Asthma

Last updated

Asthma
Two Peak Flow Meters.jpg
Peak flow meters are used to measure the peak expiratory flow rate, important in both monitoring and diagnosing asthma. [1]
Specialty Pulmonology
SymptomsRecurring episodes of wheezing, coughing, chest tightness, shortness of breath [2]
DurationLong term [3]
Causes Genetic and environmental factors [4]
Risk factors Air pollution, allergens [3]
Diagnostic method Based on symptoms, response to therapy, spirometry [5]
TreatmentAvoiding triggers, inhaled corticosteroids, salbutamol [6] [7]
Frequency358 million (2015) [8]
Deaths397,100 (2015) [9]

Asthma is a common long-term inflammatory disease of the airways of the lungs. [3] It is characterized by variable and recurring symptoms, reversible airflow obstruction, and easily triggered bronchospasms. [10] [11] Symptoms include episodes of wheezing, coughing, chest tightness, and shortness of breath. [2] These may occur a few times a day or a few times per week. [3] Depending on the person, they may become worse at night or with exercise. [3]

Inflammation signs of activation of the immune system

Inflammation is part of the complex biological response of body tissues to harmful stimuli, such as pathogens, damaged cells, or irritants, and is a protective response involving immune cells, blood vessels, and molecular mediators. The function of inflammation is to eliminate the initial cause of cell injury, clear out necrotic cells and tissues damaged from the original insult and the inflammatory process, and initiate tissue repair.

Airway obstruction is a blockage of respiration in the airway. It can be broadly classified into being either in the upper airway or lower airway.

Bronchospasm lower respiratory tract disease that affects the airways leading into the lungs

Bronchospasm or a bronchial spasm is a sudden constriction of the muscles in the walls of the bronchioles. It is caused by the release (degranulation) of substances from mast cells or basophils under the influence of anaphylatoxins. It causes difficulty in breathing which can be very mild to severe.

Contents

Asthma is thought to be caused by a combination of genetic and environmental factors. [4] Environmental factors include exposure to air pollution and allergens. [3] Other potential triggers include medications such as aspirin and beta blockers. [3] Diagnosis is usually based on the pattern of symptoms, response to therapy over time, and spirometry. [5] Asthma is classified according to the frequency of symptoms, forced expiratory volume in one second (FEV1), and peak expiratory flow rate. [12] It may also be classified as atopic or non-atopic, where atopy refers to a predisposition toward developing a type 1 hypersensitivity reaction. [13] [14]

Genetics Science of genes, heredity, and variation in living organisms

Genetics is a branch of biology concerned with the study of genes, genetic variation, and heredity in organisms.

An environmental factor, ecological factor or eco factor is any factor, abiotic or, that influences living organisms. Abiotic factors include ambient temperature, amount of sunlight, and pH of the water soil in which an organism lives. Biotic factors would include the availability of food organisms and the presence of conspecifics, competitors, predators, and parasites.

Air pollution introduction of particulates, biological molecules, or other harmful materials into the Earths atmosphere

Air pollution occurs when harmful or excessive quantities of substances including gases, particles, and biological molecules are introduced into Earth's atmosphere. It may cause diseases, allergies and even death to humans; it may also cause harm to other living organisms such as animals and food crops, and may damage the natural or built environment. Both human activity and natural processes can generate air pollution.

There is no cure for asthma. [3] Symptoms can be prevented by avoiding triggers, such as allergens and irritants, and by the use of inhaled corticosteroids. [6] [15] Long-acting beta agonists (LABA) or antileukotriene agents may be used in addition to inhaled corticosteroids if asthma symptoms remain uncontrolled. [16] [17] Treatment of rapidly worsening symptoms is usually with an inhaled short-acting beta-2 agonist such as salbutamol and corticosteroids taken by mouth. [7] In very severe cases, intravenous corticosteroids, magnesium sulfate, and hospitalization may be required. [18]

Irritation, in biology and physiology, is a state of inflammation or painful reaction to allergy or cell-lining damage. A stimulus or agent which induces the state of irritation is an irritant. Irritants are typically thought of as chemical agents but mechanical, thermal (heat), and radiative stimuli can also be irritants. Irritation also has non-clinical usages referring to bothersome physical or psychological pain or discomfort.

Corticosteroid steroid hormone

Corticosteroids are a class of steroid hormones that are produced in the adrenal cortex of vertebrates, as well as the synthetic analogues of these hormones. Two main classes of corticosteroids, glucocorticoids and mineralocorticoids, are involved in a wide range of physiological processes, including stress response, immune response, and regulation of inflammation, carbohydrate metabolism, protein catabolism, blood electrolyte levels, and behavior.

Long-acting beta-adrenoceptor agonist

Long-acting β adrenoceptor agonists are usually prescribed for moderate-to-severe persistent asthma patients or patients with chronic obstructive pulmonary disease (COPD). They are designed to reduce the need for shorter-acting β2 agonists such as salbutamol (albuterol), as they have a duration of action of approximately 12 hours in comparison with the 4-to-6-hour duration of salbutamol, making them candidates for sparing high doses of corticosteroids or treating nocturnal asthma and providing symptomatic improvement in patients with COPD. With the exception of formoterol, long-acting β2 agonists are not recommended for the treatment of acute asthma exacerbations because of their slower onset of action compared to salbutamol. Their long duration of action is due to the addition of a long, lipophilic side-chain that binds to an exosite on adrenergic receptors. This allows the active portion of the molecule to continuously bind and unbind at β2 receptors in the smooth muscle in the lungs.

In 2015, 358 million people globally had asthma, up from 183 million in 1990. [8] [19] It caused about 397,100 deaths in 2015, [9] most of which occurred in the developing world. [3] It often begins in childhood. [3] The rates of asthma have increased significantly since the 1960s. [20] Asthma was recognized as early as Ancient Egypt. [21] The word "asthma" is from the Greek ἅσθμα, ásthma, which means "panting". [22]

Ancient Egypt ancient civilization of Northeastern Africa

Ancient Egypt was a civilization of ancient North Africa, concentrated along the lower reaches of the Nile River in the place that is now the country Egypt. Ancient Egyptian civilization followed prehistoric Egypt and coalesced around 3100 BC with the political unification of Upper and Lower Egypt under Menes. The history of ancient Egypt occurred as a series of stable kingdoms, separated by periods of relative instability known as Intermediate Periods: the Old Kingdom of the Early Bronze Age, the Middle Kingdom of the Middle Bronze Age and the New Kingdom of the Late Bronze Age.

Signs and symptoms

Asthma is characterized by recurrent episodes of wheezing, shortness of breath, chest tightness, and coughing. [23] Sputum may be produced from the lung by coughing but is often hard to bring up. [24] During recovery from an attack, it may appear pus-like due to high levels of white blood cells called eosinophils. [25] Symptoms are usually worse at night and in the early morning or in response to exercise or cold air. [26] Some people with asthma rarely experience symptoms, usually in response to triggers, whereas others may have marked reactivity and persistent symptoms. [27]

Shortness of breath, also known as dyspnea, is the feeling that one cannot breathe well enough. The American Thoracic Society defines it as "a subjective experience of breathing discomfort that consists of qualitatively distinct sensations that vary in intensity", and recommends evaluating dyspnea by assessing the intensity of the distinct sensations, the degree of distress involved, and its burden or impact on activities of daily living. Distinct sensations include effort/work, chest tightness, and air hunger.

Cough medical symptom, reflex to clear large breathing passages

A cough is a sudden, and often repetitively occurring, protective reflex which helps to clear the large breathing passages from fluids, irritants, foreign particles and microbes. The cough reflex consists of three phases: an inhalation, a forced exhalation against a closed glottis, and a violent release of air from the lungs following opening of the glottis, usually accompanied by a distinctive sound.

Sputum mucus that is coughed up from the lower airways

Sputum is mucus and is the name used for the coughed-up material (phlegm) from the lower airways. In medicine, sputum samples are usually used for naked eye exam, microbiological investigations of respiratory infections, and cytological investigations of respiratory systems. It is critical that the patient not give a specimen that includes any mucoid material from the interior of the nose. Naked eye exam of sputum can be done at home by a patient in order to note the various colors. Any hint of yellow color suggests an airway infection. Such color hints are best detected when the sputum is viewed on a very white background such as white paper, a white pot, or a white sink surface. The more intense the yellow color, the more likely it is a bacterial infection.

Associated conditions

A number of other health conditions occur more frequently in those with asthma, including gastro-esophageal reflux disease (GERD), rhinosinusitis, and obstructive sleep apnea. [28] Psychological disorders are also more common, [29] with anxiety disorders occurring in between 16–52% and mood disorders in 14–41%. [30] However, it is not known whether asthma causes psychological problems or psychological problems lead to asthma. [31] Those with asthma, especially if it is poorly controlled, are at increased risk for radiocontrast reactions. [32]

Obstructive sleep apnea repeated collapse and obstruction of the upper airway during sleep, which results in reduced airflow (hypopnea) or complete airflow cessation (apnea), oxygen desaturation, and arousals from sleep.

Obstructive sleep apnea (OSA) is the most common type of sleep apnea and is caused by complete or partial obstructions of the upper airway. It is characterized by repetitive episodes of shallow or paused breathing during sleep, despite the effort to breathe, and is usually associated with a reduction in blood oxygen saturation. These episodes of decreased breathing, called "apneas", typically last 20 to 40 seconds.

Anxiety disorder cognitive disorder with an excessive, irrational dread of everyday situations

Anxiety disorders are a group of mental disorders characterized by significant feelings of anxiety and fear. Anxiety is a worry about future events, and fear is a reaction to current events. These feelings may cause physical symptoms, such as a fast heart rate and shakiness. There are several anxiety disorders, including generalized anxiety disorder, specific phobia, social anxiety disorder, separation anxiety disorder, agoraphobia, panic disorder, and selective mutism. The disorder differs by what results in the symptoms. People often have more than one anxiety disorder.

Mood disorder mental disorders which have as their most predominant feature a disturbance in affect or mood to depression or to elation

Mood disorder, also known as mood affective disorders, is a group of conditions where a disturbance in the person's mood is the main underlying feature. The classification is in the Diagnostic and Statistical Manual of Mental Disorders (DSM) and International Classification of Diseases (ICD).

Causes

Asthma is caused by a combination of complex and incompletely understood environmental and genetic interactions. [4] [33] These influence both its severity and its responsiveness to treatment. [34] 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. [35] Onset before age 12 is more likely due to genetic influence, while onset after age 12 is more likely due to environmental influence. [36]

Environmental

Many environmental factors have been associated with asthma's development and exacerbation including allergens, air pollution, and other environmental chemicals. [37] Smoking during pregnancy and after delivery is associated with a greater risk of asthma-like symptoms. [38] Low air quality from factors such as traffic pollution or high ozone levels [39] has been associated with both asthma development and increased asthma severity. [40] Over half of cases in children in the United States occur in areas with air quality below EPA standards. [41] Low air quality is more common in low-income and minority communities. [42]

Exposure to indoor volatile organic compounds may be a trigger for asthma; formaldehyde exposure, for example, has a positive association. [43] Also, phthalates in certain types of PVC are associated with asthma in both children and adults. [44] [45] While exposure to pesticides is linked to the development of asthma, a cause and effect relationship has yet to be established. [46] [47]

There is an association between acetaminophen (paracetamol) use and asthma. [48] The majority of the evidence does not, however, support a causal role. [49] A 2014 review found that the association disappeared when respiratory infections were taken into account. [50] Use by a mother during pregnancy is also associated with an increased risk as is psychological stress during pregnancy. [51] [52]

Asthma is associated with exposure to indoor allergens. [53] Common indoor allergens include dust mites, cockroaches, animal dander (fragments of fur or feathers), and mold. [54] [55] Efforts to decrease dust mites have been found to be ineffective on symptoms in sensitized subjects. [56] [57] Certain viral respiratory infections, such as respiratory syncytial virus and rhinovirus, [22] may increase the risk of developing asthma when acquired as young children. [58] Certain other infections, however, may decrease the risk. [22]

Hygiene hypothesis

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. [59] [60] 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. [61] Exposure to bacterial endotoxin in early childhood may prevent the development of asthma, but exposure at an older age may provoke bronchoconstriction. [62] Evidence supporting the hygiene hypothesis includes lower rates of asthma on farms and in households with pets. [61]

Use of antibiotics in early life has been linked to the development of asthma. [63] 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. [64] [65] There is a link between asthma and the degree of affluence which may be related to the hygiene hypothesis as less affluent individuals often have more exposure to bacteria and viruses. [66]

Genetic

CD14-endotoxin interaction based on CD14 SNP C-159T [67]
Endotoxin levelsCC genotypeTT genotype
High exposureLow riskHigh risk
Low exposureHigh riskLow risk

Family history is a risk factor for asthma, with many different genes being implicated. [68] If one identical twin is affected, the probability of the other having the disease is approximately 25%. [68] 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. [69] 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. [69] In 2006 over 100 genes were associated with asthma in one genetic association study alone; [69] more continue to be found. [70]

Some genetic variants may only cause asthma when they are combined with specific environmental exposures. [4] 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. [67]

Medical conditions

A triad of atopic eczema, allergic rhinitis and asthma is called atopy. [71] The strongest risk factor for developing asthma is a history of atopic disease; [58] with asthma occurring at a much greater rate in those who have either eczema or hay fever. [72] Asthma has been associated with eosinophilic granulomatosis with polyangiitis (formerly known as Churg–Strauss syndrome), an autoimmune disease and vasculitis. [73] Individuals with certain types of urticaria may also experience symptoms of asthma. [71]

There is a correlation between obesity and the risk of asthma with both having increased in recent years. [74] [75] 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. [76]

Beta blocker medications such as propranolol can trigger asthma in those who are susceptible. [77] Cardioselective beta-blockers, however, appear safe in those with mild or moderate disease. [78] [79] Other medications that can cause problems in asthmatics are angiotensin-converting enzyme inhibitors, aspirin, and NSAIDs. [80] Use of acid suppressing medication (proton pump inhibitors and H2 blockers) during pregnancy is associated with an increased risk of asthma in the child. [81]

Exacerbation

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. [82] Most individuals can develop severe exacerbation from a number of triggering agents. [82]

Home factors that can lead to exacerbation of asthma include dust, animal dander (especially cat and dog hair), cockroach allergens and mold. [82] [83] 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. [82] 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. [40] [84]

Pathophysiology

Asthma is the result of chronic inflammation of the conducting zone of the airways (most especially the bronchi and bronchioles), 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. [23] 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. [22]

Diagnosis

While asthma is a well-recognized condition, there is not one universal agreed upon definition. [22] 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". [23]

There is currently no precise test for the diagnosis, which is typically based on the pattern of symptoms and response to therapy over time. [5] [22] 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. [85] Spirometry is then used to confirm the diagnosis. [85] In children under the age of six the diagnosis is more difficult as they are too young for spirometry. [86]

Spirometry

Spirometry is recommended to aid in diagnosis and management. [87] [88] It is the single best test for asthma. If the FEV1 measured by this technique improves more than 12% and increases by at least 200 milliliters 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. [22] As caffeine is a bronchodilator in people with asthma, the use of caffeine before a lung function test may interfere with the results. [89] Single-breath diffusing capacity can help differentiate asthma from COPD. [22] It is reasonable to perform spirometry every one or two years to follow how well a person's asthma is controlled. [90]

Others

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. [22]

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. [91] 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. [92]

Classification

Clinical classification (≥ 12 years old) [12]
SeveritySymptom frequencyNight-time symptoms%FEV1 of predictedFEV1 variabilitySABA use
Intermittent≤2/week≤2/month≥80%<20%≤2 days/week
Mild persistent>2/week3–4/month≥80%20–30%>2 days/week
Moderate persistentDaily>1/week60–80%>30%daily
Severe persistentContinuouslyFrequent (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. [12] 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). [13] While asthma is classified based on severity, at the moment there is no clear method for classifying different subgroups of asthma beyond this system. [93] Finding ways to identify subgroups that respond well to different types of treatments is a current critical goal of asthma research. [93]

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 and emphysema. [94] 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. [95] In contrast to emphysema, asthma affects the bronchi, not the alveoli. [96]

Asthma exacerbation

Severity of an acute exacerbation [97]
Near-fatalHigh PaCO2, or requiring mechanical ventilation, or both
Life-threatening
(any one of)
Clinical signsMeasurements
Altered level of consciousness Peak flow < 33%
Exhaustion Oxygen saturation < 92%
Arrhythmia PaO2 < 8 kPa
Low blood pressure "Normal" PaCO2
Cyanosis
Silent chest
Poor respiratory effort
Acute severe
(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
ModerateWorsening symptoms
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. [22] The wheezing is most often when breathing out. [98] While these are the primary symptoms of asthma, [99] some people present primarily with coughing, and in severe cases, air motion may be significantly impaired such that no wheezing is heard. [97] In children, chest pain is often present. [100]

Signs occurring 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. [101] A blue color of the skin and nails may occur from lack of oxygen. [102]

In a mild exacerbation the peak expiratory flow rate (PEFR) is ≥200 L/min, or ≥50% of the predicted best. [103] 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. [103]

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. [104] Half of cases are due to infections with others caused by allergen, air pollution, or insufficient or inappropriate medication use. [104]

Brittle asthma is a kind of asthma distinguishable by recurrent, severe attacks. [97] 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. [97]

Exercise-induced

Exercise can trigger bronchoconstriction both in people with or without asthma. [105] It occurs in most people with asthma and up to 20% of people without asthma. [105] Exercise-induced bronchoconstriction is common in professional athletes. The highest rates are among cyclists (up to 45%), swimmers, and cross-country skiers. [106] While it may occur with any weather conditions, it is more common when it is dry and cold. [107] Inhaled beta2-agonists do not appear to improve athletic performance among those without asthma, [108] however, oral doses may improve endurance and strength. [109] [110]

Occupational

Asthma as a result of (or worsened by) workplace exposures is a commonly reported occupational disease. [111] Many cases, however, are not reported or recognized as such. [112] [113] 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. [111]

Aspirin-induced asthma

Aspirin-exacerbated respiratory disease (AERD), also known as aspirin-induced asthma, affects up to 9% of asthmatics. [114] AERD consists of asthma, nasal polyps, sinus disease, and respiratory reactions to aspirin and other NSAID medications (such as ibuprofen and naproxen). [115] People often also develop loss of smell and most experience respiratory reactions to alcohol. [116]

Alcohol-induced asthma

Alcohol may worsen asthmatic symptoms in up to a third of people. [117] This may be even more common in some ethnic groups such as the Japanese and those with aspirin-induced asthma. [117] Other studies have found improvement in asthmatic symptoms from alcohol. [117]

Nonallergic asthma

Nonallergic asthma, also known as intrinsic or nonatopic asthma, makes up between 10 and 33% of cases. There is negative skin test to common inhalant allergens and normal serum concentrations of IgE. Often it starts later in life, and women are more commonly affected than men. Usual treatments may not work as well. [118]

Differential diagnosis

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, laryngotracheomalacia, vascular rings, enlarged lymph nodes or neck masses. [119] Bronchiolitis and other viral infections may also produce wheezing. [120] 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. [119]

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. [121] 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. [122] [123]

Prevention

The evidence for the effectiveness of measures to prevent the development of asthma is weak. [124] The World Health Organization recommends decreasing risk factors such as tobacco smoke, air pollution, chemical irritants including perfume, and the number of lower respiratory infections. [125] [126] Other efforts that show promise include: limiting smoke exposure in utero, breastfeeding, and increased exposure to daycare or large families, but none are well supported enough to be recommended for this indication. [124]

Early pet exposure may be useful. [127] Results from exposure to pets at other times are inconclusive [128] and it is only recommended that pets be removed from the home if a person has allergic symptoms to said pet. [129]

Dietary restrictions during pregnancy or when breast feeding have not been found to be effective and thus are not recommended. [129] Reducing or eliminating compounds known to sensitive people from the work place may be effective. [111] It is not clear if annual influenza vaccinations affects the risk of exacerbations. [130] Immunization; however, is recommended by the World Health Organization. [131] Smoking bans are effective in decreasing exacerbations of asthma. [132]

Management

While there is no cure for asthma, symptoms can typically be improved. [133] 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. [134]

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. [135] [136]

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, a leukotriene antagonist or a mast cell stabilizer by mouth is recommended. For those who have daily attacks, a higher dose of inhaled corticosteroids is used. In a moderate or severe exacerbation, corticosteroids by mouth are added to these treatments. [7]

People with asthma have higher rates of anxiety and depression. [137] This is associated with poorer asthma control. [137] Cognitive behavioral therapy may improve quality of life, asthma control, and anxiety levels in people with asthma. [137]

Lifestyle modification

Avoidance of triggers is a key component of improving control and preventing attacks. The most common triggers include allergens, smoke (from tobacco or other sources), air pollution, non selective beta-blockers, and sulfite-containing foods. [138] [139] Cigarette smoking and second-hand smoke (passive smoke) may reduce the effectiveness of medications such as corticosteroids. [140] Laws that limit smoking decrease the number of people hospitalized for asthma. [141] Dust mite control measures, including air filtration, chemicals to kill mites, vacuuming, mattress covers and others methods had no effect on asthma symptoms. [56] Overall, exercise is beneficial in people with stable asthma. [142] Yoga could provide small improvements in quality of life and symptoms in people with asthma. [143]

Medications

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. [135] Antibiotics are generally not needed for sudden worsening of symptoms. [144]

Fast–acting

Salbutamol metered dose inhaler commonly used to treat asthma attacks. Salbutamol2.JPG
Salbutamol metered dose inhaler commonly used to treat asthma attacks.
  • Short-acting beta2-adrenoceptor agonists (SABA), such as salbutamol (albuterol USAN) are the first line treatment for asthma symptoms. [7] They are recommended before exercise in those with exercise induced symptoms. [145]
  • Anticholinergic medications, such as ipratropium bromide, provide additional benefit when used in combination with SABA in those with moderate or severe symptoms. [7] Anticholinergic bronchodilators can also be used if a person cannot tolerate a SABA. [94] If a child requires admission to hospital additional ipratropium does not appear to help over a SABA. [146]
  • Older, less selective adrenergic agonists, such as inhaled epinephrine, have similar efficacy to SABAs. [147] They are however not recommended due to concerns regarding excessive cardiac stimulation. [148]

Long–term control

Fluticasone propionate metered dose inhaler commonly used for long-term control. Fluticasone.JPG
Fluticasone propionate metered dose inhaler commonly used for long-term control.
  • Corticosteroids are generally considered the most effective treatment available for long-term control. [135] Inhaled forms such as beclomethasone are usually used except in the case of severe persistent disease, in which oral corticosteroids may be needed. [135] It is usually recommended that inhaled formulations be used once or twice daily, depending on the severity of symptoms. [149]
  • 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. [150] [151] In children this benefit is uncertain. [150] [152] [151] When used without steroids they increase the risk of severe side-effects, [153] and with corticosteroids they may slightly increase the risk. [154] [155] Evidence suggests that for children who have persistent asthma, a treatment regime that includes LABA added to inhaled corticosteroids may improve lung function but does not reduce the amount of serious exacerbations. [156] Children who require LABA as part of their asthma treatment may need to go to the hospital more frequently. [156]
  • Leukotriene receptor antagonists (anti-leukotriene agents such as montelukast and zafirlukast) may be used in addition to inhaled corticosteroids, typically also in conjunction with a LABA. [17] [135] [157] [158] Evidence is insufficient to support use in acute exacerbations. [159] [160] For adults or adolescents who have persistent asthma that is not controlled very well, the addition of anti-leukotriene agents along with daily inhaled corticosteriods improves lung function and reduces the risk of moderate and severe asthma exacerbations. [158] Anti-leukotriene agents may be effective alone for adolescents and adults, however there is no clear research suggesting which people with asthma would benefit from anti-leukotriene receptor alone. [161] In those under five years of age, anti-leukotriene agents were the preferred add-on therapy after inhaled corticosteroids by the British Thoracic Society in 2009. [162] A 2013 Cochrane systematic review concluded that anti-leukotriene agents appear to be of little benefit when added to inhaled steroids for treating children. [163] A similar class of drugs, 5-LOX inhibitors, may be used as an alternative in the chronic treatment of mild to moderate asthma among older children and adults. [17] [164] As of 2013 there is one medication in this family known as zileuton. [17]
  • Intravenous administration of the drug aminophylline does not provide an improvement in bronchodilation when compared to standard inhaled beta-2 agonist treatment. [165] Aminophylline treatment is associated with more adverse effects compared to inhaled beta-2 agonist treatment. [165]
  • Mast cell stabilizers (such as cromolyn sodium) are another non-preferred alternative to corticosteroids. [135]
  • For children with asthma which is well-controlled on combination therapy of inhaled corticosteroids (ICS) and long-acting beta2-agonists (LABA), the benefits and harms of stopping LABA and stepping down to ICS-only therapy are uncertain. [166] In adults who have stable asthma while they are taking a combination of LABA and inhaled corticosteroids (ICS), stopping LABA may increase the risk of asthma exacerbations that require treatment with corticosteroids by mouth. [167] Stopping LABA probably makes little or no important difference to asthma control or asthma-related quality of life. [167] Whether or not stopping LABA increases the risk of serious adverse events or exacerbations requiring an emergency department visit or hospitalisation is uncertain. [167]

Delivery methods

Medications are typically provided as metered-dose inhalers (MDIs) in combination with an asthma spacer or as a dry powder inhaler. The spacer is a plastic cylinder that mixes the medication with air, making it easier to receive a full dose of the drug. A nebulizer may also be used. Nebulizers and spacers are equally effective in those with mild to moderate symptoms. However, insufficient evidence is available to determine whether a difference exists in those with severe disease. [168] There is no strong evidence for the use of intravenous LABA for adults or children who have acute asthma. [169]

Adverse effects

Long-term use of inhaled corticosteroids at conventional doses carries a minor risk of adverse effects. [170] Risks include thrush, the development of cataracts, and a slightly slowed rate of growth. [170] [171] [172] Higher doses of inhaled steroids may result in lower bone mineral density. [173]

Others

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

Alternative medicine

Many people with asthma, like those with other chronic disorders, use alternative treatments; surveys show that roughly 50% use some form of unconventional therapy. [191] [192] There is little data to support the effectiveness of most of these therapies. Evidence is insufficient to support the usage of vitamin C. [193] There is tentative support for its use in exercise induced bronchospasm. [194] In people with mild to moderate asthma, treatment with vitamin D supplementation is likely to reduce the risk of asthma exacerbations. [195]

Acupuncture is not recommended for the treatment as there is insufficient evidence to support its use. [196] [197] Air ionisers show no evidence that they improve asthma symptoms or benefit lung function; this applied equally to positive and negative ion generators. [198]

Manual therapies, including osteopathic, chiropractic, physiotherapeutic and respiratory therapeutic maneuvers, have insufficient evidence to support their use in treating asthma. [199] The Buteyko breathing technique for controlling hyperventilation may result in a reduction in medication use; however, the technique does not have any effect on lung function. [136] Thus an expert panel felt that evidence was insufficient to support its use. [196]

Prognosis

Asthma deaths per million persons in 2012
.mw-parser-output .refbegin{font-size:90%;margin-bottom:0.5em}.mw-parser-output .refbegin-hanging-indents>ul{list-style-type:none;margin-left:0}.mw-parser-output .refbegin-hanging-indents>ul>li,.mw-parser-output .refbegin-hanging-indents>dl>dd{margin-left:0;padding-left:3.2em;text-indent:-3.2em;list-style:none}.mw-parser-output .refbegin-100{font-size:100%}
0-10
11-13
14-17
18-23
24-32
33-43
44-50
51-66
67-95
96-251 Asthma world map-Deaths per million persons-WHO2012.svg
Asthma deaths per million persons in 2012
  0–10
  11–13
  14–17
  18–23
  24–32
  33–43
  44–50
  51–66
  67–95
  96–251
Disability-adjusted life year for asthma per 100,000 inhabitants in 2004.
no data
<100
100-150
150-200
200-250
250-300
300-350
350-400
400-450
450-500
500-550
550-600
>600 Asthma world map - DALY - WHO2004.svg
Disability-adjusted life year for asthma per 100,000 inhabitants in 2004.

The prognosis for asthma is generally good, especially for children with mild disease. [201] Mortality has decreased over the last few decades due to better recognition and improvement in care. [202] In 2010 the death rate was 170 per million for males and 90 per million for females. [203] Rates vary between countries by 100 fold. [203]

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). [204] Of asthma diagnosed during childhood, half of cases will no longer carry the diagnosis after a decade. [68] Airway remodeling is observed, but it is unknown whether these represent harmful or beneficial changes. [205] Early treatment with corticosteroids seems to prevent or ameliorates a decline in lung function. [206] Asthma in children also has negative effects on quality of life of their parents. [207]

Epidemiology

Rates of asthma in different countries of the world as of 2004.
no data
<1%
1-2%
2-3%
3-4%
4-5%
5-6%
6-7%
7-8%
8-10%
10-12.5%
12.5-15%
>15% Prevalence of Clinical Asthma world map - GINA2004.svg
Rates of asthma in different countries of the world as of 2004.

As of 2011, 235–330 million people worldwide are affected by asthma, [208] [209] [210] and approximately 250,000–345,000 people die per year from the disease. [23] [211] Rates vary between countries with prevalences between 1 and 18%. [23] It is more common in developed than developing countries. [23] One thus sees lower rates in Asia, Eastern Europe and Africa. [22] 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. [23] The reason for these differences is not well known. [23] Low and middle income countries make up more than 80% of the mortality. [212]

While asthma is twice as common in boys as girls, [23] severe asthma occurs at equal rates. [213] In contrast adult women have a higher rate of asthma than men [23] and it is more common in the young than the old. [22] In children, asthma was the most common reason for admission to the hospital following an emergency department visit in the US in 2011. [214]

Global rates of asthma have increased significantly between the 1960s and 2008 [20] [215] with it being recognized as a major public health problem since the 1970s. [22] Rates of asthma have plateaued in the developed world since the mid-1990s with recent increases primarily in the developing world. [216] Asthma affects approximately 7% of the population of the United States [153] and 5% of people in the United Kingdom. [217] Canada, Australia and New Zealand have rates of about 14–15%. [218]

The average death rate from 2011 to 2015 from asthma in the UK was about 50% higher than the average for the European Union and had increased by about 5% in that time. [219]

Economics

From 2000 to 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. [220] 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. [220] Among both children and adults in the lowest income communities in the United States there is a higher rate of hospital stays for asthma in 2010 than those in the highest income communities. [220]

History

Ebers Papyrus detailing treatment of asthma Papyrus Ebers.png
Ebers Papyrus detailing treatment of asthma
1907 advertisement for Grimault's Indian Cigarettes, promoted as a means of relieving asthma. They contained belladonna and cannabis. Grimaults cigarette ad.jpg
1907 advertisement for Grimault's Indian Cigarettes, promoted as a means of relieving asthma. They contained belladonna and cannabis.

Asthma was recognized in ancient Egypt and was treated by drinking an incense mixture known as kyphi. [21] 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. [22] In 200 BC it was believed to be at least partly related to the emotions. [30] In the 12th century the Jewish physician-philosopher Maimonides wrote a treatise on asthma in Arabic, based partly on Arabic sources, in which he discussed the symptoms, proposed various dietary and other means of treatment, and emphasized the importance of climate and clean air. [221]

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. [222] [223] Medical treatment in 1880 included the use of intravenous doses of a drug called pilocarpine. [224] In 1886, F. H. Bosworth theorized a connection between asthma and hay fever. [225] Epinephrine was first referred to in the treatment of asthma in 1905. [226] 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. [227] [228]

A notable and well-documented case in the 19th century was that of young Theodore Roosevelt (1858–1919). 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. [229]

During the 1930s to 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. [230] 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. [230]

Related Research Articles

Sinusitis inflammation of the mucous membrane that lines the sinuses resulting in symptoms

Sinusitis, also known as a sinus infection or rhinosinusitis, is inflammation of the mucous membrane that lines the sinuses resulting in symptoms. Common symptoms include thick nasal mucus, a plugged nose, and facial pain. Other signs and symptoms may include fever, headaches, a poor sense of smell, sore throat, and a cough. The cough is often worse at night. Serious complications are rare. It is defined as acute sinusitis if it lasts less than 4 weeks, and as chronic sinusitis if it lasts for more than 12 weeks.

Pneumonia Infection of the lungs

Pneumonia is an inflammatory condition of the lung affecting primarily the small air sacs known as alveoli. Typically symptoms include some combination of productive or dry cough, chest pain, fever, and trouble breathing. Severity is variable.

A bronchodilator is a substance that dilates the bronchi and bronchioles, decreasing resistance in the respiratory airway and increasing airflow to the lungs. Bronchodilators may be endogenous, or they may be medications administered for the treatment of breathing difficulties. They are most useful in obstructive lung diseases, of which asthma and chronic obstructive pulmonary disease are the most common conditions. Although this remains somewhat controversial, they might be useful in bronchiolitis and bronchiectasis. They are often prescribed but of unproven significance in restrictive lung diseases.

Common cold common viral infection of upper respiratory tract

The common cold, also known simply as a cold, is a viral infectious disease of the upper respiratory tract that primarily affects the nose. The throat, sinuses, and larynx may also be affected. Signs and symptoms may appear less than two days after exposure to the virus. These may include coughing, sore throat, runny nose, sneezing, headache, and fever. People usually recover in seven to ten days, but some symptoms may last up to three weeks. Occasionally those with other health problems may develop pneumonia.

Cold medicine Agents whose purpose is to suppress coughing

Cold medicines are medications used by people with the common cold, cough, or related conditions. There is, however, no good evidence that cough medications reduce coughing.

Acute bronchitis short-term inflammation of the bronchi (large and medium-sized airways) of the lungs

Acute bronchitis, also known as a chest cold, is short-term inflammation of the bronchi of the lungs. The most common symptom is a cough. Other symptoms include coughing up mucus, wheezing, shortness of breath, fever, and chest discomfort. The infection may last from a few to ten days. The cough may persist for several weeks afterward with the total duration of symptoms usually around three weeks. Some have symptoms for up to six weeks.

Sore throat symptom

Sore throat, also known as throat pain, is pain or irritation of the throat.

Croup Respiratory condition that is usually triggered by an acute viral infection of the upper airway

Croup, also known as laryngotracheobronchitis, is a type of respiratory infection that is usually caused by a virus. The infection leads to swelling inside the trachea, which interferes with normal breathing and produces the classic symptoms of "barking" cough, stridor, and a hoarse voice. Fever and runny nose may also be present. These symptoms may be mild, moderate, or severe. Often it starts or is worse at night. It normally lasts one to two days.

Bronchiolitis human disease

Bronchiolitis is blockage of the small airways in the lungs due to a viral infection. It usually only occurs in children less than two years of age. Symptoms may include fever, cough, runny nose, wheezing, and breathing problems. More severe cases may be associated with nasal flaring, grunting, or the skin between the ribs pulling in with breathing. If the child has not been able to feed properly, signs of dehydration may be present.

Rhinitis irritation and inflammation of the mucous membrane inside the nose

Rhinitis, also known as coryza, is irritation and inflammation of the mucous membrane inside the nose. Common symptoms are a stuffy nose, runny nose, sneezing, and post-nasal drip.

Upper respiratory tract infection

An upper respiratory tract infection (URTI) is an illness caused by an acute infection, which involves the upper respiratory tract, including the nose, sinuses, pharynx, or larynx. This commonly includes nasal obstruction, sore throat, tonsillitis, pharyngitis, laryngitis, sinusitis, otitis media, and the common cold. Most infections are viral in nature, and in other instances, the cause is bacterial. URTIs can also be fungal or helminthic in origin, but these are far less common.

Lower respiratory tract infection

Lower respiratory tract infection (LRTI), while often used as a synonym for pneumonia, can also be applied to other types of infection including lung abscess and acute bronchitis. Symptoms include shortness of breath, weakness, fever, coughing and fatigue.

Bronchoconstriction Constriction of the airways in the lungs

Bronchoconstriction is the constriction of the airways in the lungs due to the tightening of surrounding smooth muscle, with consequent coughing, wheezing, and shortness of breath.

Occupational asthma refers to new onset asthma or the recurrence of previously quiescent asthma directly caused by exposure to an agent at workplace. It is an occupational lung disease and a type of work-related asthma. Agents that can induce occupational asthma can be grouped into sensitizers and irritants.

Bronchitis type of lower respiratory disease

Bronchitis is an inflammation of the bronchi in the lungs. Symptoms include coughing up sputum, wheezing, shortness of breath, and chest discomfort. Bronchitis is divided into two types: acute and chronic. Acute bronchitis is also known as a chest cold.

Alternative treatments used for the common cold include numerous home remedies and alternative medicines. Scientific research regarding the efficacy of each treatment is generally nonexistent or inconclusive. Current best evidence indicates prevention, including hand washing and neatness, and management of symptoms.

Acute exacerbation of chronic obstructive pulmonary disease

Acute exacerbation of COPD is a sudden worsening of COPD symptoms that typically lasts for several days. It may be triggered by an infection with bacteria or viruses or by environmental pollutants. Typically, infections cause 75% or more of the exacerbations; bacteria can roughly be found in 25% of cases, viruses in another 25%, and both viruses and bacteria in another 25%. Airway inflammation is increased during the exacerbation resulting in increased hyperinflation, reduced expiratory air flow and decreased gas exchange.

Eosinophilic bronchitis

Eosinophilic bronchitis (EB) is a type of airway inflammation due to excessive mast cell recruitment and activation in the superficial airways as opposed to the smooth muscles of the airways as seen in asthma. It often results in a chronic cough. Lung function tests are usually normal. Inhaled corticosteroids are often an effective treatment.

Chronic obstructive pulmonary disease type of lung disease characterized by long-term poor airflow

Chronic obstructive pulmonary disease (COPD) is a type of obstructive lung disease characterized by long-term breathing problems and poor airflow. The main symptoms include shortness of breath and cough with sputum production. COPD is a progressive disease, meaning it typically worsens over time. Eventually everyday activities such as walking or getting dressed, become difficult. Chronic bronchitis and emphysema are older terms used for different types of COPD. The term "chronic bronchitis" is still used to define a productive cough that is present for at least three months each year for two years.

References

  1. GINA 2011, p. 18
  2. 1 2 British Guideline 2009 , p. 4
  3. 1 2 3 4 5 6 7 8 9 10 "Asthma Fact sheet №307". WHO. November 2013. Archived from the original on June 29, 2011. Retrieved 3 March 2016.
  4. 1 2 3 4 Martinez F. D. (2007). "Genes, environments, development and asthma: a reappraisal". European Respiratory Journal. 29 (1): 179–84. doi:10.1183/09031936.00087906. PMID   17197483.
  5. 1 2 3 Lemanske, R. F.; Busse, W. W. (February 2010). "Asthma: clinical expression and molecular mechanisms". J. Allergy Clin. Immunol. 125 (2 Suppl 2): S95–102. doi:10.1016/j.jaci.2009.10.047. PMC   2853245 . PMID   20176271.
  6. 1 2 NHLBI Guideline 2007 , pp. 169–72
  7. 1 2 3 4 5 NHLBI Guideline 2007 , p. 214
  8. 1 2 GBD 2015 Disease and Injury Incidence and Prevalence, Collaborators (8 October 2016). "Global, regional, and national incidence, prevalence, and years lived with disability for 310 diseases and injuries, 1990–2015: a systematic analysis for the Global Burden of Disease Study 2015". Lancet. 388 (10053): 1545–1602. doi:10.1016/S0140-6736(16)31678-6. PMC   5055577 . PMID   27733282.
  9. 1 2 GBD 2015 Mortality and Causes of Death, Collaborators (8 October 2016). "Global, regional, and national life expectancy, all-cause mortality, and cause-specific mortality for 249 causes of death, 1980–2015: a systematic analysis for the Global Burden of Disease Study 2015". Lancet. 388 (10053): 1459–1544. doi:10.1016/S0140-6736(16)31012-1. PMC   5388903 . PMID   27733281.
  10. NHLBI Guideline 2007 , pp. 11–12
  11. GINA 2011 , p. 20,51
  12. 1 2 3 Yawn B. P. (September 2008). "Factors accounting for asthma variability: achieving optimal symptom control for individual patients" (PDF). Primary Care Respiratory Journal. 17 (3): 138–47. doi:10.3132/pcrj.2008.00004. PMID   18264646. Archived (PDF) from the original on 2010-03-04.
  13. 1 2 Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson; Aster, Jon, eds. (2010). Robbins and Cotran pathologic basis of disease (8th ed.). Saunders. p. 688. ISBN   978-1-4160-3121-5. OCLC   643462931.
  14. Stedman's Medical Dictionary (28 ed.). Lippincott Williams & Wilkins. 2005. ISBN   978-0-7817-3390-8.
  15. GINA 2011 , p. 71
  16. GINA 2011 , p. 33
  17. 1 2 3 4 Scott J. P., Peters-Golden M. (September 2013). "Antileukotriene agents for the treatment of lung disease". Am. J. Respir. Crit. Care Med. 188 (5): 538–44. doi:10.1164/rccm.201301-0023PP. PMID   23822826.CS1 maint: Uses authors parameter (link)
  18. 1 2 3 NHLBI Guideline 2007 , pp. 373–75
  19. Global Burden of Disease Study 2013, Collaborators (22 August 2015). "Global, regional, and national incidence, prevalence, and years lived with disability for 301 acute and chronic diseases and injuries in 188 countries, 1990–2013: a systematic analysis for the Global Burden of Disease Study 2013.journal=Lancet". Lancet. 386 (9995): 743–800. doi:10.1016/s0140-6736(15)60692-4. PMC   4561509 . PMID   26063472.
  20. 1 2 Anandan C., Nurmatov U., van Schayck O. C., Sheikh A. (February 2010). "Is the prevalence of asthma declining? Systematic review of epidemiological studies". Allergy. 65 (2): 152–67. doi:10.1111/j.1398-9995.2009.02244.x. PMID   19912154.CS1 maint: Uses authors parameter (link)
  21. 1 2 Manniche L. (1999). Sacred luxuries: fragrance, aromatherapy, and cosmetics in ancient Egypt. Cornell University Press. p.  49. ISBN   978-0-8014-3720-5.
  22. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 Murray, John F. (2010). "Ch. 38 Asthma". In Mason, Robert J.; Murray, John F.; Broaddus, V. Courtney; Nadel, Jay A.; Martin, Thomas R.; King, Jr., Talmadge E.; Schraufnagel, Dean E. (eds.). Murray and Nadel's textbook of respiratory medicine (5th ed.). Elsevier. ISBN   978-1-4160-4710-0.
  23. 1 2 3 4 5 6 7 8 9 10 GINA 2011 , pp. 2–5
  24. Jindal, editor-in-chief SK (2011). Textbook of pulmonary and critical care medicine. New Delhi: Jaypee Brothers Medical Publishers. p. 242. ISBN   978-93-5025-073-0. Archived from the original on 2016-04-24.CS1 maint: Extra text: authors list (link)
  25. George, Ronald B. (2005). Chest medicine : essentials of pulmonary and critical care medicine (5th ed.). Philadelphia: Lippincott Williams & Wilkins. p. 62. ISBN   978-0-7817-5273-2. Archived from the original on 2016-05-05.
  26. British Guideline 2009 , p. 14
  27. GINA 2011 , pp. 8–9
  28. Boulet L. P. (April 2009). "Influence of comorbid conditions on asthma". European Respiratory Journal. 33 (4): 897–906. doi:10.1183/09031936.00121308. PMID   19336592.
  29. Boulet, L. P.; Boulay, M. È. (June 2011). "Asthma-related comorbidities". Expert Review of Respiratory Medicine. 5 (3): 377–93. doi:10.1586/ers.11.34. PMID   21702660.
  30. 1 2 editors, Andrew Harver, Harry Kotses (2010). Asthma, health and society a public health perspective. New York: Springer. p. 315. ISBN   978-0-387-78285-0. Archived from the original on 2016-05-12.
  31. 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): 250–56. doi:10.4104/pcrj.2011.00058. PMID   21674122.
  32. Webb, edited by Henrik S. Thomsen, Judith A. W. (2014). Contrast media : safety issues and ESUR guidelines (Third ed.). Dordrecht: Springer. p. 54. ISBN   978-3-642-36724-3. Archived from the original on 2017-09-08.CS1 maint: Extra text: authors list (link)
  33. 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): 567–73. doi:10.1164/rccm.200710-1511PP. PMC   2267336 . PMID   18187692.
  34. Choudhry S; Seibold MA; Borrell LN; et al. (2007). "Dissecting complex diseases in complex populations: asthma in latino americans". Proc Am Thorac Soc. 4 (3): 226–33. doi:10.1513/pats.200701-029AW. PMC   2647623 . PMID   17607004.
  35. Dietert, RR (September 2011). "Maternal and childhood asthma: risk factors, interactions, and ramifications". Reproductive Toxicology (Elmsford, N.Y.). 32 (2): 198–204. doi:10.1016/j.reprotox.2011.04.007. PMID   21575714.
  36. Tan, DJ; Walters, EH; Perret, JL; Lodge, CJ; Lowe, AJ; Matheson, MC; Dharmage, SC (February 2015). "Age-of-asthma onset as a determinant of different asthma phenotypes in adults: a systematic review and meta-analysis of the literature". Expert Review of Respiratory Medicine. 9 (1): 109–23. doi:10.1586/17476348.2015.1000311. PMID   25584929.
  37. Kelly, FJ; Fussell, JC (August 2011). "Air pollution and airway disease". Clinical and Experimental Allergy. 41 (8): 1059–71. doi:10.1111/j.1365-2222.2011.03776.x. PMID   21623970.
  38. GINA 2011 , p. 6
  39. GINA 2011 , p. 61
  40. 1 2 Gold, D. R.; Wright, R. (2005). "Population disparities in asthma". Annu Rev Public Health. 26: 89–113. doi:10.1146/annurev.publhealth.26.021304.144528. PMID   15760282.
  41. American Lung, Association (June 2001). "Urban air pollution and health inequities: a workshop report". Environmental Health Perspectives. 109 Suppl 3: 357–74. doi:10.1289/ehp.01109s3357. PMC   1240553 . PMID   11427385.
  42. Brooks, Nancy; Sethi, Rajiv (February 1997). "The Distribution of Pollution: Community Characteristics and Exposure to Air Toxics". Journal of Environmental Economics and Management. 32 (2): 233–50. doi:10.1006/jeem.1996.0967.
  43. McGwin, G; Lienert, J; Kennedy, JI (March 2010). "Formaldehyde exposure and asthma in children: a systematic review". Environmental Health Perspectives. 118 (3): 313–17. doi:10.1289/ehp.0901143. PMC   2854756 . PMID   20064771.
  44. 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. doi:10.1289/ehp.10846. PMC   2453150 . PMID   18629304.
  45. Bornehag, CG; Nanberg, E (April 2010). "Phthalate exposure and asthma in children". International Journal of Andrology. 33 (2): 333–45. doi:10.1111/j.1365-2605.2009.01023.x. PMID   20059582.
  46. Mamane, A; Baldi, I; Tessier, JF; Raherison, C; Bouvier, G (June 2015). "Occupational exposure to pesticides and respiratory health". European Respiratory Review. 24 (136): 306–19. doi:10.1183/16000617.00006014. PMID   26028642.
  47. Mamane, A; Raherison, C; Tessier, JF; Baldi, I; Bouvier, G (September 2015). "Environmental exposure to pesticides and respiratory health". European Respiratory Review. 24 (137): 462–73. doi:10.1183/16000617.00006114. PMID   26324808.
  48. Henderson, AJ; Shaheen, SO (Mar 2013). "Acetaminophen and asthma". Paediatric Respiratory Reviews. 14 (1): 9–15, quiz 16. doi:10.1016/j.prrv.2012.04.004. PMID   23347656.
  49. 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. doi:10.1007/s00228-012-1463-7. PMC   3651816 . PMID   23292157.
  50. 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. 100 (1): 81–9. doi:10.1136/archdischild-2012-303043. PMID   25429049.
  51. 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. 41 (4): 482–89. doi:10.1111/j.1365-2222.2010.03691.x. PMID   21338428.
  52. van de Loo, KF; van Gelder, MM; Roukema, J; Roeleveld, N; Merkus, PJ; Verhaak, CM (January 2016). "Prenatal maternal psychological stress and childhood asthma and wheezing: a meta-analysis". The European Respiratory Journal. 47 (1): 133–46. doi:10.1183/13993003.00299-2015. PMID   26541526.
  53. 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. doi:10.1097/ACI.0b013e3283445921. PMID   21301330.
  54. 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. doi:10.1007/s11882-009-0082-6. PMID   20425514.
  55. Custovic, A; Simpson, A (2012). "The role of inhalant allergens in allergic airways disease". Journal of Investigational Allergology and Clinical Immunology. 22 (6): 393–401, quiz follow 401. PMID   23101182.
  56. 1 2 PC Gøtzsche; HK Johansen (2008). Gøtzsche, Peter C (ed.). "House dust mite control measures for asthma". Cochrane Database of Systematic Reviews (2): CD001187. doi:10.1002/14651858.CD001187.pub3. PMID   18425868.
  57. Calderon, Moises; et al. (2015). "Respiratory allergy caused by house dust mites: What do we really know?". Journal of Allergy and Clinical Immunology. 136 (1): 38–48. doi:10.1016/j.jaci.2014.10.012. PMID   25457152.
  58. 1 2 NHLBI Guideline 2007 , p. 11
  59. Ramsey, CD; Celedón JC (January 2005). "The hygiene hypothesis and asthma". Current Opinion in Pulmonary Medicine. 11 (1): 14–20. doi:10.1097/01.mcp.0000145791.13714.ae. PMID   15591883.
  60. Bufford, J. D.; Gern J. E. (May 2005). "The hygiene hypothesis revisited". Immunology and Allergy Clinics of North America. 25 (2): 247–62. doi:10.1016/j.iac.2005.03.005. PMID   15878454.
  61. 1 2 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): 70–77. doi:10.1097/ACI.0b013e32835ad0d2. PMID   23103806.
  62. Rao, D; Phipatanakul, W (October 2011). "Impact of environmental controls on childhood asthma". Current Allergy and Asthma Reports. 11 (5): 414–20. doi:10.1007/s11882-011-0206-7. PMC   3166452 . PMID   21710109.
  63. 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. doi:10.1542/peds.2010-2092. PMID   21606151.
  64. British Guideline 2009 , p. 72
  65. 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. doi:10.1016/j.clp.2011.03.008. PMC   3110651 . PMID   21645799.
  66. Von Hertzen, LC; Haahtela, T (February 2004). "Asthma and atopy -the price of affluence?". Allergy. 59 (2): 124–37. doi:10.1046/j.1398-9995.2003.00433.x. PMID   14763924.
  67. 1 2 Martinez FD (2007). "CD14, endotoxin, and asthma risk: actions and interactions". Proc Am Thorac Soc. 4 (3): 221–25. doi:10.1513/pats.200702-035AW. PMC   2647622 . PMID   17607003.
  68. 1 2 3 Elward, Graham Douglas, Kurtis S. (2010). Asthma. London: Manson Pub. pp. 27–29. ISBN   978-1-84076-513-7. Archived from the original on 2016-05-17.
  69. 1 2 3 Ober C, Hoffjan S (2006). "Asthma genetics 2006: the long and winding road to gene discovery". Genes Immun. 7 (2): 95–100. doi:10.1038/sj.gene.6364284. PMID   16395390.
  70. Halapi, E; Bjornsdottir, US (January 2009). "Overview on the current status of asthma genetics". The Clinical Respiratory Journal. 3 (1): 2–7. doi:10.1111/j.1752-699X.2008.00119.x. PMID   20298365.
  71. 1 2 Rapini, Ronald P.; Bolognia, Jean L.; Jorizzo, Joseph L. (2007). Dermatology: 2-Volume Set. St. Louis: Mosby. ISBN   978-1-4160-2999-1.
  72. GINA 2011 , p. 4
  73. J. C. Jennette; R. J. Falk; P. A. Bacon; et al. (January 2013). "2012 Revised International Chapel Hill Consensus Conference Nomenclature of Vasculitides". Arthritis & Rheumatism . 65 (1): 1–11. doi:10.1002/art.37715. PMID   23045170.
  74. Beuther DA (January 2010). "Recent insight into obesity and asthma". Current Opinion in Pulmonary Medicine. 16 (1): 64–70. doi:10.1097/MCP.0b013e3283338fa7. PMID   19844182.
  75. Holguin F, Fitzpatrick A (March 2010). "Obesity, asthma, and oxidative stress". J. Appl. Physiol. 108 (3): 754–59. doi:10.1152/japplphysiol.00702.2009. PMID   19926826.
  76. Wood LG, Gibson PG (July 2009). "Dietary factors lead to innate immune activation in asthma". Pharmacol. Ther. 123 (1): 37–53. doi:10.1016/j.pharmthera.2009.03.015. PMID   19375453.
  77. O'Rourke ST (October 2007). "Antianginal actions of beta-adrenoceptor antagonists". Am J Pharm Educ. 71 (5): 95. doi:10.5688/aj710595. PMC   2064893 . PMID   17998992.
  78. Salpeter, S; Ormiston, T; Salpeter, E (2002). "Cardioselective beta-blockers for reversible airway disease". The Cochrane Database of Systematic Reviews (4): CD002992. doi:10.1002/14651858.CD002992. PMID   12519582.
  79. 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. doi:10.1378/chest.13-1235. PMID   24202435.
  80. Covar, RA; Macomber, BA; Szefler, SJ (February 2005). "Medications as asthma triggers". Immunology and Allergy Clinics of North America. 25 (1): 169–90. doi:10.1016/j.iac.2004.09.009. PMID   15579370.
  81. Lai, Tianwen; Wu, Mindan; Liu, Juan; Luo, Man; He, Lulu; Wang, Xiaohui; Wu, Bin; Ying, Songmin; Chen, Zhihua; Li, Wen; Shen, Huahao (February 2018). "Acid-Suppressive Drug Use During Pregnancy and the Risk of Childhood Asthma: A Meta-analysis". Pediatrics. 141 (2): e20170889. doi:10.1542/peds.2017-0889. PMID   29326337.
  82. 1 2 3 4 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. PMC   2975603 . PMID   20568555.
  83. Sharpe, RA; Bearman, N; Thornton, CR; Husk, K; Osborne, NJ (January 2015). "Indoor fungal diversity and asthma: a meta-analysis and systematic review of risk factors". The Journal of Allergy and Clinical Immunology. 135 (1): 110–22. doi:10.1016/j.jaci.2014.07.002. PMID   25159468.
  84. Chen E, Miller GE (2007). "Stress and inflammation in exacerbations of asthma". Brain Behav. Immun. 21 (8): 993–99. doi:10.1016/j.bbi.2007.03.009. PMC   2077080 . PMID   17493786.
  85. 1 2 NHLBI Guideline 2007 , p. 42
  86. GINA 2011 , p. 20
  87. American Academy of Allergy, Asthma, and Immunology. "Five things physicians and patients should question" (PDF). Choosing Wisely: An Initiative of the ABIM Foundation. Archived from the original (PDF) on November 3, 2012. Retrieved August 14, 2012.CS1 maint: Uses authors parameter (link)
  88. 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. Archived from the original on 2011-08-27.CS1 maint: Uses authors parameter (link)
  89. Welsh, E. J.; Bara, A.; Barley, E.; Cates, C. J. (2010). Welsh, Emma J (ed.). "Caffeine for asthma" (PDF). Cochrane Database of Systematic Reviews (1): CD001112. doi:10.1002/14651858.CD001112.pub2. PMID   20091514.
  90. NHLBI Guideline 2007 , p. 58
  91. Pinnock H, Shah R (2007). "Asthma". BMJ. 334 (7598): 847–50. doi:10.1136/bmj.39140.634896.BE. PMC   1853223 . PMID   17446617.
  92. NHLBI Guideline 2007 , p. 59
  93. 1 2 Moore W. C., Pascual R. M. (June 2010). "Update in asthma 2009". American Journal of Respiratory and Critical Care Medicine. 181 (11): 1181–87. doi:10.1164/rccm.201003-0321UP. PMC   3269238 . PMID   20516492.CS1 maint: Uses authors parameter (link)
  94. 1 2 Self, Timothy; Chrisman, Cary; Finch, Christopher (2009). "22. Asthma". In Mary Anne Koda-Kimble, Brian K. Alldredge; et al. (eds.). Applied therapeutics: the clinical use of drugs (9th ed.). Philadelphia: Lippincott Williams & Wilkins. OCLC   230848069.
  95. Delacourt, C. (June 2004). "Conséquences bronchiques de l'asthme non traité" [Bronchial changes in untreated asthma]. Archives de Pédiatrie. 11 (Suppl. 2): 71s–73s. doi:10.1016/S0929-693X(04)90003-6. PMID   15301800.
  96. Schiffman, George (18 December 2009). "Chronic obstructive pulmonary disease". MedicineNet. Archived from the original on 28 August 2010. Retrieved 2 September 2010.
  97. 1 2 3 4 British Guideline 2009 , p. 54
  98. Current Review of Asthma. London: Current Medicine Group. 2003. p. 42. ISBN   978-1-4613-1095-2. Archived from the original on 2017-09-08.
  99. Barnes, P. J. (2008). "Asthma". In Fauci, Anthony S.; Braunwald, E.; Kasper, D. L. (eds.). Harrison's Principles of Internal Medicine (17th ed.). New York: McGraw-Hill. pp. 1596–607. ISBN   978-0-07-146633-2.
  100. McMahon, Maureen (2011). Pediatrics a competency-based companion. Philadelphia, PA: Saunders/Elsevier. ISBN   978-1-4160-5350-7.
  101. Maitre B., Similowski T., Derenne J. P. (September 1995). "Physical examination of the adult patient with respiratory diseases: inspection and palpation". European Respiratory Journal. 8 (9): 1584–93. PMID   8575588. Archived from the original on 2015-04-29.CS1 maint: Uses authors parameter (link)
  102. Werner, H. A. (June 2001). "Status asthmaticus in children: a review". Chest. 119 (6): 1596–607. doi:10.1378/chest.119.6.1913. PMID   11399724.
  103. 1 2 Shiber J. R., Santana J. (May 2006). "Dyspnea". Med. Clin. North Am. 90 (3): 453–79. doi:10.1016/j.mcna.2005.11.006. PMID   16473100.CS1 maint: Uses authors parameter (link)
  104. 1 2 Shah, R.; Saltoun, C. A. (May–Jun 2012). "Chapter 14: Acute severe asthma (status asthmaticus)". Allergy and Asthma Proceedings. 33 Suppl 1 (3): S47–50. doi:10.2500/aap.2012.33.3547. PMID   22794687.
  105. 1 2 Khan, D. A. (Jan–Feb 2012). "Exercise-induced bronchoconstriction: burden and prevalence". Allergy and Asthma Proceedings. 33 (1): 1–6. doi:10.2500/aap.2012.33.3507. PMID   22370526.
  106. Wuestenfeld, J. C.; Wolfarth B. (Jan 2013). "Special considerations for adolescent athletic and asthmatic patients". Open Access Journal of Sports Medicine. 4: 1–7. doi:10.2147/OAJSM.S23438. PMC   3871903 . PMID   24379703.
  107. GINA 2011 , p. 17
  108. Carlsen, K. H.; Anderson, S. D.; Bjermer, L.; Bonini, S.; Brusasco, V.; Canonica, W.; Cummiskey, J.; Delgado, L.; Del Giacco, S. R.; Drobnic, F.; Haahtela, T.; Larsson, K.; Palange, P.; Popov, T.; van Cauwenberge, P. (May 2008). European Respiratory, Society; European Academy of Allergy and Clinical, Immunology; GA(2)LEN. "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. doi:10.1111/j.1398-9995.2008.01663.x. PMID   18394123.
  109. Kindermann, W. (2007). "Do inhaled beta(2)-agonists have an ergogenic potential in non-asthmatic competitive athletes?". Sports Medicine. 37 (2): 95–102. doi:10.2165/00007256-200737020-00001. PMID   17241101.
  110. Pluim, B. M.; de Hon, O.; Staal, J. B.; Limpens, J.; Kuipers, H.; Overbeek, S. E.; Zwinderman, A. H.; Scholten, R. J. (Jan 1, 2011). "β₂-Agonists and physical performance: a systematic review and meta-analysis of randomized controlled trials". Sports Medicine. 41 (1): 39–57. doi:10.2165/11537540-000000000-00000. PMID   21142283.
  111. 1 2 3 Baur, X.; Aasen, T. B.; Burge, P. S.; Heederik, D.; Henneberger, P. K.; Maestrelli, P.; Schlünssen, V.; Vandenplas, O.; Wilken, D. (Jun 1, 2012). ERS Task Force on the Management of Work-related, Asthma. "The management of work-related asthma guidelines: a broader perspective". European Respiratory Review. 21 (124): 125–39. doi:10.1183/09059180.00004711. PMID   22654084.
  112. Kunnamo, ed.-in-chief: Ilkka (2005). Evidence-based medicine guidelines. Chichester: Wiley. p. 214. ISBN   978-0-470-01184-3. Archived from the original on 2016-05-17.CS1 maint: Extra text: authors list (link)
  113. Kraft, editors, Mario Castro, Monica (2008). Clinical asthma. Philadelphia: Mosby / Elsevier. pp. Chapter 42. ISBN   978-0-323-07081-2. Archived from the original on 2016-05-28.CS1 maint: Extra text: authors list (link)
  114. Chang, J. E.; White, A.; Simon, R. A.; Stevenson, D. D. (2012). "Aspirin-exacerbated respiratory disease: burden of disease". Allergy and Asthma Proceedings. 33 (2): 117–21. doi:10.2500/aap.2012.33.3541. PMID   22525387.
  115. "Aspirin Exacerbated Respiratory Disease (AERD)". www.aaaai.org. American Academy of Allergy Asthma & Immunology. August 3, 2018.
  116. Kennedy JL, Stoner AN, Borish L (Nov–Dec 2018). "Aspirin-exacerbated respiratory disease: Prevalence, diagnosis, treatment, and considerations for the future". American Journal of Rhinology & Allergy. 30 (6): 407–13. doi:10.2500/ajra.2016.30.4370. PMC   5108840 . PMID   28124651.
  117. 1 2 3 Adams, K. E.; Rans, T. S. (December 2013). "Adverse reactions to alcohol and alcoholic beverages". Annals of Allergy, Asthma & Immunology. 111 (6): 439–45. doi:10.1016/j.anai.2013.09.016. PMID   24267355.
  118. Peters, S. P. (2014). "Asthma phenotypes: nonallergic (intrinsic) asthma". The Journal of Allergy and Clinical Immunology. In Practice. 2 (6): 650–52. doi:10.1016/j.jaip.2014.09.006. PMID   25439352.
  119. 1 2 NHLBI Guideline 2007 , p. 46
  120. Lichtenstein, Richard (2013). Pediatric emergencies. Philadelphia: Elsevier. p. 1022. ISBN   978-0-323-22733-9. Archived from the original on 2017-09-08.
  121. Gibson PG, McDonald VM, Marks GB (September 2010). "Asthma in older adults". Lancet. 376 (9743): 803–13. doi:10.1016/S0140-6736(10)61087-2. PMID   20816547.
  122. Hargreave, FE; Parameswaran, K (August 2006). "Asthma, COPD and bronchitis are just components of airway disease". European Respiratory Journal. 28 (2): 264–67. doi:10.1183/09031936.06.00056106. PMID   16880365.
  123. Diaz, P. Knoell (2009). "23. Chronic obstructive pulmonary disease". Applied therapeutics: the clinical use of drugs (9th ed.). Philadelphia: Lippincott Williams & Wilkins.
  124. 1 2 NHLBI Guideline 2007 , pp. 184–85
  125. "Asthma". World Health Organization. April 2017. Archived from the original on 29 June 2011. Retrieved 30 May 2017.
  126. Henneberger, PK (April 2007). "Work-exacerbated asthma". Current Opinion in Allergy and Clinical Immunology. 7 (2): 146–51. doi:10.1097/ACI.0b013e328054c640. PMID   17351467.
  127. 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. doi:10.1155/2012/176484. PMC   3251799 . PMID   22235226.
  128. 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. doi:10.1016/j.ijheh.2009.12.003. PMID   20053584.
  129. 1 2 Prescott, SL; Tang, ML (May 2, 2005). Australasian Society of Clinical Immunology and, Allergy. "The Australasian Society of Clinical Immunology and Allergy position statement: Summary of allergy prevention in children". The Medical Journal of Australia. 182 (9): 464–67. PMID   15865590.
  130. Cates, CJ; Rowe, BH (Feb 28, 2013). "Vaccines for preventing influenza in people with asthma". The Cochrane Database of Systematic Reviews. 2 (2): CD000364. doi:10.1002/14651858.CD000364.pub4. PMID   23450529.
  131. "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): 301–04. Jul 24, 2009. PMID   19630186.
  132. 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. doi:10.1016/S0140-6736(14)60082-9. PMID   24680633.
  133. Ripoll, Brian C. Leutholtz, Ignacio (2011). Exercise and disease management (2nd ed.). Boca Raton: CRC Press. p. 100. ISBN   978-1-4398-2759-8. Archived from the original on 2016-05-06.
  134. GINA 2011 , p. 56
  135. 1 2 3 4 5 6 NHLBI Guideline 2007 , p. 213
  136. 1 2 "British Guideline on the Management of Asthma" (PDF). Scottish Intercollegiate Guidelines Network. 2008. Archived (PDF) from the original on 19 August 2008. Retrieved 2008-08-04.
  137. 1 2 3 Kew, Kayleigh M.; Nashed, Marina; Dulay, Valdeep; Yorke, Janelle (2016-09-21). "Cognitive behavioural therapy (CBT) for adults and adolescents with asthma". The Cochrane Database of Systematic Reviews. 9: CD011818. doi:10.1002/14651858.CD011818.pub2. ISSN   1469-493X. PMID   27649894.
  138. NHLBI Guideline 2007 , p. 69
  139. 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. doi:10.1097/00130832-200502000-00011. PMID   15643345.
  140. Stapleton M, Howard-Thompson A, George C, Hoover RM, Self TH (2011). "Smoking and asthma". J Am Board Fam Med. 24 (3): 313–22. doi:10.3122/jabfm.2011.03.100180. PMID   21551404.
  141. 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. doi:10.1016/S0140-6736(14)60082-9. PMID   24680633.
  142. Carson, KV; Chandratilleke, MG; Picot, J; Brinn, MP; Esterman, AJ; Smith, BJ (30 September 2013). "Physical training for asthma". The Cochrane Database of Systematic Reviews. 9 (9): CD001116. doi:10.1002/14651858.CD001116.pub4. PMID   24085631.
  143. Yang, Zu-Yao; Zhong, Hui-Bin; Mao, Chen; Yuan, Jin-Qiu; Huang, Ya-Fang; Wu, Xin-Yin; Gao, Yuan-Mei; Tang, Jin-Ling (27 April 2016). "Yoga for asthma". Cochrane Database of Systematic Reviews. 4: CD010346. doi:10.1002/14651858.cd010346.pub2. PMID   27115477.
  144. "QRG 153 • British guideline on the management of asthma" (PDF). SIGN. September 2016. Archived (PDF) from the original on 9 October 2016. Retrieved 6 October 2016.
  145. 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. doi:10.1164/rccm.201303-0437ST. PMID   23634861.
  146. 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 (7): CD010283. doi:10.1002/14651858.CD010283.pub2. PMID   25080126.
  147. Rodrigo GJ, Nannini LJ (2006). "Comparison between nebulized adrenaline and beta2 agonists for the treatment of acute asthma. A meta-analysis of randomized trials". Am J Emerg Med. 24 (2): 217–22. doi:10.1016/j.ajem.2005.10.008. PMID   16490653.
  148. NHLBI Guideline 2007 , p. 351
  149. NHLBI Guideline 2007 , p. 218
  150. 1 2 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. doi:10.1002/14651858.CD005535.pub2. PMC   4169792 . PMID   20464739.
  151. 1 2 Ni Chroinin, Muireann; Greenstone, Ilana; Lasserson, Toby J.; Ducharme, Francine M. (2009-10-07). "Addition of inhaled long-acting beta2-agonists to inhaled steroids as first line therapy for persistent asthma in steroid-naive adults and children". The Cochrane Database of Systematic Reviews (4): CD005307. doi:10.1002/14651858.CD005307.pub2. ISSN   1469-493X. PMC   4170786 . PMID   19821344.
  152. 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. doi:10.1002/14651858.CD005533.pub2. PMC   4169793 . PMID   20393943.
  153. 1 2 Fanta CH (March 2009). "Asthma". New England Journal of Medicine. 360 (10): 1002–14. doi:10.1056/NEJMra0804579. PMID   19264689.
  154. 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 (4): CD006923. doi:10.1002/14651858.CD006923.pub3. PMC   4017186 . PMID   22513944.
  155. 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. doi:10.1002/14651858.CD006363.pub2. PMC   4015854 . PMID   18646149.
  156. 1 2 Chauhan, Bhupendrasinh F.; Chartrand, Caroline; Ni Chroinin, Muireann; Milan, Stephen J.; Ducharme, Francine M. (2015-11-24). "Addition of long-acting beta2-agonists to inhaled corticosteroids for chronic asthma in children". The Cochrane Database of Systematic Reviews (11): CD007949. doi:10.1002/14651858.CD007949.pub2. ISSN   1469-493X. PMID   26594816.
  157. Chauhan, Bhupendrasinh F.; Ducharme, Francine M. (2014-01-24). "Addition to inhaled corticosteroids of long-acting beta2-agonists versus anti-leukotrienes for chronic asthma". The Cochrane Database of Systematic Reviews (1): CD003137. doi:10.1002/14651858.CD003137.pub5. ISSN   1469-493X. PMID   24459050.
  158. 1 2 Chauhan, Bhupendrasinh F.; Jeyaraman, Maya M.; Singh Mann, Amrinder; Lys, Justin; Abou-Setta, Ahmed M.; Zarychanski, Ryan; Ducharme, Francine M. (2017-03-16). "Addition of anti-leukotriene agents to inhaled corticosteroids for adults and adolescents with persistent asthma". The Cochrane Database of Systematic Reviews. 3: CD010347. doi:10.1002/14651858.CD010347.pub2. ISSN   1469-493X. PMID   28301050.
  159. GINA 2011 , p. 74
  160. 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 (5): CD006100. doi:10.1002/14651858.CD006100.pub2. PMID   22592708.
  161. Miligkos, Michael; Bannuru, Raveendhara R.; Alkofide, Hadeel; Kher, Sucharita R.; Schmid, Christopher H.; Balk, Ethan M. (22 September 2015). "Leukotriene-Receptor Antagonists Versus Placebo in the Treatment of Asthma in Adults and Adolescents". Annals of Internal Medicine. 163 (10): 756–67. doi:10.7326/M15-1059. PMC   4648683 . PMID   26390230.
  162. British Guideline 2009 , p. 43
  163. Chauhan, Bhupendrasinh F.; Ben Salah, Raja; Ducharme, Francine M. (2013-10-02). "Addition of anti-leukotriene agents to inhaled corticosteroids in children with persistent asthma". The Cochrane Database of Systematic Reviews (10): CD009585. doi:10.1002/14651858.CD009585.pub2. ISSN   1469-493X. PMID   24089325.
  164. "Zyflo (Zileuton tablets)" (PDF). United States Food and Drug Administration. Cornerstone Therapeutics Inc. June 2012. p. 1. Archived (PDF) from the original on 13 December 2014. Retrieved 12 December 2014.
  165. 1 2 Nair, Parameswaran; Milan, Stephen J.; Rowe, Brian H. (2012-12-12). "Addition of intravenous aminophylline to inhaled beta(2)-agonists in adults with acute asthma". The Cochrane Database of Systematic Reviews. 12: CD002742. doi:10.1002/14651858.CD002742.pub2. ISSN   1469-493X. PMID   23235591.
  166. Kew, Kayleigh M.; Beggs, Sean; Ahmad, Shaleen (2015-05-21). "Stopping long-acting beta2-agonists (LABA) for children with asthma well controlled on LABA and inhaled corticosteroids". The Cochrane Database of Systematic Reviews (5): CD011316. doi:10.1002/14651858.CD011316.pub2. ISSN   1469-493X. PMID   25997166.
  167. 1 2 3 Ahmad, Shaleen; Kew, Kayleigh M.; Normansell, Rebecca (2015-06-19). "Stopping long-acting beta2-agonists (LABA) for adults with asthma well controlled by LABA and inhaled corticosteroids". The Cochrane Database of Systematic Reviews (6): CD011306. doi:10.1002/14651858.CD011306.pub2. ISSN   1469-493X. PMID   26089258.
  168. NHLBI Guideline 2007 , p. 250
  169. Travers, Andrew H.; Milan, Stephen J.; Jones, Arthur P.; Camargo, Carlos A.; Rowe, Brian H. (2012-12-12). "Addition of intravenous beta(2)-agonists to inhaled beta(2)-agonists for acute asthma". The Cochrane Database of Systematic Reviews. 12: CD010179. doi:10.1002/14651858.CD010179. ISSN   1469-493X. PMID   23235685.
  170. 1 2 Rachelefsky, G (January 2009). "Inhaled corticosteroids and asthma control in children: assessing impairment and risk". Pediatrics. 123 (1): 353–66. doi:10.1542/peds.2007-3273. PMID   19117903.
  171. Dahl R (August 2006). "Systemic side effects of inhaled corticosteroids in patients with asthma". Respir Med. 100 (8): 1307–17. doi:10.1016/j.rmed.2005.11.020. PMID   16412623.
  172. Thomas, MS; Parolia, A; Kundabala, M; Vikram, M (June 2010). "Asthma and oral health: a review". Australian Dental Journal. 55 (2): 128–33. doi:10.1111/j.1834-7819.2010.01226.x. PMID   20604752.
  173. Skoner, DP (December 2016). "Inhaled corticosteroids: Effects on growth and bone health". Annals of Allergy, Asthma & Immunology. 117 (6): 595–600. doi:10.1016/j.anai.2016.07.043. PMID   27979015.
  174. 1 2 3 Rodrigo GJ, Rodrigo C, Hall JB (2004). "Acute asthma in adults: a review". Chest. 125 (3): 1081–102. doi:10.1378/chest.125.3.1081. PMID   15006973.
  175. 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): 493–99. doi:10.1542/peds.2013-2273. PMC   3934336 . PMID   24515516.
  176. Rowe, BH; Kirkland, SW; Vandermeer, B; Campbell, S; Newton, A; Ducharme, FM; Villa-Roel, C (March 2017). "Prioritizing Systemic Corticosteroid Treatments to Mitigate Relapse in Adults With Acute Asthma: A Systematic Review and Network Meta-analysis". Academic Emergency Medicine. 24 (3): 371–381. doi:10.1111/acem.13107. PMID   27664401.
  177. Noppen, M. (August 2002). "Magnesium Treatment for Asthma : Where Do We Stand?". Chest. 122 (2): 396–98. doi:10.1378/chest.122.2.396. PMID   12171805.
  178. Griffiths, B; Kew, KM (29 April 2016). "Intravenous magnesium sulfate for treating children with acute asthma in the emergency department" (PDF). The Cochrane Database of Systematic Reviews. 4: CD011050. doi:10.1002/14651858.CD011050.pub2. PMID   27126744.
  179. Kew, KM; Kirtchuk, L; Michell, CI (28 May 2014). "Intravenous magnesium sulfate for treating adults with acute asthma in the emergency department" (PDF). The Cochrane Database of Systematic Reviews. 5 (5): CD010909. doi:10.1002/14651858.CD010909.pub2. PMID   24865567.
  180. GINA 2011 , p. 37
  181. NHLBI Guideline 2007 , p. 399
  182. 1 2 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. doi:10.1177/1753465810367505. PMID   20435668.
  183. Boulet, LP; Laviolette, M (May–Jun 2012). "Is there a role for bronchial thermoplasty in the treatment of asthma?". Canadian Respiratory Journal. 19 (3): 191–92. doi:10.1155/2012/853731. PMC   3418092 . PMID   22679610.
  184. GINA 2011 , p. 70
  185. "Pulmonary-Allergy Drugs Advisory Committee Meeting". FDA. July 25, 2018. Retrieved May 9, 2019.
  186. Sastre, J; Dávila, I (Jun 2018). "Dupilumab: A New Paradigm for the Treatment of Allergic Diseases". Journal of Investigative Allergology and Clinical Immunology. 28 (3): 139–150. doi:10.18176/jiaci.0254. PMID   29939132.
  187. Drazen, Jeffrey M.; Israel, Elliot; Reddel, Helen K. (7 September 2017). "Severe and Difficult-to-Treat Asthma in Adults". New England Journal of Medicine. 377 (10): 965–76. doi:10.1056/NEJMra1608969. PMID   28877019.
  188. McQueen, RB; Sheehan, DN; Whittington, MD; van Boven, JFM; Campbell, JD (August 2018). "Cost-Effectiveness of Biological Asthma Treatments: A Systematic Review and Recommendations for Future Economic Evaluations". PharmacoEconomics. 36 (8): 957–971. doi:10.1007/s40273-018-0658-x. PMID   29736895.
  189. 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. doi:10.1001/jama.2013.2049. PMID   23532243. Archived from the original on 8 September 2017.
  190. Korang, SK; Feinberg, J; Wetterslev, J; Jakobsen, JC (30 September 2016). "Non-invasive positive pressure ventilation for acute asthma in children". The Cochrane Database of Systematic Reviews. 9: CD012067. doi:10.1002/14651858.CD012067.pub2. PMID   27687114.
  191. 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): 1461–67. doi:10.1378/chest.120.5.1461. PMID   11713120.
  192. 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): 252–57. doi:10.1046/j.1440-1754.2002.00770.x. PMID   12047692.
  193. Kaur B, Rowe BH, Arnold E (2009). Welsh EJ (ed.). "Vitamin C supplementation for asthma". Cochrane Database of Systematic Reviews (1): CD000993. doi:10.1002/14651858.CD000993.pub3. hdl:10138/38500. PMC   6176494 . PMID   19160185. (Retracted, see doi:10.1002/14651858.cd000993.pub4. If this is an intentional citation to a retracted paper, please replace {{Retracted}} with {{Retracted |intentional=yes}}.)
  194. Hemilä, H (2013). "Vitamin C may alleviate exercise-induced bronchoconstriction: a meta-analysis". BMJ Open . 3 (6): e002416. doi:10.1136/bmjopen-2012-002416. PMC   3686214 . PMID   23794586. Open Access logo PLoS transparent.svg
  195. Martineau, AR; Cates, CJ; Urashima, M; Jensen, M; Griffiths, AP; Nurmatov, U; Sheikh, A; Griffiths, CJ (5 September 2016). "Vitamin D for the management of asthma" (PDF). The Cochrane Database of Systematic Reviews. 9: CD011511. doi:10.1002/14651858.CD011511.pub2. PMID   27595415.
  196. 1 2 NHLBI Guideline 2007 , p. 240
  197. McCarney RW, Brinkhaus B, Lasserson TJ, Linde K (2004). McCarney RW (ed.). "Acupuncture for chronic asthma". Cochrane Database of Systematic Reviews (1): CD000008. doi:10.1002/14651858.CD000008.pub2. PMID   14973944.
  198. Blackhall, K; Appleton, S; Cates, CJ (Sep 12, 2012). Blackhall, Karen (ed.). "Ionisers for chronic asthma". Cochrane Database of Systematic Reviews. 9 (9): CD002986. doi:10.1002/14651858.CD002986.pub2. PMID   22972060.
  199. Hondras MA, Linde K, Jones AP (2005). Hondras MA (ed.). "Manual therapy for asthma". Cochrane Database of Systematic Reviews (2): CD001002. doi:10.1002/14651858.CD001002.pub2. PMID   15846609.
  200. "WHO Disease and injury country estimates". World Health Organization. 2009. Archived from the original on 11 November 2009. Retrieved November 11, 2009.
  201. Sergel, Michelle J.; Cydulka, Rita K. (September 2009). "Ch. 75: Asthma". In Wolfson, Allan B.; Harwood-Nuss, Ann (eds.). Harwood-Nuss' Clinical Practice of Emergency Medicine (5th ed.). Lippincott Williams & Wilkins. pp. 432–. ISBN   978-0-7817-8943-1.
  202. NHLBI Guideline 2007 , p. 1
  203. 1 2 "The Global Asthma Report 2014". Archived from the original on 27 April 2016. Retrieved 10 May 2016.
  204. Organization, World Health (2008). The global burden of disease : 2004 update ([Online-Ausg.] ed.). Geneva: World Health Organization. p. 35. ISBN   978-92-4-156371-0.
  205. Maddox L, Schwartz DA (2002). "The pathophysiology of asthma". Annu. Rev. Med. 53: 477–98. doi:10.1146/annurev.med.53.082901.103921. PMID   11818486.
  206. Beckett PA, Howarth PH (2003). "Pharmacotherapy and airway remodelling in asthma?". Thorax. 58 (2): 163–74. doi:10.1136/thorax.58.2.163. PMC   1746582 . PMID   12554904.
  207. Silva, N; Carona, C; Crespo, C; Canavarro, MC (June 2015). "Quality of life in pediatric asthma patients and their parents: a meta-analysis on 20 years of research". Expert Review of Pharmacoeconomics & Outcomes Research . 15 (3): 499–519. doi:10.1586/14737167.2015.1008459. hdl:10316/45410. PMID   25651982.
  208. "World Health Organization Fact Sheet Fact sheet No 307: Asthma". 2011. Archived from the original on 2011-06-29. Retrieved Jan 17, 2013.
  209. GINA 2011 , p. 3
  210. 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. doi:10.1016/S0140-6736(12)61729-2. PMID   23245607.
  211. 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. doi:10.1016/S0140-6736(12)61728-0. hdl:10536/DRO/DU:30050819. PMID   23245604.
  212. World Health Organization. "WHO: Asthma". Archived from the original on 15 December 2007. Retrieved 2007-12-29.
  213. Bush A, Menzies-Gow A (December 2009). "Phenotypic differences between pediatric and adult asthma". Proc Am Thorac Soc. 6 (8): 712–19. doi:10.1513/pats.200906-046DP. PMID   20008882.
  214. 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. Archived from the original on 2014-08-03.
  215. Grant EN, Wagner R, Weiss KB (August 1999). "Observations on emerging patterns of asthma in our society". J Allergy Clin Immunol . 104 (2 Pt 2): S1–S9. doi:10.1016/S0091-6749(99)70268-X. PMID   10452783.
  216. 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. PMC   2626301 . PMID   16175830.
  217. Anderson, HR; Gupta R; Strachan DP; Limb ES (January 2007). "50 years of asthma: UK trends from 1955 to 2004". Thorax. 62 (1): 85–90. doi:10.1136/thx.2006.066407. PMC   2111282 . PMID   17189533.
  218. Masoli, Matthew (2004). Global Burden of Asthma (PDF). p. 9. Archived from the original (PDF) on 2013-05-02.
  219. "Asthma-related death rate in UK among highest in Europe, charity analysis finds". Pharmaceutical Journal. 3 May 2018. Retrieved 13 August 2018.
  220. 1 2 3 Barrett ML, Wier LM, 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. Archived from the original on 2014-03-28.
  221. Rosner, Fred (2002). "The Life of Moses Maimonides, a Prominent Medieval Physician" (PDF). Einstein Quart J Biol Med. 19 (3): 125–28. Archived (PDF) from the original on 2009-03-05.
  222. Thorowgood JC (November 1873). "On bronchial asthma". British Medical Journal . 2 (673): 600. doi:10.1136/bmj.2.673.600. PMC   2294647 . PMID   20747287.
  223. Gaskoin G (March 1872). "On the treatment of asthma". British Medical Journal . 1 (587): 339. doi:10.1136/bmj.1.587.339. PMC   2297349 . PMID   20746575.
  224. Berkart JB (June 1880). "The treatment of asthma". British Medical Journal . 1 (1016): 917–18. doi:10.1136/bmj.1.1016.917. PMC   2240555 . PMID   20749537.
    Berkart JB (June 1880). "The treatment of asthma". British Medical Journal . 1 (1017): 960–62. doi:10.1136/bmj.1.1017.960. PMC   2240530 . PMID   20749546.
  225. Bosworth FH (1886). "Hay fever, asthma, and allied affections". Transactions of the Annual Meeting of the American Climatological Association. 2: 151–70. PMC   2526599 . PMID   21407325.
  226. Doig RL (February 1905). "Epinephrin; especially in asthma". California State Journal of Medicine. 3 (2): 54–55. PMC   1650334 . PMID   18733372.
  227. 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. doi:10.1056/NEJMra1102783. PMID   22375974.
  228. 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. doi:10.1016/j.pcrj.2006.09.002. PMID   17092772.
  229. David McCullough (1981). Mornings on Horseback: The Story of an Extraordinary Family, a Vanished Way of Life and the Unique Child Who Became Theodore Roosevelt. Simon and Schuster. pp. 93–108. ISBN   978-0-7432-1830-6. Archived from the original on 2015-04-07.
  230. 1 2 Opolski M, Wilson I (September 2005). "Asthma and depression: a pragmatic review of the literature and recommendations for future research". Clin Pract Epidemiol Ment Health. 1: 18. doi:10.1186/1745-0179-1-18. PMC   1253523 . PMID   16185365.

Notes

Classification
D
External resources