|Classification and external resources|
Peak flow meters are used to measure the peak expiratory flow rate, important in both monitoring and diagnosing asthma.
Asthma (from the Greek ἅσθμα, ásthma, "panting") is a common chronic inflammatory disease of the airways characterized by variable and recurring symptoms, reversible airflow obstruction and bronchospasm. Common symptoms include wheezing, coughing, chest tightness, and shortness of breath.
Asthma is thought to be caused by a combination of genetic and environmental factors. Its diagnosis is usually based on the pattern of symptoms, response to therapy over time and spirometry. It is clinically classified according to the frequency of symptoms, forced expiratory volume in one second (FEV1), and peak expiratory flow rate. Asthma may also be classified as atopic (extrinsic) or non-atopic (intrinsic) where atopy refers to a predisposition toward developing type 1 hypersensitivity reactions.
Treatment of acute symptoms is usually with an inhaled short-acting beta-2 agonist (such as salbutamol) and oral corticosteroids. In very severe cases, intravenous corticosteroids, magnesium sulfate, and hospitalization may be required. Symptoms can be prevented by avoiding triggers, such as allergens and irritants, and by the use of inhaled corticosteroids. Long-acting beta agonists (LABA) or leukotriene antagonists may be used in addition to inhaled corticosteroids if asthma symptoms remain uncontrolled. The occurrence of asthma has increased significantly since the 1970s. In 2011, 235–300 million people globally have been diagnosed with asthma, and it caused 250,000 deaths.
Signs and symptoms 1
- Associated conditions 1.1
- Hygiene hypothesis 2.1.1
- Genetic 2.2
- Medical conditions 2.3
- Exacerbation 2.4
- Environmental 2.1
- Pathophysiology 3
- Spirometry 4.1
- Others 4.2
- Asthma exacerbation 4.3.1
- Exercise-induced 4.3.2
- Occupational 4.3.3
- Differential diagnosis 4.4
- Prevention 5
- Lifestyle modification 6.1
- Fast–acting 6.2.1
- Long–term control 6.2.2
- Delivery methods 6.2.3
- Adverse effects 6.2.4
- Others 6.3
- Alternative medicine 6.4
- Prognosis 7
- Epidemiology 8
- Economics 9
- History 10
- Notes 11
- External links 12
Signs and symptoms
The sound of wheezing as heard with a stethoscope.
|Problems playing this file? See .|
Asthma is characterized by recurrent episodes of wheezing, shortness of breath, chest tightness, and coughing. Sputum may be produced from the lung by coughing but is often hard to bring up. During recovery from an attack, it may appear pus-like due to high levels of white blood cells called eosinophils. Symptoms are usually worse at night and in the early morning or in response to exercise or cold air. Some people with asthma rarely experience symptoms, usually in response to triggers, whereas others may have marked and persistent symptoms.
A number of other health conditions occur more frequently in those with asthma, including gastro-esophageal reflux disease (GERD), rhinosinusitis, and obstructive sleep apnea. Psychological disorders are also more common, with anxiety disorders occurring in between 16–52% and mood disorders in 14–41%. However, it is not known if asthma causes psychological problems or if psychological problems lead to asthma.
Asthma is caused by a combination of complex and incompletely understood environmental and genetic interactions. These factors influence both its severity and its responsiveness to treatment. It is believed that the recent increased rates of asthma are due to changing epigenetics (heritable factors other than those related to the DNA sequence) and a changing living environment.
Many environmental factors have been associated with asthma's development and exacerbation including allergens, air pollution, and other environmental chemicals. formaldehyde exposure, for example, has a positive association. Also, phthalates in certain types of PVC are associated with asthma in children and adults. There is an association between acetaminophen (paracetamol) use and asthma. The majority of the evidence does not; however, support a causal role. A 2014 review found that the association disappeared when respiratory infections were taken into account. Use by a mother during pregnancy is also associated with an increased risk. Asthma is associated with exposure to indoor allergens. Common indoor allergens include: dust mites, cockroaches, animal dander, and mold. Efforts to decrease dust mites have been found to be ineffective. Certain viral respiratory infections, such as respiratory syncytial virus and rhinovirus, may increase the risk of developing asthma when acquired as young children. Certain other infections, however, may decrease the risk.
The hygiene hypothesis attempts to explain the increased rates of asthma worldwide as a direct and unintended result of reduced exposure, during childhood, to non-pathogenic bacteria and viruses. It has been proposed that the reduced exposure to bacteria and viruses is due, in part, to increased cleanliness and decreased family size in modern societies. Exposure to bacterial endotoxin in early childhood may prevent the development of asthma, but exposure at an older age may provoke bronchoconstriction. Evidence supporting the hygiene hypothesis includes lower rates of asthma on farms and in households with pets.
Use of antibiotics in early life has been linked to the development of asthma. Also, delivery via caesarean section is associated with an increased risk (estimated at 20–80%) of asthma—this increased risk is attributed to the lack of healthy bacterial colonization that the newborn would have acquired from passage through the birth canal. There is a link between asthma and the degree of affluence.
|Endotoxin levels||CC genotype||TT genotype|
|High exposure||Low risk||High risk|
|Low exposure||High risk||Low risk|
Family history is a risk factor for asthma, with many different genes being implicated. If one identical twin is affected, the probability of the other having the disease is approximately 25%. By the end of 2005, 25 genes had been associated with asthma in six or more separate populations, including GSTM1, IL10, CTLA-4, SPINK5, LTC4S, IL4R and ADAM33, among others. Many of these genes are related to the immune system or modulating inflammation. Even among this list of genes supported by highly replicated studies, results have not been consistent among all populations tested. In 2006 over 100 genes were associated with asthma in one genetic association study alone; more continue to be found.
Some genetic variants may only cause asthma when they are combined with specific environmental exposures. An example is a specific single nucleotide polymorphism in the CD14 region and exposure to endotoxin (a bacterial product). Endotoxin exposure can come from several environmental sources including tobacco smoke, dogs, and farms. Risk for asthma, then, is determined by both a person's genetics and the level of endotoxin exposure.
A triad of atopic eczema, allergic rhinitis and asthma is called atopy. The strongest risk factor for developing asthma is a history of atopic disease; with asthma occurring at a much greater rate in those who have either eczema or hay fever. Asthma has been associated with Churg–Strauss syndrome, an autoimmune disease and vasculitis. Individuals with certain types of urticaria may also experience symptoms of asthma.
There is a correlation between obesity and the risk of asthma with both having increased in recent years. Several factors may be at play including decreased respiratory function due to a buildup of fat and the fact that adipose tissue leads to a pro-inflammatory state.
Beta blocker medications such as propranolol can trigger asthma in those who are susceptible. Cardioselective beta-blockers, however, appear safe in those with mild or moderate disease. Other medications that can cause problems in same are ASA, NSAIDs, and angiotensin-converting enzyme inhibitors. COX-2 inhibitors do not appear to be a concern.
Some individuals will have stable asthma for weeks or months and then suddenly develop an episode of acute asthma. Different individuals react to various factors in different ways. Most individuals can develop severe exacerbation from a number of triggering agents.
Home factors that can lead to exacerbation of asthma include dust, animal dander (especially cat and dog hair), cockroach allergens and mold. Perfumes are a common cause of acute attacks in women and children. Both viral and bacterial infections of the upper respiratory tract can worsen the disease. Psychological stress may worsen symptoms—it is thought that stress alters the immune system and thus increases the airway inflammatory response to allergens and irritants.
Asthma is the result of chronic inflammation of the airways which subsequently results in increased contractability of the surrounding smooth muscles. This among other factors leads to bouts of narrowing of the airway and the classic symptoms of wheezing. The narrowing is typically reversible with or without treatment. Occasionally the airways themselves change. Typical changes in the airways include an increase in eosinophils and thickening of the lamina reticularis. Chronically the airways' smooth muscle may increase in size along with an increase in the numbers of mucous glands. Other cell types involved include: T lymphocytes, macrophages, and neutrophils. There may also be involvement of other components of the immune system including: cytokines, chemokines, histamine, and leukotrienes among others.
While asthma is a well recognized condition, there is not one universal agreed upon definition. It is defined by the Global Initiative for Asthma as "a chronic inflammatory disorder of the airways in which many cells and cellular elements play a role. The chronic inflammation is associated with airway hyper-responsiveness that leads to recurrent episodes of wheezing, breathlessness, chest tightness and coughing particularly at night or in the early morning. These episodes are usually associated with widespread but variable airflow obstruction within the lung that is often reversible either spontaneously or with treatment".
There is currently no precise test with the diagnosis typically based on the pattern of symptoms and response to therapy over time. A diagnosis of asthma should be suspected if there is a history of: recurrent wheezing, coughing or difficulty breathing and these symptoms occur or worsen due to exercise, viral infections, allergens or air pollution. Spirometry is then used to confirm the diagnosis. In children under the age of six the diagnosis is more difficult as they are too young for spirometry.
Spirometry is recommended to aid in diagnosis and management. It is the single best test for asthma. If the FEV1 measured by this technique improves more than 12% following administration of a bronchodilator such as salbutamol, this is supportive of the diagnosis. It however may be normal in those with a history of mild asthma, not currently acting up. As caffeine is a bronchodilator in people with asthma, the use of caffeine before a lung function test may interfere with the results. Single-breath diffusing capacity can help differentiate asthma from COPD. It is reasonable to perform spirometry every one or two years to follow how well a person's asthma is controlled.
The methacholine challenge involves the inhalation of increasing concentrations of a substance that causes airway narrowing in those predisposed. If negative it means that a person does not have asthma; if positive, however, it is not specific for the disease.
Other supportive evidence includes: a ≥20% difference in peak expiratory flow rate on at least three days in a week for at least two weeks, a ≥20% improvement of peak flow following treatment with either salbutamol, inhaled corticosteroids or prednisone, or a ≥20% decrease in peak flow following exposure to a trigger. Testing peak expiratory flow is more variable than spirometry, however, and thus not recommended for routine diagnosis. It may be useful for daily self-monitoring in those with moderate to severe disease and for checking the effectiveness of new medications. It may also be helpful in guiding treatment in those with acute exacerbations.
|Severity||Symptom frequency||Night time symptoms||%FEV1 of predicted||FEV1 Variability||SABA use|
|Mild persistent||>2/week||3–4/month||≥80%||20–30%||>2 days/week|
|Severe persistent||Continuously||Frequent (7×/week)||<60%||>30%||≥twice/day|
Asthma is clinically classified according to the frequency of symptoms, forced expiratory volume in one second (FEV1), and peak expiratory flow rate. 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). While asthma is classified based on severity, at the moment there is no clear method for classifying different subgroups of asthma beyond this system. Finding ways to identify subgroups that respond well to different types of treatments is a current critical goal of asthma research.
Although asthma is a chronic obstructive condition, it is not considered as a part of chronic obstructive pulmonary disease as this term refers specifically to combinations of disease that are irreversible such as bronchiectasis, chronic bronchitis, and emphysema. Unlike these diseases, the airway obstruction in asthma is usually reversible; however, if left untreated, the chronic inflammation from asthma can lead the lungs to become irreversibly obstructed due to airway remodeling. In contrast to emphysema, asthma affects the bronchi, not the alveoli.
|Near-fatal||High PaCO2 and/or requiring mechanical ventilation|
(any one of)
|Altered level of consciousness||Peak flow < 33%|
|Exhaustion||Oxygen saturation < 92%|
|Arrhythmia||PaO2 < 8 kPa|
|Low blood pressure||"Normal" PaCO2|
|Poor respiratory effort|
(any one of)
|Peak flow 33–50%|
|Respiratory rate ≥ 25 breaths per minute|
|Heart rate ≥ 110 beats per minute|
|Unable to complete sentences in one breath|
|Peak flow 50–80% best or predicted|
|No features of acute severe asthma|
An acute asthma exacerbation is commonly referred to as an asthma attack. The classic symptoms are shortness of breath, wheezing, and chest tightness. While these are the primary symptoms of asthma, some people present primarily with coughing, and in severe cases, air motion may be significantly impaired such that no wheezing is heard.
Signs which occur during an asthma attack include the use of accessory muscles of respiration (sternocleidomastoid and scalene muscles of the neck), there may be a paradoxical pulse (a pulse that is weaker during inhalation and stronger during exhalation), and over-inflation of the chest. A blue color of the skin and nails may occur from lack of oxygen.
In a mild exacerbation the peak expiratory flow rate (PEFR) is ≥200 L/min or ≥50% of the predicted best. 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.
Acute severe asthma, previously known as status asthmaticus, is an acute exacerbation of asthma that does not respond to standard treatments of bronchodilators and corticosteroids. Half of cases are due to infections with others caused by allergen, air pollution, or insufficient or inappropriate medication use.
Brittle asthma is a kind of asthma distinguishable by recurrent, severe attacks. Type 1 brittle asthma is a disease with wide peak flow variability, despite intense medication. Type 2 brittle asthma is background well-controlled asthma with sudden severe exacerbations.
Exercise can trigger bronchoconstriction in both people with and without asthma. It occurs in most people with asthma and up to 20% of people without asthma. In athletes is diagnosed more commonly in elite athletes, with rates varying from 3% for bobsled racers to 50% for cycling and 60% for cross-country skiing. While it may occur with any weather conditions it is more common when it is dry and cold. Inhaled beta2-agonists do not appear to improve athletic performance among those without asthma however oral doses may improve endurance and strength.
Asthma as a result of (or worsened by) workplace exposures, is a commonly reported occupational disease. Many cases however are not reported or recognized as such. It is estimated that 5–25% of asthma cases in adults are work–related. A few hundred different agents have been implicated with the most common being: isocyanates, grain and wood dust, colophony, soldering flux, latex, animals, and aldehydes. The employment associated with the highest risk of problems include: those who spray paint, bakers and those who process food, nurses, chemical workers, those who work with animals, welders, hairdressers and timber workers.
Many other conditions can cause symptoms similar to those of asthma. In children, other upper airway diseases such as allergic rhinitis and sinusitis should be considered as well as other causes of airway obstruction including: foreign body aspiration, tracheal stenosis or laryngotracheomalacia, vascular rings, enlarged lymph nodes or neck masses. In adults, COPD, congestive heart failure, airway masses, as well as drug-induced coughing due to ACE inhibitors should be considered. In both populations vocal cord dysfunction may present similarly.
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. It closely resembles asthma in symptoms, is correlated with more exposure to cigarette smoke, an older age, less symptom reversibility after bronchodilator administration, and decreased likelihood of family history of atopy.
The evidence for the effectiveness of measures to prevent the development of asthma is weak. Some show promise including: limiting smoke exposure both
- Asthma at DMOZ
- National Asthma Education and Prevention Program (NAEPP) (2007). "Expert Panel Report 3: Guidelines for the Diagnosis and Management of Asthma" (PDF).
- "British Guideline on the Management of Asthma" (PDF).
- "Global Strategy for Asthma Management and Prevention" (PDF). Global Initiative for Asthma. 2011.
- GINA 2011, p. 18
- NHLBI Guideline 2007, pp. 11–12
- British Guideline 2009, p. 4
- Martinez FD (2007). "Genes, environments, development and asthma: a reappraisal". European Respiratory Journal 29 (1): 179–84.
- Lemanske, R.F.; Busse, W.W. (February 2010). "Asthma: clinical expression and molecular mechanisms". J. Allergy Clin. Immunol. 125 (2 Suppl 2): S95–102.
- Yawn BP (September 2008). "Factors accounting for asthma variability: achieving optimal symptom control for individual patients". Primary Care Respiratory Journal 17 (3): 138–147.
- Kumar, Vinay; Abbas, Abul K; Fausto, Nelson et al., eds. (2010). Robbins and Cotran pathologic basis of disease (8th ed.). Saunders. p. 688.
- Stedman's Medical Dictionary (28 ed.). Lippincott Williams and Wilkins. 2005.
- NHLBI Guideline 2007, p. 214
- NHLBI Guideline 2007, pp. 373–375
- NHLBI Guideline 2007, pp. 169–172
- GINA 2011, p. 71
- GINA 2011, p. 33
- "World Health Organization Fact Sheet Fact sheet No 307: Asthma". 2011. Retrieved Jan 17, 2013.
- GINA 2011, p. 3
- GINA 2011, pp. 2–5
- Jindal, editor-in-chief SK (2011). Textbook of pulmonary and critical care medicine. New Delhi: Jaypee Brothers Medical Publishers. p. 242.
- George, Ronald B. (2005). Chest medicine : essentials of pulmonary and critical care medicine (5th ed.). Philadelphia, PA: Lippincott Williams & Wilkins. p. 62.
- British Guideline 2009, p. 14
- GINA 2011, pp. 8–9
- Boulet LP (April 2009). "Influence of comorbid conditions on asthma". European Respiratory Journal 33 (4): 897–906.
- Boulet, LP; Boulay, MÈ (June 2011). "Asthma-related comorbidities". Expert review of respiratory medicine 5 (3): 377–93.
- editors, Andrew Harver, Harry Kotses, (2010). Asthma, health and society a public health perspective. New York: Springer. p. 315.
- Thomas, M; Bruton, A; Moffat, M; Cleland, J (September 2011). "Asthma and psychological dysfunction". Primary care respiratory journal : journal of the General Practice Airways Group 20 (3): 250–6.
- Miller, RL; Ho SM (March 2008). "Environmental epigenetics and asthma: current concepts and call for studies". American Journal of Respiratory and Critical Care Medicine 177 (6): 567–573.
- Choudhry S, Seibold MA, Borrell LN "" et al. (2007). "Dissecting complex diseases in complex populations: asthma in latino americans". Proc Am Thorac Soc 4 (3): 226–33.
- Dietert, RR (September 2011). "Maternal and childhood asthma: risk factors, interactions, and ramifications". Reproductive toxicology (Elmsford, N.Y.) 32 (2): 198–204.
- Kelly, FJ; Fussell, JC (August 2011). "Air pollution and airway disease". Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology 41 (8): 1059–71.
- GINA 2011, p. 6
- GINA 2011, p. 61
- Gold, D.R.; Wright, R. (2005). "Population disparities in asthma". Annu Rev Public Health 26: 89–113.
- McGwin, G; Lienert, J; Kennedy, JI (March 2010). "Formaldehyde exposure and asthma in children: a systematic review". Environmental health perspectives 118 (3): 313–7.
- Jaakkola, J.J.; Knight, T.L. (July 2008). "The role of exposure to phthalates from polyvinyl chloride products in the development of asthma and allergies: a systematic review and meta-analysis". Environ Health Perspect 116 (7): 845–53.
- Bornehag, CG; Nanberg, E (April 2010). "Phthalate exposure and asthma in children". International journal of andrology 33 (2): 333–45.
- Henderson, AJ; Shaheen, SO (Mar 2013). "Acetaminophen and asthma.". Paediatric Respiratory Reviews 14 (1): 9–15; quiz 16.
- Heintze, K; Petersen, KU (Jun 2013). "The case of drug causation of childhood asthma: antibiotics and paracetamol.". European journal of clinical pharmacology 69 (6): 1197–209.
- Cheelo, M; Lodge, CJ; Dharmage, SC; Simpson, JA; Matheson, M; Heinrich, J; Lowe, AJ (26 November 2014). "Paracetamol exposure in pregnancy and early childhood and development of childhood asthma: a systematic review and meta-analysis.". Archives of disease in childhood.
- Eyers, S; Weatherall, M; Jefferies, S; Beasley, R (Apr 2011). "Paracetamol in pregnancy and the risk of wheezing in offspring: a systematic review and meta-analysis.". Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology 41 (4): 482–9.
- Ahluwalia, SK; Matsui, EC (April 2011). "The indoor environment and its effects on childhood asthma". Current Opinion in Allergy and Clinical Immunology 11 (2): 137–43.
- Arshad, SH (January 2010). "Does exposure to indoor allergens contribute to the development of asthma and allergy?". Current allergy and asthma reports 10 (1): 49–55.
- Custovic, A; Simpson, A (2012). "The role of inhalant allergens in allergic airways disease". Journal of investigational allergology & clinical immunology : official organ of the International Association of Asthmology (INTERASMA) and Sociedad Latinoamericana de Alergia e Inmunologia 22 (6): 393–401; qiuz follow 401.
- Murray, John F. (2010). "Ch. 38 Asthma". In Mason, Robert J.; Murray, John F.; Broaddus, V. Courtney et al. Murray and Nadel's textbook of respiratory medicine (5th ed.). Elsevier.
- NHLBI Guideline 2007, p. 11
- Ramsey, CD; Celedón JC (January 2005). "The hygiene hypothesis and asthma". Current Opinion in Pulmonary Medicine 11 (1): 14–20.
- Bufford, JD; Gern JE (May 2005). "The hygiene hypothesis revisited". Immunology and Allergy Clinics of North America 25 (2): 247–262.
- Brooks, C; Pearce, N; Douwes, J (February 2013). "The hygiene hypothesis in allergy and asthma: an update". Current Opinion in Allergy and Clinical Immunology 13 (1): 70–7.
- Rao, D; Phipatanakul, W (October 2011). "Impact of environmental controls on childhood asthma.". Current allergy and asthma reports 11 (5): 414–20.
- Murk, W; Risnes, KR; Bracken, MB (June 2011). "Prenatal or early-life exposure to antibiotics and risk of childhood asthma: a systematic review". Pediatrics 127 (6): 1125–38.
- British Guideline 2009, p. 72
- Neu, J; Rushing, J (June 2011). "Cesarean versus vaginal delivery: long-term infant outcomes and the hygiene hypothesis". Clinics in perinatology 38 (2): 321–31.
- Von Hertzen, LC; Haahtela, T (February 2004). "Asthma and atopy -the price of affluence?". Allergy 59 (2): 124–37.
- Martinez FD (2007). "CD14, endotoxin, and asthma risk: actions and interactions". Proc Am Thorac Soc 4 (3): 221–5.
- Elward, Graham Douglas, Kurtis S. (2010). Asthma. London: Manson Pub. pp. 27–29.
- Ober C, Hoffjan S (2006). "Asthma genetics 2006: the long and winding road to gene discovery". Genes Immun 7 (2): 95–100.
- Halapi, E; Bjornsdottir, US (January 2009). "Overview on the current status of asthma genetics". The clinical respiratory journal 3 (1): 2–7.
- Rapini, Ronald P.; Bolognia, Jean L.; Jorizzo, Joseph L. (2007). Dermatology: 2-Volume Set. St. Louis: Mosby.
- GINA 2011, p. 4
- Beuther DA (January 2010). "Recent insight into obesity and asthma". Current Opinion in Pulmonary Medicine 16 (1): 64–70.
- Holguin F, Fitzpatrick A (March 2010). "Obesity, asthma, and oxidative stress". J. Appl. Physiol. 108 (3): 754–9.
- Wood LG, Gibson PG (July 2009). "Dietary factors lead to innate immune activation in asthma". Pharmacol. Ther. 123 (1): 37–53.
- O'Rourke ST (October 2007). "Antianginal actions of beta-adrenoceptor antagonists". Am J Pharm Educ 71 (5): 95.
- Salpeter, S; Ormiston, T; Salpeter, E (2001). Salpeter, Shelley R, ed. "Cardioselective beta-blocker use in patients with reversible airway disease". Cochrane Database of Systematic Reviews (2): CD002992.
- Morales, DR; Jackson, C; Lipworth, BJ; Donnan, PT; Guthrie, B (Nov 7, 2013). "Adverse respiratory effect of acute beta-blocker exposure in asthma: a systematic review and meta-analysis of randomized controlled trials.". Chest 145 (4): 779–86.
- Covar, RA; Macomber, BA; Szefler, SJ (February 2005). "Medications as asthma trigers". Immunology and allergy clinics of North America 25 (1): 169–90.
- Morales, DR; Lipworth, BJ; Guthrie, B; Jackson, C; Donnan, PT; Santiago, VH (July 2014). "Safety risks for patients with aspirin-exacerbated respiratory disease after acute exposure to selective nonsteroidal anti-inflammatory drugs and COX-2 inhibitors: Meta-analysis of controlled clinical trials.". The Journal of allergy and clinical immunology 134 (1): 40–45.e10.
- Baxi SN, Phipatanakul W (April 2010). "The role of allergen exposure and avoidance in asthma". Adolesc Med State Art Rev 21 (1): 57–71, viii–ix.
- Chen E, Miller GE (2007). "Stress and inflammation in exacerbations of asthma". Brain Behav Immun. 21 (8): 993–9.
- NHLBI Guideline 2007, p. 42
- GINA 2011, p. 20
- Third Expert Panel on the Diagnosis and Management of Asthma (2007). Guidelines for the diagnosis and management of asthma. National Heart, Lung, and Blood Institute (US). 07-4051.
- Welsh, EJ.; Bara, A.; Barley, E.; Cates, CJ. (2010). Welsh, Emma J, ed. "Caffeine for asthma". Cochrane Database of Systematic Reviews: CD001112.
- NHLBI Guideline 2007, p. 58
- Pinnock H, Shah R (2007). "Asthma". BMJ 334 (7598): 847–50.
- NHLBI Guideline 2007, p. 59
- Moore WC, Pascual RM (June 2010). "Update in asthma 2009". American Journal of Respiratory and Critical Care Medicine 181 (11): 1181–7.
- Self, Timothy; Chrisman, Cary; Finch, Christopher (2009). "22. Asthma". In Mary Anne Koda-Kimble, Brian K Alldredge, et al. Applied therapeutics: the clinical use of drugs (9th ed.). Philadelphia: Lippincott Williams & Wilkins.
- Delacourt, C (June 2004). "Conséquences bronchiques de l'asthme non traité" [Bronchial changes in untreated asthma]. Archives de Pédiatrie 11 (Suppl. 2): 71s–73s.
- Schiffman, George (18 December 2009). "Chronic obstructive pulmonary disease". MedicineNet. Archived from the original on 28 August 2010. Retrieved 2 September 2010.
- British Guideline 2009, p. 54
- Barnes, PJ (2008). "Asthma". In Fauci, Anthony S; Braunwald, E,; Kasper, DL. Harrison's Principles of Internal Medicine (17th ed.). New York: McGraw-Hill. pp. 1596–1607.
- Maitre B, Similowski T, Derenne JP (September 1995). "Physical examination of the adult patient with respiratory diseases: inspection and palpation". European Respiratory Journal 8 (9): 1584–93.
- Werner, HA (June 2001). "Status asthmaticus in children: a review". Chest 119 (6): 1596–1607.
- Shiber JR, Santana J (May 2006). "Dyspnea". Med. Clin. North Am. 90 (3): 453–79.
- Shah, R; Saltoun, CA (May–Jun 2012). "Chapter 14: Acute severe asthma (status asthmaticus)". Allergy and asthma proceedings : the official journal of regional and state allergy societies. 33 Suppl 1 (3): S47–50.
- Khan, DA (Jan–Feb 2012). "Exercise-induced bronchoconstriction: burden and prevalence". Allergy and asthma proceedings : the official journal of regional and state allergy societies 33 (1): 1–6.
- GINA 2011, p. 17
- Carlsen, KH; Anderson, SD; Bjermer, L; Bonini, S; Brusasco, V; Canonica, W; Cummiskey, J; Delgado, L; Del Giacco, SR; Drobnic, F; Haahtela, T; Larsson, K; Palange, P; Popov, T; van Cauwenberge, P; European Respiratory, Society; European Academy of Allergy and Clinical, Immunology; GA(2)LEN, (May 2008). "Treatment of exercise-induced asthma, respiratory and allergic disorders in sports and the relationship to doping: Part II of the report from the Joint Task Force of European Respiratory Society (ERS) and European Academy of Allergy and Clinical Immunology (EAACI) in cooperation with GA(2)LEN". Allergy 63 (5): 492–505.
- Kindermann, W (2007). "Do inhaled beta(2)-agonists have an ergogenic potential in non-asthmatic competitive athletes?". Sports medicine (Auckland, N.Z.) 37 (2): 95–102.
- Pluim, BM; de Hon, O; Staal, JB; Limpens, J; Kuipers, H; Overbeek, SE; Zwinderman, AH; Scholten, RJ (Jan 1, 2011). "β₂-Agonists and physical performance: a systematic review and meta-analysis of randomized controlled trials". Sports medicine (Auckland, N.Z.) 41 (1): 39–57.
- Baur, X; Aasen, TB; Burge, PS; Heederik, D; Henneberger, PK; Maestrelli, P; Schlünssen, V; Vandenplas, O; Wilken, D; ERS Task Force on the Management of Work-related, Asthma (Jun 1, 2012). "The management of work-related asthma guidelines: a broader perspective". European Respiratory Review 21 (124): 125–39.
- Kunnamo, ed.-in-chief: Ilkka (2005). Evidence-based medicine guidelines. Chichester: Wiley. p. 214.
- Kraft, editors, Mario Castro, Monica (2008). Clinical asthma. Philadelphia: Mosby / Elsevier. pp. Chapter 42.
- NHLBI Guideline 2007, p. 46
- Gibson PG, McDonald VM, Marks GB (September 2010). "Asthma in older adults". Lancet 376 (9743): 803–13.
- Hargreave, FE; Parameswaran, K (August 2006). "Asthma, COPD and bronchitis are just components of airway disease". European Respiratory Journal 28 (2): 264–7.
- Diaz, P. Knoell (2009). "23. Chronic obstructive pulmonary disease". Applied therapeutics: the clinical use of drugs (9th ed.). Philadelphia: Lippincott Williams & Wilkins.
- NHLBI Guideline 2007, pp. 184–5
- Lodge, CJ; Allen, KJ; Lowe, AJ; Hill, DJ; Hosking, CS; Abramson, MJ; Dharmage, SC (2012). "Perinatal cat and dog exposure and the risk of asthma and allergy in the urban environment: a systematic review of longitudinal studies". Clinical & developmental immunology 2012: 176484.
- Chen, CM; Tischer, C; Schnappinger, M; Heinrich, J (January 2010). "The role of cats and dogs in asthma and allergy—a systematic review". International journal of hygiene and environmental health 213 (1): 1–31.
- Prescott, SL; Tang, ML; Australasian Society of Clinical Immunology and, Allergy (May 2, 2005). "The Australasian Society of Clinical Immunology and Allergy position statement: Summary of allergy prevention in children". The Medical journal of Australia 182 (9): 464–7.
- Cates, CJ; Rowe, BH (Feb 28, 2013). "Vaccines for preventing influenza in people with asthma.". The Cochrane database of systematic reviews 2: CD000364.
- "Strategic Advisory Group of Experts on Immunization – report of the extraordinary meeting on the influenza A (H1N1) 2009 pandemic, 7 July 2009.". Wkly Epidemiol Rec 84 (30): 301–4. Jul 24, 2009.
- Been, JV; Nurmatov, UB; Cox, B; Nawrot, TS; van Schayck, CP; Sheikh, A (May 3, 2014). "Effect of smoke-free legislation on perinatal and child health: a systematic review and meta-analysis.". Lancet 383 (9928): 1549–60.
- Ripoll, Brian C. Leutholtz, Ignacio (2011). Exercise and disease management (2nd ed.). Boca Raton: CRC Press. p. 100.
- GINA 2011, p. 56
- NHLBI Guideline 2007, p. 213
- "British Guideline on the Management of Asthma" (PDF). Scottish Intercollegiate Guidelines Network. 2008. Archived from the original on 19 August 2008. Retrieved 2008-08-04.
- NHLBI Guideline 2007, p. 69
- Thomson NC, Spears M (2005). "The influence of smoking on the treatment response in patients with asthma". Current Opinion in Allergy and Clinical Immunology 5 (1): 57–63.
- Stapleton M, Howard-Thompson A, George C, Hoover RM, Self TH (2011). "Smoking and asthma". J Am Board Fam Med 24 (3): 313–22.
- Been, Jasper (Mar 28, 2014). "Effect of smoke-free legislation on perinatal and child health: a systematic review and meta-analysis". Lancet 383 (9928): 1549–60.
- Chandratilleke, MG; Carson, KV; Picot, J; Brinn, MP; Esterman, AJ; Smith, BJ (May 16, 2012). Carson, Kristin V, ed. "Physical training for asthma". Cochrane Database of Systematic Reviews 5: CD001116.
- Parsons JP, Hallstrand TS, Mastronarde JG, et al. (May 2013). "An official American Thoracic Society clinical practice guideline: exercise-induced bronchoconstriction". Am. J. Respir. Crit. Care Med. 187 (9): 1016–27.
- Vézina, K; Chauhan, BF; Ducharme, FM (Jul 31, 2014). "Inhaled anticholinergics and short-acting beta(2)-agonists versus short-acting beta2-agonists alone for children with acute asthma in hospital.". The Cochrane database of systematic reviews 7: CD010283.
- Rodrigo GJ, Nannini LJ (2006). "Comparison between nebulized adrenaline and beta2 agonists for the treatment of acute asthma. A meta-analysis of randomized trials". Am J Emerg Med 24 (2): 217–22.
- NHLBI Guideline 2007, p. 351
- NHLBI Guideline 2007, p. 218
- Ducharme, FM; Ni Chroinin, M; Greenstone, I; Lasserson, TJ (May 12, 2010). Ducharme, Francine M, ed. "Addition of long-acting beta2-agonists to inhaled corticosteroids versus same dose inhaled corticosteroids for chronic asthma in adults and children". Cochrane Database of Systematic Reviews (5): CD005535.
- Ducharme, FM; Ni Chroinin, M; Greenstone, I; Lasserson, TJ (Apr 14, 2010). Ducharme, Francine M, ed. "Addition of long-acting beta2-agonists to inhaled steroids versus higher dose inhaled corticosteroids in adults and children with persistent asthma". Cochrane Database of Systematic Reviews (4): CD005533.
- Fanta CH (March 2009). "Asthma". New England Journal of Medicine 360 (10): 1002–14.
- Cates, CJ; Cates, MJ (Apr 18, 2012). Cates, Christopher J, ed. "Regular treatment with formoterol for chronic asthma: serious adverse events". Cochrane Database of Systematic Reviews 4: CD006923.
- Cates, CJ; Cates, MJ (Jul 16, 2008). Cates, Christopher J, ed. "Regular treatment with salmeterol for chronic asthma: serious adverse events". Cochrane Database of Systematic Reviews (3): CD006363.
- GINA 2011, p. 74
- Watts, K; Chavasse, RJ (May 16, 2012). Watts, Kirsty, ed. "Leukotriene receptor antagonists in addition to usual care for acute asthma in adults and children". Cochrane Database of Systematic Reviews 5: CD006100.
- Chauhan, BF; Ben Salah, R; Ducharme, FM (Oct 2, 2013). "Addition of anti-leukotriene agents to inhaled corticosteroids in children with persistent asthma.". The Cochrane database of systematic reviews 10: CD009585.
- British Guideline 2009, p. 43
- NHLBI Guideline 2007, p. 250
- Rachelefsky, G (January 2009). "Inhaled corticosteroids and asthma control in children: assessing impairment and risk". Pediatrics 123 (1): 353–66.
- Dahl R (August 2006). "Systemic side effects of inhaled corticosteroids in patients with asthma". Respir Med 100 (8): 1307–17.
- Rodrigo GJ, Rodrigo C, Hall JB (2004). "Acute asthma in adults: a review". Chest 125 (3): 1081–102.
- Keeney, GE; Gray, MP; Morrison, AK; Levas, MN; Kessler, EA; Hill, GD; Gorelick, MH; Jackson, JL (Mar 2014). "Dexamethasone for acute asthma exacerbations in children: a meta-analysis.". Pediatrics 133 (3): 493–9.
- Noppen, M. (August 2002). "Magnesium Treatment for Asthma : Where Do We Stand?". Chest 122 (2): 396–8.
- GINA 2011, p. 37
- NHLBI Guideline 2007, p. 399
- Castro, M; Musani, AI; Mayse, ML; Shargill, NS (April 2010). "Bronchial thermoplasty: a novel technique in the treatment of severe asthma". Therapeutic advances in respiratory disease 4 (2): 101–16.
- Boulet, LP; Laviolette, M (May–Jun 2012). "Is there a role for bronchial thermoplasty in the treatment of asthma?". Canadian respiratory journal : journal of the Canadian Thoracic Society 19 (3): 191–2.
- GINA 2011, p. 70
- Lin, SY; Erekosima, N; Kim, JM; Ramanathan, M; Suarez-Cuervo, C; Chelladurai, Y; Ward, D; Segal, JB (27 March 2013). "Sublingual Immunotherapy for the Treatment of Allergic Rhinoconjunctivitis and Asthma A Systematic Review". JAMA 309 (12): 1278–88.
- Blanc PD, Trupin L, Earnest G, Katz PP, Yelin EH, Eisner MD (2001). "Alternative therapies among adults with a reported diagnosis of asthma or rhinosinusitis : data from a population-based survey". Chest 120 (5): 1461–7.
- Shenfield G, Lim E, Allen H (2002). "Survey of the use of complementary medicines and therapies in children with asthma". J Paediatr Child Health 38 (3): 252–7.
- Kaur B, Rowe BH, Arnold E (2009). Welsh, Emma J, ed. "Vitamin C supplementation for asthma". Cochrane Database of Systematic Reviews (1): CD000993.
- Hemilä, H (2013). "Vitamin C may alleviate exercise-induced bronchoconstriction: a meta-analysis.". BMJ open 3 (6).
- NHLBI Guideline 2007, p. 240
- McCarney RW, Brinkhaus B, Lasserson TJ, Linde K (2004). McCarney, Robert W, ed. "Acupuncture for chronic asthma". Cochrane Database of Systematic Reviews (1): CD000008.
- Blackhall, K; Appleton, S; Cates, CJ (Sep 12, 2012). Blackhall, Karen, ed. "Ionisers for chronic asthma". Cochrane Database of Systematic Reviews 9: CD002986.
- Hondras MA, Linde K, Jones AP (2005). Hondras, Maria A, ed. "Manual therapy for asthma". Cochrane Database of Systematic Reviews (2): CD001002.
- "WHO Disease and injury country estimates". World Health Organization. 2009. Archived from the original on 11 November 2009. Retrieved November 11, 2009.
- Sergel, Michelle J.; Cydulka, Rita K. (September 2009). "Ch. 75: Asthma". In Wolfson, Allan B.; Harwood-Nuss, Ann. Harwood-Nuss' Clinical Practice of Emergency Medicine (5th ed.). Lippincott Williams & Wilkins. pp. 432–.
- NHLBI Guideline 2007, p. 1
- Organization, World Health (2008). The global burden of disease : 2004 update. ([Online-Ausg.] ed.). Geneva, Switzerland: World Health Organization. p. 35.
- Maddox L, Schwartz DA (2002). "The pathophysiology of asthma". Annu. Rev. Med. 53: 477–98.
- Beckett PA, Howarth PH (2003). "Pharmacotherapy and airway remodelling in asthma?". Thorax 58 (2): 163–74.
- Vos, T; et al (December 2012). "Years lived with disability (YLDs) for 1160 sequelae of 289 diseases and injuries 1990–2010: a systematic analysis for the Global Burden of Disease Study 2010". Lancet 380 (9859): 2163–96.
- Lozano, R (Dec 15, 2012). "Global and regional mortality from 235 causes of death for 20 age groups in 1990 and 2010: a systematic analysis for the Global Burden of Disease Study 2010.". Lancet 380 (9859): 2095–128.
- Bush A, Menzies-Gow A (December 2009). "Phenotypic differences between pediatric and adult asthma". Proc Am Thorac Soc 6 (8): 712–9.
- Weiss AJ, Wier LM, Stocks C, Blanchard J (June 2014). "Overview of Emergency Department Visits in the United States, 2011". HCUP Statistical Brief #174. Rockville, MD: Agency for Healthcare Research and Quality.
- Grant EN, Wagner R, Weiss KB (August 1999). "Observations on emerging patterns of asthma in our society".
- Anandan C, Nurmatov U, van Schayck OC, Sheikh A (February 2010). "Is the prevalence of asthma declining? Systematic review of epidemiological studies". Allergy 65 (2): 152–67.
- Bousquet, J; Bousquet, PJ; Godard, P; Daures, JP (July 2005). "The public health implications of asthma". Bulletin of the World Health Organization 83 (7): 548–54.
- Anderson, HR; Gupta R; Strachan DP; Limb ES (January 2007). "50 years of asthma: UK trends from 1955 to 2004". Thorax 62 (1): 85–90.
- Masoli, Matthew (2004). Global Burden of Asthma. p. 9.
- Barrett ML, Wier LM, and Washington R. (January 2014). "Trends in Pediatric and Adult Hospital Stays for Asthma, 2000–2010.". HCUP Statistical Brief #169. Rockville, MD: Agency for Healthcare Research and Quality.
- Manniche L (1999). Sacred luxuries: fragrance, aromatherapy, and cosmetics in ancient Egypt.
- Thorowgood JC (November 1873). "On bronchial asthma".
- Gaskoin G (March 1872). "On the treatment of asthma".
Berkart JB (June 1880). "The treatment of asthma".
Berkart JB (June 1880). "The treatment of asthma".
- Bosworth FH (1886). "Hay fever, asthma, and allied affections". Transactions of the Annual Meeting of the American Climatological Association 2: 151–70.
- Doig RL (February 1905). "Epinephrin; especially in asthma". California State Journal of Medicine 3 (2): 54–5.
- von Mutius, E; Drazen, JM (Mar 1, 2012). "A patient with asthma seeks medical advice in 1828, 1928, and 2012". New England Journal of Medicine 366 (9): 827–34.
- Crompton G (December 2006). "A brief history of inhaled asthma therapy over the last fifty years". Primary care respiratory journal : journal of the General Practice Airways Group 15 (6): 326–31.
- David McCullough (1981). Mornings on Horseback: The Story of an Extraordinary Faimly, a Vanished Way of Life and the Unique Child Who Became Theodore Roosevelt. Simon and Schuster. pp. 93–108.
- Opolski M, Wilson I (September 2005). "Asthma and depression: a pragmatic review of the literature and recommendations for future research". Clin Pract Epidemol Ment Health 1: 18.
During the 1930s–1950s, asthma was known as one of the "holy seven" psychosomatic illnesses. Its cause was considered to be psychological, with treatment often based on psychoanalysis and other talking cures. As these psychoanalysts interpreted the asthmatic wheeze as the suppressed cry of the child for its mother, they considered the treatment of depression to be especially important for individuals with asthma.
A notable and well-documented case in the 19th century was that of young Theodore Roosevelt (1857–1919). At that time there was no effective treatment. Roosevelt's youth was in large part shaped by his poor health partly related to his asthma. He experienced recurring nighttime asthma attacks that caused the experience of being smothered to death, terrifying the boy and his parents.
In 1873, one of the first papers in modern medicine on the subject tried to explain the pathophysiology of the disease while one in 1872, concluded that asthma can be cured by rubbing the chest with chloroform liniment. Medical treatment in 1880, included the use of intravenous doses of a drug called pilocarpin. In 1886, F.H. Bosworth theorized a connection between asthma and hay fever. Epinephrine was first referred to in the treatment of asthma in 1905. Oral corticosteroids began to be used for this condition in the 1950s while inhaled corticosteroids and selective short acting beta agonist came into wide use in the 1960s.
Asthma was recognized in Ancient Egypt and was treated by drinking an incense mixture known as kyphi. It was officially named as a specific respiratory problem by Hippocrates circa 450 BC, with the Greek word for "panting" forming the basis of our modern name. In 200 BC it was believed to be at least partly related to the emotions.
From 2000–2010, the average cost per asthma-related hospital stay in the United States for children remained relatively stable at about $3,600, whereas the average cost per asthma-related hospital stay for adults increased from $5,200 to $6,600. In 2010, Medicaid was the most frequent primary payer among children and adults aged 18–44 years in the United States; private insurance was the second most frequent payer. Among both children and adults in the lowest income communities in the United States there is a higher rates of hospital stays for asthma in 2010 than those in the highest income communities.
Global rates of asthma have increased significantly between the 1960s and 2008 with it being recognized as a major public health problem since the 1970s. Rates of asthma have plateaued in the developed world since the mid-1990s with recent increases primarily in the developing world. Asthma affects approximately 7% of the population of the United States and 5% of people in the United Kingdom. Canada, Australia and New Zealand have rates of about 14–15%.
While asthma is twice as common in boys as girls, severe asthma occurs at equal rates. In contrast adult women have a higher rate of asthma than men and it is more common in the young than the old. In children, asthma was the most common reason for admission to the hospital following an emergency department visit in the US in 2011.
As of 2011, 235–330 million people worldwide are affected by asthma, and approximately 250,000–345,000 people die per year from the disease. Rates vary between countries with prevalences between 1 and 18%. It is more common in developed than developing countries. One thus sees lower rates in Asia, Eastern Europe and Africa. Within developed countries it is more common in those who are economically disadvantaged while in contrast in developing countries it is more common in the affluent. The reason for these differences is not well known. Low and middle income countries make up more than 80% of the mortality.
The prognosis for asthma is generally good, especially for children with mild disease. Mortality has decreased over the last few decades due to better recognition and improvement in care. Globally it causes moderate or severe disability in 19.4 million people as of 2004 (16 million of which are in low and middle income countries). Of asthma diagnosed during childhood, half of cases will no longer carry the diagnosis after a decade. Airway remodeling is observed, but it is unknown whether these represent harmful or beneficial changes. Early treatment with corticosteroids seems to prevent or ameliorates a decline in lung function.
"Manual therapies", including osteopathic, chiropractic, physiotherapeutic and respiratory therapeutic maneuvers, have insufficient evidence to support their use in treating asthma. The Buteyko breathing technique for controlling hyperventilation may result in a reduction in medications use however does not have any effect on lung function. Thus an expert panel felt that evidence was insufficient to support its use.
Many people with asthma, like those with other chronic disorders, use alternative treatments; surveys show that roughly 50% use some form of unconventional therapy. There is little data to support the effectiveness of most of these therapies. Evidence is insufficient to support the usage of Vitamin C. There is tentative support for its use in exercise induced brochospasm. Acupuncture is not recommended for the treatment as there is insufficient evidence to support its use. Air ionisers show no evidence that they improve asthma symptoms or benefit lung function; this applied equally to positive and negative ion generators.
For those with severe persistent asthma not controlled by inhaled corticosteroids and LABAs, bronchial thermoplasty may be an option. It involves the delivery of controlled thermal energy to the airway wall during a series of bronchoscopies. While it may increase exacerbation frequency in the first few months it appears to decrease the subsequent rate. Effects beyond one year are unknown. Evidence suggests that sublingual immunotherapy in those with both allergic rhinitis and asthma improve outcomes.
- Oxygen to alleviate hypoxia if saturations fall below 92%.
- Oral corticosteroid are recommended with five days of prednisone being the same 2 days of dexamethasone.
- Magnesium sulfate intravenous treatment has been shown to provide a bronchodilating effect when used in addition to other treatment in severe acute asthma attacks.
- Heliox, a mixture of helium and oxygen, may also be considered in severe unresponsive cases.
- Intravenous salbutamol is not supported by available evidence and is thus used only in extreme cases.
- Methylxanthines (such as theophylline) were once widely used, but do not add significantly to the effects of inhaled beta-agonists. Their use in acute exacerbations is controversial.
- 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.
When asthma is unresponsive to usual medications, other options are available for both emergency management and prevention of flareups. For emergency management other options include:
Long-term use of inhaled corticosteroids at conventional doses carries a minor risk of adverse effects. Risks include the development of cataracts and a mild regression in stature.
Medications are typically provided as metered-dose inhalers (MDIs) in combination with an asthma spacer or as a dry powder inhaler. The spacer is a plastic cylinder that mixes the medication with air, making it easier to receive a full dose of the drug. A nebulizer may also be used. Nebulizers and spacers are equally effective in those with mild to moderate symptoms. However insufficient evidence is available to determine whether a difference exists in those with severe disease.
- Corticosteroids are generally considered the most effective treatment available for long-term control. Inhaled forms such as beclomethasone are usually used except in the case of severe persistent disease, in which oral corticosteroids may be needed. It is usually recommended that inhaled formulations be used once or twice daily, depending on the severity of symptoms.
- Long-acting beta-adrenoceptor agonists (LABA) such as salmeterol and formoterol can improve asthma control, at least in adults, when given in combination with inhaled corticosteroids. In children this benefit is uncertain. When used without steroids they increase the risk of severe side-effects and even with corticosteroids they may slightly increase the risk.
- Leukotriene antagonists (such as montelukast and zafirlukast) may be used in addition to inhaled corticosteroids, typically also in conjunction with LABA. Evidence is insufficient to support use in acute exacerbations. In children they appear to be of little benefit when added to inhaled steroids. In those under five years of age, they were the preferred add-on therapy after inhaled corticosteroids by the British Thoracic Society in 2009.
- Mast cell stabilizers (such as cromolyn sodium) are another non-preferred alternative to corticosteroids.
- Short-acting beta2-adrenoceptor agonists (SABA), such as salbutamol (albuterol USAN) are the first line treatment for asthma symptoms. They are recommended before exercise in those with exercise induced symptoms.
- Anticholinergic medications, such as ipratropium bromide, provide additional benefit when used in combination with SABA in those with moderate or severe symptoms. Anticholinergic bronchodilators can also be used if a person cannot tolerate a SABA. If a child requires admission to hospital additional ipratropium does not appear to help over a SABA.
- Older, less selective adrenergic agonists, such as inhaled epinephrine, have similar efficacy to SABAs. They are however not recommended due to concerns regarding excessive cardiac stimulation.
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.
Avoidance of triggers is a key component of improving control and preventing attacks. The most common triggers include allergens, smoke (tobacco and other), air pollution, non selective beta-blockers, and sulfite-containing foods. Cigarette smoking and second-hand smoke (passive smoke) may reduce the effectiveness of medications such as corticosteroids. Laws that limit smoking decrease the number of people hospitalized for asthma. Dust mite control measures, including air filtration, chemicals to kill mites, vacuuming, mattress covers and others methods had no effect on asthma symptoms. Overall exercise, however is beneficial in people with stable asthma.
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 corticosteroids or alternatively, an oral leukotriene antagonist or a mast cell stabilizer is recommended. For those who have daily attacks, a higher dose of inhaled corticosteroids is used. In a moderate or severe exacerbation, oral corticosteroids are added to these treatments.
The most effective treatment for asthma is identifying triggers, such as cigarette smoke, pets, or aspirin, and eliminating exposure to them. If trigger avoidance is insufficient, the use of medication is recommended. Pharmaceutical drugs are selected based on, among other things, the severity of illness and the frequency of symptoms. Specific medications for asthma are broadly classified into fast-acting and long-acting categories.
While there is no cure for asthma, symptoms can typically be improved. A specific, customized plan for proactively monitoring and managing symptoms should be created. This plan should include the reduction of exposure to allergens, testing to assess the severity of symptoms, and the usage of medications. The treatment plan should be written down and advise adjustments to treatment according to changes in symptoms.
 Smoking bans are effective in decreasing exacerbations of asthma.