* Omalizumab, an IgE blocker, can help patients with severe allergic asthma that is not well controlled with other drugs. It is expensive, but not compared with hospitalization(s). It requires regular injections.
* Methotrexate is occasionally used in some difficult-to-treat patients.
* If chronic acid indigestion (GERD) contributes to a patient's asthma, it should also be treated, because it may prolong the respiratory problem.
* Chronic sinus disease may be a contributing factor in difficult to control asthma, and should be evaluated.

[edit] Trigger avoidance

As is common with respiratory disease, smoking is believed to adversely affect asthmatics in several ways, including an increased severity of symptoms (likely due to increased inflammation[98]), a more rapid decline of lung function, and decreased response to preventive medications.[99] Automobile emissions are considered an even more significant cause and aggravating factor.[citation needed] Asthmatics who smoke or who live near traffic[citation needed] typically require additional medications to help control their disease. Furthermore, exposure of both non-smokers and smokers to wood smoke, gas stove fumes and second-hand smoke is detrimental, resulting in more severe asthma, more emergency room visits, and more asthma-related hospital admissions.[100] Smoking cessation and avoidance of second-hand smoke is strongly encouraged in asthmatics.[101] Air filters and room air cleaners may help prevent some asthma symptoms.[102] Ozone is also considered as a major factor in increasing asthma.[103]

For those in whom exercise can trigger an asthma attack (exercise-induced asthma), higher levels of ventilation and cold, dry air tend to exacerbate attacks. For this reason, activities in which a patient breathes large amounts of cold air, such as skiing and running, tend to be worse for asthmatics, whereas swimming in an indoor, heated pool with warm, humid air is less likely to provoke a response.[8]

[edit] Diet and Supplements
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Eating a healthy balanced diet with plenty of fruits and vegetables is important to staying healthy, particularly for people with asthma. Recent clinical studies have shown that people with asthma tend to eat fewer fruits and vegetables and are often deficient in nutrients such as Vitamin C, Magnesium and Selenium[citation needed]. In addition, increased intake of Omega 3 Fatty Acids has been shown to decrease inflammation[citation needed].

Vitamin C is a key vitamin antioxidant present in the extracellular fluid lining the lungs. Low intake of Vitamin C has been related to pulmonary dysfunction and several studies have shown that increasing Vitamin C intake may improve lung function in people with asthma and provide a protective effect against exercise-induced asthma.[104] While results have been positive, it is unlikely that Vitamin C alone will attenuate the effects of asthma. Larger and methodologically stronger studies are necessary before Vitamin C can be recommended for people with asthma.[105]

Magnesium is an essential mineral that has been shown to provide bronchodilating effects in people with asthma[citation needed]. In addition, clinical studies have shown that people with asthma may be deficient in Magnesium and that this mineral may play a role in asthma[citation needed]. However, it has not yet been unequivocally established that all asthmatics are deficient in this important mineral, because it is difficult to measure. More studies are needed to determine the role of Magnesium supplementation in the treatment for asthma. It is proven, however, that Magnesium sulfate intravenous treatment greatly improves pulmonary function when used in addition to conventional treatment in severe acute asthma attacks.[106]

Selenium is a trace mineral that is essential to good health. It is thought that deficiency of selenium may play some role in the development of asthma[citation needed]. Because selenium is important to the production of antioxidants, it is said that selenium deficiency may increase oxidative stress on the body, which may be a factor in chronic diseases such as asthma[citation needed]. Some clinical studies suggest that selenium supplementation for people with chronic asthma may help to improve symptoms[citation needed], however more research is needed to confirm these results.[107]

[edit] Treatment

Perhaps the most important step in controlling asthma is establishing a partnership between doctor and patient (whether child or adult) to create a specific, customized plan for proactively monitoring and managing symptoms. It is essential to be certain that someone who has asthma understands (and takes an active part in deciding) what needs to be accomplished, including reducing exposure to allergens, taking medical tests to assess the severity of symptoms, and possibly using medications. The treatment plan should be written down, consulted at every visit, and adjusted according to changes in symptoms.[108]

The most effective treatment for asthma is identifying triggers, such as pets or aspirin, and limiting or eliminating exposure to them. If trigger avoidance is insufficient, medical treatment is available. Desensitization has been suggested as a possible cure.[109] Additionally, some trial subjects were able to remove their symptoms by retraining their breathing habits with the Buteyko method.[110]

Other forms of treatment include relief medication, prevention medication, long-acting β2-agonists, and emergency treatment.

[edit] Medical