Asthma: Difference between revisions
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{{Infobox disease |
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| Name = Asthma |
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| DiseasesDB = 1006 |
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| Image = Two Peak Flow Meters.jpg |
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| Caption = Peak flow meters are used to measure one's [[peak expiratory flow]] rate |
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| ICD10 = {{ICD10|J|45||j|40}} |
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| ICD9 = {{ICD9|493}} |
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| ICDO = |
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| OMIM = 600807 |
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| MedlinePlus = 000141 |
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| eMedicineSubj = article |
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| eMedicineTopic = 806890 |
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| eMedicine_mult = {{eMedicine2|article|796274}} {{eMedicine2|article|800119}} {{eMedicine2|article|137501}} {{eMedicine2|article|296301}} {{eMedicine2|article|1000997}} {{eMedicine2|article|353436}} {{eMedicine2|article|88849}} |
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| MeshName = Asthma allergy |
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| MeshNumber = C08.127.108 |
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}} |
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'''Asthma''' (from the Greek άσθμα, ''ásthma'', "panting") is a common [[chronic (medicine)|chronic]] inflammatory [[disease]] of the [[bronchi|airways]] characterized by variable and recurring symptoms, reversible airflow obstruction, and [[bronchospasm]].<ref name="nhlbi2007p11-12" /> Symptoms include [[wheezing]], [[coughing]], chest tightness, and [[shortness of breath]].<ref name="bts2009p3" /> |
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Treatment of acute symptoms is usually with an inhaled short-acting [[Beta2-adrenergic agonist|beta-2 agonist]] (such as [[salbutamol]]).<ref name="nhlbi2007p214" /> Symptoms can be prevented by avoiding triggers, such as [[allergens]]<ref name="nhlbi2007p169" /> and [[irritants]], and by inhaling [[corticosteroids]].<ref name="gina2009p69" /> [[Leukotriene antagonist]]s are less effective than [[corticosteroids]] and thus less preferred.<ref>{{cite journal |author=Fanta CH |title=Asthma |journal=N Engl J Med |volume=360 |issue=10 |pages=1002–14 |year=2009 |month=March |pmid=19264689 |doi=10.1056/NEJMra0804579}}</ref> |
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The prevalence of asthma has increased significantly since the 1970s. As of 2009, 300 million people were affected worldwide.<ref name="gina2009p2" /> In 2009 asthma caused 250,000 deaths globally.<ref name="gina2009p2" /> Despite this, with proper control of asthma with step down therapy, prognosis is generally good. |
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{{TOC limit|limit=3}} |
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==Classification== |
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{| class="wikitable" style = "float: right; margin-left:1em; text-align:center" |
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|+ Clinical classification of severity<ref name="Yawn2008" /> |
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|- |
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! scope="col" style="width:10em;" | Severity in patients ≥ 12 years of age <ref name="Self, Timothy 2009">Self, Timothy. Chrisman,Cary. Finch, Christopher. "Applied Therapeutics: The Clinical Use of Drugs, 9th Edition" Philadelphia: Lippincott Williams & Wilkins, 2009. Chapter 22 (Asthma)</ref> |
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! scope="col" style="width:7em;" | Symptom frequency |
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! scope="col" style="width:7em;" | Nighttime symptoms |
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! scope="col" style="width:6em;" | %FEV<sub>1</sub> of predicted |
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! scope="col" style="width:6em;" | FEV<sub>1</sub> Variability |
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! scope="col" style="width:10em;" | Use of short-acting beta<sub>2</sub> agonist for symptom control (not for prevention of EIB) |
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|- |
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! scope="row" | Intermittent |
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| ≤2 per week |
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| ≤2 per month |
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| ≥80% |
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| <20% |
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| ≤2 days per week |
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|- |
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! scope="row" | Mild persistent |
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| >2 per week<br />but not daily |
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| 3-4 per month |
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| ≥80% |
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| 20–30% |
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| >2 days/week<br />but not daily |
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|- |
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! scope="row" | Moderate persistent |
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| Daily |
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| >1 per week but not nightly |
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| 60–80% |
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| >30% |
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| Daily |
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|- |
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! scope="row" | Severe persistent |
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| Throughout the day |
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| Frequent (often 7x/week) |
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| <60% |
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| >30% |
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| Several times per day |
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|} |
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Asthma is clinically classified according to the frequency of symptoms, forced expiratory volume in 1 second ([[spirometry|FEV<sub>1</sub>]]), and [[peak expiratory flow rate]].<ref name="Yawn2008" /> 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).<ref name="RobbinsCotran2010" /> |
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While asthma is classified based on severity, at the moment there is no clear method for classifying different subgroups of asthma beyond this system.<ref name="Moore2010" /> 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.<ref name="Moore2010" /> Finding ways to identify subgroups that respond well to different types of treatments is a current critical goal of asthma research.<ref name="Moore2010" /> |
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Although asthma is a [[chronic (medicine)|chronic]] [[obstructive lung disease|obstructive]] condition, it is not considered as a part of [[chronic obstructive pulmonary disease]] as this term refers specifically to combinations of disease that are irreversible such as [[bronchiectasis]], [[chronic bronchitis]], and [[emphysema]].<ref name="Self, Timothy 2009"/> Unlike these diseases, the airway obstruction in asthma is usually reversible; however, if left untreated, the chronic inflammation of the lungs during asthma can become irreversible obstruction due to airway remodeling.<ref name="Delacourt2004" /> In contrast to [[emphysema]], asthma affects the bronchi, not the [[alveoli]].<ref name="Schiffman2009" /> |
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===Brittle asthma=== |
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{{Main|Brittle asthma}} |
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Brittle asthma is a term used to describe two types of asthma, distinguishable by recurrent, severe attacks.<ref name="BTS54" /> 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.<ref name="BTS54"/> |
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===Asthma attack=== |
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An acute asthma exacerbation is commonly referred to as an ''asthma attack''. The classic symptoms are [[shortness of breath]], [[wheeze|wheezing]], and chest tightness.<ref name="Mason2005" /> While these are the primary symptoms of asthma,<ref name="Barnes" /> some people present primarily with [[cough]]ing, and in severe cases, air motion may be significantly impaired such that no wheezing is heard.<ref name="BTS54"/> |
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Signs which occur during an asthma attack include the use of accessory [[muscle]]s of respiration ([[sternocleidomastoid]] and [[scalene muscles]] of the neck), there may be a [[pulsus paradoxus|paradoxical pulse]] (a pulse that is weaker during inhalation and stronger during exhalation), and over-inflation of the chest.,<ref name="AbuHilal2010" /> a [[cyanosis|blue color]] of the skin and nails may occur from lack of oxygen.<ref name="Werner2001" /> |
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In a mild exacerbation the [[peak expiratory flow rate]] (PEFR) is ≥200 L/min or ≥50% of the predicted best.<ref name=Shiber2006>{{cite journal |author=Shiber JR, Santana J |title=Dyspnea |journal=Med. Clin. North Am. |volume=90 |issue=3 |pages=453–79 |year=2006 |month=May |pmid=16473100 |doi=10.1016/j.mcna.2005.11.006 |url=}}</ref> Moderate is defined as between 80 and 200 L/min or 25% and 50% of the predicted best while severe is defined as ≤ 80 L/min or ≤25% of the predicted best.<ref name=Shiber2006/> |
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Insufficient levels of vitamin D are linked with severe asthma attacks.<ref>http://www.reuters.com/article/idUSTRE65M5E920100623</ref> |
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===Status asthmaticus=== |
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{{Main|Status asthmaticus}} |
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Status asthmaticus is an acute exacerbation of asthma that does not respond to standard treatments of bronchodilators and steroids. Nonselective beta blockers (such as Timolol) have caused fatal status asthmaticus.<ref name=Asthma >{{cite book|author= Dipiro J.T. Talbert R.L. Yee G.C. Matzke G.R. Wells B.G. Posey L.M., |title= Pharmacotherpay. a pathophysiologic approach|edition =7|pages=524|year=2008| state=New York|unused_data= publishing company=McGraw-Hill}}</ref> |
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===Exercise induced=== |
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{{Main|Exercise-induced asthma}} |
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A diagnosis of asthma is common among top athletes. 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.<ref name=olympics>{{cite journal |author=Weiler JM, Layton T, Hunt M |title=Asthma in United States Olympic athletes who participated in the 1996 Summer Games |journal=J. Allergy Clin. Immunol. |volume=102 |issue=5 |pages=722–6 |year=1998 |pmid=9819287| doi = 10.1016/S0091-6749(98)70010-7}}</ref> |
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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.<ref name=olympics /><ref name=athletes>{{cite journal |author=Helenius I, Haahtela T |title=Allergy and asthma in elite summer sport athletes |journal=J. Allergy Clin. Immunol. |volume=106 |issue=3 |pages=444–52 |year=2000 |pmid=10984362 |doi=10.1067/mai.2000.107749}}</ref> |
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Exercise induced asthma can be treated with the use of a short-acting beta2 agonist.<ref name="Self, Timothy 2009"/> |
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===Occupational=== |
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{{Main|Occupational asthma}} |
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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.<ref name=chartbook>{{cite web | title=Fatal and Nonfatal Injuries, and Selected Illnesses and Conditions: Respiratory Diseases | work=Worker Health Chartbook 2004 | publisher=National Institute for Occupational Safety and Health |date = September 2004| url=http://www.cdc.gov/niosh/docs/2004-146/ch2/ch2-10.asp.htm | accessdate=December 17, 2008}}</ref> In one study monitoring workplace asthma by occupation, the highest percentage of cases occurred among [[Operator (profession)|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 [[service (economics)|services]] (34.2%) industries.<ref name=chartbook /> 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.<ref>{{cite web | title=Asthma and Allergies | publisher=National Institute for Occupational Safety and Health | date=September 22, 2008 | url=http://www.cdc.gov/niosh/topics/asthma/ | accessdate=March 23, 2009 }}</ref> |
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==Signs and symptoms== |
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{{listen |
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| filename = |
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Wheeze2O.ogg | title = Wheezing |
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| description = The sound of wheezing as heard with a stethoscope. |
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| format = [[Ogg]] |
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}} |
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Common symptoms of asthma include [[wheezing]], [[shortness of breath]], chest tightness and [[cough]]ing. Symptoms are often worse at night or in the early morning, or in response to exercise or cold air.<ref name="bts2009p12" /> Some people with asthma only rarely experience symptoms, usually in response to triggers, whereas other may have marked persistent airflow obstruction.<ref name="gina2009p9" /> |
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===Gastro-esophageal reflux disease=== |
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[[Gastro-esophageal reflux disease]] coexists with asthma in 80% of people with asthma, with similar symptoms. This is due to increased lung pressures, promoting bronchoconstriction, and through chronic aspiration.<ref name="Boulet 2009">{{cite journal |author=Boulet LP |title=Influence of comorbid conditions on asthma |journal=Eur Respir J |volume=33 |issue=4 |pages=897–906 |year=2009 |month=April |pmid=19336592 |doi=10.1183/09031936.00121308 |url=}}</ref> |
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===Sleep Disorders=== |
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Due to altered anatomy of the respiratory tract: increased upper airway adipose deposition, altered pharynx skeletal morphology, and extension of the pharyngeal airway; leading to upper airway collapse.<ref name="Harrington 2007">{{cite journal |author=Harrington JJ, Lee-Chiong T |title=Sleep and older patients |journal=Clin Chest Med |volume=28 |issue=4 |pages=673–84, v |year=2007 |month=December |pmid=17967287 |doi=10.1016/j.ccm.2007.07.002 |url=}}</ref> |
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==Cause== |
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Asthma is caused by environmental and genetic factors.<ref name=Martinez_geneenvir>{{cite journal |author=Martinez FD |title=Genes, environments, development and asthma: a reappraisal |journal=Eur Respir J |volume=29 |issue=1 |pages=179–84 |year=2007 |pmid=17197483 |doi=10.1183/09031936.00087906}}</ref> These factors influence how severe asthma is and how well it responds to medication.<ref>{{cite journal |author=Choudhry S, Seibold MA, Borrell LN "et al." |title=Dissecting complex diseases in complex populations: asthma in latino americans |journal=Proc Am Thorac Soc |volume=4 |issue=3 |pages=226–33 |year=2007 |pmid=17607004 |doi=10.1513/pats.200701-029AW |pmc=2647623}}</ref> The interaction is complex and not fully understood.<ref>{{cite journal | last=Miller | first=RL | coauthors=Ho SM |title=Environmental epigenetics and asthma: current concepts and call for studies | journal=American Journal of Respiratory and Critical Care Medicine | volume=177 | issue=6 | pages=567–573 | year=2008 | month=March | pmid=18187692 |url=http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2267336/?tool=pubmed | doi=10.1164/rccm.200710-1511PP | pmc=2267336 }}</ref> |
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Studying the prevalence of asthma and related diseases such as [[eczema]] and [[rhinitis|hay fever]] have yielded important clues about some key risk factors.<ref>GINA 2009. p.4</ref> The strongest risk factor for developing asthma is a history of [[atopy|atopic disease]];<ref name="NHLBI 11"/> this increases one's risk of hay fever by up to 5x and the [[risk]] of asthma by 3-4x.<ref>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.</ref> In children between the ages of 3-14, a positive skin test for [[allergy|allergies]] and an increase in [[Antibody|immunoglobulin E]] increases the chance of having asthma.<ref>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.</ref> In adults, the more allergens one reacts positively to in a skin test, the higher the odds of having asthma.<ref>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.</ref> |
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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.<ref>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.</ref><ref>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.</ref> 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.<ref>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.</ref><ref>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.</ref><ref>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.</ref><ref>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.</ref> 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.<ref>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.</ref><ref>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.</ref><ref>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.</ref> |
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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.<ref>{{cite journal |author=Beuther DA |title=Recent insight into obesity and asthma |journal=Curr Opin Pulm Med |volume=16 |issue=1 |pages=64–70 |year=2010 |month=January |pmid=19844182 |doi=10.1097/MCP.0b013e3283338fa7 |url=}}</ref><ref name=holguin>{{cite journal |author=Holguin F, Fitzpatrick A |title=Obesity, asthma, and oxidative stress |journal=J. Appl. Physiol. |volume=108 |issue=3 |pages=754–9 |year=2010 |month=March |pmid=19926826 |doi=10.1152/japplphysiol.00702.2009 |url=}}</ref><ref>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.</ref><ref>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.</ref> In Taiwan, symptoms of allergies and airway hyper-reactivity increased in correlation with each 20% increase in [[body-mass index]].<ref>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.</ref> Several factors associated with obesity may play a role in the pathogenesis of asthma, including decreased respiratory function due to a buildup of adipose tissue (fat) and the fact that adipose tissue leads to a pro-inflammatory state, which has been associated with non-eosinophilic asthma.<ref name="Woods 2009">{{cite journal |author=Wood LG, Gibson PG |title=Dietary factors lead to innate immune activation in asthma |journal=Pharmacol. Ther.|volume=123 |issue=1 |pages=37–53 |year=2009 |month=July |pmid=19375453 |doi=10.1016/j.pharmthera.2009.03.015 |url=}}</ref> |
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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.<ref name="Bolognia">{{cite book |author=Rapini, Ronald P.; Bolognia, Jean L.; Jorizzo, Joseph L. |title=Dermatology: 2-Volume Set |publisher=Mosby |location=St. Louis |year=2007 |pages= |isbn=1-4160-2999-0 |oclc= |doi= |accessdate=}}</ref> Additionally, adult-onset asthma has been associated with periocular [[xanthogranuloma]]s.<ref>PMID: 8140711; URL: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1298462/</ref> |
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===Environmental=== |
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Many environmental [[risk factor]]s have been associated with asthma development and morbidity in children. |
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Maternal tobacco smoking during pregnancy and after delivery is associated with a greater risk of asthma-like symptoms, wheezing, and respiratory infections during childhood.<ref>GINA 2009. p.6</ref> Low [[air Quality Index|air quality]], from traffic pollution or high [[ozone]] levels,<ref>GINA 2009. p.56</ref> has been repeatedly associated with increased asthma [[morbidity]] and has a suggested association with asthma development that needs further research.<ref name=Gold>{{cite journal |author=Gold DR,Wright R |title=Population disparities in asthma |journal=Annu Rev Public Health |volume=26 |pages=89–113 |year=2005 |pmid=15760282 |doi=10.1146/annurev.publhealth.26.021304.144528 |last2=Wright |first2=R}}</ref><ref name=childrens_health_study>{{cite web | url=http://www.arb.ca.gov/research/chs/chs.htm | title=California Children's Health Study }}</ref> |
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Recent studies show a relationship between exposure to air pollutants (e.g. from traffic) and childhood asthma.<ref>M Salam et al., [http://journals.lww.com/co-pulmonarymedicine/Fulltext/2008/01000/Recent_evidence_for_adverse_effects_of_residential.3.aspx "Recent evidence for adverse effects of residential proximity to traffic sources on asthma"], Current Opinion Pulmonary Medicine, 2008, Vol. 14, Issue 1</ref> This research finds that both the occurrence of the disease and exacerbation of childhood asthma are affected by outdoor air pollutants. High levels of [[endotoxin]] exposure may contribute to asthma risk.<ref>{{cite journal |author=Liu AH |title=Something old, something new: indoor endotoxin, allergens and asthma |journal=Paediatr Respir Rev |volume=5 Suppl A |issue= |pages=S65–71 |year=2004 |pmid=14980246 |doi= |url=}}</ref> |
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Viral respiratory infections are not only one of the leading triggers of an exacerbation but may increase one's risk of developing asthma especially in young children.<ref name="Self, Timothy 2009"/><ref name="NHLBI 11">NHLBI 2007. p.11</ref> |
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Psychological [[stress (biological)|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.<ref name=Gold /><ref name="Chen2007">{{cite journal |author=Chen E, Miller GE |title=Stress and inflammation in exacerbations of asthma. |journal=Brain Behav Immun. |volume=21 |issue=8 |pages=993–9 |year=2007 |pmid=17493786 |doi=10.1016/j.bbi.2007.03.009 |pmc=2077080}}</ref> |
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[[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).<ref>{{cite journal | last=Droste | first=JH | coauthors=Wieringa MH, Weyler JJ, Nelen VJ et al. | title=Does the use of antibiotics in early childhood increase the risk of asthma and allergic disease? | journal=Clinical and Experimental Allergy | volume=30 | issue=11 | pages=1547–1553 | month=November | year=2000 | pmid=11069562 }}</ref> The [[hygiene hypothesis]] ([[asthma#Hygiene hypothesis|see below]]) is a [[hypothesis]] about the cause of asthma and other allergic disease, and is supported by epidemiologic data for asthma.<ref>{{cite journal | last=Bufford | first=JD | coauthors=Gern JE | title=The hygiene hypothesis revisited | journal=Immunology and Allergy Clinics of North America | volume=25 | issue=2 | pages=247–262 | month=May | year=2005 | pmid=15878454 | doi=10.1016/j.iac.2005.03.005 }}</ref> 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. |
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[[Caesarean section]]s have been associated with asthma, possibly because of modifications to the immune system (as described by the hygiene hypothesis).<ref>BTS 2009 p.72</ref> |
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Respiratory infections such as [[rhinovirus]], ''[[Chlamydia pneumoniae]]'' and ''[[Bordetella pertussis]]'' are correlated with asthma exacerbations.<ref name="Thorax2006-Terttu">{{cite journal |author=Harju TH, Leinonen M, Nokso-Koivisto J, ''et al.'' |title=Pathogenic bacteria and viruses in induced sputum or pharyngeal secretions of adults with stable asthma |journal=Thorax |volume=61 |issue=7 |pages=579–84 |year=2006 |pmid=16517571 |doi=10.1136/thx.2005.056291 |pmc=2104650}}</ref> |
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[[Beta blocker]] medications such as metoprolol may trigger asthma in those who are susceptible.<ref>{{cite journal |author=O'Rourke ST |title=Antianginal actions of beta-adrenoceptor antagonists |journal=Am J Pharm Educ |volume=71 |issue=5 |pages=95 |year=2007 |month=October |pmid=17998992 |pmc=2064893 |doi= |url=}}</ref> |
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Observational studies have found that indoor exposure to [[volatile organic compounds]] (VOCs) may be one of the triggers of asthma, however experimental studies have not confirmed these observations.<ref>{{cite journal |author=Dales R, Raizenne M |title=Residential exposure to volatile organic compounds and asthma |journal=J Asthma |volume=41 |issue=3 |pages=259–70 |year=2004 |pmid=15260458 |doi= |url=}}</ref> Even VOC exposure at low levels has been associated with an increase in the risk of pediatric asthma. Because there are so many VOCs in the air, measuring total VOC concentrations in the indoor environment may not represent the exposure of individual compounds.<ref>{{cite journal |author=Rumchev K, Spickett J, Bulsara M, et al. |title=Association of domestic exposure to volatile organic compounds with asthma in young children. |journal=british medical journal |volume=59 |issue=9 |pages=746–751 |year=2004|month=April|pmid= |pmc= |doi= |url=}}</ref><ref>{{cite journal |author= Jeong-Hee Kim,1 Ja-Kyoung Kim,1 Byong-Kwan Son, |title= Effects of Air Pollutants on Childhood Asthma |journal= Yonsei Med J.|volume=46 |issue=2|pages=239–244 |year=2005|month=April |pmid=PMC2823020 |pmc= |doi= |url=}}</ref> Exposure to VOCs is associated with an increase in the IL-4 producing Th2 cells and a reduction in IFN-γ producing Th1 cells. Thus the mechanism of action of VOC exposure may be allergic sensitization mediated by a Th2 cell phenotype.<ref>{{cite journal |author= Lehmann I, Rehwagen M, Diez U, |title= Enhanced in vivo IgE production and T cell polarization toward the type 2 phenotype in association with indoor exposure to VOC: results of the LARS study |journal= International Journal of Hygiene and Environmental Health |volume=204 |issue=4 |pages=211–221 |year=2001 |month= |pmid= |pmc= |doi= 10.1078/1438-4639-00100 |url=}}</ref> Different individual variations in discomfort, from no response to excessive response, were seen in one of the studies. These variations may be due to the development of tolerance during exposure.<ref>{{cite journal |author=Harving H, Dahl R, Mølhave L. |title=Lung function and bronchial reactivity in asthmatics during exposure to volatile organic compounds. |journal=Am Rev Respir Dis. |volume=143 |issue=4 |pages=751–4 |year=1991 |month=October |pmid=2008987 |pmc= |doi= |url=}}</ref> Another study has concluded that formaldehyde may cause asthma-like symptoms. Low VOC emitting materials should be used while doing repairs or renovations which decreases the symptoms related to asthma caused by VOCs and formaldehyde.<ref>{{cite journal |author=D Norbäck, E Björnsson, C Janson, et al.|title=Asthmatic symptoms and volatile organic compounds, formaldehyde, and carbon dioxide in dwellings. |journal=Occup Environ Med |volume=52 |issue=6 |pages=388–395 |year=1995 |month=October |pmid= |pmc= |doi= 10.1136/oem.52.6.388|url=}}</ref> In another study "the indoor concentration of aliphatic compounds (C8-C11), butanols, and 2,2,4-trimethyl 1,3-pentanediol diisobutyrate (TXIB) was significantly elevated in newly painted dwellings. The total indoor VOC was about 100 micrograms/m3 higher in dwellings painted in the last year". The author concluded that some VOCs may cause inflammatory reactions in the airways and may be the reason for asthmatic symptoms.<ref>{{cite journal |author=Wieslander G, Norbäck D, Björnsson E, et al. |title=Asthma and the indoor environment: the significance of emission of formaldehyde and volatile organic compounds from newly painted indoor surfaces. |journal=Int Arch Occup Environ Health|volume=69 |issue=2 |pages=115–24|year=1997 |month= |pmid=9001918|pmc= |doi= |url=}}</ref><ref>{{cite journal |author=Wieslander G, Norbäck D, Edling C, |title=AIRWAY SYMPTOMS AMONG HOUSE PAINTERS IN RELATION TO EXPOSURE TO VOLATILE ORGANIC COMPOUNDS (VOCS)—A LONGITUDINAL STUDY |journal=The Annals of Occupational Hygiene|volume=41 |issue=2 |pages=155–166|year=1996 |month= |pmid=|pmc= |doi= 10.1093/annhyg/41.2.155|url=}}</ref> |
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There is a significant association between asthma-like symptoms (wheezing) among preschool children and the concentration of DEHP (pthalates) in indoor environment.<ref>{{cite journal |author= Barbara Kolarik,Kiril Naydenov, Malin Larsson, |title= The Association between Phthalates in Dust and Allergic Diseases among Bulgarian Children |journal= Environ Health Perspect |volume=116 |issue=1|pages=98–103 |year=2008 |month=October |pmid=17998992 |pmc= 2199301 |doi= |url=}}</ref> DEHP (di-ethylhexyl phthalate) is a plasticizer that is commonly used in building material. The hydrolysis product of DEHP (di-ethylhexyl phthalate) is MEHP (Mono-ethylhexyl phthalate) which mimics the prostaglandins and thromboxanes in the airway leading to symptoms related to asthma.<ref>{{cite journal |author=Oeie, L. Hersoug, L.-G. Madsen, J. O. |title=Residential Exposure to Plasticizers and Its Possible Role in the Pathogenesis of Asthma |journal=ENVIRONMENTAL HEALTH PERSPECTIVES|volume=105 |issue=9|pages=972–978 |year=1997 |month= |issn=0091-6765|pmc= |doi= |url=}}</ref> Another mechanism that has been studied regarding phthalates causation of asthma is that high phthalates level can "modulate the murine immune response to a coallergen". Asthma can develop in the adults who come in contact with heated PVC fumes.<ref>{{cite journal |author= Jaakkola JJ, Knight TL. |title= The role of exposure to phthalates from polyvinyl chloride products in the development of asthma and allergies: a systematic review and meta-analysis.|journal= ENVIRONMENTAL HEALTH PERSPECTIVES |volume=116 |issue=7 |pages=845–53 |year=2008 |month=July |pmid= 18629304 |pmc= PMC2453150 |doi= |url=}}</ref> Two main type of phthalates, namely n-butyl benzyl phthalate (BBzP) and di(2-ethylhexyl) phthalate (DEHP), have been associated between the concentration of polyvinyl chloride (PVC) used as flooring and the dust concentrations. Water leakage were associated more with BBzP, and buildings construction were associated with high concentrations of DEHP.<ref>{{cite journal |author= C-G Bornehag, B Lundgren, C J. Weschler, et al |title= Phthalates in Indoor Dust and Their Association with Building Characteristics |journal= Environ Health Perspect. |volume=113 |issue=10|pages=1399–1404 |year=2005 |month=October |pmid=PMC1281287 |pmc=|doi= |url=}}</ref> Asthma has been shown to have a relationship with plaster wall materials and wall-to wall carpeting. The onset of asthma was also related to the floor–leveling plaster at home. Therefore, it is important to understand the health aspect of these materials in the indoor surfaces.<ref>{{cite journal |author=O'Rourke ST |title= Interior Surface Materials and Asthma in Adults: A Population-based Incident Case-Control Study |journal= American Journal of Epidemiology |volume=164 |issue=8 |pages=742–749 |year=2006 |month=March |pmid= |pmc= |doi= 10.1093/aje/kwj249 |url=}}</ref> |
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===Genetic=== |
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Over 100 [[gene]]s have been associated with asthma in at least one [[genetic association]] study.<ref name=Hoffjan>{{cite journal |author=Ober C,Hoffjan S |title=Asthma genetics 2006: the long and winding road to gene discovery |journal=Genes Immun |volume=7 |issue=2 |pages=95–100 |year=2006 |pmid=16395390 |doi=10.1038/sj.gene.6364284 |last2=Hoffjan |first2=S}}</ref> 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:<ref name=Hoffjan /> |
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{{Multicol}} |
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<small> |
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*[[Glutathione S-transferase Mu 1|GSTM1]] |
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*[[Interleukin 10|IL10]] |
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*[[CTLA-4]] |
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*[[SPINK5]] |
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*[[Leukotriene C4 synthase|LTC4S]] |
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{{Multicol-break}} |
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<small> |
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*[[lymphotoxin alpha|LTA]] |
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*[[GRPA]] |
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*[[NOD1]] |
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*[[CC16]] |
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*[[GSTP1]] |
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{{Multicol-break}} |
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<small> |
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*[[STAT6]] |
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*[[NOS1]] |
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*[[CCL5]] |
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*[[Thromboxane receptor|TBXA2R]] |
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*[[TGFB1]] |
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{{Multicol-break}} |
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<small> |
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*[[Interleukin 4|IL4]] |
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*[[Interleukin 13|IL13]] |
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*[[CD14]] |
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*[[Beta-2 adrenergic receptor|ADRB2]] (β-2 adrenergic receptor) |
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*[[HLA-DRB1]] |
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{{Multicol-break}} |
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<small> |
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*[[HLA-DQB1]] |
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*[[Tumor necrosis factors|TNF]] |
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*[[FCER1B]] |
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*[[Interleukin-4 receptor|IL4R]] |
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*[[ADAM33]] |
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{{Multicol-end}} |
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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.<ref name=Hoffjan /> 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|date=May 2010}} For example, one group of genetic differences ([[single nucleotide polymorphism]]s in [[Chromosome 17 (human)|17q21]]) was associated with asthma that develops in childhood.<ref name="pmid18923164">{{cite journal |author=Bouzigon E, Corda E, Aschard H, ''et al.'' |title=Effect of 17q21 Variants and Smoking Exposure in Early-Onset Asthma |journal=The New England journal of medicine |volume= 359|issue= 19|page= 1985|year=2008 |month=October |pmid=18923164 |doi=10.1056/NEJMoa0806604 |url=}}</ref> |
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===Gene–environment interactions=== |
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{| class="wikitable" style = "float: right; margin-left:15px; text-align:center" |
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|+ CD14-endotoxin interaction based on CD14 SNP C-159T<ref name=Martinez_CD14 /> |
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|- |
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! Endotoxin levels !! CC genotype !! TT genotype |
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|- |
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! High exposure |
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| Low risk || High risk |
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|- |
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! Low exposure |
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|High risk || Low risk |
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|} |
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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.<ref name=Martinez_geneenvir /> |
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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.<ref name=Martinez_CD14>{{cite journal |author=Martinez FD |title=CD14, endotoxin, and asthma risk: actions and interactions |journal=Proc Am Thorac Soc |volume=4 |issue=3 |pages=221–5 |year=2007 |pmid=17607003 |doi=10.1513/pats.200702-035AW |pmc=2647622}}</ref> |
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===Exacerbation=== |
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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.<ref name=baxi>{{cite journal |author=Baxi SN, Phipatanakul W |title=The role of allergen exposure and avoidance in asthma |journal=Adolesc Med State Art Rev |volume=21 |issue=1 |pages=57–71, viii–ix |year=2010 |month=April |pmid=20568555 |pmc=2975603 |doi= |url=}}</ref> However, most individuals can develop severe exacerbation of asthma from several triggering agents.<ref name=baxi/><ref>[http://www.mayoclinic.com/health/asthma/DS00021 Asthma definition] Mayo Clinic. Retrieved on 2010-02-08</ref> |
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Home factors that can lead to exacerbation include [[dust]], [[house dust mite|house mites]], animal [[dander]] (especially cat and dog hair), cockroach [[allergen]]s and [[mold]]s at any given home.<ref name=baxi/> [[Perfume]]s are a common cause of acute attacks in females and children. Both [[virus]] and bacterial [[infection]]s of the upper respiratory tract infection can worsen asthma.<ref name=baxi/> |
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===Hygiene hypothesis=== |
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{{Main|Hygiene hypothesis}} |
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One theory for the cause of the increase in asthma prevalence worldwide is the "[[hygiene hypothesis]]"<ref name="Self, Timothy 2009"/> —that the rise in the prevalence of allergies and asthma is a direct and unintended result of reduced exposure to a wide variety of different bacteria and virus types in modern societies, or modern hygienic practices preventing childhood infections.<ref>{{cite journal | last=Ramsey | first=CD | coauthors=Celedón JC | title=The hygiene hypothesis and asthma | journal=Current Opinion in Pulmonary Medicine | volume=11 | issue=1 | pages=14–20 | month=January | year=2005 | pmid=15591883 | doi=10.1097/01.mcp.0000145791.13714.ae }}</ref> Children living in less hygienic environments (East Germany vs. West Germany,<ref>{{cite journal | last=de Lara | first=C | coauthors=Noble A | title=Dishing the dirt on asthma: What we can learn from poor hygiene | journal=Biologics | volume=1 | issue=2 | pages=139–150 | month=June | year=2007 | url=http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2721305/?tool=pubmed | pmid=19707324 | pmc=2721305 }}</ref> families with many children,<ref>Strachan DP: "Hay fever, hygiene, and household size." ''BMJ '' 1989; 299:1259-1260.</ref><ref>Von Mutius E, Martinez FD, Fritzsch C, et al.: "Skin test reactivity and number of siblings." ''BMJ '' 1994; 308:692-695.</ref><ref>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.</ref> day care environments<ref>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)</ref>) 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.<ref>Pattemore PK, Johnston SL, Bardin PG: "Viruses as precipitants of asthma symptoms. I Epidemiology." ''Clin Exp Allergy'' 1992; 22:325-336.</ref><ref>Nicholson KG, Kent J,chloes loves kurt Ireland DC: "Respiratory viruses and exacerbations of asthma in adults." ''BMJ '' 1993; 307:982-996.</ref><ref>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.</ref> 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.<ref>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.</ref> 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.<ref>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.</ref> |
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===Socioeconomic factors=== |
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The incidence of asthma is highest among low-income populations worldwide{{specify|date=November 2010}}. Asthma deaths are most common in low and middle income countries,<ref>{{cite web|url=http://www.who.int/mediacentre/factsheets/fs307/en/ |title=WHO | Asthma |publisher=Who.int |date=2008-06-03 |accessdate=2010-04-16}}</ref> and in the Western world, it is found in those low-income neighborhoods whose populations consist of large percentages of ethnic minorities.<ref name=AAAAAI>{{cite web | title=Patient/Public Education: Fast Facts — Asthma Demographics/Statistics | publisher= American Academy of Allergy Asthma & Immunology | url=http://www.aaaai.org/patients/resources/fastfacts/asthma_demographics.stm | accessdate=2006-05-02}}</ref> Additionally, asthma has been strongly associated with the presence of [[cockroach]]es in living quarters; these insects are more likely to be found in those same neighborhoods.<ref name="EPA">{{cite web | author=Environmental Protection Agency | title=Cockroaches and Pests — Indoor Environmental Asthma Triggers | accessdate=23 November 2009 | publisher=Environmental Protection Agency | url=http://www.epa.gov/asthma/pests.html}}</ref> |
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Most likely due to income and geography, the incidence of and treatment quality for asthma varies among different racial groups.<ref name="CDC2002"/> The prevalence of "severe persistent" asthma is also greater in low-income communities than those with better access to treatment.<ref name="CDC2002">{{cite web | author=National Center for Health Statistics | title=Asthma Prevalence, Health Care Use and Mortality, 2002 | date=7 April 2006 | publisher=Centers for Disease Control and Prevention | url=http://www.cdc.gov/nchs/data/hestat/asthma/asthma.htm}}</ref><ref name="NIH2004">{{cite journal | author=National Heart, Lung, and Blood Institute | title=Morbidity & Mortality: 2004 Chart Book On Cardiovascular, Lung, and Blood Diseases | month=May | year=2004 | publisher=National Institutes of Health}}</ref> |
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==Diagnosis== |
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{| border="1" cellpadding="5" cellspacing="0" align="center" class="wikitable" style="float: right; margin-left:15px" |
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|+ '''Severity of acute asthma exacerbations'''<ref name="BTS54"/> |
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|- |
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! style="border-top: 3px solid darkgray;" | Near-fatal asthma |
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| colspan="2" style="border-top: 3px solid darkgray;" | High [[Arterial blood gas|PaCO<sub>2</sub>]] and/or requiring mechanical ventilation |
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|- |
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! rowspan="9" style="border-top: 3px solid darkgray;" | Life threatening asthma |
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| colspan="2" style="border-top: 3px solid darkgray;" | Any one of the following in a person with severe asthma:- |
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|- |
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! Clinical signs |
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! Measurements |
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|- |
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| Altered [[level of consciousness]] |
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| [[Peak flow]] < 33% |
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|- |
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| Exhaustion |
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| [[Oxygen saturation]] < 92% |
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|- |
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| [[Arrhythmia]] |
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| [[Arterial blood gas|PaO<sub>2</sub>]] < 8 kPa |
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|- |
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| Low [[blood pressure]] |
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| "Normal" PaCO<sub>2</sub> |
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|- |
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| [[Cyanosis]] |
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|- |
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| Silent chest |
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|- |
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| Poor respiratory effort |
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|- |
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! rowspan="5" style="border-top: 3px solid darkgray;" | Acute severe asthma |
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| colspan="2" style="border-top: 3px solid darkgray;" | Any one of:- |
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|- |
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| colspan="2" | Peak flow 33-50% |
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|- |
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| colspan="2" | Respiratory rate ≥ 25 breaths per minute |
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|- |
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| colspan="2" | Heart rate ≥ 110 beats per minute |
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|- |
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| colspan="2" | Unable to complete sentences in one breath |
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|- |
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! rowspan="3" style="border-top: 3px solid darkgray; border-bottom: 3 px solid darkgray;" | Moderate asthma exacerbation |
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| colspan="2" style="border-top: 3px solid darkgray;" | Worsening symptoms |
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|- |
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| colspan="2" | Peak flow 80%-50% best or predicted |
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|- |
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| colspan="2" style="border-bottom: 3 px solid darkgray;" | No features of acute severe asthma |
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|} |
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[[Image:Asthma .jpg|thumb|Obstruction of the lumen of the bronchiole by mucoid exudate, goblet cell metaplasia, epithelial basement membrane thickening and severe inflammation of bronchiole in a patient with asthma.]] |
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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.<ref name=lemanske>{{cite journal |author=Lemanske RF, Busse WW |title=Asthma: clinical expression and molecular mechanisms |journal=J. Allergy Clin. Immunol. |volume=125 |issue=2 Suppl 2 |pages=S95–102 |year=2010 |month=February |pmid=20176271 |pmc=2853245 |doi=10.1016/j.jaci.2009.10.047 |url=}}</ref> |
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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]] or [[spirometer]], and the following diagnostic criteria are used by the [[British Thoracic Society]]:<ref>{{cite journal |author=Pinnock H, Shah R |title=Asthma |journal=BMJ |volume=334 |issue=7598 |pages=847–50 |year=2007 |pmid=17446617 |doi=10.1136/bmj.39140.634896.BE |pmc=1853223}}</ref> |
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*≥20% difference on at least three days in a week for at least two weeks; |
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*≥20% improvement of peak flow following treatment, for example: |
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**10 minutes of inhaled β-agonist (e.g., [[salbutamol]]); |
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**six weeks of inhaled [[corticosteroid]] (e.g., [[beclometasone dipropionate|beclometasone]]); |
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**14 days of 30 mg [[prednisolone]]. |
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*≥20% decrease in peak flow following exposure to a trigger (e.g., exercise). |
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In contrast, the US National Asthma Education and Prevention Program (NAEPP) uses a ‘symptom patterns’ approach.<ref name=naepp>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</ref> 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.<ref name=naepp/><ref name="Tippets1">{{cite journal |author=Tippets B, Guilbert TW |title=Managing Asthma in Children: Part 1: Making the Diagnosis, Assessing Severity |journal=Consultant for Pediatricians|volume=8 |issue=5 |year=2009 |url=http://www.consultantlive.com/asthma/article/10162/1414747}}</ref> 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.<ref name=naepp/> Spirometry is needed to establish a diagnosis of asthma.<ref name=naepp/> |
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*Wheezing—high-pitched whistling sounds when breathing out—especially in children. (Lack of wheezing and a normal chest examination do not exclude asthma.) |
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*history of any of the following: |
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**Cough, worse particularly at night |
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**Recurrent wheeze |
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**Recurrent difficulty in breathing |
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**Recurrent chest tightness |
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*Symptoms occur or worsen in the presence of: |
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**Exercise |
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**Viral infection |
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**Animals with fur or hair |
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**House-dust mites (in mattresses, pillows, upholstered furniture, carpets) |
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**Mold |
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**Smoke (tobacco, wood) |
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**Pollen |
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**Changes in weather |
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**Strong emotional expression (laughing or crying hard) |
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**Airborne chemicals or dusts |
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**Menstrual cycles |
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*Symptoms occur or worsen at night, awakening the patient |
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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.<ref name="Sapp">{{cite journal |author=Sapp J and Niven AS |title=Making the most of pulmonary function testing in the diagnosis of asthma |journal=Journal of Respiratory Diseases |date=April 7, 2008 |url=http://www.consultantlive.com/asthma/article/1145425/1404762}}</ref> 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.<ref name="Sapp" /> 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.<ref>{{cite web |title='Be in control' pack |url=http://www.asthma.org.uk/document.rm?id=29 |publisher=Asthma UK |format=PDF |accessdate=2007-11-19}}</ref> |
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===Differential diagnosis=== |
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Differential diagnoses include:<ref name=naepp/> |
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*Infants and Children |
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**Upper airway diseases |
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***Allergic rhinitis and sinusitis |
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**Obstructions involving large airways |
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*** Foreign body in trachea or bronchus |
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*** Vocal cord dysfunction |
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***Vascular rings or laryngeal webs |
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***Laryngotracheomalacia, tracheal stenosis, or bronchostenosis |
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***Enlarged lymph nodes or tumor |
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**Obstructions involving small airways |
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***Viral bronchiolitis or obliterative bronchiolitis |
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***Cystic fibrosis |
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*** Bronchopulmonary dysplasia |
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*** Heart disease |
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**Other causes |
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***Recurrent cough not due to asthma |
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***Aspiration from swallowing mechanism dysfunction or gastroesophageal reflux |
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***Medication induced |
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*Adults |
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**COPD (e.g., chronic bronchitis or emphysema) |
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** Congestive heart failure |
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**Pulmonary embolism |
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** Mechanical obstruction of the airways (benign and malignant tumors) |
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**Pulmonary infiltration with eosinophilia |
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** Cough secondary to drugs (e.g., angiotensin-converting enzyme (ACE) inhibitors) |
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**Vocal cord dysfunction |
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Before diagnosing asthma, [[differential diagnosis|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 blocker|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.<ref>{{cite journal |author=deShazo RD and Stupko JE|title=Diagnosing asthma in seniors: An algorithmic approach|journal=Journal of Respiratory Diseases |date=October 1, 2008 |url=http://www.consultantlive.com/asthma/article/1145425/1405157}}</ref> |
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====Chronic Obstructive Pulmonary Disease==== |
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[[Chronic obstructive pulmonary disease]] can coexist with asthma and can occur as a complication of chronic asthma. After the age of 65 most people with obstructive airway disease will have asthma and COPD. In this setting, COPD can be differentiated by increased airway neutrophils, abnormally increased wall thickness, and increased smooth muscle in the bronchi. However, this level of investigation is not performed due to COPD and asthma sharing similar principles of management: corticosteroids, long acting beta agonists, and smoking cessation.<ref name=Gibson>{{cite journal |author=Gibson PG, McDonald VM, Marks GB |title=Asthma in older adults |journal=Lancet |volume=376 |issue=9743 |pages=803–13 |year=2010 |month=September |pmid=20816547 |doi=10.1016/S0140-6736(10)61087-2 |url=}}</ref> It closely resembles asthma in symptoms, 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]].<ref name="Hargreave">{{cite journal | last=Hargreave | first=FE | coauthors=Parameswaran K | title=Asthma, COPD and bronchitis are just components of airway disease | journal=European Respiratory Journal | volume=28 | issue=2 | pages=264–267 | month=August | year=2006 | url=http://erj.ersjournals.com/cgi/content/full/28/2/264 | pmid=16880365 | doi=10.1183/09031936.06.00056106 }}</ref><ref name="Applied Therapeutics 2009">Diaz, P. Knoell. "Applied Therapeutics: The Clinical Use of Drugs, 9th Edition" Philadelphia: Lippincott Williams & Wilkins, 2009. Chapter 23 (Chronic Obstructive Pulmonary Disease)</ref> |
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====Others==== |
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The term "atopy" was coined to describe this triad of [[atopic eczema]], [[allergic rhinitis]] and asthma.<ref name="Bolognia"/> |
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[[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|date=May 2010}} |
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==Prevention== |
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The evidence for the effectiveness of measures to prevent the development of asthma is weak.<ref name="nhlbi2007p184"/> Ones which show some promise include: limiting smoke exposure both [[in utero]] and after delivery, [[breastfeeding]], increased exposure to respiratory infection per the [[hygiene hypothesis]] (such as in those who attend daycare or are from large families).<ref name="nhlbi2007p184"/> |
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==Management== |
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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.<ref>{{cite journal |author=Tippets B Guilbert TW|title=Managing Asthma in Children, Part 2: Achieving and Maintaining Control |journal=Consultant for Pediatricians |volume=8 |issue=6 |year=2009 |url=http://pediatrics.consultantlive.com/display/article/1145470/1418640}}</ref> |
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The most effective treatment for asthma is identifying triggers, such as [[Health effects of tobacco smoking|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.<ref>NHBLI 2007, p.213</ref><ref>{{cite web |url=http://www.sign.ac.uk/pdf/sign101.pdf |title=British Guideline on the Management of Asthma|format=PDF|publisher=Scottish Intercollegiate Guidelines Network|year=2008 |work= |accessdate=2008-08-04}}</ref> |
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[[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.<ref name=naepp/> |
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===Lifestyle modification=== |
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Avoidance of triggers is a key component of improving control and preventing attacks. The most common triggers include: [[allergen]]s, smoke (tobacco and other), air pollution, [[Beta_blocker#Non-selective_agents|non selective beta-blockers]], and sulfite-containing foods.<ref name=naepp/><ref name=thomson>{{cite journal |author=Thomson NC, Spears M |title=The influence of smoking on the treatment response in patients with asthma |journal=Curr Opin Allergy Clin Immunol |volume=5 |issue=1 |pages=57–63 |year=2005 |pmid=15643345 |doi=10.1097/00130832-200502000-00011}}</ref> |
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===Medications=== |
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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.<ref>NHLBI 2007,p.213</ref> |
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;Fast acting |
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[[Image:Salbutamol2.JPG|thumb|[[Salbutamol]] metered dose inhaler commonly used to treat asthma attacks.]] |
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*Short acting [[beta2-adrenergic agonist|beta<sub>2</sub>-adrenoceptor agonists]] (SABA), such as [[salbutamol]] (''albuterol'' [[United States Adopted Name|USAN]]) are the first line treatment for asthma symptoms.<ref name="nhlbi2007p214" /> |
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*[[Anticholinergic]] medications, such as [[ipratropium|ipratropium bromide]] provide addition benefit when used in combination with SABA in those with moderate or severe symptoms.<ref name="nhlbi2007p214" /> Anticholinergic bronchodilators can also be used if a person cannot tolerate a SABA.<ref name="Self, Timothy 2009"/> |
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* Older, less selective [[adrenergic receptor|adrenergic agonists]], such as inhaled [[epinephrine]], have similar efficacy to SABAs.<ref name=Rodrigo>{{cite journal |author=Rodrigo GJ, Nannini LJ |title=Comparison between nebulized adrenaline and beta2 agonists for the treatment of acute asthma. A meta-analysis of randomized trials |journal=Am J Emerg Med |volume=24 |issue=2 |pages=217–22 |year=2006 |pmid=16490653 |doi=10.1016/j.ajem.2005.10.008}}</ref> They are however not recommended due to concerns regarding excessive cardiac stimulation.<ref name="nhlbi2007p351">[[#NHLBI|NHLBI 2007]] p.351</ref> |
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;Long term control |
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[[Image:Fluticasone.JPG|thumb|[[Fluticasone propionate]] metered dose inhaler commonly used for long term control.]] |
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* [[Glucocorticoid]]s are the most effective treatment available for long term control.<ref name="nhlbi2007p213"/> Inhaled forms are usually used except in the case of severe persistent disease, in which oral steroids may be needed.<ref name="nhlbi2007p213"/> Inhaled formulations may be used once or twice daily, depending on the severity of symptoms.<ref name="nhlbi2007p218"/> |
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*[[Long acting beta-adrenoceptor agonist]]s (LABA) 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.<ref name="Fanta2009" /><ref>{{cite journal |author=Cates CJ, Lasserson TJ, Jaeschke R |title=Regular treatment with salmeterol and inhaled steroids for chronic asthma: serious adverse events |journal=Cochrane Database Syst Rev |volume= |issue=3 |pages=CD006922 |year=2009 |pmid=19588410 |doi=10.1002/14651858.CD006922.pub2 |url=}}</ref><ref>{{cite journal |author=Cates CJ, Cates MJ |title=Regular treatment with salmeterol for chronic asthma: serious adverse events |journal=Cochrane Database Syst Rev |volume= |issue=3 |pages=CD006363 |year=2008 |pmid=18646149 |doi=10.1002/14651858.CD006363.pub2 |url=}}</ref> 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.<ref>{{cite web |url=http://news.yahoo.com/s/nm/20081205/hl_nm/us_drugs_asthma_1 |title=FDA sees asthma drug risks — Yahoo! News |work= |accessdate=December 5, 2008}} {{Dead link|date=September 2010|bot=H3llBot}}</ref> |
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*[[Leukotriene antagonist]]s ( such as [[zafirlukast]]) are an alternative to inhaled glucocorticoids, but are not preferred. They may also be used in addition to inhaled glucocorticoids but in this role are second line to LABA.<ref name="nhlbi2007p213"/> |
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*[[Mast cell stabilizer]]s (such as [[cromolyn sodium]]) are another non-preferred alternative to glucocorticoids.<ref name="nhlbi2007p213"/> |
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;Delivery methods |
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Medications are typically provided as [[metered-dose inhaler]]s (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.<ref name="nhlbi2007p250">[[#NHLBI|NHLBI 2007]] p.250</ref> |
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;Safety and adverse effects |
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Long-term use of glucocorticoids carries a significant potential for adverse effects. The incidence of [[cataract]]s is increased in people undergoing treatment for asthma with corticosteroids, due to altered regulation of lens epithelial cells.<ref name="Wang 2009">{{cite journal |author=Wang JJ, Rochtchina E, Tan AG, Cumming RG, Leeder SR, Mitchell P |title=Use of inhaled and oral corticosteroids and the long-term risk of cataract |journal=Ophthalmology |volume=116|issue=4 |pages=652–7 |year=2009 |month=April|pmid=19243828 |doi=10.1016/j.ophtha.2008.12.001}}</ref> The incidence of [[osteoporosis]] is also increased, due to changes in[[bone remodeling]].<ref>{{cite journal |author=Dahl R |title=Systemic side effects of inhaled corticosteroids in patients with asthma |journal=Respir Med |volume=100 |issue=8 |pages=1307–17 |year=2006 |month=August |pmid=16412623|doi=10.1016/j.rmed.2005.11.020}}</ref><ref>{{cite journal |doi=10.1007/s007740070008 |author=Nishimura J, Ikuyama S |title=Glucocorticoid-induced osteoporosis: pathogenesis and management |journal=J Bone Miner Metab |volume=18 |issue=6 |pages=350–2 |year=2000|pmid=11052469}}</ref> |
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<!--add information on LABA safety--> |
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===Other=== |
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When an asthma attack is unresponsive to usual medications, other options are available for emergency management. |
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* [[Oxygen]] is used to alleviate [[hypoxia (medical)|hypoxia]] if [[oxygen saturation|saturations]] fall below 92%.<ref name=rodrigo>{{cite journal |author=Rodrigo GJ, Rodrigo C, Hall JB |title=Acute asthma in adults: a review |journal=Chest |volume=125 |issue=3 |pages=1081–102 |year=2004 |pmid=15006973| doi = 10.1378/chest.125.3.1081}}</ref> |
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* [[Magnesium sulfate]] intravenous treatment has been shown to provide a bronchodilating effect when used in addition to other treatment in severe acute asthma attacks.<ref>10.1378/chest.122.2.396 CHEST August 2002 vol. 122 no. 2 396-398</ref><ref name="nhlbi2007p373"/> |
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* [[Heliox]], a mixture of helium and oxygen, may also be considered in severe unresponsive cases.<ref name="nhlbi2007p373"/> |
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* Intravenous salbutamol is not supported by available evidence and is thus used only in extreme cases.<ref name=rodrigo/> |
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* [[Methylxanthines]] (such as [[theophylline]]) were once widely used, but do not add significantly to the effects of inhaled beta-agonists.<ref name=rodrigo/> |
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* The dissociative anesthetic [[ketamine]] is theoretically useful if [[intubation]] and [[mechanical ventilation]] is needed in people who are approaching respiratory arrest; however, there is no evidence from clinical trials to support this.<ref name="nhlbi2007p399"/> |
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===Complementary medicine=== |
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Many asthma patients, like those who suffer from other chronic disorders, use [[alternative medicine|alternative treatments]]; surveys show that roughly 50% of asthma patients use some form of unconventional therapy.<ref name=blanc>{{cite journal |author=Blanc PD, Trupin L, Earnest G, Katz PP, Yelin EH, Eisner MD |title=Alternative therapies among adults with a reported diagnosis of asthma or rhinosinusitis : data from a population-based survey |journal=Chest |volume=120 |issue=5 |pages=1461–7 |year=2001 |pmid=11713120| doi = 10.1378/chest.120.5.1461}}</ref><ref name=shenfield>{{cite journal |author=Shenfield G, Lim E, Allen H |title=Survey of the use of complementary medicines and therapies in children with asthma |journal=J Paediatr Child Health |volume=38 |issue=3 |pages=252–7 |year=2002 |pmid=12047692| doi = 10.1046/j.1440-1754.2002.00770.x}}</ref> There is little data to support the effectiveness of most of these therapies. Evidence is insufficient to support the usage of Vitamin C.<ref>{{cite journal | unused_data=coauthorsRowe BH, Arnold E | last=Kaur | first=B | title=Vitamin C supplementation for asthma | journal=Cochrane Database Syst Rev | issue=1 | pages=CD000993 | year=2009 | pmid=19160185 | doi=10.1002/14651858.CD000993.pub3 | coauthors=Rowe BH, Arnold E }}</ref> [[Acupuncture]] is not recommended for the treatment as there is insufficient evidence to support its use.<ref name="nhlbi2007p240"/><ref name=mccartney>{{cite journal |author=McCarney RW, Brinkhaus B, Lasserson TJ, Linde K |title=Acupuncture for chronic asthma |journal=Cochrane Database Syst Rev |volume= |issue=1 |pages=CD000008 |year=2004 |pmid=14973944 |doi=10.1002/14651858.CD000008.pub2}}</ref> [[Air ioniser]]s show no evidence that they improve asthma symptoms or benefit lung function; this applied equally to positive and negative ion generators.<ref name=blackhall>{{cite journal |author=Blackhall K, Appleton S, Cates CJ |title=Ionisers for chronic asthma |journal=Cochrane Database Syst Rev |volume= |issue=3 |pages=CD002986 |year=2003 |pmid=12917939 |doi=10.1002/14651858.CD002986}}</ref> |
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Dust mite control measures, including air filtration, chemicals to kill mites, vacuuming, mattress covers and others methods had no effect on asthma symptoms.<ref name="Gøtzsche">{{cite journal |author=[[Peter C. Gøtzsche|PC Gøtzsche]], HK Johansen |title=House dust mite control measures for asthma|journal=Cochrane Database Syst Rev |volume= |issue=2 |pages=CD001187 |year=2008 |doi=10.1002/14651858.CD001187.pub3 |pmid=18425868}}</ref> 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).<ref>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.</ref> Washing laundry/rugs in hot water was also found to improve control of allergens.<ref name="Self, Timothy 2009"/> |
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A study of "manual therapies" for asthma, including [[osteopathy|osteopathic]], [[chiropractic]], [[physical therapy|physiotherapeutic]] and [[respiratory therapy|respiratory therapeutic]] manoeuvres, found there is insufficient evidence to support or refute their use in treating.<ref name=hondras>{{cite journal |author=Hondras MA, Linde K, Jones AP |title=Manual therapy for asthma |journal=Cochrane Database Syst Rev |volume= |issue=2 |pages=CD001002 |year=2005 |pmid=15846609 |doi=10.1002/14651858.CD001002.pub2}}</ref> The [[Buteyko breathing technique]] for controlling hyperventilation may result in a reduction in medications use however does not have any effect on lung function.<ref name="SIGN">{{cite web |url=http://www.sign.ac.uk/pdf/sign101.pdf |title=www.sign.ac.uk |format=PDF |page=37 |date=May 2008}}</ref> Thus an expert panel felt that evidence was insufficient to support its use.<ref name="nhlbi2007p240"/> |
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==Prognosis== |
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The prognosis for asthma is good, especially for children with mild disease.<ref name="Tippets1" />{{Failed verification|date=May 2010}} Of asthma diagnosed during childhood, 54% of cases will no longer carry the diagnosis after a decade.{{Citation needed|date=May 2010}} 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.<ref name=Maddox>{{cite journal |author=Maddox L, Schwartz DA |title=The pathophysiology of asthma |journal=Annu. Rev. Med. |volume=53 |issue= |pages=477–98 |year=2002 |pmid=11818486 |doi=10.1146/annurev.med.53.082901.103921}}</ref> 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.<ref name=beckett>{{cite journal |author=Beckett PA, Howarth PH |title=Pharmacotherapy and airway remodelling in asthma? |journal=Thorax |volume=58 |issue=2 |pages=163–74 |year=2003 |pmid=12554904| doi = 10.1136/thorax.58.2.163 |pmc=1746582}}</ref> |
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For those who continue to suffer from mild symptoms, corticosteroids can help most to live their lives with few [[disability|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|date=May 2010}} Though they (delayed) also had good functional control of asthma, they were observed to exhibit slightly less optimal disease control and more signs of airway inflammation.{{Citation needed|date=May 2010}} |
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Asthma mortality has decreased over the last few decades due to better recognition and improvement in care.<ref>NHBLI 2007, p.1</ref> |
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==Epidemiology== |
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[[File:Asthma world map - DALY - WHO2004.svg|thumb|350px|[[Disability-adjusted life year]] for asthma per 100,000 inhabitants in 2004.<ref>{{cite web |url=http://www.who.int/healthinfo/global_burden_disease/estimates_country/en/index.html |title=WHO Disease and injury country estimates |year=2009 |work=World Health Organization |accessdate=November 11, 2009}}</ref><div class="references-small" style="-moz-column-count:3; column-count:3;"> |
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{{legend|#b3b3b3|no data}} |
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{{legend|#ffff65|<100}} |
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{{legend|#fff200|100–150}} |
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{{legend|#ffdc00|150–200}} |
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{{legend|#ffc600|200–250}} |
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{{legend|#ffb000|250–300}} |
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{{legend|#ff9a00|300–350}} |
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{{legend|#ff8400|350–400}} |
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{{legend|#ff6e00|400–450}} |
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{{legend|#ff5800|450–500}} |
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{{legend|#ff4200|500–550}} |
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{{legend|#ff2c00|550–600}} |
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{{legend|#cb0000|>600}} |
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</div>]] |
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[[File:asthma prevalence.png|thumb|right|The [[prevalence]] of childhood asthma in the United States has increased since 1980, especially in younger children.]] |
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As of 2009, 300 million people worldwide were affected by asthma leading to approximately 250,000 deaths per year.<ref name="gina2009p2" /><ref name="Fanta2009" /><ref name="WHO2009" /><ref>{{cite journal |author=Braman SS |title=The global burden of asthma |journal=Chest |volume=130 |issue=1 Suppl |pages=4S–12S |year=2006 |month=July |pmid=16840363 |doi=10.1378/chest.130.1_suppl.4S |url=}}</ref> |
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It is estimated that asthma has a 7-10% prevalence worldwide.<ref name="NEJM"/> As of 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 country|developed]] and [[western world|westernized]] countries having higher rates of asthma.<ref name="ISAAC">{{cite journal |author= |title=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 |journal=Lancet |volume=351 |issue=9111 |pages=1225–32 |year=1998 |month=April |pmid=9643741 |doi= |url=}}</ref> 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.<ref name=Gold /> Mortality however is most common in low to middle income countries,<ref>{{cite web |author=World Health Organization |authorlink=World Health Organization |title=WHO: Asthma |url=http://www.who.int/mediacentre/factsheets/fs307/en/ |accessdate=2007-12-29}}</ref> while 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.<ref name="ISAAC" />{{Update after|2010|11}} |
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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|date=May 2010}} In the U.S., urban residents, Hispanics, and African Americans are affected more than the population as a whole.{{Citation needed|date=May 2010}} Striking increases in asthma prevalence have been observed in populations migrating from a rural environment to an urban one,<ref>{{cite journal |author=Ng'ang'a LW, Odhiambo JA, Mungai MW, ''et al.'' |title=Prevalence of exercise induced bronchospasm in Kenyan school children: An urban-rural comparison |journal=[[Thorax (journal)|Thorax]] |year=1998 |month=November |volume=53 |issue=11 |pages=919–26 |pmid=10193388 |pmc=1745121 |doi=10.1136/thx.53.11.919}}</ref>{{Update after|2010|11}} or from a third-world country to Westernized one.<ref>{{cite journal |author=Waite DA, Eyles EF, Tonkin SL, O'Donnell TV |title=Asthma prevalence in Tokelauan children in two environments |journal=Clin Allergy |year=1980 |month=January |volume=10 |issue=1 |pages=71–5 |pmid=7363447 |doi=10.1111/j.1365-2222.1980.tb02082.x}}</ref>{{Update after|2010|11}} |
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Asthma affects approximately 7% of the population of the United States<ref name="Fanta2009" /> and 5% of people in the United Kingdom.<ref name="Anderson2007" /> Asthma causes 4,210 deaths per year in the United States.<ref name="NEJM">{{cite journal |author=Lazarus SC |title=Clinical practice. Emergency treatment of asthma |journal=N. Engl. J. Med. |volume=363 |issue=8 |pages=755–64 |year=2010 |month=August |pmid=20818877 |doi=10.1056/NEJMcp1003469 |url= |accessdate=2010-10-26}}</ref><ref name="Getahun2005" /> In 2005 in the United States asthma affected more than 22 million people including 6 million children.<ref name="NHLBI 2007, p.1">NHLBI 2007, p.1</ref> It accounted for nearly 1/2 million hospitalizations<ref name="NHLBI 2007, p.1"/>{{When|date=November 2010}}. More boys have asthma than girls, but more women have it than men.<ref>{{cite web |author=Hayden, Merrill |title=Asthma Guide |url=http://www.webmd.com/asthma/guide/how-we-breath |date=19 September 2009 }}</ref> Of all children, [[African Americans]] and [[Latinos]] who live in cities are more at risk for developing asthma.{{Citation needed|date=May 2010}} 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|date=May 2010}} In some Latino neighborhoods, as many as one in three children has been found to have asthma.<ref name="Corbett, Sara 2005">{{cite news |author=Corbett, Sara |title=The Asthma Trap |date=March/April 2005 |work=Mother Jones |url=http://motherjones.com/print/16323}}</ref> |
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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.<ref name="Simpson2010">{{cite journal |author= Simpson CR, Sheikh A |title= Trends in the epidemiology of asthma in England: a national study of 333,294 patients |journal=J R Soc Med |volume=103| pages=98–106 | year=2010 | pmid=20200181 | doi=10.1258/jrsm.2009.090348 |issue= 3 }}</ref> |
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The frequency of atopic dermatitis, asthma, urticaria and allergic contact dermatitis has been found to be lower in [[psoriasis|psoriatic]] patients.<ref name="Bolognia"/> |
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===Increasing frequency=== |
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Rates of asthma have increased significantly between the 1960s and 2008.<ref>{{cite journal |author=Grant EN, Wagner R, Weiss KB |title=Observations on emerging patterns of asthma in our society |journal=[[J Allergy Clin Immunol]] |year=1999 |month=August |volume=104 |pages=S1–S9 |pmid=10452783 |doi=10.1016/S0091-6749(99)70268-X |issue=2 Pt 2}}</ref><ref>{{cite journal |author=Anandan C, Nurmatov U, van Schayck OC, Sheikh A |title=Is the prevalence of asthma declining? Systematic review of epidemiological studies |journal=Allergy |volume=65 |issue=2 |pages=152–67 |year=2010 |month=February |pmid=19912154 |doi=10.1111/j.1398-9995.2009.02244.x |url=}}</ref> 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,<ref name=WHO>{{cite web |author=World Health Organization |authorlink=World Health Organization |title=Global surveillance, prevention and control of chronic respiratory diseases: a comprehensive approach |format=PDF |pages=15–20, 49 |year=2007 |url=http://www.who.int/gard/publications/GARD_Manual/en/index.html |accessdate=2010-05-14 |isbn=9789241563468 }}</ref> compared with just 2% some 25–30 years ago. |
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===Variability=== |
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Asthma prevalence in the US is higher than in most other countries in the world, but varies drastically between diverse US populations.<ref name=Gold /> In the US, asthma prevalence is highest in Puerto Ricans, African Americans, Filipinos, Irish Americans, and Native Hawaiians, and lowest in Mexicans and Koreans.<ref>{{cite journal |author=Lara M, Akinbami L, Flores G,Morgenstern H |title=Heterogeneity of childhood asthma among Hispanic children: Puerto Rican children bear a disproportionate burden |journal=Pediatrics |volume=117 |issue=1 |pages=43–53 |year=2006 |pmid=16396859 |doi=10.1542/peds.2004-1714}}</ref><ref>{{cite journal |author=Davis AM, Kreutzer R, Lipsett M, King G,Shaikh N |title=Asthma prevalence in Hispanic and Asian American ethnic subgroups: results from the California Healthy Kids Survey |journal=Pediatrics |volume=118 |issue=2 |pages=e363–70 |year=2006 |pmid=16882779 |doi=10.1542/peds.2005-2687}}</ref><ref>{{cite journal |author=Johnson DB, Oyama N, LeMarchand L,Wilkens L |title=Native Hawaiians mortality, morbidity, and lifestyle: comparing data from 1982, 1990, and 2000 |journal=Pac Health Dialog |volume=11 |issue=2 |pages=120–30 |year=2004 |pmid=16281689}}</ref> Mortality rates follow similar trends, and response to [[salbutamol]] is lower in Puerto Ricans than in African Americans or Mexicans.<ref>{{cite journal |author=Naqvi M, Thyne S, Choudhry S "et al." |title=Ethnic-specific differences in bronchodilator responsiveness among african americans, puerto ricans, and mexicans with asthma |journal=J Asthma |volume=44| issue=8 |pages=639–48 |year=2007 |pmid=17943575 |doi=10.1080/02770900701554441}}</ref><ref>{{cite journal |author=Burchard EG, Avila PC, Nazario S "et al." |title=Lower bronchodilator responsiveness in Puerto Rican than in Mexican subjects with asthma |journal=Am J Respir Crit Care Med |volume=169 |issue=3 |pages=386–92 |year=2004 |pmid=14617512 |doi=10.1164/rccm.200309-1293OC}}</ref> 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. |
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Asthma prevalence also differs between populations of the same ethnicity who are born and live in different places.<ref>{{cite journal |author=Gold DR,Acevedo-Garcia D| title=Immigration to the United States and acculturation as risk factors for asthma and allergy| journal=J Allergy Clin Immunol |volume=116 |issue=1 |pages=38–41| year=2005| pmid=15990770 |doi=10.1016/j.jaci.2005.04.033 |last2=Acevedo-Garcia |first2=D}}</ref> US-born Mexican populations, for example, have higher asthma rates than non-US born Mexican populations that are living in the US.<ref>{{cite journal |author=Eldeirawi KM,Persky VW| title=Associations of acculturation and country of birth with asthma and wheezing in Mexican American youths |journal=J Asthma |volume=43 |issue=4 |pages=279–86 |year=2006 |pmid=16809241 |doi=10.1080/0277090060022869 |last2=Persky |first2=VW}}</ref> |
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There is no correlation between asthma and gender in children. More adult women are diagnosed with asthma than adult men, but this does not necessarily mean that more adult women have asthma.<ref>{{cite journal |author=Bush A, Menzies-Gow A |title=Phenotypic differences between pediatric and adult asthma |journal=Proc Am Thorac Soc |volume=6 |issue=8 |pages=712–9 |year=2009 |month=December |pmid=20008882 |doi=10.1513/pats.200906-046DP |url=}}</ref> |
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==History== |
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{{Expand section|date=December 2008}} |
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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 illness]]es. Its [[Etiology|aetiology]] was considered to be psychological, with treatment often based on psychoanalysis and other '[[talking cure]]s'.<ref name="pmid16185365"/> 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.<ref name="pmid16185365">{{cite journal |author=Opolski M, Wilson I |title=Asthma and depression: a pragmatic review of the literature and recommendations for future research |journal=Clin Pract Epidemol Ment Health |volume=1 |page=18 |year=2005 |month=September |pmid=16185365 |pmc=1253523 |doi=10.1186/1745-0179-1-18 }}</ref> |
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==Research== |
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* The [[University of Maryland School of Medicine]] announced in 2010 that bitter taste receptors had been discovered on smooth muscle in human lung [[bronchi]]. These smooth muscles control airway contraction and dilation - contrary to expectation, bitter substances such as [[quinine]] or [[chloroquine]] opened contracted airways, offering new insight into asthma.<ref>http://www.physorg.com/news/2010-10-discovery-receptors-lungs-people-asthma.html</ref> |
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==References== |
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{{Reflist|colwidth=30em|refs= |
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<ref name="nhlbi2007p11-12">[[#NHLBI|NHLBI 2007]] p.11–12</ref> |
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<ref name="bts2009p3">[[#BTS|BTS 2009]] p.3</ref> |
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<ref name="nhlbi2007p184">[[#NHLBI|NHLBI 2007]] p.184-185</ref> |
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<ref name="nhlbi2007p213">[[#NHLBI|NHLBI 2007]] p.560</ref> |
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<ref name="nhlbi2007p214">[[#NHLBI|NHLBI 2007]] p.214</ref> |
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<ref name="nhlbi2007p218">[[#NHLBI|NHLBI 2007]] p.218</ref> |
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<ref name="nhlbi2007p240">[[#NHLBI|NHLBI 2007]] p.240</ref> |
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<ref name="nhlbi2007p373">[[#NHLBI|NHLBI 2007]] p.373</ref> |
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<ref name="nhlbi2007p399">[[#NHLBI|NHLBI 2007]] p.399</ref> |
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<ref name="nhlbi2007p169">[[#NHLBI|NHLBI 2007]] p.169–172</ref> |
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<ref name="gina2009p69">[[#GINA|GINA 2009]] p.69</ref> |
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<ref name="Anderson2007">{{cite journal | last=Anderson | first=HR | coauthors=Gupta R, Strachan DP, Limb ES | title=50 years of asthma: UK trends from 1955 to 2004 | journal=Thorax | volume=62 | issue=1 | pages=85–90 | month=January | year=2007 | url=http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2111282/pdf/85.pdf | pmid=17189533 | doi=10.1136/thx.2006.066407 | pmc=2111282 }}</ref> |
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<ref name="WHO2009">{{cite web |title=World Health Organization Fact Sheet Fact sheet No 307: Asthma |year=2009 |url=http://www.who.int/mediacentre/factsheets/fs307/en/print.html |accessdate=2 September 2010}}</ref> |
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<ref name="Fanta2009">{{cite journal |author=Fanta CH |title=Asthma |journal=New England Journal of Medicine |volume=360 |issue=10 |pages=1002–14 |year=2009 |month=March |pmid=19264689 |doi=10.1056/NEJMra0804579 }}</ref> |
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<ref name="Getahun2005">{{cite journal |author=Getahun D, Demissie K, Rhoads GG |title=Recent trends in asthma hospitalization and mortality in the United States |journal=Journal of asthma |volume=42 |issue=5 |pages=373–8 |year=2005 |pmid=16036412 |doi=10.1081/JAS-62995 }}</ref> |
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<ref name="gina2009p2">[[#GINA|GINA 2009]] p.2</ref> |
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<ref name="Yawn2008">{{cite journal | last=Yawn | first=BP | title=Factors accounting for asthma variability: achieving optimal symptom control for individual patients | journal=Primary Care Respiratory Journal | volume=17 | issue=3 | pages=138–147 | month=September | year=2008 | url=http://www.thepcrj.org/journ/vol17/17_3_138_147.pdf | pmid=18264646 | doi=10.3132/pcrj.2008.00004 }}</ref> |
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<ref name="RobbinsCotran2010">{{cite book |last=Kumar |first=Vinay |last2=Abbas |first2=Abul K |last3=Fausto |first3=Nelson |last4=Aster |first4=Jon |title=Robbins and Cotran Pathologic Basis of Disease |publisher=Saunders |edition=8th |year=2010 |isbn=9781416031215 |page=688}}</ref> |
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<ref name="Moore2010">{{cite journal |author=Moore WC, Pascual RM |title=Update in asthma 2009 |journal=American journal of respiratory and critical care medicine |volume=181 |issue=11 |pages=1181–7 |year=2010 |month=June |pmid=20516492 |doi=10.1164/rccm.201003-0321UP}}</ref> |
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<ref name="Delacourt2004">{{cite journal |last=Delacourt |first=C |title=Bronchial changes in untreated asthma |journal=Archives de Pédiatrie |volume=11 |issue=Suppl. 2 |pages=71s–73s |month=June |year=2004 | pmid=15301800 }}</ref> |
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<ref name="Schiffman2009">{{cite web |url=http://www.medicinenet.com/chronic_obstructive_pulmonary_disease_copd/article.htm |title=Chronic Obstructive Pulmonary Disease |first=George |last=Schiffman |date=18 December 2009 |publisher=MedicineNet |accessdate=2 September 2010}}</ref> |
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<ref name="BTS54">[[#BTS|BTS 2009]] p.54</ref> |
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<ref name="gina2009p9">[[#GINA|GINA 2009]] p.8–9</ref> |
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<ref name="bts2009p12">[[#BTS|BTS 2009]] p.12</ref> |
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<ref name="Mason2005">{{cite book |first1=Robert J |last1=Mason |first2=V Courtney |last2=Broaddus |first3=John F |last3=Murray |first4=Jay A |last4=Nadel |title=Murray and Nadel's Textbook of Respiratory Medicine |publisher=Elsevier |edition=4th |year=2005 |chapter=Asthma |isbn=978-0721603278}}</ref> |
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<ref name="Barnes">{{cite book |last=Barnes |first=PJ |chapter=Asthma |title=Harrison's Principles of Internal Medicine |editor1-last=Fauci |editor1-first=Anthony S |editor2-last=Braunwald |editor2-first=E, |editor3-last=Kasper |editor3-first=DL |location=New York |publisher=McGraw-Hill |year=2008 |edition=17th |isbn=9780071466332 |pages=1596–1607}}</ref> |
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<ref name="AbuHilal2010">{{cite journal |last1=Abu-Hilal |first1=MA |last2=Mookadam |first2=F |title=Pulsus paradoxus; historical and clinical perspectives |journal=International Journal of Cardiology |volume=138 |issue=3 |pages=229–32 |year=2010 |month=February |pmid=19464740 |doi=10.1016/j.ijcard.2009.04.045}}</ref> |
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<ref name="Werner2001">{{cite journal |last=Werner |first=HA |title=Status asthmaticus in children: a review |journal=Chest |volume=119 |issue=6 |pages=1596–1607 |year=2001 |month=June |url=http://chestjournal.chestpubs.org/content/119/6/1913.long |pmid=11399724 |doi=10.1378/chest.119.6.1913 }}</ref> |
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}} |
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;Bibliography |
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{{Refbegin}} |
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*{{cite web | url=http://www.nhlbi.nih.gov/guidelines/asthma/asthgdln.pdf | title=Expert Panel Report 3: Guidelines for the Diagnosis and Management of Asthma | format=PDF | work=[[National Heart Lung and Blood Institute]] | year=2007 |ref=NHLBI}} |
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*{{cite web | url=http://www.brit-thoracic.org.uk/Portals/0/Clinical%20Information/Asthma/Guidelines/sign101%20revised%20June%2009.pdf | title=British Guideline on the Management of Asthma | format=pdf | work=[[British Thoracic Society]] | year=2009 |ref=BTS}} |
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*{{cite web | url=http://www.ginasthma.org/Guidelineitem.asp??l1=2&l2=1&intId=1561 | title=Global Initiative for Asthma | year=2009 |ref=GINA}} |
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{{Refend}} |
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==External links== |
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*[http://www.who.int/respiratory/asthma/en/ World Health Organization site on asthma] |
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*[http://www.nhlbi.nih.gov/health/public/lung/index.htm#asthma National Heart, Lung, and Blood Institute — Asthma] – U.S. NHLBI Information for Patients and the Public page. |
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*[http://www.nlm.nih.gov/medlineplus/asthma.html MedLinePlus: Asthma] – a U.S. National Library of Medicine page |
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*[http://www.nationalasthma.org.au/cms/index.php Asthma Management Handbook 2006] National Asthma Council Australia |
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*[http://www.ginasthma.org the Global Initiative for Asthma (GINA)] |
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*[http://www.cks.nhs.uk/asthma NHS Guidance for the management of Asthma] |
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*[http://www.nhs.uk/conditions/asthma/Pages/Introduction.aspx Types of Asthma by NHS] |
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*[http://www.childhoodasthma.co.uk Childhood Asthma] |
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*[http://eng.mapofmedicine.com/evidence/map/acute_asthma1.html Acute Asthma care map] Map of Medicine |
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Revision as of 19:14, 9 February 2011
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