WordNet
- the process of thickening by dehydration
- relating to or associated with the bronchi; "bronchial tubes"; "bronchial pneumonia"
- respiratory disorder characterized by wheezing; usually of allergic origin (同)asthma attack, bronchial_asthma
PrepTutorEJDIC
- 気管支の
- 喘息(ぜんそく)
- bronchusの複数形
Wikipedia preview
出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2013/05/14 18:47:17」(JST)
wiki en
For other uses, see Asthma (disambiguation).
| Asthma | |
|---|---|
| Classification and external resources | |
Peak flow meters are used to measure the peak expiratory flow rate, important in both monitoring and diagnosing asthma.[1] |
|
| ICD-10 | J45 |
| ICD-9 | 493 |
| OMIM | 600807 |
| DiseasesDB | 1006 |
| MedlinePlus | 000141 |
| eMedicine | article/806890 |
| MeSH | D001249 |
Asthma (from the Greek ἅσθμα, ásthma, "panting") is a common chronic inflammatory disease of the airways characterized by variable and recurring symptoms, reversible airflow obstruction, and bronchospasm.[2] Common symptoms include wheezing, coughing, chest tightness, and shortness of breath.[3]
Asthma is thought to be caused by a combination of genetic and environmental factors.[4] Its diagnosis is usually based on the pattern of symptoms, response to therapy over time, and spirometry.[5] It is clinically classified according to the frequency of symptoms, forced expiratory volume in one second (FEV1), and peak expiratory flow rate.[6] Asthma may also be classified as atopic (extrinsic) or non-atopic (intrinsic)[7] where atopy refers to a predisposition toward developing type 1 hypersensitivity reactions.[8]
Treatment of acute symptoms is usually with an inhaled short-acting beta-2 agonist (such as salbutamol) and oral corticosteroids.[9] In very severe cases intravenous corticosteroids, magnesium sulfate and hospitalization maybe required.[10] Symptoms can be prevented by avoiding triggers, such as allergens[11] and irritants, and by the use of inhaled corticosteroids.[12] Long-acting beta agonists (LABA) or leukotriene antagonists may be used in addition to inhaled corticosteroids if asthma symptoms remain uncontrolled.[13] The prevalence of asthma has increased significantly since the 1970s. As of 2011, 235–300 million people were affected globally,[14][15] including about 250,000 deaths.[15]
Contents
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Signs and symptoms
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Wheezing
The sound of wheezing as heard with a stethoscope.
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| Problems listening to this file? See media help. | |
Asthma is characterized by recurrent episodes of wheezing, shortness of breath, chest tightness, and coughing.[16] Sputum may be produced from the lung by coughing but is often hard to bring up.[17] During recovery from an attack it may appear pus like due to high levels of white blood cells called eosinophils.[18] Symptoms are usually worse at night and in the early morning or in response to exercise or cold air.[19] Some people with asthma rarely experience symptoms, usually in response to triggers, whereas others may have marked and persistent symptoms.[20]
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.[21] Psychological disorders are also more common[22] with anxiety disorders occurring in between 16–52% and mood disorders in 14–41%.[23] It however is not known if asthma causes psychological problems or if psychological problems lead to asthma.[24]
Causes
Asthma is caused by a combination of complex and incompletely understood environmental and genetic interactions.[4][25] These factors influence both its severity and its responsiveness to treatment.[26] 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.[27]
Environmental
Many environmental factors have been associated with asthma's development and exacerbation including: allergens, air pollution, and other environmental chemicals.[28] Smoking during pregnancy and after delivery is associated with a greater risk of asthma-like symptoms.[29] Low air quality, from traffic pollution or high ozone levels,[30] has been associated with both asthma development and increased asthma severity.[31] Exposure to indoor volatile organic compounds may be a trigger for asthma; formaldehyde exposure, for example, has a positive association.[32] Also, phthalates in PVC are associated with asthma in children and adults[33][34] as are high levels of endotoxin exposure.[35]
Asthma is associated with exposure to indoor allergens.[36] Common indoor allergens include: dust mites, cockroaches, animal dander, and mold.[37][38] Efforts to decrease dust mites have been found to be ineffective.[39] Certain viral respiratory infections may increase the risk of developing asthma when acquired as young children such as:[40] respiratory syncytial virus and rhinovirus.[41] Certain other infections however may decrease the risk.[41]
Hygiene hypothesis
The hygiene hypothesis is a theory which 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.[42][43] 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.[44] Evidence supporting the hygiene hypothesis includes lower rates of asthma on farms and in households with pets.[44]
Use of antibiotics in early life has been linked to the development of asthma.[45] Also, delivery via 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.[46][47] There is a link between asthma and the degree of affluence.[48]
Genetic
| Endotoxin levels | CC genotype | TT genotype |
|---|---|---|
| High exposure | Low risk | High risk |
| Low exposure | High risk | Low risk |
Family history is a risk factor for asthma with many different genes being implicated.[50] If one identical twin is affected, the probability of the other having the disease is approximately 25%.[50] 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.[51] 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.[51] In 2006 over 100 genes were associated with asthma in one genetic association study alone;[51] more continue to be found.[52]
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.[49]
Medical conditions
A triad of atopic eczema, allergic rhinitis and asthma is called atopy.[53] The strongest risk factor for developing asthma is a history of atopic disease;[40] with asthma occurring at a much greater rate in those who have either eczema or hay fever.[54] Asthma has been associated with Churg–Strauss syndrome, an autoimmune disease and vasculitis. Individuals with certain types of urticaria may also experience symptoms of asthma.[53]
There is a correlation between obesity and the risk of asthma with both having increased in recent years.[55][56] 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.[57]
Beta blocker medications such as propranolol can trigger asthma in those who are susceptible.[58] Cardioselective beta-blockers, however, appear safe in those with mild or moderate disease.[59] Other medications that can cause problems are ASA, NSAIDs, and angiotensin-converting enzyme inhibitors.[60]
Exacerbation
Some individuals will have stable asthma for weeks or months and then suddenly develop an episode of acute asthma. Different individuals react differently to various factors.[61] Most individuals can develop severe exacerbation from a number of triggering agents.[61]
Home factors that can lead to exacerbation of asthma include dust, animal dander (especially cat and dog hair), cockroach allergens and mold.[61] Perfumes are a common cause of acute attacks in women and children. Both viral and bacterial infections of the upper respiratory tract can worsen the disease.[61] 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.[31][62]
Pathophysiology
Main article: Pathophysiology of asthma
Obstruction of the lumen of a bronchiole by mucoid exudate, goblet cell metaplasia, and epithelial basement membrane thickening in a person with asthma.
Asthma is the result of chronic inflammation of the airways which subsequently results in increased contractability of the surrounding smooth muscles. This among other factors leads to bouts of narrowing of the airway and the classic symptoms of wheezing. The narrowing is typically reversible with or without treatment. Occasionally the airways themselves change.[16] 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.[41]
Diagnosis
While asthma is a well recognized condition, there is not one universal agreed upon definition.[41] 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".[16]
There is currently no precise test with the diagnosis typically based on the pattern of symptoms and response to therapy over time.[5][41] 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.[63] Spirometry is then used to confirm the diagnosis.[63] In children under the age of six the diagnosis is more difficult as they are too young for spirometry.[64]
Spirometry
Spirometry is recommended to aid in diagnosis and management.[65][66] It is the single best test for asthma. If the FEV1 measured by this technique improves more than 12% following administration of a bronchodilator such as salbutamol, this is supportive of the diagnosis.[67] It however may be normal in those with a history of mild asthma, not currently acting up. Single-breath diffusing capacity can help differentiate asthma from COPD.[41] It is reasonable to perform spirometry every one or two years to follow how well a person's asthma is controlled.[68]
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.[41]
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.[69] 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.[70]
Classification
| Severity | Symptom frequency | Night time symptoms | %FEV1 of predicted | FEV1 Variability | SABA use |
|---|---|---|---|---|---|
| Intermittent | ≤2/week | ≤2/month | ≥80% | <20% | ≤2 days/week |
| Mild persistent | >2/week | 3–4/month | ≥80% | 20–30% | >2 days/week |
| Moderate persistent | Daily | >1/week | 60–80% | >30% | daily |
| Severe persistent | Continuously | Frequent (7×/week) | <60% | >30% | ≥twice/day |
Asthma is clinically classified according to the frequency of symptoms, forced expiratory volume in one second (FEV1), and peak expiratory flow rate.[6] 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).[7] While asthma is classified based on severity, at the moment there is no clear method for classifying different subgroups of asthma beyond this system.[71] Finding ways to identify subgroups that respond well to different types of treatments is a current critical goal of asthma research.[71]
Although asthma is a chronic obstructive condition, it is not considered as a part of chronic obstructive pulmonary disease as this term refers specifically to combinations of disease that are irreversible such as bronchiectasis, chronic bronchitis, and emphysema.[72] 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.[73] In contrast to emphysema, asthma affects the bronchi, not the alveoli.[74]
Asthma exacerbation
| Near-fatal | High PaCO2 and/or requiring mechanical ventilation | |
|---|---|---|
| Life threatening (any one of) |
||
| Clinical signs | Measurements | |
| 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 | ||
| Moderate | Worsening 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.[41] While these are the primary symptoms of asthma,[76] some people present primarily with coughing, and in severe cases, air motion may be significantly impaired such that no wheezing is heard.[75]
Signs which occur during an asthma attack include the use of accessory muscles of respiration (sternocleidomastoid and scalene muscles of the neck), there may be a paradoxical pulse (a pulse that is weaker during inhalation and stronger during exhalation), and over-inflation of the chest.[77] A blue color of the skin and nails may occur from lack of oxygen.[78]
In a mild exacerbation the peak expiratory flow rate (PEFR) is ≥200 L/min or ≥50% of the predicted best.[79] 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.[79]
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.[80] Half of cases are due to infections with others caused by allergen, air pollution, or insufficient or inappropriate medication use.[80]
Brittle asthma is a kind of asthma distinguishable by recurrent, severe attacks.[75] Type 1 brittle asthma is a disease with wide peak flow variability, despite intense medication. Type 2 brittle asthma is background well-controlled asthma with sudden severe exacerbations.[75]
Exercise-induced
Main article: Exercise-induced bronchoconstriction
Exercise can trigger bronchoconstriction in both people with and without asthma.[81] It occurs in most people with asthma and up to 20% of people without asthma.[81] In athletes it occurs more common in elite athletes, with rates varying from 3% for bobsled racers to 50% for cycling and 60% for cross-country skiing.[81] While it may occur with any weather conditions it is more common when it is dry and cold.[82] Inhaled beta2-agonists do not appear to improve athletic performance among those without asthma[83] however oral doses may improve endurance and strength.[84][85]
Occupational
Main article: Occupational asthma
Asthma as a result of (or worsened by) workplace exposures, is a commonly reported occupational disease.[86] Many cases however are not reported or recognized as such.[87][88] It is estimated that 5–25% of asthma 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.[86]
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 or laryngotracheomalacia, vascular rings, enlarged lymph nodes or neck masses. In adults, COPD, congestive heart failure, airway masses, as well as drug-induced coughing due to ACE inhibitors should be considered. In both populations vocal cord dysfunction may present similarly.[89]
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.[90] 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.[91][92]
Prevention
The evidence for the effectiveness of measures to prevent the development of asthma is weak.[93] Some show promise including: limiting smoke exposure both in utero and after delivery, breastfeeding, and increased exposure to daycare or large families but none are well supported enough to be recommended for this indication.[93] Early pet exposure may be useful.[94] Results from exposure to pets at other times are inconclusive[95] and it is only recommended that pets be removed from the home if a person has allergic symptoms to said pet.[96] Dietary restrictions during pregnancy or when breast feeding have not been found to be effective and thus are not recommended.[96] Reducing or eliminating compounds known to sensitive people from the work place may be effective.[86]
Management
While there is no cure for asthma, symptoms can typically be improved.[97] 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 treament according to changes in symptoms.[98]
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.[99][100]
Bronchodilators are recommended for short-term relief of symptoms. In those with occasional attacks, no other medication is needed. If mild persistent disease is present (more than two attacks a week), low-dose inhaled corticosteroids or alternatively, an oral leukotriene antagonist or a mast cell stabilizer is recommended. For those who have daily attacks, a higher dose of inhaled corticosteroids is used. In a moderate or severe exacerbation, oral corticosteroids are added to these treatments.[9]
Lifestyle modification
Avoidance of triggers is a key component of improving control and preventing attacks. The most common triggers include allergens, smoke (tobacco and other), air pollution, non selective beta-blockers, and sulfite-containing foods.[101][102] Cigarette smoking and second-hand smoke (passive smoke) may reduce the effectiveness of medications such as corticosteroids.[103] Dust mite control measures, including air filtration, chemicals to kill mites, vacuuming, mattress covers and others methods had no effect on asthma symptoms.[39]
Medications
Medications used to treat asthma are divided into two general classes: quick-relief medications used to treat acute symptoms; and long-term control medications used to prevent further exacerbation.[99]
- Fast–acting
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.[9]
- Anticholinergic medications, such as ipratropium bromide, provide additional benefit when used in combination with SABA in those with moderate or severe symptoms.[9] Anticholinergic bronchodilators can also be used if a person cannot tolerate a SABA.[72]
- Older, less selective adrenergic agonists, such as inhaled epinephrine, have similar efficacy to SABAs.[104] They are however not recommended due to concerns regarding excessive cardiac stimulation.[105]
- Long–term control
Fluticasone propionate metered dose inhaler commonly used for long-term control.
- Corticosteroids are generally considered the most effective treatment available for long-term control.[99] Inhaled forms such as beclomethasone are usually used except in the case of severe persistent disease, in which oral corticosteroids may be needed.[99] It is usually recommended that inhaled formulations be used once or twice daily, depending on the severity of symptoms.[106]
- 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.[107] In children this benefit is uncertain.[107][108] When used without steroids they increase the risk of severe side-effects[109] and even with corticosteroids they may slightly increase the risk.[110][111]
- Leukotriene antagonists (such as montelukast and zafirlukast) may be used in addition to inhaled corticosteroids, typically also in conjunction with LABA.[99] Evidence is insufficient to support use in acute exacerbations.[112][113] In children under five years of age, they are the preferred add-on therapy after inhaled corticosteroids.[114]
- Mast cell stabilizers (such as cromolyn sodium) are another non-preferred alternative to corticosteroids.[99]
- Delivery methods
Medications are typically provided as metered-dose inhalers (MDIs) in combination with an asthma spacer or as a dry powder inhaler. The spacer is a plastic cylinder that mixes the medication with air, making it easier to receive a full dose of the drug. A nebulizer may also be used. Nebulizers and spacers are equally effective in those with mild to moderate symptoms however insufficient evidence is available to determine whether or not a difference exists in those severe symptomatology.[115]
- Adverse effects
Long-term use of inhaled corticosteroids at conventional doses carries a minor risk of adverse effects.[116] Risks include the development of cataracts and a mild regression in stature.[116][117]
Others
When asthma is unresponsive to usual medications, other options are available for both emergency management and prevention of flareups. For emergency management other options include:
- Oxygen to alleviate hypoxia if saturations fall below 92%.[118]
- Magnesium sulfate intravenous treatment has been shown to provide a bronchodilating effect when used in addition to other treatment in severe acute asthma attacks.[10][119]
- Heliox, a mixture of helium and oxygen, may also be considered in severe unresponsive cases.[10]
- Intravenous salbutamol is not supported by available evidence and is thus used only in extreme cases.[118]
- Methylxanthines (such as theophylline) were once widely used, but do not add significantly to the effects of inhaled beta-agonists.[118] Their use in acute exacerbations is controversial.[120]
- The dissociative anesthetic ketamine is theoretically useful if intubation and mechanical ventilation is needed in people who are approaching respiratory arrest; however, there is no evidence from clinical trials to support this.[121]
For those with severe persistent asthma not controlled by inhaled corticosteroids and LABAs bronchial thermoplasty may be an option.[122] It involves the delivery of controlled thermal energy to the airway wall during a series of bronchoscopies.[122] While it may increase exacerbation frequency in the first few months it appears to decrease the subsequent rate. Effects beyond one year are unknown.[123] Evidence suggests that sublingual immunotherapy in those with both allergic rhinitis and asthma improve outcomes.[124]
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.[125][126] There is little data to support the effectiveness of most of these therapies. Evidence is insufficient to support the usage of Vitamin C.[127] Acupuncture is not recommended for the treatment as there is insufficient evidence to support its use.[128][129] Air ionisers show no evidence that they improve asthma symptoms or benefit lung function; this applied equally to positive and negative ion generators.[130]
"Manual therapies", including osteopathic, chiropractic, physiotherapeutic and respiratory therapeutic maneuvers, have insufficient evidence to support their use in treating asthma.[131] The Buteyko breathing technique for controlling hyperventilation may result in a reduction in medications use however does not have any effect on lung function.[100] Thus an expert panel felt that evidence was insufficient to support its use.[128]
Prognosis
Disability-adjusted life year for asthma per 100,000 inhabitants in 2004.[132]
|
no data
<100
100–150
150–200
200–250
250–300
300–350
|
350–400
400–450
450–500
500–550
550–600
>600
|
The prognosis for asthma is generally good, especially for children with mild disease.[133] Mortality has decreased over the last few decades due to better recognition and improvement in care.[134] 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).[135] Of asthma diagnosed during childhood, half of cases will no longer carry the diagnosis after a decade.[50] Airway remodeling is observed, but it is unknown whether these represent harmful or beneficial changes.[136] Early treatment with corticosteroids seems to prevent or ameliorates a decline in lung function.[137]
Epidemiology
Main article: Epidemiology of asthma
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%
|
As of 2011, 235–300 million people worldwide are affected by asthma,[14][15] and approximately 250,000 people die per year from the disease.[16] Rates vary between countries with prevalences between 1 and 18%.[16] It is more common in developed than developing countries.[16] One thus sees lower rates in Asia, Eastern Europe and Africa.[41] 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.[16] The reason for these differences is not well known.[16] Low and middle income countries make up more than 80% of the mortality.[138]
While asthma is twice as common in boys as girls,[16] severe asthma occurs at equal rates.[139] In contrast adult women have a higher rate of asthma than men[16] and it is more common in the young than the old.[41]
Global rates of asthma have increased significantly between the 1960s and 2008[140][141] with it being recognized as a major public health problem since the 1970s.[41] Rates of asthma have plateaued in the developed world since the mid-1990s with recent increases primarily in the developing world.[142] Asthma affects approximately 7% of the population of the United States[109] and 5% of people in the United Kingdom.[143] Canada, Australia and New Zealand have rates of about 14–15%.[144]
History
Asthma was recognized in Ancient Egypt and was treated by drinking an incense mixture known as kyphi.[145] 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.[41] In 200 BC it was believed to be at least partly related to the emotions.[23]
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.[146][147] Medical treatment in 1880, included the use of intravenous doses of a drug called pilocarpin.[148] In 1886, F.H. Bosworth theorized a connection between asthma and hay fever.[149] Epinephrine was first referred to in the treatment of asthma in 1905.[150] 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.[151][152]
During the 1930s–1950s, asthma was known as one of the "holy seven" psychosomatic illnesses. Its cause was considered to be psychological, with treatment often based on psychoanalysis and other talking cures.[153] As these psychoanalysts interpreted the asthmatic wheeze as the suppressed cry of the child for its mother, they considered the treatment of depression to be especially important for individuals with asthma.[153]
Notes
- ^ GINA 2011, p. 18
- ^ NHLBI Guideline 2007, pp. 11–12
- ^ British Guideline 2009, p. 4
- ^ a b c Martinez FD (2007). "Genes, environments, development and asthma: a reappraisal". Eur Respir J 29 (1): 179–84. doi:10.1183/09031936.00087906. PMID 17197483.
- ^ a b Lemanske RF, Busse WW (February 2010). "Asthma: clinical expression and molecular mechanisms". J. Allergy Clin. Immunol. 125 (2 Suppl 2): S95–102. doi:10.1016/j.jaci.2009.10.047. PMC 2853245. PMID 20176271.
- ^ a b c Yawn BP (September 2008). "Factors accounting for asthma variability: achieving optimal symptom control for individual patients". Primary Care Respiratory Journal 17 (3): 138–147. doi:10.3132/pcrj.2008.00004. PMID 18264646. Archived from the original on 2010-03-04.
- ^ a b Kumar, Vinay; Abbas, Abul K; Fausto, Nelson et al., eds. (2010). Robbins and Cotran pathologic basis of disease (8th ed.). Saunders. p. 688. ISBN 978-1-4160-3121-5. OCLC 643462931.
|displayeditors=suggested (help) - ^ Stedman's Medical Dictionary (28 ed.). Lippincott Williams and Wilkins. 2005. ISBN 0-7817-3390-1.
- ^ a b c d NHLBI Guideline 2007, p. 214
- ^ a b c NHLBI Guideline 2007, pp. 373–375
- ^ NHLBI Guideline 2007, pp. 169–172
- ^ GINA 2011, p. 71
- ^ GINA 2011, p. 33
- ^ a b "World Health Organization Fact Sheet Fact sheet No 307: Asthma". 2011. Retrieved Jan 17th,2013.
- ^ a b c GINA 2011, p. 3
- ^ a b c d e f g h i j GINA 2011, pp. 2–5
- ^ Jindal, editor-in-chief SK. Textbook of pulmonary and critical care medicine. New Delhi: Jaypee Brothers Medical Publishers. p. 242. ISBN 978-93-5025-073-0.
- ^ George, Ronald B. (2005). Chest medicine : essentials of pulmonary and critical care medicine (5th ed. ed.). Philadelphia, PA: Lippincott Williams & Wilkins. p. 62. ISBN 978-0-7817-5273-2.
- ^ British Guideline 2009, p. 14
- ^ GINA 2011, pp. 8–9
- ^ Boulet LP (April 2009). "Influence of comorbid conditions on asthma". Eur Respir J 33 (4): 897–906. doi:10.1183/09031936.00121308. PMID 19336592.
- ^ Boulet, LP; Boulay, MÈ (2011 Jun). "Asthma-related comorbidities.". Expert review of respiratory medicine 5 (3): 377–93. PMID 21702660.
- ^ a b 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.
- ^ Thomas, M; Bruton, A; Moffat, M; Cleland, J (2011 Sep). "Asthma and psychological dysfunction.". Primary care respiratory journal : journal of the General Practice Airways Group 20 (3): 250–6. PMID 21674122.
- ^ Miller, RL; Ho SM (March 2008). "Environmental epigenetics and asthma: current concepts and call for studies". American Journal of Respiratory and Critical Care Medicine 177 (6): 567–573. doi:10.1164/rccm.200710-1511PP. PMC 2267336. PMID 18187692.
- ^ 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.
- ^ Dietert, RR (2011 Sep). "Maternal and childhood asthma: risk factors, interactions, and ramifications.". Reproductive toxicology (Elmsford, N.Y.) 32 (2): 198–204. PMID 21575714.
- ^ Kelly, FJ; Fussell, JC (2011 Aug). "Air pollution and airway disease.". Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology 41 (8): 1059–71. PMID 21623970.
- ^ GINA 2011, p. 6
- ^ GINA 2011, p. 61
- ^ a b Gold DR, Wright R (2005). "Population disparities in asthma". Annu Rev Public Health 26: 89–113. doi:10.1146/annurev.publhealth.26.021304.144528. PMID 15760282.
- ^ McGwin, G; Lienert, J; Kennedy, JI (2010 Mar). "Formaldehyde exposure and asthma in children: a systematic review.". Environmental health perspectives 118 (3): 313–7. PMID 20064771.
- ^ Jaakkola JJ, Knight TL. (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.
- ^ Bornehag, CG; Nanberg, E (2010 Apr). "Phthalate exposure and asthma in children.". International journal of andrology 33 (2): 333–45. PMID 20059582.
- ^ Liu AH (2004). "Something old, something new: indoor endotoxin, allergens and asthma". Paediatr Respir Rev 5 (Suppl A): S65–71. doi:10.1016/S1526-0542(04)90013-9. PMID 14980246.
- ^ 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. PMID 21301330.
- ^ 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. PMID 20425514.
- ^ Custovic, A; Simpson, A (2012). "The role of inhalant allergens in allergic airways disease.". Journal of investigational allergology & clinical immunology : official organ of the International Association of Asthmology (INTERASMA) and Sociedad Latinoamericana de Alergia e Inmunologia 22 (6): 393–401; qiuz follow 401. PMID 23101182.
- ^ a b PC Gøtzsche, HK Johansen (2008). "House dust mite control measures for asthma". In Gøtzsche, Peter C. Cochrane Database Syst Rev (2): CD001187. doi:10.1002/14651858.CD001187.pub3. PMID 18425868.
- ^ a b NHLBI Guideline 2007, p. 11
- ^ a b c d e f g h i j k l Murray and Nadel's textbook of respiratory medicine. (5th ed. ed.). Philadelphia, PA: Saunders/Elsevier. 2010. pp. Chapter 38. ISBN 1-4160-4710-7.
- ^ 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.
- ^ Bufford, JD; Gern JE (May 2005). "The hygiene hypothesis revisited". Immunology and Allergy Clinics of North America 25 (2): 247–262. doi:10.1016/j.iac.2005.03.005. PMID 15878454.
- ^ a b Brooks, C; Pearce, N; Douwes, J (2013 Feb). "The hygiene hypothesis in allergy and asthma: an update.". Current opinion in allergy and clinical immunology 13 (1): 70–7. PMID 23103806.
- ^ Murk, W; Risnes, KR, Bracken, MB (2011 Jun). "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.
- ^ British Guideline 2009, p. 72
- ^ Neu, J; Rushing, J (2011 Jun). "Cesarean versus vaginal delivery: long-term infant outcomes and the hygiene hypothesis.". Clinics in perinatology 38 (2): 321–31. PMID 21645799.
- ^ Von Hertzen, LC; Haahtela, T (2004 Feb). "Asthma and atopy -the price of affluence?". Allergy 59 (2): 124–37. PMID 14763924.
- ^ a b Martinez FD (2007). "CD14, endotoxin, and asthma risk: actions and interactions". Proc Am Thorac Soc 4 (3): 221–5. doi:10.1513/pats.200702-035AW. PMC 2647622. PMID 17607003.
- ^ a b c Elward, Graham Douglas, Kurtis S. (2010). Asthma. London: Manson Pub. pp. 27–29. ISBN 978-1-84076-513-7.
- ^ a b c 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.
- ^ Halapi, E; Bjornsdottir, US (2009 Jan). "Overview on the current status of asthma genetics.". The clinical respiratory journal 3 (1): 2–7. PMID 20298365.
- ^ a b Rapini, Ronald P.; Bolognia, Jean L.; Jorizzo, Joseph L. (2007). Dermatology: 2-Volume Set. St. Louis: Mosby. ISBN 1-4160-2999-0.
- ^ GINA 2011, p. 4
- ^ Beuther DA (January 2010). "Recent insight into obesity and asthma". Curr Opin Pulm Med 16 (1): 64–70. doi:10.1097/MCP.0b013e3283338fa7. PMID 19844182.
- ^ Holguin F, Fitzpatrick A (March 2010). "Obesity, asthma, and oxidative stress". J. Appl. Physiol. 108 (3): 754–9. doi:10.1152/japplphysiol.00702.2009. PMID 19926826.
- ^ 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.
- ^ O'Rourke ST (October 2007). "Antianginal actions of beta-adrenoceptor antagonists". Am J Pharm Educ 71 (5): 95. PMC 2064893. PMID 17998992.
- ^ Salpeter, S; Ormiston, T; Salpeter, E (2001). "Cardioselective beta-blocker use in patients with reversible airway disease.". Cochrane database of systematic reviews (Online) (2): CD002992. PMID 11406056.
- ^ Covar, RA; Macomber, BA; Szefler, SJ (2005 Feb). "Medications as asthma trigers.". Immunology and allergy clinics of North America 25 (1): 169–90. PMID 15579370.
- ^ a b c d Baxi SN, Phipatanakul W (April 2010). "The role of allergen exposure and avoidance in asthma". Adolesc Med State Art Rev 21 (1): 57–71, viii–ix. PMC 2975603. PMID 20568555.
- ^ Chen E, Miller GE (2007). "Stress and inflammation in exacerbations of asthma". Brain Behav Immun. 21 (8): 993–9. doi:10.1016/j.bbi.2007.03.009. PMC 2077080. PMID 17493786.
- ^ a b NHLBI Guideline 2007, p. 42
- ^ GINA 2011, p. 20
- ^ American Academy of Allergy, Asthma, and Immunology, "Five things physicians and patients should question", Choosing wisely: an initiative of the ABIM Foundation (American Academy of Allergy, Asthma, and Immunology), retrieved August 14, 2012
- ^ 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).
- ^ Perez, LL (March–April 2013). "Office spirometry". Osteopathic Family Physician 5 (2): 65–69. doi:10.1016/j.osfp.2012.09.003.
- ^ NHLBI Guideline 2007, p. 58
- ^ Pinnock H, Shah R (2007). "Asthma". BMJ 334 (7598): 847–50. doi:10.1136/bmj.39140.634896.BE. PMC 1853223. PMID 17446617.
- ^ NHLBI Guideline 2007, p. 59
- ^ a b Moore WC, Pascual RM (June 2010). "Update in asthma 2009". American Journal of Respiratory and Critical Care Medicine 181 (11): 1181–7. doi:10.1164/rccm.201003-0321UP. PMID 20516492.
- ^ a b Self, Timothy; Chrisman, Cary; Finch, Christopher (2009). "22. Asthma". In Mary Anne Koda-Kimble, Brian K Alldredge, et al. Applied therapeutics: the clinical use of drugs (9th ed.). Philadelphia: Lippincott Williams & Wilkins. OCLC 230848069.
- ^ Delacourt, C (June 2004). "Conséquences bronchiques de l'asthme non traité" [Bronchial changes in untreated asthma]. Archives de Pédiatrie 11 (Suppl. 2): 71s–73s. PMID 15301800.
- ^ Schiffman, George (18 December 2009). "Chronic obstructive pulmonary disease". MedicineNet. Archived from the original on 28 August 2010. Retrieved 2 September 2010.
- ^ a b c d British Guideline 2009, p. 54
- ^ Barnes, PJ (2008). "Asthma". In Fauci, Anthony S; Braunwald, E,; Kasper, DL. Harrison's Principles of Internal Medicine (17th ed.). New York: McGraw-Hill. pp. 1596–1607. ISBN 978-0-07-146633-2.
- ^ Maitre B, Similowski T, Derenne JP (September 1995). "Physical examination of the adult patient with respiratory diseases: inspection and palpation". Eur. Respir. J. 8 (9): 1584–93. PMID 8575588.
- ^ Werner, HA (June 2001). "Status asthmaticus in children: a review". Chest 119 (6): 1596–1607. doi:10.1378/chest.119.6.1913. PMID 11399724.
- ^ a b Shiber JR, Santana J (May 2006). "Dyspnea". Med. Clin. North Am. 90 (3): 453–79. doi:10.1016/j.mcna.2005.11.006. PMID 16473100.
- ^ a b Shah, R; Saltoun, CA (2012 May–Jun). "Chapter 14: Acute severe asthma (status asthmaticus).". Allergy and asthma proceedings : the official journal of regional and state allergy societies. 33 Suppl 1: S47–50. PMID 22794687.
- ^ a b c Khan, DA (2012 Jan–Feb). "Exercise-induced bronchoconstriction: burden and prevalence.". Allergy and asthma proceedings : the official journal of regional and state allergy societies 33 (1): 1–6. PMID 22370526.
- ^ GINA 2011, p. 17
- ^ Carlsen, KH; Anderson, SD; Bjermer, L; Bonini, S; Brusasco, V; Canonica, W; Cummiskey, J; Delgado, L; Del Giacco, SR; Drobnic, F; Haahtela, T; Larsson, K; Palange, P; Popov, T; van Cauwenberge, P; European Respiratory, Society; European Academy of Allergy and Clinical, Immunology; GA(2)LEN, (2008 May). "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. PMID 18394123.
- ^ Kindermann, W (2007). "Do inhaled beta(2)-agonists have an ergogenic potential in non-asthmatic competitive athletes?". Sports medicine (Auckland, N.Z.) 37 (2): 95–102. PMID 17241101.
- ^ Pluim, BM; de Hon, O; Staal, JB; Limpens, J; Kuipers, H; Overbeek, SE; Zwinderman, AH; Scholten, RJ (2011 Jan 1). "β₂-Agonists and physical performance: a systematic review and meta-analysis of randomized controlled trials.". Sports medicine (Auckland, N.Z.) 41 (1): 39–57. PMID 21142283.
- ^ a b c Baur, X; Aasen, TB; Burge, PS; Heederik, D; Henneberger, PK; Maestrelli, P; Schlünssen, V; Vandenplas, O; Wilken, D; ERS Task Force on the Management of Work-related, Asthma (2012 Jun 1). "The management of work-related asthma guidelines: a broader perspective.". European respiratory review : an official journal of the European Respiratory Society 21 (124): 125–39. PMID 22654084.
- ^ Kunnamo, ed.-in-chief: Ilkka (2005). Evidence-based medicine guidelines. Chichester: Wiley. p. 214. ISBN 978-0-470-01184-3.
- ^ Kraft, editors, Mario Castro, Monica (2008). Clinical asthma. Philadelphia: Mosby / Elsevier. pp. Chapter 42. ISBN 978-0-323-07081-2.
- ^ NHLBI Guideline 2007, p. 46
- ^ 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.
- ^ Hargreave FE; Parameswaran K (August 2006). "Asthma, COPD and bronchitis are just components of airway disease". European Respiratory Journal 28 (2): 264–267. doi:10.1183/09031936.06.00056106. PMID 16880365.
- ^ Diaz, P. Knoell (2009). "23. Chronic obstructive pulmonary disease". Applied therapeutics: the clinical use of drugs (9th ed.). Philadelphia: Lippincott Williams & Wilkins.
- ^ a b NHLBI Guideline 2007, pp. 184–5
- ^ Lodge, CJ; Allen, KJ; Lowe, AJ; Hill, DJ; Hosking, CS; Abramson, MJ; Dharmage, SC (2012). "Perinatal cat and dog exposure and the risk of asthma and allergy in the urban environment: a systematic review of longitudinal studies.". Clinical & developmental immunology 2012: 176484. PMID 22235226.
- ^ Chen, CM; Tischer, C; Schnappinger, M; Heinrich, J (2010 Jan). "The role of cats and dogs in asthma and allergy—a systematic review.". International journal of hygiene and environmental health 213 (1): 1–31. PMID 20053584.
- ^ a b Prescott, SL; Tang, ML; Australasian Society of Clinical Immunology and, Allergy (2005 May 2). "The Australasian Society of Clinical Immunology and Allergy position statement: Summary of allergy prevention in children.". The Medical journal of Australia 182 (9): 464–7. PMID 15865590.
- ^ Ripoll, Brian C. Leutholtz, Ignacio. Exercise and disease management (2nd ed. ed.). Boca Raton: CRC Press. p. 100. ISBN 978-1-4398-2759-8.
- ^ GINA 2011, p. 56
- ^ a b c d e f NHLBI Guideline 2007, p. 213
- ^ a b "British Guideline on the Management of Asthma" (PDF). Scottish Intercollegiate Guidelines Network. 2008. Archived from the original on 19 August 2008. Retrieved 2008-08-04.
- ^ NHLBI Guideline 2007, p. 69
- ^ Thomson NC, Spears M (2005). "The influence of smoking on the treatment response in patients with asthma". Curr Opin Allergy Clin Immunol 5 (1): 57–63. doi:10.1097/00130832-200502000-00011. PMID 15643345.
- ^ 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.
- ^ 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.
- ^ NHLBI Guideline 2007, p. 351
- ^ NHLBI Guideline 2007, p. 218
- ^ a b Ducharme, FM; Ni Chroinin, M; Greenstone, I; Lasserson, TJ (2010 May 12). "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 (Online) (5): CD005535. PMID 20464739.
- ^ Ducharme, FM; Ni Chroinin, M; Greenstone, I; Lasserson, TJ (2010 Apr 14). "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 (Online) (4): CD005533. PMID 20393943.
- ^ a b Fanta CH (March 2009). "Asthma". New England Journal of Medicine 360 (10): 1002–14. doi:10.1056/NEJMra0804579. PMID 19264689.
- ^ Cates, CJ; Cates, MJ (2012 Apr 18). "Regular treatment with formoterol for chronic asthma: serious adverse events.". Cochrane database of systematic reviews (Online) 4: CD006923. PMID 22513944.
- ^ Cates, CJ; Cates, MJ (2008 Jul 16). "Regular treatment with salmeterol for chronic asthma: serious adverse events.". Cochrane database of systematic reviews (Online) (3): CD006363. PMID 18646149.
- ^ GINA 2011, p. 74
- ^ Watts, K; Chavasse, RJ (2012 May 16). "Leukotriene receptor antagonists in addition to usual care for acute asthma in adults and children.". Cochrane database of systematic reviews (Online) 5: CD006100. PMID 22592708.
- ^ British Guideline 2009, p. 43
- ^ NHLBI Guideline 2007, p. 250
- ^ a b Rachelefsky, G (2009 Jan). "Inhaled corticosteroids and asthma control in children: assessing impairment and risk.". Pediatrics 123 (1): 353–66. doi:10.1542/peds.2007-3273. PMID 19117903.
- ^ 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.
- ^ a b c Rodrigo GJ, Rodrigo C, Hall JB (2004). "Acute asthma in adults: a review". Chest 125 (3): 1081–102. doi:10.1378/chest.125.3.1081. PMID 15006973.
- ^ Noppen, M. (August 2002). "Magnesium Treatment for Asthma : Where Do We Stand?". Chest 122 (2): 396–8. doi:10.1378/chest.122.2.396. PMID 12171805.
- ^ GINA 2011, p. 37
- ^ NHLBI Guideline 2007, p. 399
- ^ a b Castro, M; Musani, AI, Mayse, ML, Shargill, NS (2010 Apr). "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.
- ^ GINA 2011, p. 70
- ^ Lin, Sandra (27). "Sublingual Immunotherapy for the Treatment of Allergic Rhinoconjunctivitis and Asthma A Systematic Review". JAMA 309 (12): 1278–1288. doi:10.1001/jama.2013.2049.
- ^ Blanc PD, Trupin L, Earnest G, Katz PP, Yelin EH, Eisner MD (2001). "Alternative therapies among adults with a reported diagnosis of asthma or rhinosinusitis : data from a population-based survey". Chest 120 (5): 1461–7. doi:10.1378/chest.120.5.1461. PMID 11713120.
- ^ Shenfield G, Lim E, Allen H (2002). "Survey of the use of complementary medicines and therapies in children with asthma". J Paediatr Child Health 38 (3): 252–7. doi:10.1046/j.1440-1754.2002.00770.x. PMID 12047692.
- ^ Kaur, B; Rowe BH, Arnold E (2009). "Vitamin C supplementation for asthma". In Arnold, Elizabeth. Cochrane Database Syst Rev (1): CD000993. doi:10.1002/14651858.CD000993.pub3. PMID 19160185. Unknown parameter
|unused_data=ignored (help) - ^ a b NHLBI Guideline 2007, p. 240
- ^ McCarney RW, Brinkhaus B, Lasserson TJ, Linde K (2004). "Acupuncture for chronic asthma". In McCarney, Robert W. Cochrane Database Syst Rev (1): CD000008. doi:10.1002/14651858.CD000008.pub2. PMID 14973944.
- ^ Blackhall, K; Appleton, S; Cates, CJ (2012 Sep 12). "Ionisers for chronic asthma.". Cochrane database of systematic reviews (Online) 9: CD002986. PMID 22972060.
- ^ Hondras MA, Linde K, Jones AP (2005). "Manual therapy for asthma". In Hondras, Maria A. Cochrane Database Syst Rev (2): CD001002. doi:10.1002/14651858.CD001002.pub2. PMID 15846609.
- ^ "WHO Disease and injury country estimates". World Health Organization. 2009. Archived from the original on 11 November 2009. Retrieved November 11, 2009.
- ^ Sergel, Michelle J.; Cydulka, Rita K. (September 2009). "Ch. 75: Asthma". In Wolfson, Allan B.; Harwood-Nuss, Ann. Harwood-Nuss' Clinical Practice of Emergency Medicine (5th ed.). Lippincott Williams & Wilkins. pp. 432–. ISBN 978-0-7817-8943-1.
- ^ NHLBI Guideline 2007, p. 1
- ^ Organization, World Health (2008). The global burden of disease : 2004 update. ([Online-Ausg.] ed.). Geneva, Switzerland: World Health Organization. p. 35. ISBN 978-92-4-156371-0.
- ^ 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.
- ^ 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.
- ^ World Health Organization. "WHO: Asthma". Archived from the original on 15 December 2007. Retrieved 2007-12-29.
- ^ Bush A, Menzies-Gow A (December 2009). "Phenotypic differences between pediatric and adult asthma". Proc Am Thorac Soc 6 (8): 712–9. doi:10.1513/pats.200906-046DP. PMID 20008882.
- ^ 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.
- ^ Anandan C, Nurmatov U, van Schayck OC, Sheikh A (February 2010). "Is the prevalence of asthma declining? Systematic review of epidemiological studies". Allergy 65 (2): 152–67. doi:10.1111/j.1398-9995.2009.02244.x. PMID 19912154.
- ^ Bousquet, J; Bousquet, PJ; Godard, P; Daures, JP (2005 Jul). "The public health implications of asthma.". Bulletin of the World Health Organization 83 (7): 548–54. PMID 16175830.
- ^ 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.
- ^ Masoli, Matthew (2004). Global Burden of Asthma. p. 9.
- ^ Manniche L (1999). Sacred luxuries: fragrance, aromatherapy, and cosmetics in ancient Egypt. Cornell University Press. pp. 49. ISBN 978-0-8014-3720-5.
- ^ Thorowgood JC (November 1873). "On bronchial asthma". British Medical Journal 2 (673): 600. doi:10.1136/bmj.2.673.600. PMC 2294647. PMID 20747287.
- ^ 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.
- ^ Berkart JB (June 1880). "The treatment of asthma". British Medical Journal 1 (1016): 917–8. doi:10.1136/bmj.1.1016.917. PMC 2240555. PMID 20749537.
Berkart JB (June 1880). "The treatment of asthma". British Medical Journal 1 (1017): 960–2. doi:10.1136/bmj.1.1017.960. PMC 2240530. PMID 20749546. - ^ 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.
- ^ Doig RL (February 1905). "Epinephrin; especially in asthma". California State Journal of Medicine 3 (2): 54–5. PMC 1650334. PMID 18733372.
- ^ von Mutius, E; Drazen, JM (2012 Mar 1). "A patient with asthma seeks medical advice in 1828, 1928, and 2012.". New England Journal of Medicine 366 (9): 827–34. PMID 22375974.
- ^ Crompton G (2006 Dec). "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. PMID 17092772.
- ^ a b Opolski M, Wilson I (September 2005). "Asthma and depression: a pragmatic review of the literature and recommendations for future research". Clin Pract Epidemol Ment Health 1: 18. doi:10.1186/1745-0179-1-18. PMC 1253523. PMID 16185365.
- References
- National Asthma Education and Prevention Program (NAEPP) (2007). "Expert Panel Report 3: Guidelines for the Diagnosis and Management of Asthma" (PDF). National Heart Lung and Blood Institute.
- "British Guideline on the Management of Asthma" (PDF). British Thoracic Society. 2008 (revised 2012).
- "Global Strategy for Asthma Management and Prevention" (PDF). Global Initiative for Asthma. 2011.
External links
- Asthma at the Open Directory Project
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UpToDate Contents
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- 1. 喘息のマネージメントの概要 an overview of asthma management
- 2. 成人における喘息の急性増悪の治療 treatment of acute exacerbations of asthma in adults
- 3. 思春期および成人における喘息の診断 diagnosis of asthma in adolescents and adults
- 4. Acute asthma exacerbations in children: Emergency department management
- 5. ウイルス誘発性の喘鳴および喘息：概要 virus induced wheezing and asthma an overview
English Journal
- The role of selenium in inflammation and immunity: from molecular mechanisms to therapeutic opportunities.
- Huang Z, Rose AH, Hoffmann PR.Source1 Department of Cell and Molecular Biology, John A. Burns School of Medicine, University of Hawaii , Honolulu, Hawaii.
- Antioxidants & redox signaling.Antioxid Redox Signal.2012 Apr 1;16(7):705-43. Epub 2012 Jan 9.
- Abstract Dietary selenium (]Se), mainly through its incorporation into selenoproteins, plays an important role in inflammation and immunity. Adequate levels of Se are important for initiating immunity, but they are also involved in regulating excessive immune responses and chronic inflammation. Ev
- PMID 21955027
- MKP-1: A negative feedback effector that represses MAPK-mediated pro-inflammatory signaling pathways and cytokine secretion in human airway smooth muscle cells.
- Manetsch M, Che W, Seidel P, Chen Y, Ammit AJ.SourceRespiratory Research Group, Faculty of Pharmacy, University of Sydney, NSW 2006, Australia.
- Cellular signalling.Cell Signal.2012 Apr;24(4):907-13. Epub 2011 Dec 19.
- Airway smooth muscle (ASM) plays an important immunomodulatory role in airway inflammation in asthma. In our previous in vitro studies in ASM cells delineating the pro-inflammatory mitogen-activated protein kinase (MAPK) signaling pathways activated by tumor necrosis factor α (TNFα), we observed t
- PMID 22200679
- Inhibition airway remodeling and transforming growth factor-β1/Smad signaling pathway by astragalus extract in asthmatic mice.
- Qu ZH, Yang ZC, Chen L, Lv ZD, Yi MJ, Ran N.SourceDepartment of Pediatrics, The Affiliated Hospital of Qingdao University Medical College, Qingdao 266003, Shandong Province, P.R. China.
- International journal of molecular medicine.Int J Mol Med.2012 Apr;29(4):564-8. doi: 10.3892/ijmm.2011.868. Epub 2011 Dec 23.
- Airway remodeling is characterized by airway wall thickening, subepithelial fibrosis, increased smooth muscle mass, angiogenesis and increased mucous glands, which can lead to a chronic and obstinate asthma with pulmonary function depression. In the present study
- PMID 22200784
Japanese Journal
- 気管支喘息に対する鍼治療の効果の検討-運動誘発性喘息を対象として-
- 豊福 伸幸
- 明治国際医療大学誌 (05), 13-24, 2011-11-01
- NAID 110008672476
- Two cases of Schizophyllum asthma: Is this a new clinical entity or a precursor of ABPM?
- Ogawa Haruhiko,Fujimura Masaki,Takeuchi Yasuo,Makimura Koichi
- Pulmonary Pharmacology and Therapeutics 24(5), 559-562, 2011-10-01
- … Background: There is a close link between fungal sensitization and asthma severity. … commune, "suehirotake" in Japanese), one of the basidiomycetous (BM) fungi, is a fungus that can cause allergic bronchopulmonary mycosis (ABPM) and allergic fungal sinusitis (AFS), whether the fungus causes or sensitizes subjects to asthma is unclear. … Methods: The bronchial provocation test using S. …
- NAID 120003239434
- 喘息児における肥満改善に伴う呼吸機能への影響
- 増本 夏子,小田嶋 博,嶋田 清隆,村上 洋子,本村 知華子,本荘 哲,岡田 賢司
- アレルギー 60(8), 983-992, 2011-08-30
- 【目的】肥満の気管支喘息(以下,喘息と略す)への関与は,小児においても数多くの報告があるが,そのメカニズムについては必ずしも明らかではなく,我が国での検討,報告は少ない.今回,我々は肥満症を合併した喘息児を対象とし,肥満の改善に伴う呼吸機能の変化について検討した.【方法】当科で入院による肥満治療を行った喘息を有する児10名(男児8:女児2,平均年齢10歳)に対し,肥満改善プログラムの前後で身長,体 …
- NAID 110008722814
Related Links
- asthma [az´mah] a condition marked by recurrent attacks of dyspnea, with airway inflammation and wheezing due to spasmodic constriction of the bronchi; it is also known as bronchial asthma. Attacks vary greatly from occasional ...
- What Is Bronchial Asthma?. Bronchial asthma, also called asthma, is a lung disease in which the airways that carry air into and out of the lungs become inflamed and narrow. People of all ages can get bronchial asthma ...
Related Pictures
★リンクテーブル★
| リンク元 | 「気管支喘息」「inspissation」「BA」 |
| 関連記事 | 「bronchial」「asthma」 |
「気管支喘息」
- 英
- bronchial asthma
- 同
- 喘息 asthma
- 関
- 喘息発作(喘息の急性増悪)
概念
- 気道の慢性炎症、気道過敏性、可逆性の気道閉塞を呈する
疫学
病型
- アトピー型：小児に多く、60-70%は成人になる前に寛解
- 感染型
- 混合型
病態生理
- 遺伝子素因を背景とした気道過敏性が存在し、ある誘因により気道閉塞が起こる。これが喘息症状を引きおこす。
- ここに気管炎症が加わると、気道過敏性亢進、気道閉塞を直接引きおこすほか、気道リモデリングを促してさらに気道過敏性亢進・気道閉塞を亢進させる。
- この病態の中で、気道に起こっている変化は次のようにまとめられる。
- 可逆的変化 ：気道上皮細胞の剥離、粘液栓、炎症細胞(好酸球など)の浸潤、粘膜・粘膜下の浮腫、うっ血
- 不可逆的変化：平滑筋の肥厚、気道上皮下の線維性肥厚、気道上皮での杯細胞の過形成、気道粘膜下の血管新生
気流制限をきたす機序
- 気流制限は4つの機序により成立
- (1)気道平滑筋収縮、(2)気管壁の浮腫、(3)気道粘液分泌、(4)気道壁リモデリング
気管炎症
- 好酸球性気道炎症：好酸球、肥満細胞、リンパ球などの炎症細胞がサイトカインと化学伝達物質などを介して炎症を惹起する。
- リンパ球
- 肥満細胞
- 好酸球
- 気道上皮細胞
- 気管支平滑筋
- 気管支分泌腺
気管壁リモデリング
- 慢性の炎症状態 → 永続的な気道壁の肥厚 → 不可逆的な気流制限
- (1) 基底膜下にコラーゲンが沈着 → 気道粘膜の線維化
- (2) 気管支平滑筋の肥厚、過形成
- (3) 粘膜下線過形成
気道過敏性
- 非特異的な刺激により気管支平滑筋が容易に収縮する状態
- ヒスタミン、アセチルコリン、メサコリンの希釈系列を投与してFEV1.0が20%以上低下する閾値を測定して評価
- 気道過敏性と喘息の重症度が相関する。
検査
- IgE：
- 高値であることが多く、その場合には抗原の同定を行う。
- IgEの値と症状には相関関係がない。
- 喀痰：好酸球増加、クルシュマンらせん体、シャルコー・ライデン結晶、クレオラ小体
症状
身体所見
- 聴診：
- 大発作の際には呼吸音の減弱が認められる。
診断
成人喘息での診断の目安
- 参考1
- 成人喘息の診断基準はない
- 1．発作性の呼吸困難、喘鳴、咳(夜間、早朝に出現する傾向)の反復
- 2．可逆性気流制限：自然に、あるいは治療により寛解する。PEF値の日内変動20%以上、β2刺激薬吸入により1秒量が12%以上増加かつ絶対量で200mL以上増加
- 3．気道過敏性の亢進：アセチルコリン、ヒスタミン、メサコリンに対する気道収縮反応の亢進
- 4．アトピー素因：環境アレルゲンに対するIgE抗体の存在
- 5．気道炎症の存在：喀痰、末梢血中の好酸球数の増加、ECP高値、クレオラ体の証明、呼気中NO濃度上昇
- 6．鑑別診断疾患の除外：症状が他の心肺疾患によらない
治療
- (1)原因の除去と(2)薬物療法
- 薬物療法
- 気管支拡張薬：SABA
-
- β2受容体に結合→Gsα活性化→[cAMP]i↑
- 副作用：振戦、動悸
- PDE阻害→[cAMP]i↑。抗炎症作用もあるらしい(T細胞、好酸球に対する作用(SPU.241))
- 安全域(有効安全治療濃度閾)が狭いので、血中濃度モニタリングが必要。5-15μg/ml
- 副作用：悪心、嘔吐、頻脈、不整脈
- 抗コリン薬
- M3受容体に拮抗して作用を発現。作用力、即時性ともにβ2作動薬より劣る。(SPU.242)
- β2作動薬と併用するらしい。
- イプラトロピウム
- 抗炎症薬
- ステロイド
- 抗アレルギー薬
- 化学伝達物質遊離抑制薬、ヒスタミンH1機構薬、ロイコトリエン拮抗薬、トロンボキサンA2阻害薬。
- 減感作療法 (SPU.242)
薬物療法に用いられる薬剤
| 長期管理薬 (コントローラー) |
・ステロイド薬(吸入、経口) |
| ・テオフィリン徐放製剤 | |
| ・長時間作用性β2刺激薬(吸入、経口、貼付) | |
| ・抗アレルギー薬 | |
| ・ロイコトリエン受容体拮抗薬 | |
| ・メディエーター遊離抑制薬 | |
| ・ヒスタミンH1拮抗薬 | |
| ・トロンボキサン阻害薬 | |
| ・Th2サイトカイン阻害薬 | |
| 発作治療薬 (リリーバー) |
・ステロイド薬(注射・経口) |
| ・短時間作用性β2刺激薬(吸入・経口・注射) | |
| ・アミノフィリン点滴静注 | |
| ・短時間作用性テオフィリン製剤(経口) | |
| ・抗コリン薬(吸入) |
ガイドライン
- 1. 一般臨床医のための喘息治療ガイドライン2007
国試
「inspissation」
- n.
-
- Systemic administration of belladonna alkaloids or their derivatives for bronchial asthma or chronic obstructive pulmonary disease carries the disadvantage of reducing bronchial secretions and inspissation of the residual secretions.(GOO.195)
「BA」
「bronchial」
- adj.
- 気管支の
「asthma」