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Classification and external resources

Peak flow meters are used to measure one's peak expiratory flow rate
ICD-10 J45.
ICD-9 493
OMIM 600807
DiseasesDB 1006
MedlinePlus 000141
eMedicine article/806890 article/796274 article/800119 article/137501 article/296301 article/1000997 article/353436 article/88849
MeSH C08.127.108

Asthma, from the Greek î�σî�î�î� (�¡sthma), meaning gasp, is a common chronic inflammatory disease of the airways characterized by variable and recurring symptoms, airflow obstruction, and bronchospasm.[1] Symptoms include wheezing, coughing, chest tightness, and shortness of breath.[2]

Treatment of acute symptoms is usually with an inhaled short-acting beta-2 agonist (such as salbutamol).[3] Symptoms can be prevented by avoiding triggering such as allergens[4] and irritants and by using inhaled corticosteroids.[5] Leukotriene antagonists are less effective than corticosteroids and thus less preferred.

As of 2009, 300 million people worldwide were affected by asthma leading to 250,000 deaths per year.[6] Rates have increased significantly over the last 40 years. Prognosis is good with treatment.

[edit] Classification

Clinical classification of severity[7]
Severity Symptom frequency Nighttime symptoms  %FEV1 of predicted FEV1 Variability
Intermittent <1 per week '2 per month '80% <20%
Mild persistent >1 per week
but <1 per day
>2 per month '80% 20'30%
Moderate persistent Daily >1 per week 60'80% >30%
Severe persistent Daily Frequent <60% >30%

Asthma is clinically classified according to the frequency of symptoms, forced expiratory volume in 1 second (FEV1), and peak expiratory flow rate.[7] Asthma may also be classified as atopic (extrinsic) or non-atopic (intrinsic), based on whether symptoms are precipitated by allergens (atopic) or not (non-atopic).[8]

While asthma is classified based on severity, at the moment there is no clear method for classifying different subgroups of asthma beyond this system.[9] Within the classifications described above, although the cases of asthma respond to the same treatment differs, thus it is clear that the cases within a classification have significant differences.[9] Finding ways to identify subgroups that respond well to different types of treatments is a current critical goal of asthma research.[9]

Although asthma is a chronic obstructive condition, it is not considered as a part of chronic obstructive pulmonary disease as this term refers specifically to combinations of bronchiectasis, chronic bronchitis, and emphysema. Unlike these diseases, the airway obstruction in asthma is usually reversible; however, if left untreated, asthma can result in chronic inflammation of the lungs and irreversible obstruction.[10] In contrast to emphysema, asthma affects the bronchi, not the alveoli.[11]

[edit] Brittle asthma

Brittle asthma is a term used to describe two types of asthma, distinguishable by recurrent, severe attacks.[12] Type 1 brittle asthma refers to disease with wide peak flow variability, despite intense medication. Type 2 brittle asthma describes background well-controlled asthma, with sudden severe exacerbations.[12]

[edit] Asthma attack

Severity of acute asthma exacerbations[12]
Near-fatal asthma High PaCO2 and/or requiring mechanical ventilation
Life threatening asthma Any one of the following in a person with severe asthma:-
Clinical signs Measurements
Altered conscious level Peak flow < 33%
Exhaustion Oxygen saturation < 92%
Arrhythmia PaO2 < 8 kPa
Low blood pressure "Normal" PaCO2
Silent chest
Poor respiratory effort
Acute severe asthma Any one of:-
Peak flow 33-50%
Respiratory rate ' 25 breaths per minute
Heart rate ' 110 beats per minute
Unable to complete sentences in one breath
Moderate asthma exacerbation Worsening symptoms
Peak flow > 50% best or predicted
No features of acute severe asthma

An acute exacerbation of asthma is commonly referred to as an asthma attack. The classic symptoms are shortness of breath, wheezing, and chest tightness.[13] While these are the primary symptom of asthma,[14] some people present primarily with coughing, and in severe cases, air motion may be significantly impaired such that no wheezing is heard.[12]

Signs which occur during an asthma attack include the use of accessory muscles of respiration (sternocleidomastoid and scalene muscles of the neck), there may be a paradoxical pulse (a pulse that is weaker during inhalation and stronger during exhalation), and over-inflation of the chest.[15], a blue color of the skin and nails may occur from lack of oxygen.[16]

[edit] Status asthmaticus

Status asthmaticus is an acute exacerbation of asthma that does not respond to standard treatments of bronchodilators and steroids.

[edit] Signs and symptoms

Common symptoms of asthma include wheezing, shortness of breath, chest tightness and coughing. Symptoms are often worse at night or in the early morning, or in response to exercise or cold air.[17] Some people with asthma only rarely experience symptoms, usually in response to triggers, where as other may have marked persistent airflow obstruction.[18]

[edit] Cause

Asthma is caused by environmental and genetic factors.[19] These factors influence how severe asthma is and how well it responds to medication.[20] The interaction is complex and not fully understood.[21]

[edit] Environmental

Many environmental risk factors have been associated with asthma development and morbidity in children.

Environmental tobacco smoke, especially maternal cigarette smoking, is associated with high risk of asthma prevalence and asthma morbidity, wheeze, and respiratory infections.[22] Low air quality, from traffic pollution or high ozone levels,[23] has been repeatedly associated with increased asthma morbidity and has a suggested association with asthma development that needs further research.[24][25]

Recent studies show a relationship between exposure to air pollutants (e.g. from traffic) and childhood asthma.[26] This research finds that both the occurrence of the disease and exacerbation of childhood asthma are affected by outdoor air pollutants.

Viral respiratory infections are not only one of the leading triggers of an exacerbation but may increase one's risk of developing asthma.[27]

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.[24][28]

Antibiotic use early in life has been linked to development of asthma in several examples; it is thought that antibiotics make children who are predisposed to atopic immune responses susceptible to development of asthma because they modify gut flora, and thus the immune system (as described by the hygiene hypothesis).[29] The hygiene hypothesis (see below) is a hypothesis about the cause of asthma and other allergic disease, and is supported by epidemiologic data for asthma.[30] 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 an increased risk for asthma and allergy.

Caesarean sections have been associated with asthma, possibly because of modifications to the immune system (as described by the hygiene hypothesis).[31]

Respiratory infections such as rhinovirus, Chlamydia pneumoniae and Bordetella pertussis are correlated with asthma exacerbations.[32]

[edit] Genetic

Over 100 genes have been associated with asthma in at least one genetic association study.[33] 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:[33]

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.[33] 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.[citation needed] For example, one group of genetic differences (single nucleotide polymorphisms in 17q21) was associated with asthma that develops in childhood.[34]

[edit] Gene'environment interactions

CD14-endotoxin interaction based on CD14 SNP C-159T[35]
Endotoxin levels CC genotype TT genotype
High exposure Low risk High risk
Low exposure High risk Low risk

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.[19]

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.[35]

[edit] Exacerbation

Some individuals will have stable asthma for weeks or months and then suddenly develop an episode of acute asthma. Different asthmatic individuals react differently to various factors.[36] However, most individuals can develop severe exacerbation of asthma from several triggering agents.[36][37]

Home factors that can lead to exacerbation include dust, house mites, animal dander (especially cat and dog hair), cockroach allergens and molds at any given home.[36] Perfumes are a common cause of acute attacks in females and children. Both virus and bacterial infections of the upper respiratory tract infection can worsen asthma.[36]

[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.[38] The strongest risk factor for developing asthma is a history of atopic disease;[27] this increases one's risk of hay fever by up to 5x and the risk of asthma by 3-4x.[39] 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.[40] In adults, the more allergens one reacts positively to in a skin test, the higher the odds of having asthma.[41]

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.[42][43] 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.[44][45][46][47] 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.[48][49][50]

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.[51][52][53][54] In Taiwan, symptoms of allergies and airway hyper-reactivity increased in correlation with each 20% increase in body-mass index.[55]

Asthma has been associated with Churg'Strauss syndrome, and individuals with immunologically mediated urticaria may also experience systemic symptoms with generalized urticaria, rhino-conjunctivitis, orolaryngeal and gastrointestinal symptoms, asthma, and, at worst, anaphylaxis.[56] Additionally, adult-onset asthma has been associated with periocular xanthogranulomas.[57]

[edit] 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.[58] Children living in less hygienic environments (East Germany vs. West Germany,[59] families with many children,[60][61][62] day care environments[63]) tend to have 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.[64][65][66] 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.[67] 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.[68]

[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.[24] In the US, asthma prevalence is highest in Puerto Ricans, African Americans, Filipinos, Irish Americans, and Native Hawaiians, and lowest in Mexicans and Koreans.[69][70][71] Mortality rates follow similar trends, and response to Salbutamol is lower in Puerto Ricans than in African Americans or Mexicans.[72][73] 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.[74] US-born Mexican populations, for example, have higher asthma rates than non-US born Mexican populations that are living in the US.[75]

There is no correlation between asthma and gender in children, but more adult women are diagnosed with asthma than adult men.[76]

[edit] Socioeconomic factors

The incidence of asthma is highest among low-income populations both nationally[specify] and worldwide. Asthma deaths are most common in low and middle income countries,[77] and in the Western world, it is found in those low-income neighborhoods whose populations consist of large percentages of ethnic minorities[78].Additionally, asthma has been strongly associated with the presence of cockroaches in living quarters; these insects are more likely to be found in those same neighborhoods.[79]

Most likely due to income and geography, the incidence of and treatment quality for asthma varies among different racial groups.[80] For example, African Americans are less likely to receive outpatient treatment for asthma despite their higher prevalence of the disease. They are much more likely to require an emergency room visit or hospitalization for their asthma symptoms which is probably a contributing factor to their higher likelihood as a race of dying from an asthma attack compared to whites. The prevalence of "severe persistent" asthma is also greater in low-income communities than those with better access to treatment.[80][81]

[edit] Athletics

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.[82]

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.[82][83]

[edit] Occupation

Asthma as a result of (or worsened by) workplace exposures is a 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.[84] 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.[84] 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.[85]

[edit] Diagnosis

There is currently not a precise physiologic, immunologic, or histologic test for diagnosing asthma. The diagnosis is usually made based on the pattern of symptoms (airways obstruction and hyperresponsiveness) and/or response to therapy (partial or complete reversibility) over time.[86]

The British Thoracic Society determines a diagnosis of asthma using a 'response to therapy' approach. If the patient responds to treatment, then this is considered to be a confirmation of the diagnosis of asthma. The response measured is the reversibility of airway obstruction after treatment. Airflow in the airways is measured with a peak flow meter, and the following diagnostic criteria are used by the British Thoracic Society:[87]

  • '20% difference on at least three days in a week for at least two weeks;
  • '20% improvement of peak flow following treatment, for example:
  • '20% decrease in peak flow following exposure to a trigger (e.g., exercise).

In contrast, the US National Asthma Education and Prevention Program (NAEPP) uses a 'symptom patterns' approach.[88] Their guidelines for the diagnosis and management of asthma state that a diagnosis of asthma begins by assessing if any of the following list of indicators is present.[88][89] While the indicators are not sufficient to support a diagnosis of asthma, the presence of multiple key indicators increases the probability of a diagnosis of asthma.[88] Spirometry is needed to establish a diagnosis of asthma.[88]

  • Wheezing'high-pitched whistling sounds when breathing out'especially in children. (Lack of wheezing and a normal chest examination do not exclude asthma.)
  • history of any of the following:
    • Cough, worse particularly at night
    • Recurrent wheeze
    • Recurrent difficulty in breathing
    • Recurrent chest tightness
  • Symptoms occur or worsen in the presence of:
    • Exercise
    • Viral infection
    • Animals with fur or hair
    • House-dust mites (in mattresses, pillows, upholstered furniture, carpets)
    • Mold
    • Smoke (tobacco, wood)
    • Pollen
    • Changes in weather
    • Strong emotional expression (laughing or crying hard)
    • Airborne chemicals or dusts
    • Menstrual cycles
  • Symptoms occur or worsen at night, awakening the patient

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.[90] 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 patients who may experience only exercise-induced asthma. It may also be useful for daily self-monitoring and for checking the effects of new medications.[90] Peak flow readings can be charted 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.[91]

[edit] Differential diagnosis

Differential diagnoses include:[88]

  • Infants and Children
    • Upper airway diseases
      • Allergic rhinitis and sinusitis
    • Obstructions involving large airways
      • Foreign body in trachea or bronchus
      • Vocal cord dysfunction
      • Vascular rings or laryngeal webs
      • Laryngotracheomalacia, tracheal stenosis, or bronchostenosis
      • Enlarged lymph nodes or tumor
    • Obstructions involving small airways
      • Viral bronchiolitis or obliterative bronchiolitis
      • Cystic fibrosis
      • Bronchopulmonary dysplasia
      • Heart disease
    • Other causes
      • Recurrent cough not due to asthma
      • Aspiration from swallowing mechanism dysfunction or gastroesophageal reflux
  • Adults
    • COPD (e.g., chronic bronchitis or emphysema)
    • Congestive heart failure
    • Pulmonary embolism
    • Mechanical obstruction of the airways (benign and malignant tumors)
    • Pulmonary infiltration with eosinophilia
    • Cough secondary to drugs (e.g., angiotensin-converting enzyme (ACE) inhibitors)
    • Vocal cord dysfunction

Before diagnosing asthma, alternative possibilities should be considered such as the use of known bronchoconstrictors (substances that cause narrowing of the airways, e.g. certain anti-inflammatory agents or beta-blockers). Among elderly people, the presenting symptom may be fatigue, cough, or difficulty breathing, all of which may be erroneously attributed to Chronic obstructive pulmonary disease(COPD), congestive heart failure, or simple aging.[92]

Chronic obstructive pulmonary disease closely resembles asthma, is correlated with more exposure to cigarette smoke, an older age, less symptom reversibility after bronchodilator administration (as measured by spirometry), and decreased likelihood of family history of atopy.[93][citation needed]

The term "atopy" was coined to describe this triad of atopic eczema, allergic rhinitis and asthma.[56]

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. If the aspiration is indirect (from acid reflux), then treatment is directed at this is indicated.[citation needed]

[edit] Prevention

Fluticasone propionate metered dose inhaler commonly used to prevent asthma attacks.

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 first step is establishing a plan of action to prevent episodes of asthma by avoiding triggers and allergens, regularly testing for lung function, and using preventive medications.[88]

Controller treatments for the long term treatment of asthma include:

  • Inhaled corticosteroids are the most widely used prevention medications and normally come as inhalers.[88]
  • Leukotriene modifiers such as montelukast provide both anti-spasm and anti-inflammatory effects.[88]
  • Mast cell stabilizers such as (cromoglicate (cromolyn), and nedocromil). These medications are believed to prevent the initiation of the allergy reaction, by stabilizing the mast cell.[88]
  • Methylxanthines (theophylline and aminophylline). These agents are bronchodilators with minimal anti-inflammatory effect.[88]
  • LABAs, such as Salmeterol and formoterol are bronchodilators that have a duration of bronchodilation of at least 12 hours after a single dose.[88]
  • Immunomodulators such as Omalizumab (anti-IgE), which is a monoclonal antibody that prevents binding of IgE to the high-affinity receptors on basophils and mast cells.[88]
  • 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.[88]

[edit] Trigger avoidance

People with asthma should avoid all triggers, i.e.:

  • Reduce exposure to allergens to which the person is sensitive[88]
  • Avoid exposure to environmental tobacco smoke, smoke from wood-burning stoves and fireplaces, and substances with strong odors[88][94]
  • Avoid exertion outdoors when levels of air pollution are high[88]
  • Avoid use of nonselective beta-blockers[88]
  • Avoid sulfite-containing and other foods to which they are sensitive[88]
  • Consider allergen immunotherapy when there is clear evidence of a relationship[88]

For those in whom exercise can trigger an asthma attack, higher levels of ventilation and cold, dry air tend to exacerbate attacks.[14] For this reason, activities in which a patient breathes large amounts of cold air, such as skiing and running, tend to be worse for people with asthma, whereas swimming in an indoor, heated pool with warm, humid air is less likely to provoke a response.[14]

[edit] Management

A specific, customized plan for proactively monitoring and managing symptoms should be created. Someone who has asthma should understand the importance of reducing exposure to allergens, testing to assess the severity of symptoms, and the usage of medications. The treatment plan should be written down and adjusted according to changes in symptoms.[95]

The most effective treatment for asthma is identifying triggers, such as cigarette smoke, pets, or aspirin, and eliminating exposure to them. If trigger avoidance is insufficient, medical treatment is recommended. Medical treatments used depends on the severity of illness and the frequency of symptoms. Specific medications for asthma are broadly classified in to fast acting and long acting.[96][97]

Bronchodilators are recommended for short-term relief of symptoms. In those with occasional attacks, no other medication is needed. If mild persistent disease is present (more than two attacks a week), low-dose inhaled glucocorticoids or alternatively, an oral leukotriene antagonist or a mast cell stabilizer is recommended. For those who suffer daily attacks, a higher dose of inhaled glucocorticoid is used. In a severe asthma exacerbation, oral glucocorticoids are added to these treatments.[88]

[edit] Medications

Salbutamol metered dose inhaler commonly used to treat asthma attacks.

Medications used to treat asthma are divided into two general classes: quick-relief medications used to treat acute symptoms; and long-term control medications used to prevent further exacerbation.[98]

Fast acting
Long term control
  • Glucocorticoids are the most effective treatment available for long term control.[101] Inhaled forms are usually used except in the case of severe persitent disease in which oral steroids may be needed.[101] The inhaled formulation may be used once or twice daily depending on the severity of symptoms.[102]
  • Long acting beta-adrenoceptor agonists (LABD) have at least a 12-hour effect. They are however not to be used without a steroid due to an increased risk of severe symptoms.[103][104][105] In December 2008, members of the FDA's drug-safety office recommended withdrawing approval for these medications in children. Discussion is ongoing about their use in adults.[106]
  • Leukotriene antagonist ( such as zafirlukast) are an alternative to inhaled glucocorticoids, but are not preferred. They may also be used in addition to inhaled glucocorticoids but are second line to LABD.[101]
  • Mast cell stabilizers ( such as cromolyn sodium) are another none preferred alternative to glucocorticoids.[101]
Delivery methods

Medications are typically provided as metered-dose inhalers (MDIs) in combination with an asthma spacer or as a dry powder inhaler. The spacer is a plastic cylinder that mixes the medication with air, making it easier to receive a full dose of the drug. A nebulizer may also be used. Nebulizers and spacers are equally effective in those with mild to moderate symptoms however insufficient evidence is available to determine whether or not a difference exist in those severe symptomatology.[107]

[edit] Other

When an asthma attack is unresponsive to usual medications, other options available for emergency management may include:

  • Oxygen used to alleviate hypoxia if the saturation is less than 92%.[108]
  • Magnesium sulfate intravenous treatment has been shown to provide a bronchodilating effect when used in addition to other treatment in severe acute asthma attacks.[109][110]
  • Heliox, a mixture of helium and oxygen, may also be considered in severe unresponsive cases.[110]
  • Intravenous salbutamol is not supported by the evidence and thus only used in extremes.[108]
  • Methylxanthines (such as theophylline) do not add significantly to the effects of inhaled beta-agonists.[108]
  • The dissociative anesthetic ketamine is theoretically useful if intubation and mechanical ventilation is needed in people who are approaching respiratory arrest however evidence from trials does not exist.[111]

[edit] Complementary medicine

Many asthma patients, like those who suffer from other chronic disorders, use alternative treatments; surveys show that roughly 50% of asthma patients use some form of unconventional therapy.[112][113] There is little data to support the effectiveness of most of these therapies. Evidence is insufficient to support the usage of Vitamin C.[114] Acupuncture is not recommended for the treatment as there is insufficient evidence to support its use.[115][116] Air ionisers show no evidence that they improve asthma symptoms or benefit lung function; this applied equally to positive and negative ion generators.[117]

Dust mite control measures, including air filtration, chemicals to kill mites, vacuuming, mattress covers and others methods had no effect on asthma symptoms.[118] However, a review of 30 studies found that "bedding encasement might be an effective asthma treatment under some conditions" (when the patient is highly allergic to dust mite and the intervention reduces the dust mite exposure level from high levels to low levels).[119]

A study of "manual therapies" for asthma, including osteopathic, chiropractic, physiotherapeutic and respiratory therapeutic manoeuvres, found there is insufficient evidence to support or refute their use in treating.[120] The Buteyko breathing technique for controlling hyperventilation may result in a reduction in medications use however does not have any effect on lung function.[121] Thus an expert panel felt that evidence was insufficent to support its use.[115]

[edit] Prognosis

The prognosis for asthma is good, especially for children with mild disease.[89][not in citation given] Of asthma diagnosed during childhood, 54% of cases will no longer carry the diagnosis after a decade.[citation needed] The extent of permanent lung damage in people with asthma is unclear. Airway remodeling is observed, but it is unknown whether these represent harmful or beneficial changes.[122] Although conclusions from studies are mixed, most studies show that early treatment with glucocorticoids prevents or ameliorates decline in lung function as measured by several parameters.[123] For those who continue to suffer from mild symptoms, corticosteroids can help most to live their lives with few disabilities. It is more likely to consider immediate medication of inhaled corticosteroids as soon as asthma attacks occur. According to studies conducted, patients with relatively mild asthma who have received inhaled corticosteroids within 12 months of their first asthma symptoms achieved good functional control of asthma after 10 years of individualized therapy as compared to patients who received this medication after 2 years (or more) from their first attacks.[citation needed] Though they (delayed) also had good functional control of asthma, they were observed to exhibited slightly less optimal disease control and more signs of airway inflammation.[citation needed]

Asthma mortality has decreased over the last few decades due to better recognition and improvement in care.[124]

[edit] Epidemiology

Disability-adjusted life year for asthma per 100,000 inhabitants in 2004.[125]
     no data      <100      100'150      150'200      200'250      250'300      300'350      350'400      400'450      450'500      500'550      550'600      >600
The prevalence of childhood asthma in the United States has increased since 1980, especially in younger children.

As of 2009, 300 million people worldwide were affected by asthma leading to approximately 250,000 deaths per year.[126][103][6][127]

A 1998 there was a great disparity in prevalence worldwide across the world (as high as a 20 to 60-fold difference), with a trend toward more developed and westernized countries having higher rates of asthma.[128] Westernization however does not explain the entire difference in asthma prevalence between countries, and the disparities may also be affected by differences in genetic, social and environmental risk factors.[24] Mortality however is most common in low to middle income countries,[129] well symptoms were most prevalent (as much as 20%) in the United Kingdom, Australia, New Zealand, and Republic of Ireland; they were lowest (as low as 2'3%) in Eastern Europe, Indonesia, Greece, Uzbekistan, India, and Ethiopia.[128][dated info]

While asthma is more common in affluent countries, it is by no means a restricted problem; the WHO estimate that there are between 15 and 20 million people with asthma in India.[citation needed] In the U.S., urban residents, Hispanics, and African Americans are affected more than the population as a whole.[citation needed] Striking increases in asthma prevalence have been observed in populations migrating from a rural environment to an urban one,[130][dated info] or from a third-world country to Westernized one.[131][dated info]

It affects 7% of the population of the United States,[132] 5% of British people.[133] Asthma causes 4,000 deaths per year in the United States.[134] In 2005 in the United States asthma affected more than 22 million people including 6 million children.[135] It accounted for nearly 1/2 million hospitalizations,[135] and 14 million missed days of school annually.[citation needed] More boys have asthma than girls, but more women have it than men.[136] Of all children, African Americans and Latinos who live in cities are more at risk for developing asthma.[citation needed] African American children in the U.S. are four times more likely to die of asthma and three times more likely to be hospitalized, compared to their white counterparts.[citation needed] In some Latino neighborhoods, as many as one in three children has been found to have asthma.[137]

In England, an estimated 261,400 people were newly diagnosed with asthma in 2005; 5.7 million people had an asthma diagnosis and were prescribed 32.6 million asthma-related prescriptions.[138]

The frequency of atopic dermatitis, asthma, urticaria and allergic contact dermatitis has been found to be lower in psoriatic patients.[56]

[edit] Increasing frequency

Rates of asthma have increased significantly between the 1960s and 2008.[139][140] Some 9% of US children had asthma in 2001, compared with just 3.6% in 1980. The World Health Organization (WHO) reports that some 10% of the Swiss population suffers from asthma today,[141] compared with just 2% some 25'30 years ago.

[edit] History

Asthma was first recognized and named by Hippocrates circa 450 BC. During the 1930s'50s, asthma was considered as being one of the 'holy seven' psychosomatic illnesses. Its aetiology was considered to be psychological, with treatment often based on psychoanalysis and other 'talking cures'.[142] As these psychoanalysts interpreted the asthmatic wheeze as the suppressed cry of the child for its mother, so they considered that the treatment of depression was especially important for individuals with asthma.[142]

[edit] See also

[edit] References

  1. ^ NHLBI 2007 p.11'12
  2. ^ BTS 2009 p.3
  3. ^ a b c NHLBI 2007 p.214
  4. ^ NHLBI 2007 p.169'172
  5. ^ GINA 2009 p.69
  6. ^ a b GINA 2009 p.2
  7. ^ a b Yawn, BP (September 2008). "Factors accounting for asthma variability: achieving optimal symptom control for individual patients". Primary Care Respiratory Journal 17 (3): 138'147. doi:10.3132/pcrj.2008.00004. PMID 18264646. http://www.thepcrj.org/journ/vol17/17_3_138_147.pdf. 
  8. ^ Kumar, Vinay; Abbas, Abul K; Fausto, Nelson; Aster, Jon (2010). Robbins and Cotran Pathologic Basis of Disease (8th ed.). Saunders. p. 688. ISBN 9781416031215. 
  9. ^ a b c Moore WC, Pascual RM (June 2010). "Update in asthma 2009". American journal of respiratory and critical care medicine 181 (11): 1181'7. doi:10.1164/rccm.201003-0321UP. PMID 20516492. 
  10. ^ Delacourt, C (June 2004). "Bronchial changes in untreated asthma". Archives de Pédiatrie 11 (Suppl. 2): 71s'73s. PMID 15301800. 
  11. ^ Schiffman, George (18 December 2009). "Chronic Obstructive Pulmonary Disease". MedicineNet. http://www.medicinenet.com/chronic_obstructive_pulmonary_disease_copd/article.htm. Retrieved 2 September 2010. 
  12. ^ a b c d BTS 2009 p.54
  13. ^ Mason, Robert J; Broaddus, V Courtney; Murray, John F; Nadel, Jay A (2005). "Asthma". Murray and Nadel's Textbook of Respiratory Medicine (4th ed.). Elsevier. ISBN 978-0721603278. 
  14. ^ a b c Barnes, PJ (2008). "Asthma". in Fauci, Anthony S; Braunwald, E,; Kasper, DL. Harrison's Principles of Internal Medicine (17th ed.). New York: McGraw-Hill. pp. 1596'1607. ISBN 9780071466332. 
  15. ^ Abu-Hilal, MA; Mookadam, F (February 2010). "Pulsus paradoxus; historical and clinical perspectives". International Journal of Cardiology 138 (3): 229'32. doi:10.1016/j.ijcard.2009.04.045. PMID 19464740. 
  16. ^ Werner, HA (June 2001). "Status asthmaticus in children: a review". Chest 119 (6): 1596'1607. doi:10.1378/chest.119.6.1913. PMID 11399724. http://chestjournal.chestpubs.org/content/119/6/1913.long. 
  17. ^ BTS 2009 p.12
  18. ^ GINA 2009 p.8'9
  19. ^ a b Martinez FD (2007). "Genes, environments, development and asthma: a reappraisal". Eur Respir J 29 (1): 179'84. doi:10.1183/09031936.00087906. PMID 17197483. 
  20. ^ Choudhry S, Seibold MA, Borrell LN "et al." (2007). "Dissecting complex diseases in complex populations: asthma in latino americans". Proc Am Thorac Soc 4 (3): 226'33. doi:10.1513/pats.200701-029AW. PMID 17607004. 
  21. ^ Miller, RL; Ho SM (March 2008). "Environmental epigenetics and asthma: current concepts and call for studies". American Journal of Respiratory and Critical Care Medicine 177 (6): 567'573. doi:10.1164/rccm.200710-1511PP. PMID 18187692. PMC 2267336. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2267336/?tool=pubmed. 
  22. ^ GINA 2009. p.6
  23. ^ GINA 2009. p.56
  24. ^ a b c d Gold DR,Wright R; Wright, R (2005). "Population disparities in asthma". Annu Rev Public Health 26: 89'113. doi:10.1146/annurev.publhealth.26.021304.144528. PMID 15760282. 
  25. ^ "California Children's Health Study". http://www.arb.ca.gov/research/chs/chs.htm. 
  26. ^ M Salam et al., "Recent evidence for adverse effects of residential proximity to traffic sources on asthma", Current Opinion Pulmonary Medicine, 2008, Vol. 14, Issue 1
  27. ^ a b NHLBI 2007. p.11
  28. ^ Chen E, Miller GE (2007). "Stress and inflammation in exacerbations of asthma.". Brain Behav Immun. 21 (8): 993'9. doi:10.1016/j.bbi.2007.03.009. PMID 17493786. 
  29. ^ Droste, JH; Wieringa MH, Weyler JJ, Nelen VJ et al. (November 2000). "Does the use of antibiotics in early childhood increase the risk of asthma and allergic disease?". Clinical and Experimental Allergy 30 (11): 1547'1553. PMID 11069562. 
  30. ^ Bufford, JD; Gern JE (May 2005). "The hygiene hypothesis revisited". Immunology and Allergy Clinics of North America 25 (2): 247'262. doi:10.1016/j.iac.2005.03.005. PMID 15878454. 
  31. ^ BTS 2009 p.72
  32. ^ Harju TH, Leinonen M, Nokso-Koivisto J, et al. (2006). "Pathogenic bacteria and viruses in induced sputum or pharyngeal secretions of adults with stable asthma". Thorax 61 (7): 579'84. doi:10.1136/thx.2005.056291. PMID 16517571. 
  33. ^ a b c Ober C,Hoffjan S; Hoffjan, S (2006). "Asthma genetics 2006: the long and winding road to gene discovery". Genes Immun 7 (2): 95'100. doi:10.1038/sj.gene.6364284. PMID 16395390. 
  34. ^ Bouzigon E, Corda E, Aschard H, et al. (October 2008). "Effect of 17q21 Variants and Smoking Exposure in Early-Onset Asthma". The New England journal of medicine 359 (19): 1985. doi:10.1056/NEJMoa0806604. PMID 18923164. 
  35. ^ a b Martinez FD (2007). "CD14, endotoxin, and asthma risk: actions and interactions". Proc Am Thorac Soc 4 (3): 221'5. doi:10.1513/pats.200702-035AW. PMID 17607003. 
  36. ^ a b c d Baxi SN, Phipatanakul W (April 2010). "The role of allergen exposure and avoidance in asthma". Adolesc Med State Art Rev 21 (1): 57'71, viii'ix. PMID 20568555. 
  37. ^ Asthma definition Mayo Clinic. Retrieved on 2010-02-08
  38. ^ GINA 2009. p.4
  39. ^ Ronmark E, Lundback B, Jonsson EA, et al.: "Incidence of asthma in adults: Report from the obstructive lung disease in northern Sweden study." Allergy 1997; 52:1071-1081.
  40. ^ Burrows B, Martinez FD, Holonen M, et al.: "Association of asthma with serum IgE levels and skin-test reactivity to allergens." N Engl J Med 1989; 320:271-277.
  41. ^ Simpson BM, Custovic A, Simpson A, et al.: NAC Manchester Asthma and Allergy Study (NACMAAS): "Risk factors for asthma and allergic disorders in adults." Clin Exp Allergy 2001; 31:391-399.
  42. ^ Peat JK, Tovey E, Toelle BG, et al.: "House dust mite allergens: A major risk factor for childhood asthma in Australia." Am J Respir Crit Care Med 1996; 153:141-146.
  43. ^ Custovic A, Smith AC, Woodcock A: "Indoor allergens are a primary cause of asthma: Asthma and the environment." Eur Respir Rev 1998; 53:155-158.
  44. ^ Chan-Yeung M, Manfreda J, Dimich-Ward H, et al.: "A randomized controlled study on the effectiveness of a multifaceted intervention program in the primary prevention of asthma in high-risk infants." Arch Pediatr Adolesc Med 2000; 154:657-663.
  45. ^ Custovic A, Simpson BM, Simpson A, et al.: "Effect of environmental manipulation in pregnancy and early life on respiratory symptoms and atopy during first year of life: A randomised trial." Lancet 2001; 358:188-193.
  46. ^ Arshad SH, Bojarskas J, Tsitoura S, et al.: "Prevention of sensitization to house dust mite by allergen avoidance in school age children: A randomized controlled study." Clin Exp Allergy 2002; 32:843-849.
  47. ^ Arshad SH, Bateman B, Matthews SM: "Primary prevention of asthma and atopy during childhood by allergen avoidance in infancy: A randomised controlled study." Thorax 2003; 58:489-493.
  48. ^ Celedon JC, Litonjua AA, Ryan L, et al.: "Exposure to cat allergen, maternal history of asthma, and wheezing in first 5 years of life." Lancet 2002; 360:781-782.
  49. ^ Ownby DR, Johnson CC, Peterson EL: "Exposure to dogs and cats in the first year of life and risk of allergic sensitization at 6 to 7 years of age." JAMA 2002; 288:963-972.
  50. ^ Perzanowski MS, Ronmark E, Platts-Mills TA, Lundback B: "Effect of cat and dog ownership on sensitization and development of asthma among preteenage children." Am J Respir Crit Care Med 2002; 166:696-702.
  51. ^ Beuther DA (January 2010). "Recent insight into obesity and asthma". Curr Opin Pulm Med 16 (1): 64'70. doi:10.1097/MCP.0b013e3283338fa7. PMID 19844182. 
  52. ^ Holguin F, Fitzpatrick A (March 2010). "Obesity, asthma, and oxidative stress". J. Appl. Physiol. 108 (3): 754'9. doi:10.1152/japplphysiol.00702.2009. PMID 19926826. 
  53. ^ Kuczmarski RJ, Flegal KM, Campbell SM, Johnson CL: "Increasing prevalence of overweight among US adults: The National Health and Nutrition Examination Surveys, 1960'1991." JAMA 1994; 272:205-211.
  54. ^ Troiano RP, Flegal KM, Kuczmarski RJ, et al.: "Overweight prevalence and trends for children and adolescents: The National Health and Nutrition Examination Surveys, 1963'1991." Arch Pediatr Adolesc Med 1995; 149:1085-1091.
  55. ^ Huang S-L, Shiao GM, Chou P: "Association between body mass index and allergy in teenage girls in Taiwan." Clin Exp Allergy 1998; 29:323-329.
  56. ^ a b c Rapini, Ronald P.; Bolognia, Jean L.; Jorizzo, Joseph L. (2007). Dermatology: 2-Volume Set. St. Louis: Mosby. ISBN 1-4160-2999-0. 
  57. ^ PMID: 8140711; URL: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1298462/
  58. ^ Ramsey, CD; Celedón JC (January 2005). "The hygiene hypothesis and asthma". Current Opinion in Pulmonary Medicine 11 (1): 14'20. doi:10.1097/01.mcp.0000145791.13714.ae. PMID 15591883. 
  59. ^ de Lara, C; Noble A (June 2007). "Dishing the dirt on asthma: What we can learn from poor hygiene". Biologics 1 (2): 139'150. PMID 19707324. PMC 2721305. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2721305/?tool=pubmed. 
  60. ^ Strachan DP: "Hay fever, hygiene, and household size." BMJ 1989; 299:1259-1260.
  61. ^ Von Mutius E, Martinez FD, Fritzsch C, et al.: "Skin test reactivity and number of siblings." BMJ 1994; 308:692-695.
  62. ^ Jarvis D, Chinn S, Luczynska C, Burney P: "The association of family size with atopy and atopic disease." Clin Exp Allergy 1997; 27:240-245.
  63. ^ Ball TM, Castro-Rodriguez JA, Griffith KA, et al.: "Siblings, day-care attendance, and the risk of asthma and wheezing during childhood. N Engl J Med 2000; 343:538-543. etc)
  64. ^ Pattemore PK, Johnston SL, Bardin PG: "Viruses as precipitants of asthma symptoms. I Epidemiology." Clin Exp Allergy 1992; 22:325-336.
  65. ^ Nicholson KG, Kent J,chloes loves kurt Ireland DC: "Respiratory viruses and exacerbations of asthma in adults." BMJ 1993; 307:982-996.
  66. ^ Tan WC, Xiang X, Qiu D, et al.: "Epidemiology of respiratory viruses in patients hospitalized with near-fatal asthma, acute exacerbations of asthma, or chronic obstructive pulmonary disease." Am J Med 2003; 115:272-277.
  67. ^ Weiss ST, Tager IB, Munoz A, Speizer FE: "The relationship of respiratory infections in early childhood to the occurrence of increased levels of bronchial responsiveness and atopy." Am Rev Respir Dis 1985; 131:573-578.
  68. ^ Illi S, von Mutius E, Lau S, et al.: "Early childhood infectious diseases and the development of asthma up to school age: A birth cohort study." BMJ 2001; 322:390-395.
  69. ^ Lara M, Akinbami L, Flores G,Morgenstern H (2006). "Heterogeneity of childhood asthma among Hispanic children: Puerto Rican children bear a disproportionate burden". Pediatrics 117 (1): 43'53. doi:10.1542/peds.2004-1714. PMID 16396859. 
  70. ^ Davis AM, Kreutzer R, Lipsett M, King G,Shaikh N (2006). "Asthma prevalence in Hispanic and Asian American ethnic subgroups: results from the California Healthy Kids Survey". Pediatrics 118 (2): e363'70. doi:10.1542/peds.2005-2687. PMID 16882779. 
  71. ^ Johnson DB, Oyama N, LeMarchand L,Wilkens L (2004). "Native Hawaiians mortality, morbidity, and lifestyle: comparing data from 1982, 1990, and 2000". Pac Health Dialog 11 (2): 120'30. PMID 16281689. 
  72. ^ Naqvi M, Thyne S, Choudhry S "et al." (2007). "Ethnic-specific differences in bronchodilator responsiveness among african americans, puerto ricans, and mexicans with asthma". J Asthma 44 (8): 639'48. doi:10.1080/02770900701554441. PMID 17943575. 
  73. ^ Burchard EG, Avila PC, Nazario S "et al." (2004). "Lower bronchodilator responsiveness in Puerto Rican than in Mexican subjects with asthma". Am J Respir Crit Care Med 169 (3): 386'92. doi:10.1164/rccm.200309-1293OC. PMID 14617512. 
  74. ^ Gold DR,Acevedo-Garcia D; Acevedo-Garcia, D (2005). "Immigration to the United States and acculturation as risk factors for asthma and allergy". J Allergy Clin Immunol 116 (1): 38'41. doi:10.1016/j.jaci.2005.04.033. PMID 15990770. 
  75. ^ Eldeirawi KM,Persky VW; Persky, VW (2006). "Associations of acculturation and country of birth with asthma and wheezing in Mexican American youths". J Asthma 43 (4): 279'86. doi:10.1080/0277090060022869. PMID 16809241. 
  76. ^ Bush A, Menzies-Gow A (December 2009). "Phenotypic differences between pediatric and adult asthma". Proc Am Thorac Soc 6 (8): 712'9. doi:10.1513/pats.200906-046DP. PMID 20008882. 
  77. ^ "WHO | Asthma". Who.int. 2008-06-03. http://www.who.int/mediacentre/factsheets/fs307/en/. Retrieved 2010-04-16. 
  78. ^ "Patient/Public Education: Fast Facts ' Asthma Demographics/Statistics". American Academy of Allergy Asthma & Immunology. http://www.aaaai.org/patients/resources/fastfacts/asthma_demographics.stm. Retrieved 2006-05-02. 
  79. ^ Environmental Protection Agency. "Cockroaches and Pests ' Indoor Environmental Asthma Triggers". Environmental Protection Agency. http://www.epa.gov/asthma/pests.html. Retrieved 23 November 2009. 
  80. ^ a b National Center for Health Statistics (7 April 2006). "Asthma Prevalence, Health Care Use and Mortality, 2002". Centers for Disease Control and Prevention. http://www.cdc.gov/nchs/data/hestat/asthma/asthma.htm. 
  81. ^ National Heart, Lung, and Blood Institute (May 2004). Morbidity & Mortality: 2004 Chart Book On Cardiovascular, Lung, and Blood Diseases. National Institutes of Health. 
  82. ^ a b Weiler JM, Layton T, Hunt M (1998). "Asthma in United States Olympic athletes who participated in the 1996 Summer Games". J. Allergy Clin. Immunol. 102 (5): 722'6. doi:10.1016/S0091-6749(98)70010-7. PMID 9819287. 
  83. ^ Helenius I, Haahtela T (2000). "Allergy and asthma in elite summer sport athletes". J. Allergy Clin. Immunol. 106 (3): 444'52. doi:10.1067/mai.2000.107749. PMID 10984362. 
  84. ^ a b "Fatal and Nonfatal Injuries, and Selected Illnesses and Conditions: Respiratory Diseases". Worker Health Chartbook 2004. National Institute for Occupational Safety and Health. September 2004. http://www.cdc.gov/niosh/docs/2004-146/ch2/ch2-10.asp.htm. Retrieved December 17, 2008. 
  85. ^ "Asthma and Allergies". National Institute for Occupational Safety and Health. September 22, 2008. http://www.cdc.gov/niosh/topics/asthma/. Retrieved March 23, 2009. 
  86. ^ Lemanske RF, Busse WW (February 2010). "Asthma: clinical expression and molecular mechanisms". J. Allergy Clin. Immunol. 125 (2 Suppl 2): S95'102. doi:10.1016/j.jaci.2009.10.047. PMID 20176271. 
  87. ^ Pinnock H, Shah R (2007). "Asthma". BMJ 334 (7598): 847'50. doi:10.1136/bmj.39140.634896.BE. PMID 17446617. 
  88. ^ a b c d e f g h i j k l m n o p q r s t National Asthma Education and Prevention Program (NAEPP). Expert panel report 3: guidelines for the diagnosis and management of asthma. Bethesda (MD): National Heart, Lung, and Blood Institute; 2007.http://www.nhlbi.nih.gov/guidelines/asthma/asthgdln.pdf
  89. ^ a b Tippets B, Guilbert TW (2009). "Managing Asthma in Children: Part 1: Making the Diagnosis, Assessing Severity". Consultant for Pediatricians 8 (5). http://www.consultantlive.com/asthma/article/10162/1414747. 
  90. ^ a b Sapp J and Niven AS (April 7, 2008). "Making the most of pulmonary function testing in the diagnosis of asthma". Journal of Respiratory Diseases. http://www.consultantlive.com/asthma/article/1145425/1404762. 
  91. ^ "'Be in control' pack" (PDF). Asthma UK. http://www.asthma.org.uk/document.rm?id=29. Retrieved 2007-11-19. 
  92. ^ deShazo RD and Stupko JE (October 1, 2008). "Diagnosing asthma in seniors: An algorithmic approach". Journal of Respiratory Diseases. http://www.consultantlive.com/asthma/article/1145425/1405157. 
  93. ^ Hargreave, FE; Parameswaran K (August 2006). "Asthma, COPD and bronchitis are just components of airway disease". European Respiratory Journal 28 (2): 264'267. doi:10.1183/09031936.06.00056106. PMID 16880365. http://erj.ersjournals.com/cgi/content/full/28/2/264. 
  94. ^ Thomson NC, Spears M (2005). "The influence of smoking on the treatment response in patients with asthma". Curr Opin Allergy Clin Immunol 5 (1): 57'63. doi:10.1097/00130832-200502000-00011. PMID 15643345. 
  95. ^ Tippets B Guilbert TW (2009). "Managing Asthma in Children, Part 2: Achieving and Maintaining Control". Consultant for Pediatricians 8 (6). http://pediatrics.consultantlive.com/display/article/1145470/1418640. 
  96. ^ NHBLI 2007, p.213
  97. ^ "British Guideline on the Management of Asthma" (PDF). Scottish Intercollegiate Guidelines Network. 2008. http://www.sign.ac.uk/pdf/sign101.pdf. Retrieved 2008-08-04. 
  98. ^ NHLBI 2007,p.213
  99. ^ Rodrigo GJ, Nannini LJ (2006). "Comparison between nebulized adrenaline and beta2 agonists for the treatment of acute asthma. A meta-analysis of randomized trials". Am J Emerg Med 24 (2): 217'22. doi:10.1016/j.ajem.2005.10.008. PMID 16490653. 
  100. ^ NHLBI 2007 p.351
  101. ^ a b c d NHLBI 2007 p.213
  102. ^ NHLBI 2007 p.218
  103. ^ a b Fanta CH (March 2009). "Asthma". New England Journal of Medicine 360 (10): 1002'14. doi:10.1056/NEJMra0804579. PMID 19264689. 
  104. ^ Cates CJ, Lasserson TJ, Jaeschke R (2009). "Regular treatment with salmeterol and inhaled steroids for chronic asthma: serious adverse events". Cochrane Database Syst Rev (3): CD006922. doi:10.1002/14651858.CD006922.pub2. PMID 19588410. 
  105. ^ Cates CJ, Cates MJ (2008). "Regular treatment with salmeterol for chronic asthma: serious adverse events". Cochrane Database Syst Rev (3): CD006363. doi:10.1002/14651858.CD006363.pub2. PMID 18646149. 
  106. ^ "FDA sees asthma drug risks ' Yahoo! News". http://news.yahoo.com/s/nm/20081205/hl_nm/us_drugs_asthma_1. Retrieved December 5, 2008. 
  107. ^ NHLBI 2007 p.250
  108. ^ a b c Rodrigo GJ, Rodrigo C, Hall JB (2004). "Acute asthma in adults: a review". Chest 125 (3): 1081'102. doi:10.1378/chest.125.3.1081. PMID 15006973. 
  109. ^ 10.1378/chest.122.2.396 CHEST August 2002 vol. 122 no. 2 396-398
  110. ^ a b NHLBI 2007 p.373
  111. ^ NHLBI 2007 p.399
  112. ^ Blanc PD, Trupin L, Earnest G, Katz PP, Yelin EH, Eisner MD (2001). "Alternative therapies among adults with a reported diagnosis of asthma or rhinosinusitis : data from a population-based survey". Chest 120 (5): 1461'7. doi:10.1378/chest.120.5.1461. PMID 11713120. 
  113. ^ Shenfield G, Lim E, Allen H (2002). "Survey of the use of complementary medicines and therapies in children with asthma". J Paediatr Child Health 38 (3): 252'7. doi:10.1046/j.1440-1754.2002.00770.x. PMID 12047692. 
  114. ^ Kaur, B; Rowe BH, Arnold E (2009). "Vitamin C supplementation for asthma". Cochrane Database Syst Rev (1): CD000993. doi:10.1002/14651858.CD000993.pub3. PMID 19160185. 
  115. ^ a b NHLBI 2007 p.240
  116. ^ McCarney RW, Brinkhaus B, Lasserson TJ, Linde K (2004). "Acupuncture for chronic asthma". Cochrane Database Syst Rev (1): CD000008. doi:10.1002/14651858.CD000008.pub2. PMID 14973944. 
  117. ^ Blackhall K, Appleton S, Cates CJ (2003). "Ionisers for chronic asthma". Cochrane Database Syst Rev (3): CD002986. doi:10.1002/14651858.CD002986. PMID 12917939. 
  118. ^ PC Gøtzsche, HK Johansen (2008). "House dust mite control measures for asthma". Cochrane Database Syst Rev (2): CD001187. doi:10.1002/14651858.CD001187.pub3. PMID 18425868. 
  119. ^ Author=Recer GM; title=A review of the effects of impermeable bedding encasements on dust-mite allergen exposure and bronchial hyper-responsiveness in dust-mite-sensitized patients; journal= Clin Exp Allergy; 2004 Feb;34(2):268-75.
  120. ^ Hondras MA, Linde K, Jones AP (2005). "Manual therapy for asthma". Cochrane Database Syst Rev (2): CD001002. doi:10.1002/14651858.CD001002.pub2. PMID 15846609. 
  121. ^ "www.sign.ac.uk" (PDF). May 2008. p. 37. http://www.sign.ac.uk/pdf/sign101.pdf. 
  122. ^ Maddox L, Schwartz DA (2002). "The pathophysiology of asthma". Annu. Rev. Med. 53: 477'98. doi:10.1146/annurev.med.53.082901.103921. PMID 11818486. 
  123. ^ Beckett PA, Howarth PH (2003). "Pharmacotherapy and airway remodelling in asthma?". Thorax 58 (2): 163'74. doi:10.1136/thorax.58.2.163. PMID 12554904. 
  124. ^ NHBLI 2007, p.1
  125. ^ "WHO Disease and injury country estimates". World Health Organization. 2009. http://www.who.int/healthinfo/global_burden_disease/estimates_country/en/index.html. Retrieved November 11, 2009. 
  126. ^ "World Health Organization Fact Sheet Fact sheet No 307: Asthma". 2009. http://www.who.int/mediacentre/factsheets/fs307/en/print.html. Retrieved 2 September 2010. 
  127. ^ Braman SS (July 2006). "The global burden of asthma". Chest 130 (1 Suppl): 4S'12S. doi:10.1378/chest.130.1_suppl.4S. PMID 16840363. 
  128. ^ a b "Worldwide variation in prevalence of symptoms of asthma, allergic rhinoconjunctivitis, and atopic eczema: ISAAC. The International Study of Asthma and Allergies in Childhood (ISAAC) Steering Committee". Lancet 351 (9111): 1225'32. April 1998. PMID 9643741. 
  129. ^ World Health Organization. "WHO: Asthma". http://www.who.int/mediacentre/factsheets/fs307/en/. Retrieved 2007-12-29. 
  130. ^ Ng'ang'a LW, Odhiambo JA, Mungai MW, et al. (November 1998). "Prevalence of exercise induced bronchospasm in Kenyan school children: An urban-rural comparison". Thorax 53 (11): 919'26. doi:10.1136/thx.53.11.919. PMID 10193388. 
  131. ^ Waite DA, Eyles EF, Tonkin SL, O'Donnell TV (January 1980). "Asthma prevalence in Tokelauan children in two environments". Clin Allergy 10 (1): 71'5. doi:10.1111/j.1365-2222.1980.tb02082.x. PMID 7363447. 
  132. ^ "Asthma: Lung and Airway Disorders: Merck Manual Home Edition". http://www.merck.com/mmhe/sec04/ch044/ch044a.html. 
  133. ^ Anderson, HR; Gupta R, Strachan DP, Limb ES (January 2007). "50 years of asthma: UK trends from 1955 to 2004". Thorax 62 (1): 85'90. doi:10.1136/thx.2006.066407. PMID 17189533. PMC 2111282. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2111282/pdf/85.pdf. 
  134. ^ Getahun D, Demissie K, Rhoads GG (2005). "Recent trends in asthma hospitalization and mortality in the United States". Journal of asthma 42 (5): 373'8. doi:10.1081/JAS-62995. PMID 16036412. 
  135. ^ a b NHLBI 2007, p.1
  136. ^ Hayden, Merrill (19 September 2009). "Asthma Guide". http://www.webmd.com/asthma/guide/how-we-breath. 
  137. ^ Corbett, Sara (March/April 2005). "The Asthma Trap". Mother Jones. http://motherjones.com/print/16323. 
  138. ^ Simpson CR, Sheikh A (2010). "Trends in the epidemiology of asthma in England: a national study of 333,294 patients". J R Soc Med 103 (3): 98'106. doi:10.1258/jrsm.2009.090348. PMID 20200181. 
  139. ^ Grant EN, Wagner R, Weiss KB (August 1999). "Observations on emerging patterns of asthma in our society". J Allergy Clin Immunol 104 (2 Pt 2): S1'S9. doi:10.1016/S0091-6749(99)70268-X. PMID 10452783. 
  140. ^ Anandan C, Nurmatov U, van Schayck OC, Sheikh A (February 2010). "Is the prevalence of asthma declining? Systematic review of epidemiological studies". Allergy 65 (2): 152'67. doi:10.1111/j.1398-9995.2009.02244.x. PMID 19912154. 
  141. ^ World Health Organization (2007). "Global surveillance, prevention and control of chronic respiratory diseases: a comprehensive approach" (PDF). pp. 15'20, 49. http://www.who.int/gard/publications/GARD_Manual/en/index.html. Retrieved 2010-05-14. 
  142. ^ a b Opolski M, Wilson I (September 2005). "Asthma and depression: a pragmatic review of the literature and recommendations for future research". Clin Pract Epidemol Ment Health 1: 18. doi:10.1186/1745-0179-1-18. PMID 16185365. 

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