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AsthmaClassification and external resources

Peak flow meters are used to measure the peak expiratory flow rate,important in both monitoring and diagnosing asthma.[1]

ICD-10 J45(http://apps.who.int/classifications/icd10/browse/2010/en#/J45)

ICD-9 493 (http://www.icd9data.com/getICD9Code.ashx?icd9=493)

OMIM 600807 (http://omim.org/entry/600807)

DiseasesDB 1006 (http://www.diseasesdatabase.com/ddb1006.htm)

MedlinePlus 000141(http://www.nlm.nih.gov/medlineplus/ency/article/000141.htm)

eMedicine article/806890 (http://emedicine.medscape.com/article/806890-overview)

MeSH D001249 (http://www.nlm.nih.gov/cgi/mesh/2013/MB_cgi?field=uid&term=D001249)

AsthmaFrom Wikipedia, the free encyclopedia

Asthma (from the Greek ἅσθμα,ásthma, "panting") is a commonchronic inflammatory disease of theairways characterized by variableand recurring symptoms, reversibleairflow obstruction, andbronchospasm.[2] Commonsymptoms include wheezing,coughing, chest tightness, andshortness of breath.[3]

Asthma is thought to be caused bya combination of genetic andenvironmental factors.[4] Itsdiagnosis is usually based on thepattern of symptoms, response totherapy over time, andspirometry.[5] It is clinicallyclassified according to thefrequency of symptoms, forcedexpiratory volume in one second(FEV1), and peak expiratory flowrate.[6] Asthma may also beclassified as atopic (extrinsic) ornon-atopic (intrinsic)[7] whereatopy refers to a predispositiontoward developing type 1hypersensitivity reactions.[8]

Treatment of acute symptoms isusually with an inhaled short-actingbeta-2 agonist (such as salbutamol)and oral corticosteroids.[9] In very severe cases intravenous corticosteroids, magnesium sulfate andhospitalization maybe required.[10] Symptoms can be prevented by avoiding triggers, such as allergens[11] andirritants, and by the use of inhaled corticosteroids.[12] Long-acting beta agonists (LABA) or leukotrieneantagonists may be used in addition to inhaled corticosteroids if asthma symptoms remain uncontrolled.[13]

The prevalence of asthma has increased significantly since the 1970s. As of 2011, 235–300 million peoplewere affected globally,[14][15] including about 250,000 deaths.[15]

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Contents1 Signs and symptoms

1.1 Associated conditions2 Causes

2.1 Environmental2.2 Genetic2.3 Medical conditions2.4 Exacerbation

3 Pathophysiology4 Diagnosis

4.1 Spirometry4.2 Others4.3 Classification4.4 Differential diagnosis

5 Prevention6 Management

6.1 Lifestyle modification6.2 Medications6.3 Others6.4 Alternative medicine

7 Prognosis8 Epidemiology9 History10 Notes11 External links

Signs and symptomsAsthma is characterized by recurrent episodes of wheezing, shortness of breath, chest tightness, andcoughing.[16] Sputum may be produced from the lung by coughing but is often hard to bring up.[17] Duringrecovery from an attack it may appear pus like due to high levels of white blood cells called eosinophils.[18]

Symptoms are usually worse at night and in the early morning or in response to exercise or cold air.[19] Somepeople with asthma rarely experience symptoms, usually in response to triggers, whereas others may havemarked and persistent symptoms.[20]

Associated conditions

A number of other health conditions occur more frequently in those with asthma including: gastro-esophagealreflux disease (GERD), rhinosinusitis, and obstructive sleep apnea.[21] Psychological disorders are also morecommon[22] with anxiety disorders occurring in between 16–52% and mood disorders in 14–41%.[23] Ithowever is not known if asthma causes psychological problems or if psychological problems lead toasthma.[24]

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CausesAsthma is caused by a combination of complex and incompletely understood environmental and geneticinteractions.[4][25] These factors influence both its severity and its responsiveness to treatment.[26] It isbelieved that the recent increased rates of asthma are due to changing epigenetics (heritable factors other thanthose related to the DNA sequence) and a changing living environment.[27]

Environmental

Many environmental factors have been associated with asthma's development and exacerbation including:allergens, air pollution, and other environmental chemicals.[28] Smoking during pregnancy and after deliveryis associated with a greater risk of asthma-like symptoms.[29] Low air quality, from traffic pollution or highozone levels,[30] has been associated with both asthma development and increased asthma severity.[31]

Exposure to indoor volatile organic compounds may be a trigger for asthma; formaldehyde exposure, forexample, has a positive association.[32] Also, phthalates in PVC are associated with asthma in children andadults[33][34] as are high levels of endotoxin exposure.[35]

Asthma is associated with exposure to indoor allergens.[36] Common indoor allergens include: dust mites,cockroaches, animal dander, and mold.[37][38] Efforts to decrease dust mites have been found to beineffective.[39] Certain viral respiratory infections may increase the risk of developing asthma when acquiredas young children such as:[40] respiratory syncytial virus and rhinovirus.[41] Certain other infections howevermay decrease the risk.[41]

Hygiene hypothesis

The hygiene hypothesis is a theory which attempts to explain the increased rates of asthma worldwide as adirect and unintended result of reduced exposure, during childhood, to non–pathogenic bacteria andviruses.[42][43] It has been proposed that the reduced exposure to bacteria and viruses is due, in part, toincreased cleanliness and decreased family size in modern societies.[44] Evidence supporting the hygienehypothesis includes lower rates of asthma on farms and in households with pets.[44]

Use of antibiotics in early life has been linked to the development of asthma.[45] Also, delivery via caesareansection is associated with an increased risk (estimated at 20–80%) of asthma—this increased risk is attributedto the lack of healthy bacterial colonization that the newborn would have acquired from passage through thebirth canal.[46][47] There is a link between asthma and the degree of affluence.[48]

Genetic

Family history is a risk factor for asthma with many different genes being implicated.[50] If one identical twinis affected, the probability of the other having the disease is approximately 25%.[50] By the end of 2005, 25genes had been associated with asthma in six or more separate populations including:GSTM1, IL10, CTLA-4,SPINK5,LTC4S, IL4R and ADAM33 among others.[51] Many of these genes are related to the immune system

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CD14-endotoxin interaction based on CD14SNP C-159T[49]

Endotoxin levels CC genotype TT genotypeHigh exposure Low risk High risk

Low exposure High risk Low risk

or modulating inflammation. Even among this list of genessupported by highly replicated studies, results have notbeen consistent among all populations tested.[51] In 2006over 100 genes were associated with asthma in one geneticassociation study alone;[51] more continue to be found.[52]

Some genetic variants may only cause asthma when theyare combined with specific environmental exposures.[4]

An example is a specific single nucleotide polymorphismin the CD14 region and exposure to endotoxin (a bacterial product). Endotoxin exposure can come fromseveral environmental sources including tobacco smoke, dogs, and farms. Risk for asthma, then, is determinedby both a person's genetics and the level of endotoxin exposure.[49]

Medical conditions

A triad of atopic eczema, allergic rhinitis and asthma is called atopy.[53] The strongest risk factor fordeveloping asthma is a history of atopic disease;[40] with asthma occurring at a much greater rate in those whohave either eczema or hay fever.[54] Asthma has been associated with Churg–Strauss syndrome, anautoimmune disease and vasculitis. Individuals with certain types of urticaria may also experience symptomsof asthma.[53]

There is a correlation between obesity and the risk of asthma with both having increased in recentyears.[55][56] Several factors may be at play including decreased respiratory function due to a buildup of fatand the fact that adipose tissue leads to a pro-inflammatory state.[57]

Beta blocker medications such as propranolol can trigger asthma in those who are susceptible.[58]

Cardioselective beta-blockers, however, appear safe in those with mild or moderate disease.[59] Othermedications that can cause problems are ASA, NSAIDs, and angiotensin-converting enzyme inhibitors.[60]

Exacerbation

Some individuals will have stable asthma for weeks or months and then suddenly develop an episode of acuteasthma. Different individuals react differently to various factors.[61] Most individuals can develop severeexacerbation from a number of triggering agents.[61]

Home factors that can lead to exacerbation of asthma include dust, animal dander (especially cat and dog hair),cockroach allergens and mold.[61] Perfumes are a common cause of acute attacks in women and children.Both viral and bacterial infections of the upper respiratory tract can worsen the disease.[61] Psychologicalstress may worsen symptoms—it is thought that stress alters the immune system and thus increases the airwayinflammatory response to allergens and irritants.[31][62]

Pathophysiology

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Obstruction of the lumen of abronchiole by mucoid exudate, gobletcell metaplasia, and epithelialbasement membrane thickening in aperson with asthma.

Main article: Pathophysiology of asthma

Asthma is the result of chronic inflammation of the airways whichsubsequently results in increased contractability of the surroundingsmooth muscles. This among other factors leads to bouts of narrowingof the airway and the classic symptoms of wheezing. The narrowingis typically reversible with or without treatment. Occasionally theairways themselves change.[16] Typical changes in the airwaysinclude an increase in eosinophils and thickening of the laminareticularis. Chronically the airways' smooth muscle may increase insize along with an increase in the numbers of mucous glands. Othercell types involved include: T lymphocytes, macrophages, andneutrophils. There may also be involvement of other components ofthe immune system including: cytokines, chemokines, histamine, andleukotrienes among others.[41]

Diagnosis

While asthma is a well recognized condition, there is not one universal agreed upon definition.[41] It is definedby the Global Initiative for Asthma as "a chronic inflammatory disorder of the airways in which many cellsand cellular elements play a role. The chronic inflammation is associated with airway hyper-responsivenessthat leads to recurrent episodes of wheezing, breathlessness, chest tightness and coughing particularly at nightor in the early morning. These episodes are usually associated with widespread but variable airflowobstruction within the lung that is often reversible either spontaneously or with treatment".[16]

There is currently no precise test with the diagnosis typically based on the pattern of symptoms and responseto therapy over time.[5][41] A diagnosis of asthma should be suspected if there is a history of: recurrentwheezing, coughing or difficulty breathing and these symptoms occur or worsen due to exercise, viralinfections, allergens or air pollution.[63] Spirometry is then used to confirm the diagnosis.[63] In children underthe age of six the diagnosis is more difficult as they are too young for spirometry.[64]

Spirometry

Spirometry is recommended to aid in diagnosis and management.[65][66] It is the single best test for asthma. Ifthe FEV1 measured by this technique improves more than 12% following administration of a bronchodilatorsuch as salbutamol, this is supportive of the diagnosis.[67] It however may be normal in those with a history ofmild asthma, not currently acting up. Single-breath diffusing capacity can help differentiate asthma fromCOPD.[41] It is reasonable to perform spirometry every one or two years to follow how well a person's asthmais controlled.[68]

Others

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Clinical classification (≥ 12 years old)[6]

Severity Symptomfrequency

Night timesymptoms

%FEV1 ofpredicted

FEV1Variability SABA use

Intermittent ≤2/week ≤2/month ≥80% <20% ≤2 days/weekMild persistent >2/week 3–4/month ≥80% 20–30% >2 days/week

Moderatepersistent Daily >1/week 60–80% >30% daily

Severe persistent Continuously Frequent(7×/week) <60% >30% ≥twice/day

The methacholine challenge involves the inhalation of increasing concentrations of a substance that causesairway narrowing in those predisposed. If negative it means that a person does not have asthma; if positive,however, it is not specific for the disease.[41]

Other supportive evidence includes: a ≥20% difference in peak expiratory flow rate on at least three days in aweek for at least two weeks, a ≥20% improvement of peak flow following treatment with either salbutamol,inhaled corticosteroids or prednisone, or a ≥20% decrease in peak flow following exposure to a trigger.[69]

Testing peak expiratory flow is more variable than spirometry, however, and thus not recommended forroutine diagnosis. It may be useful for daily self-monitoring in those with moderate to severe disease and forchecking the effectiveness of new medications. It may also be helpful in guiding treatment in those with acuteexacerbations.[70]

Classification

Asthma isclinicallyclassifiedaccordingto thefrequencyof

symptoms, forced expiratory volume in one second (FEV1), and peak expiratory flow rate.[6] Asthma mayalso be classified as atopic (extrinsic) or non-atopic (intrinsic), based on whether symptoms are precipitated byallergens (atopic) or not (non-atopic).[7] While asthma is classified based on severity, at the moment there is noclear method for classifying different subgroups of asthma beyond this system.[71] Finding ways to identifysubgroups that respond well to different types of treatments is a current critical goal of asthma research.[71]

Although asthma is a chronic obstructive condition, it is not considered as a part of chronic obstructivepulmonary disease as this term refers specifically to combinations of disease that are irreversible such asbronchiectasis, chronic bronchitis, and emphysema.[72] Unlike these diseases, the airway obstruction in asthmais usually reversible; however, if left untreated, the chronic inflammation from asthma can lead the lungs tobecome irreversibly obstructed due to airway remodeling.[73] In contrast to emphysema, asthma affects thebronchi, not the alveoli.[74]

Asthma exacerbation

An acute asthma exacerbation is commonly referred to as an asthma attack. The classic symptoms areshortness of breath, wheezing, and chest tightness.[41] While these are the primary symptoms of asthma,[76]

some people present primarily with coughing, and in severe cases, air motion may be significantly impaired

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Severity of an acute exacerbation[75]

Near-fatal High PaCO2 and/or requiring mechanical ventilation

Life threatening(any one of)

Clinical signs MeasurementsAltered level of consciousness Peak flow < 33%

Exhaustion Oxygen saturation < 92%Arrhythmia PaO2 < 8 kPa

Low blood pressure "Normal" PaCO2

CyanosisSilent chest

Poor respiratory effort

Acute severe(any one of)

Peak flow 33–50%Respiratory rate ≥ 25 breaths per minute

Heart rate ≥ 110 beats per minuteUnable to complete sentences in one breath

ModerateWorsening symptoms

Peak flow 50–80% best or predictedNo features of acute severe asthma

such that no wheezing isheard.[75]

Signs which occur during anasthma attack include the useof accessory muscles ofrespiration(sternocleidomastoid andscalene muscles of the neck),there may be a paradoxicalpulse (a pulse that is weakerduring inhalation and strongerduring exhalation), and over-inflation of the chest.[77] Ablue color of the skin and nailsmay occur from lack ofoxygen.[78]

In a mild exacerbation the peakexpiratory flow rate (PEFR) is≥200 L/min or ≥50% of thepredicted best.[79] Moderate isdefined as between 80 and200 L/min or 25% and 50% ofthe predicted best while severeis defined as ≤ 80 L/min or≤25% of the predicted best.[79]

Acute severe asthma, previously known as status asthmaticus, is an acute exacerbation of asthma that does notrespond to standard treatments of bronchodilators and corticosteroids.[80] Half of cases are due to infectionswith others caused by allergen, air pollution, or insufficient or inappropriate medication use.[80]

Brittle asthma is a kind of asthma distinguishable by recurrent, severe attacks.[75] Type 1 brittle asthma is adisease with wide peak flow variability, despite intense medication. Type 2 brittle asthma is background well-controlled asthma with sudden severe exacerbations.[75]

Exercise-induced

Main article: Exercise-induced bronchoconstriction

Exercise can trigger bronchoconstriction in both people with and without asthma.[81] It occurs in most peoplewith asthma and up to 20% of people without asthma.[81] In athletes it occurs more common in elite athletes,with rates varying from 3% for bobsled racers to 50% for cycling and 60% for cross-country skiing.[81] While

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it may occur with any weather conditions it is more common when it is dry and cold.[82] Inhaled beta2-agonists do not appear to improve athletic performance among those without asthma[83] however oral dosesmay improve endurance and strength.[84][85]

Occupational

Main article: Occupational asthma

Asthma as a result of (or worsened by) workplace exposures, is a commonly reported occupational disease.[86]

Many cases however are not reported or recognized as such.[87][88] It is estimated that 5–25% of asthma casesin adults are work–related. A few hundred different agents have been implicated with the most common being:isocyanates, grain and wood dust, colophony, soldering flux, latex, animals, and aldehydes. The employmentassociated with the highest risk of problems include: those who spray paint, bakers and those who processfood, nurses, chemical workers, those who work with animals, welders, hairdressers and timber workers.[86]

Differential diagnosis

Many other conditions can cause symptoms similar to those of asthma. In children, other upper airwaydiseases such as allergic rhinitis and sinusitis should be considered as well as other causes of airwayobstruction including: foreign body aspiration, tracheal stenosis or laryngotracheomalacia, vascular rings,enlarged lymph nodes or neck masses. In adults, COPD, congestive heart failure, airway masses, as well asdrug-induced coughing due to ACE inhibitors should be considered. In both populations vocal corddysfunction may present similarly.[89]

Chronic obstructive pulmonary disease can coexist with asthma and can occur as a complication of chronicasthma. After the age of 65 most people with obstructive airway disease will have asthma and COPD. In thissetting, COPD can be differentiated by increased airway neutrophils, abnormally increased wall thickness, andincreased smooth muscle in the bronchi. However, this level of investigation is not performed due to COPDand asthma sharing similar principles of management: corticosteroids, long acting beta agonists, and smokingcessation.[90] It closely resembles asthma in symptoms, is correlated with more exposure to cigarette smoke, anolder age, less symptom reversibility after bronchodilator administration, and decreased likelihood of familyhistory of atopy.[91][92]

Prevention

The evidence for the effectiveness of measures to prevent the development of asthma is weak.[93] Some showpromise including: limiting smoke exposure both in utero and after delivery, breastfeeding, and increasedexposure to daycare or large families but none are well supported enough to be recommended for thisindication.[93] Early pet exposure may be useful.[94] Results from exposure to pets at other times areinconclusive[95] and it is only recommended that pets be removed from the home if a person has allergicsymptoms to said pet.[96] Dietary restrictions during pregnancy or when breast feeding have not been found tobe effective and thus are not recommended.[96] Reducing or eliminating compounds known to sensitivepeople from the work place may be effective.[86]

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Management

While there is no cure for asthma, symptoms can typically be improved.[97] A specific, customized plan forproactively monitoring and managing symptoms should be created. This plan should include the reduction ofexposure to allergens, testing to assess the severity of symptoms, and the usage of medications. The treatmentplan should be written down and advise adjustments to treament according to changes in symptoms.[98]

The most effective treatment for asthma is identifying triggers, such as cigarette smoke, pets, or aspirin, andeliminating exposure to them. If trigger avoidance is insufficient, the use of medication is recommended.Pharmaceutical drugs are selected based on, among other things, the severity of illness and the frequency ofsymptoms. Specific medications for asthma are broadly classified into fast-acting and long-actingcategories.[99][100]

Bronchodilators are recommended for short-term relief of symptoms. In those with occasional attacks, no othermedication is needed. If mild persistent disease is present (more than two attacks a week), low-dose inhaledcorticosteroids or alternatively, an oral leukotriene antagonist or a mast cell stabilizer is recommended. Forthose who have daily attacks, a higher dose of inhaled corticosteroids is used. In a moderate or severeexacerbation, oral corticosteroids are added to these treatments.[9]

Lifestyle modification

Avoidance of triggers is a key component of improving control and preventing attacks. The most commontriggers include allergens, smoke (tobacco and other), air pollution, non selective beta-blockers, and sulfite-containing foods.[101][102] Cigarette smoking and second-hand smoke (passive smoke) may reduce theeffectiveness of medications such as corticosteroids.[103] Dust mite control measures, including air filtration,chemicals to kill mites, vacuuming, mattress covers and others methods had no effect on asthma symptoms.[39]

Medications

Medications used to treat asthma are divided into two general classes: quick-relief medications used to treatacute symptoms; and long-term control medications used to prevent further exacerbation.[99]

Fast–acting

Short-acting beta2-adrenoceptor agonists (SABA), such as salbutamol (albuterol USAN) are the firstline treatment for asthma symptoms.[9]

Anticholinergic medications, such as ipratropium bromide, provide additional benefit when used incombination with SABA in those with moderate or severe symptoms.[9] Anticholinergicbronchodilators can also be used if a person cannot tolerate a SABA.[72]

Older, less selective adrenergic agonists, such as inhaled epinephrine, have similar efficacy toSABAs.[104] They are however not recommended due to concerns regarding excessive cardiacstimulation.[105]

Long–term control

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Salbutamol metered dose inhalercommonly used to treat asthmaattacks.

Corticosteroids are generally considered the most effective treatment available for long-term control.[99]

Inhaled forms such as beclomethasone are usually used except in the case of severe persistent disease, inwhich oral corticosteroids may be needed.[99] It is usually recommended that inhaled formulations beused once or twice daily, depending on the severity of symptoms.[106]

Long-acting beta-adrenoceptor agonists (LABA) such as salmeterol and formoterol can improve asthmacontrol, at least in adults, when given in combination with inhaled corticosteroids.[107] In children thisbenefit is uncertain.[107][108] When used without steroids they increase the risk of severe side-effects[109] and even with corticosteroids they may slightly increase the risk.[110][111]

Leukotriene antagonists (such as montelukast and zafirlukast) may be used in addition to inhaledcorticosteroids, typically also in conjunction with LABA.[99] Evidence is insufficient to support use inacute exacerbations.[112][113] In children under five years ofage, they are the preferred add-on therapy after inhaledcorticosteroids.[114]

Mast cell stabilizers (such as cromolyn sodium) are anothernon-preferred alternative to corticosteroids.[99]

Delivery methods

Medications are typically provided as metered-dose inhalers (MDIs) incombination with an asthma spacer or as a dry powder inhaler. Thespacer is a plastic cylinder that mixes the medication with air, makingit easier to receive a full dose of the drug. A nebulizer may also beused. Nebulizers and spacers are equally effective in those with mildto moderate symptoms however insufficient evidence is available todetermine whether or not a difference exists in those severesymptomatology.[115]

Adverse effects

Long-term use of inhaled corticosteroids at conventional doses carriesa minor risk of adverse effects.[116] Risks include the development ofcataracts and a mild regression in stature.[116][117]

Others

When asthma is unresponsive to usual medications, other options are available for both emergencymanagement and prevention of flareups. For emergency management other options include:

Oxygen to alleviate hypoxia if saturations fall below 92%.[118]

Magnesium sulfate intravenous treatment has been shown to provide a bronchodilating effect when usedin addition to other treatment in severe acute asthma attacks.[10][119]

Heliox, a mixture of helium and oxygen, may also be considered in severe unresponsive cases.[10]

Intravenous salbutamol is not supported by available evidence and is thus used only in extremecases.[118]

Methylxanthines (such as theophylline) were once widely used, but do not add significantly to the

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Fluticasone propionate metered doseinhaler commonly used for long-termcontrol.

effects of inhaled beta-agonists.[118] Their use in acute exacerbations is controversial.[120]

The dissociative anesthetic ketamine is theoretically useful if intubation and mechanical ventilation isneeded in people who are approaching respiratory arrest; however, there is no evidence from clinicaltrials to support this.[121]

For those with severe persistent asthma not controlled by inhaled corticosteroids and LABAs bronchialthermoplasty may be an option.[122] It involves the delivery of controlled thermal energy to the airway wallduring a series of bronchoscopies.[122] While it may increase exacerbation frequency in the first few months itappears to decrease the subsequent rate. Effects beyond one year are unknown.[123] Evidence suggests thatsublingual immunotherapy in those with both allergic rhinitis and asthma improve outcomes.[124]

Alternative medicine

Many people with asthma, like those with other chronic disorders, usealternative treatments; surveys show that roughly 50% use some formof unconventional therapy.[125][126] There is little data to support theeffectiveness of most of these therapies. Evidence is insufficient tosupport the usage of Vitamin C.[127] Acupuncture is notrecommended for the treatment as there is insufficient evidence tosupport its use.[128][129] Air ionisers show no evidence that theyimprove asthma symptoms or benefit lung function; this appliedequally to positive and negative ion generators.[130]

"Manual therapies", including osteopathic, chiropractic,physiotherapeutic and respiratory therapeutic maneuvers, haveinsufficient evidence to support their use in treating asthma.[131] TheButeyko breathing technique for controlling hyperventilation mayresult in a reduction in medications use however does not have anyeffect on lung function.[100] Thus an expert panel felt that evidencewas insufficient to support its use.[128]

Prognosis

The prognosis for asthma is generally good, especially for children with mild disease.[133] Mortality hasdecreased over the last few decades due to better recognition and improvement in care.[134] Globally it causesmoderate or severe disability in 19.4 million people as of 2004 (16 million of which are in low and middleincome countries).[135] Of asthma diagnosed during childhood, half of cases will no longer carry the diagnosisafter a decade.[50] Airway remodeling is observed, but it is unknown whether these represent harmful orbeneficial changes.[136] Early treatment with corticosteroids seems to prevent or ameliorates a decline in lungfunction.[137]

Epidemiology

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Disability-adjusted life year forasthma per 100,000 inhabitants in2004.[132]

no data

<100

100–150

150–200

200–250

250–300

300–350

350–400

400–450

450–500

500–550

550–600

>600

Rates of asthma in different countriesof the world as of 2004.

no data

<1%

1-2%

2-3%

3-4%

4-5%

5-6%

6-7%

7-8%

8-10%

10-12.5%

12.5–15%

>15%

Main article: Epidemiology of asthma

As of 2011, 235–300 millionpeople worldwide are affectedby asthma,[14][15] andapproximately 250,000people die per year from thedisease.[16] Rates varybetween countries withprevalences between 1 and18%.[16] It is more commonin developed than developingcountries.[16] One thus seeslower rates in Asia, EasternEurope and Africa.[41] Withindeveloped countries it is morecommon in those who areeconomically disadvantagedwhile in contrast indeveloping countries it is

more common in the affluent.[16] The reason for these differences is not well known.[16] Low and middleincome countries make up more than 80% of the mortality.[138]

While asthma is twice as common in boys as girls,[16] severe asthma occurs at equal rates.[139] In contrastadult women have a higher rate of asthma than men[16] and it is more common in the young than the old.[41]

Global rates of asthma have increased significantly between the 1960s and 2008[140][141] with it beingrecognized as a major public health problem since the 1970s.[41] Rates of asthma have plateaued in thedeveloped world since the mid-1990s with recent increases primarily in the developing world.[142] Asthmaaffects approximately 7% of the population of the United States[109] and 5% of people in the UnitedKingdom.[143] Canada, Australia and New Zealand have rates of about 14–15%.[144]

HistoryAsthma was recognized in Ancient Egypt and was treated by drinking an incense mixture known askyphi.[145] It was officially named as a specific respiratory problem by Hippocrates circa 450 BC, with theGreek word for "panting" forming the basis of our modern name.[41] In 200 BC it was believed to be at leastpartly related to the emotions.[23]

In 1873, one of the first papers in modern medicine on the subject tried to explain the pathophysiology of thedisease while one in 1872, concluded that asthma can be cured by rubbing the chest with chloroformliniment.[146][147] Medical treatment in 1880, included the use of intravenous doses of a drug calledpilocarpin.[148] In 1886, F.H. Bosworth theorized a connection between asthma and hay fever.[149]

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Epinephrine was first referred to in the treatment of asthma in 1905.[150] Oral corticosteroids began to be usedfor this condition in the 1950s while inhaled corticosteroids and selective short acting beta agonist came intowide use in the 1960s.[151][152]

During the 1930s–1950s, asthma was known as one of the "holy seven" psychosomatic illnesses. Its causewas considered to be psychological, with treatment often based on psychoanalysis and other talking cures.[153]

As these psychoanalysts interpreted the asthmatic wheeze as the suppressed cry of the child for its mother,they considered the treatment of depression to be especially important for individuals with asthma.[153]

Notes

1. ^ GINA 2011, p. 182. ^ NHLBI Guideline 2007, pp. 11–123. ^ British Guideline 2009, p. 44. ^ a b c Martinez FD (2007). "Genes, environments, development and asthma: a reappraisal". Eur Respir J 29 (1):

179–84. doi:10.1183/09031936.00087906 (http://dx.doi.org/10.1183%2F09031936.00087906). PMID 17197483(//www.ncbi.nlm.nih.gov/pubmed/17197483).

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References

National Asthma Education and Prevention Program (NAEPP) (2007). "Expert Panel Report 3: Guidelines for theDiagnosis and Management of Asthma" (http://www.nhlbi.nih.gov/guidelines/asthma/asthgdln.pdf) (PDF).National Heart Lung and Blood Institute."British Guideline on the Management of Asthma" (http://www.sign.ac.uk/pdf/sign101.pdf) (PDF). BritishThoracic Society. 2008 (revised 2012)."Global Strategy for Asthma Management and Prevention"(http://www.ginasthma.org/uploads/users/files/GINA_Report2011_May4.pdf) (PDF). Global Initiative for Asthma.2011.

External linksAsthma (http://www.dmoz.org/Health/Conditions_and_Diseases/Respiratory_Disorders/Asthma//) at the OpenDirectory Project

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