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विकिपिडिया नं
ब्रोंकियल आज्मा
वर्गीकरण व पिनेयागु श्रोत
ICD-10 J45.
ICD-9 493
OMIM ६००८०७
DiseasesDB १००६6
MedlinePlus ०००१४
eMedicine med/१७७  emerg/43
MeSH C08.127.108

आज्मा वा आस्थ्मा रेस्पिरेटरी सिस्टमयागु छगु क्रोनिक ल्वे ख। थ्व ल्वेय् मनुयागु एअरवे कन्स्ट्रिक्ट जुइ, इन्फ्लामेसन जुइ व सोंय् म्युकस प्येपुना च्वनि। थन्यागु इपिसोड थ्व ल्वे छगु वा येक्व ट्रिगरं याना जुइ। थ्व ल्वेयागु ट्रिगर एलरजेन, ख्वांगु फे, मोइस्ट फे, व्यायाम, एक्जर्सन, इमोसनल स्ट्रेस आदि ख। मचातेगु दथुइ थ्व ल्वय् भाइरल संक्रमणं (गथे कि-सेखं चाइगु याना अप्व जुगु खने दु)। [१] थ्व कथंया एअरवे न्यारोविङ (airway narrowing)तेसं व्हीज, डिस्प्निया, नुगःपा कस्सेजुइगु, व मुसु वैगु थेंन्यागु लक्षण क्येनि। थ्व लक्षणतेत ब्रोंकोडाइलेटर बिया लंके ज्यु। थन्यागु एपिसोडतेगु दथुइ अप्व उसाँय् मदुपिं बांलागु थें जुइ तर गब्लें-गब्लें सासः ल्हाय् थाकुगु थें जुइफु।

The symptoms of asthma, which can range from mild to life threatening, can usually be controlled with a combination of drugs and environmental changes.

Public attention in the developed world has recently focused on asthma because of its rapidly increasing prevalence, affecting up to one in four urban children.[२]


आज्मा धागु खंग्व युनानी खंग्व आजीन नं वगु ख,थ्व खंग्वयाग अर्थ "शार्प (sharp) सासः" ख। थ्व खँग्व दक्ले न्ह्य होमरयागु इलियाडय् च्वयातगु खने दु।[३] हिपोक्रेटिज नं थ्व खँग्वयात ल्वेयागु रुपे ४५० बी सीय् दक्ले न्ह्य छ्येलादिल। हिप्पोक्रेटिजयागु विचा कथं थ्व ल्वे अप्व याना टेलर, एन्ग्लर्स व मेटलवर्करय् खने दु। ६ शताब्दी धुंका ग्यालेननं आज्मायागु बारेय् येक्व च्वव्या दिल। वेकलं थ्व ल्वे ब्रोंकसयागु आंशिक वा पूर्ण रुपे अब्स्ट्रक्सन जुया जुइगु धैगु खं विचा याना दिल। ११९० ए डीय् मोसेस मोइमोनिडेज, छम्ह मध्ययुगीय र्‍याबाइ, दार्शनिक, व चिकित्सकं थुकियागु बारेय् येक्व च्वया दिल व थ्व अवस्थायागु प्रिभेन्सन, डायग्नोसिस् व ट्रिट्मेन्टयागु बारेय् च्वया दिल।[४] १७औं शताव्दीय् बर्नार्डिनो रामाजिनी नं अर्ग्यानिक धु व थ्व ल्वेयागु छुं सम्बन्ध दुगु खं सीका दिल। ब्रोंकोडाइलेटरयागु छ्येलेज्या १९०१ निसें न्ह्येथन तर १९६०यागु दशक तक्क नं थ्व ल्वेयागु इन्फ्लामेटरी भागयागु बारेय् चिकित्सकत अनभिज्ञ जुल। थ्व भाग सी धुंका एन्टि-इन्फ्लामेटरी वास नं थ्व ल्वेयागु रेजिमेनय् तेनिगु ज्या जुल।


छुं मनुय् आज्मा क्रोनिक रेस्पिरेटरी इम्पेयरमेन्टयागु रुपे खने दै। मेमेपिंय् थ्व ल्वे इन्टर्मिटेन्ट ल्वेयागु रुपे खने दै व थ्व ल्वेयागु लक्षण इन्टरमिटेन्ट कथलं अपर रेस्पिरेटरी संक्रमण, तनाव, वायुय् दैगु एलर्जेन, वायु प्रदुषक (दसु कुं) वा व्यायामं याना जुइ।

आज्मायागु एक्युट एट्याकयाट आज्मा अट्याक धाई। थन्यागु अट्याकयागु हलमार्क डिस्प्नियाव्हीज वा स्ट्राइडरय् छगु जुइ। Although the former is "often regarded as the sine qua non of asthma,"[५] some patients present primarily with coughing, and in the late stages of an attack, air motion may be so impaired that no wheezing may be heard. When present the cough may sometimes produce clear sputum. The onset may be sudden, with a sense of constriction in the chest, breathing becomes difficult, and wheezing occurs (primarily upon expiration, but can be in both respiratory phases).

Signs of an asthmatic episode include wheezing, rapid breathing (tachypnea), prolonged expiration, a rapid heart rate (tachycardia), rhonchous lung sounds (audible through a stethoscope), and over-inflation of the chest. During a serious asthma attack, the accessory muscles of respiration (sternocleidomastoid and scalene muscles of the neck) may be used, shown as in-drawing of tissues between the ribs and above the sternum and clavicles, and the presence of a paradoxical pulse (a pulse that is weaker during inhalation and stronger during exhalation).

During very severe attacks, an asthma sufferer can turn blue from lack of oxygen, and can experience chest pain or even loss of consciousness. Just before loss of consciousness, there is a chance that the patient will feel numbness in the limbs and palms may start to sweat. Feet may become icy cold. Severe asthma attacks may lead to respiratory arrest and death. Despite the severity of symptoms during an asthmatic episode, between attacks an asthmatic may show few signs of the disease.[६]


आज्मायात छगु रिभर्सिबल एअरवे अब्स्ट्रक्सनया कथं परिभाषित यानातगु दु। Reversibility थमंतुं (spontaneously) वा निदान (treatment) याना जुइ। थुकिया दक्ले आधारभूत पीक एक्स्पिरेटरी फ्लो रेटया लनेज्या व क्वय् बियातगु क्राइटेरियायात ब्रिटिस थोर्‍यासिक सोसाइटी नं आज्माया डायग्नोसिसया आधार कागु दु:[७]

In many cases, a physician can diagnose asthma on the basis of typical findings in a patient's clinical history and examination. Asthma is strongly suspected if a patient suffers from eczema or other allergic conditions—suggesting a general atopic constitution—or has a family history of asthma. While measurement of airway function is possible for adults, most new cases are diagnosed in children who are unable to perform such tests. Diagnosis in children is based on a careful compilation and analysis of the patient's medical history and subsequent improvement with an inhaled bronchodilator medication. In adults, diagnosis can be made with a peak flow meter (which tests airway restriction), looking at both the diurnal variation and any reversibility following inhaled bronchodilator medication.

Testing peak flow at rest (or baseline) and after exercise can be helpful, especially in young asthmatics who may experience only exercise-induced asthma. If the diagnosis is in doubt, a more formal lung function test may be conducted. Once a diagnosis of asthma is made, a patient can use peak flow meter testing to monitor the severity of the disease.

In the Emergency Department doctors may use a capnography PMID 16187465 which measures the amount of exhaled carbon dioxide along with pulse oximetry which shows the amount of oxygen dissolved in the blood, to determine the severity of an asthma attack as well as the response to treatment.

Differential diagnosis[सम्पादन]

Before diagnosing someone as asthmatic, alternative possibilities should be considered. A physician taking a history should check whether the patient is using any known bronchoconstrictors (substances that cause narrowing of the airways, e.g., certain anti-inflammatory agents or beta-blockers).

Chronic obstructive pulmonary disease, which closely resembles asthma, is correlated with more exposure to cigarette smoke, an older patient, less symptom reversibility after bronchodilator administration (as measured by spirometry), and decreased likelihood of family history of atopy.

Pulmonary aspiration, whether direct due to dysphagia (swallowing disorder) or indirect (due to acid reflux), can show similar symptoms to asthma. However, with aspiration, fevers might also indicate aspiration pneumonia. Direct aspiration (dysphagia) can be diagnosed by performing a Modified Barium Swallow test and treated with feeding therapy by a qualified speech therapist. If the aspiration is indirect (from acid reflux) then treatment directed at this is indicated.

A majority of children who are asthma sufferers have an identifiable allergy trigger. Specifically, in a 2004 study, 71% had positive test results for more than 1 allergen, and 42% had positive test results for more than 3 allergens.[८]

The majority of these triggers can often be identified from the history; for instance, asthmatics with hay fever or pollen allergy will have seasonal symptoms, those with allergies to pets may experience an abatement of symptoms when away from home, and those with occupational asthma may improve during leave from work. Occasionally, allergy tests are warranted and, if positive, may help in identifying avoidable symptom triggers.

After a pulmonary function test has been carried out, radiological tests, such as a chest X-ray or CT scan, may be required to exclude the possibility of other lung diseases. In some people, asthma may be triggered by gastroesophageal reflux disease, which can be treated with suitable antacids. Very occasionally, specialized tests after inhalation of methacholine — or, even less commonly, histamine — may be performed.

Asthma is categorized by the United States National Heart, Lung and Blood Institute as falling into one of four categories: mild intermittent, mild persistent, moderate persistent and severe persistent. The diagnosis of "severe persistent asthma" occurs when symptoms are continual with frequent exacerbations and frequent nighttime symptoms, result in limited physical activity and when lung function as measured by PEV or FEV1 tests is less than 60% predicted with PEF variability greater than 30%.

There is no cure for asthma. Doctors have only found ways to prevent attacks and relieve the symptoms such as tightness of the chest and trouble breathing.


Inflamed airways and bronchoconstriction in asthma. Airways narrowed as a result of the inflammatory response cause wheezing.


During an asthma episode, inflamed airways react to environmental triggers such as smoke, dust, or pollen. The airways narrow and produce excess mucus, making it difficult to breathe. In essence, asthma is the result of an immune response in the bronchial airways.[९]

The airways of asthmatics are "hypersensitive" to certain triggers, also known as stimuli (see below). In response to exposure to these triggers, the bronchi (large airways) contract into spasm (an "asthma attack"). Inflammation soon follows, leading to a further narrowing of the airways and excessive mucus production, which leads to coughing and other breathing difficulties.


There are many different categories of stimuli:

Bronchial inflammation[सम्पादन]

The mechanisms behind allergic asthma—i.e., asthma resulting from an immune response to inhaled allergens—are the best understood of the causal factors. In both asthmatics and non-asthmatics, inhaled allergens that find their way to the inner airways are ingested by a type of cell known as antigen presenting cells, or APCs. APCs then "present" pieces of the allergen to other immune system cells. In most people, these other immune cells (TH0 cells) "check" and usually ignore the allergen molecules. In asthmatics, however, these cells transform into a different type of cell (TH2), for reasons that are not well understood. The resultant TH2 cells activate an important arm of the immune system, known as the humoral immune system. The humoral immune system produces antibodies against the inhaled allergen. Later, when an asthmatic inhales the same allergen, these antibodies "recognize" it and activate a humoral response. Inflammation results: chemicals are produced that cause the airways to constrict and release more mucus, and the cell-mediated arm of the immune system is activated. The inflammatory response is responsible for the clinical manifestations of an asthma attack. The following section describes this complex series of events in more detail.


The fundamental problem in asthma appears to be immunological: young children in the early stages of asthma show signs of excessive inflammation in their airways. Epidemiological findings give clues as to the pathogenesis: the incidence of asthma seems to be increasing worldwide, and asthma is now very much more common in affluent countries.

In 1968 Andor Szentivanyi first described The Beta Adrenergic Theory of Asthma; in which blockage of the Beta-2 receptors of pulmonary smooth muscle cells causes asthma.[१२] Szentivanyi's Beta Adrenergic Theory is a citation classic[१३] and has been cited more times than any other article in the history of the Journal of Allergy.

In 1995 Szentivanyi and colleagues demonstrated that IgE blocks beta-2 receptors.[१४] Since overproduction of IgE is central to all atopic diseases, this was a watershed moment in the world of Allergy.[१५]

The Beta-Adrenergic Theory has been cited in the scholarship of such noted investigators as Richard F. Lockey (former President of the American Academy of Allergy, Asthma, and Immunology),[१६] Charles Reed (Chief of Allergy at Mayo Medical School),[१७] and Craig Venter (Human Genome Project).[१८]


येक्व स्टडिज कथलं मस्तय् आज्मा, ब्रोंकाइटिस, व एक्युट रेस्पिरेटरी ल्वेयात वायुयागु क्वालिटी नाप स्वापू दुगु खं क्यंगु दु।[१९] One of the largest of these studies is the California Children's Health Study.[२०] From the press release [१]

The study showed that children in the high ozone communities who played three or more sports developed asthma at a rate three times higher than those in the low ozone communities. Because participation in some sports can result in a child drawing up to 17 times the “normal” amount of air into the lungs, young athletes are more likely to develop asthma.

Note that concentrations of ozone have risen steadily in Europe since 1870. [२]

Another theory of pathogenesis is that asthma is a disease of hygiene. In nature, babies are exposed to bacteria and other antigens soon after birth, "switching on" the TH1 lymphocyte cells of the immune system that deal with bacterial infection. If this stimulus is insufficient, as it may be in modern, clean environments, then TH2 cells predominate, and asthma and other allergic diseases may develop. This "hygiene hypothesis" may explain the increase in asthma in affluent populations. The TH2 lymphocytes and eosinophil cells that protect us against parasites and other infectious agents are the same cells responsible for the allergic reaction. The Charcot-Leyden crystals are formed when the crystalline material in eosinophils coalesce. These crystals are significant in sputum samples of people with asthma. In the developed world, these parasites are now rarely encountered, but the immune response remains and is wrongly triggered in some individuals by certain allergens.

Finally, it has been postulated that some forms of asthma may be related to infection, in particular by Chlamydia pneumoniae.[२१] This issue remains controversial, as the relationship is not borne out by meta-analysis of the research.[२२] The correlation seems to be not with the onset, but rather with accelerated loss of lung function in adults with new onset of non-atopic asthma.[२३] One possible explanation is that some asthmatics may have altered immune response that facilitates long-term chlamydia pneumonia infection.[२४] The response to targeting with macrolide antibiotics has been investigated, but the temporary benefit reported in some studies may reflect just their anti-inflammatory activities rather than their antimicrobic action.[२२]

Asthma and sleep apnea[सम्पादन]

मू पौ: sleep apnea

It is recognized with increasing frequency, that patients who have both obstructive sleep apnea (OSA) and bronchial asthma, often improve tremendously when the sleep apnea is diagnosed and treated.[२५] CPAP is not effective in patients with nocturnal asthma only.[२६]

Asthma and gastro-esophageal reflux disease[सम्पादन]

If gastro-esophageal reflux disease is present, the patient may have repetitive episodes of acid aspiration, which results in airway inflammation and "irritant-induced" asthma.[पुष्टि(साइटेसन) मागु] GERD may be common in difficult-to-control asthma, but generally speaking, treating it does not seem to affect the asthma.[२७]


The most effective treatment for asthma is identifying triggers, such as pets or aspirin, and limiting or eliminating exposure to them. Desensitization to allergens has been shown to be a treatment option for certain patients.[२८]

As is common with respiratory disease, smoking adversely affects asthmatics in several ways, including an increased severity of symptoms, a more rapid decline of lung function, and decreased response to preventive medications.[२९] Asthmatics who smoke typically require additional medications to help control their disease. Furthermore, exposure of both non-smokers and smokers to second-hand smoke is detrimental, resulting in more severe asthma, more emergency room visits, and more asthma-related hospital admissions.[३०] Smoking cessation and avoidance of second-hand smoke is strongly encouraged in asthmatics.[३१]

The specific medical treatment recommended to patients with asthma depends on the severity of their illness and the frequency of their symptoms. Specific treatments for asthma are broadly classified as relievers, preventers and emergency treatment. The Expert Panel Report 2: Guidelines for the Diagnosis and Management of Asthma (EPR-2)[३१] of the U.S. National Asthma Education and Prevention Program, and the British Guideline on the Management of Asthma[३२] are broadly used and supported by many doctors. A new draft Full Report of Expert Panel: Guidelines fo the Diagnosis and Management of Asthma (EPR-3) was posted on the NHLBI web site for public review and comment but has been withdrawn from the NIH website pending formal dissemination, although comments submitted by the American College of Allergy, Asthma and Immunology about the proposed revised NHLBI asthma guidelines are still available online. Bronchodilators are recommended for short-term relief in all patients. For those who experience occasional attacks, no other medication is needed. For those with mild persistent disease (more than two attacks a week), low-dose inhaled glucocorticoids or alternatively, an oral leukotriene modifier, a mast-cell stabilizer, or theophylline may be administered. For those who suffer daily attacks, a higher dose of glucocorticoid in conjunction with a long-acting inhaled β-2 agonist may be prescribed; alternatively, a leukotriene modifier or theophylline may substitute for the β-2 agonist. In severe asthmatics, oral glucocorticoids may be added to these treatments during severe attacks.

For those in whom exercise can trigger an asthma attack (exercise-induced asthma), higher levels of ventilation and cold, dry air tend to exacerbate attacks. For this reason, activities in which a patient breathes large amounts of cold air, such as skiing and running, tend to be worse for asthmatics, whereas swimming in an indoor, heated pool, with warm, humid air, is less likely to provoke a response.[५]

Researchers at Harvard Medical School (HMS) have come up with convincing evidence that the answer to what causes asthma lies in a special type of natural "killer" cell. This finding means that physicians may not be treating asthma sufferers with the right kinds of drugs. For example, natural killer T cells seem to be resistant to the corticosteroids in widely used inhalers.[३३]

A novel therapeutic target currently under investigation is the A2B receptor, a cell surface G-protein coupled receptor expressed in the lungs and in inflammatory cells expressed in asthma. Several animal models have confirmed the a critical role for A2B antagonists in pulmonary inflammation, fibrosis and airway remodelling.[३४]

Relief medication[सम्पादन]

Symptomatic control of episodes of wheezing and shortness of breath is generally achieved with fast-acting bronchodilators. These are typically provided in pocket-sized, metered-dose inhalers (MDIs). In young sufferers, who may have difficulty with the coordination necessary to use inhalers, or those with a poor ability to hold their breath for 10 seconds after inhaler use (generally the elderly), an asthma spacer (see top image) is used. The spacer is a plastic cylinder that mixes the medication with air in a simple tube, making it easier for patients to receive a full dose of the drug and allows for the active agent to be dispersed into smaller, more fully inhaled bits. A nebulizer which provides a larger, continuous dose can also be used. Nebulizers work by vaporizing a dose of medication in a saline solution into a steady stream of foggy vapour, which the patient inhales continuously until the full dosage is administered. There is no clear evidence, however, that they are more effective than inhalers used with a spacer. Nebulizers may be helpful to some patients experiencing a severe attack. Such patients may not be able to inhale deeply, so regular inhalers may not deliver medication deeply into the lungs, even on repeated attempts. Since a nebulizer delivers the medication continuously, it is thought that the first few inhalations may relax the airways enough to allow the following inhalations to draw in more medication.

Relievers include:

  • Short-acting, selective beta2-adrenoceptor agonists, such as salbutamol (albuterol USAN), levalbuterol, terbutaline and bitolterol.
    Tremors, the major side effect, have been greatly reduced by inhaled delivery, which allows the drug to target the lungs specifically; oral and injected medications are delivered throughout the body. There may also be cardiac side effects at higher doses (due to Beta-1 agonist activity), such as elevated heart rate or blood pressure; with the advent of selective agents, these side effects have become less common. Patients must be cautioned against using these medicines too frequently, as with such use their efficacy may decline, producing desensitization resulting in an exacerbation of symptoms which may lead to refractory asthma and death.
  • Older, less selective adrenergic agonists, such as inhaled epinephrine and ephedrine tablets, have also been used. Cardiac side effects occur with these agents at either similar or lesser rates to albuterol.[३५] [३६] When used solely as a relief medication, inhaled epinephrine has been shown to be an effective agent to terminate an acute asthmatic exacerbation.[३५] In emergencies, these drugs were sometimes administered by injection. Their use via injection has declined due to related adverse effects.
  • Anticholinergic medications, such as ipratropium bromide may be used instead. They have no cardiac side effects and thus can be used in patients with heart disease; however, they take up to an hour to achieve their full effect and are not as powerful as the β2-adrenoreceptor agonists.

Prevention medication[सम्पादन]

Current treatment protocols recommend prevention medications such as an inhaled corticosteroid, which helps to suppress inflammation and reduces the swelling of the lining of the airways, in anyone who has frequent (greater than twice a week) need of relievers or who has severe symptoms. If symptoms persist, additional preventive drugs are added until the asthma is controlled. With the proper use of prevention drugs, asthmatics can avoid the complications that result from overuse of relief medications.

Asthmatics sometimes stop taking their preventive medication when they feel fine and have no problems breathing. This often results in further attacks, and no long-term improvement.

Preventive agents include the following.

  • Inhaled glucocorticoids are the most widely used of the prevention medications and normally come as inhaler devices (ciclesonide, beclomethasone, budesonide, flunisolide, fluticasone, mometasone, and triamcinolone).
    Long-term use of corticosteroids can have many side effects including a redistribution of fat, increased appetite, blood glucose problems and weight gain. In particular high doses of steroids may cause osteoporosis. For this reasons inhaled steroids are generally used for prevention, as their smaller doses are targeted to the lungs unlike the higher doses of oral preparations. Nevertheless, patients on high doses of inhaled steroids may still require prophylactic treatment to prevent osteoporosis.
    Deposition of steroids in the mouth may cause a hoarse voice or oral thrush (due to decreased immunity). This may be minimised by rinsing the mouth with water after inhaler use, as well as by using a spacer which increases the amount of drug that reaches the lungs.
  • Leukotriene modifiers (montelukast, zafirlukast, pranlukast, and zileuton).
  • Mast cell stabilizers (cromoglicate (cromolyn), and nedocromil).
  • Antimuscarinics/anticholinergics (ipratropium, oxitropium, and tiotropium), which have a mixed reliever and preventer effect. (These are rarely used in preventive treatment of asthma, except in patients who do not tolerate beta-2-agonists.)
  • Methylxanthines (theophylline and aminophylline), which are sometimes considered if sufficient control cannot be achieved with inhaled glucocorticoids and long-acting β-agonists alone.
  • Antihistamines, often used to treat allergic symptoms that may underlie the chronic inflammation. In more severe cases, hyposensitization ("allergy shots") may be recommended.
  • Omalizumab, an IgE blocker; this can help patients with severe allergic asthma that does not respond to other drugs. However, it is expensive and must be injected.
  • Methotrexate is occasionally used in some difficult-to-treat patients.
  • If chronic acid indigestion (GERD) contributes to a patient's asthma, it should also be treated, because it may prolong the respiratory problem.

Additionally, the antidepressant tianeptine has shown significant efficacy in children with asthma.

Long-acting β2-agonists[सम्पादन]

A typical inhaler, of Serevent (salmeterol), a long-acting bronchodilator.

Long-acting bronchodilators (LABD) are similar in structure to short-acting selective beta2-adrenoceptor agonists, but have much longer sidechains resulting in a 12-hour effect, and are used to give a smoothed symptomatic relief (used morning and night). While patients report improved symptom control, these drugs do not replace the need for routine preventers, and their slow onset means the short-acting dilators may still be required. In November of 2005, the American FDA released a health advisory alerting the public to findings that show the use of long-acting β2-agonists could lead to a worsening of symptoms, and in some cases death.[३७]

Currently available long-acting beta2-adrenoceptor agonists include salmeterol, formoterol, bambuterol, and sustained-release oral albuterol. Combinations of inhaled steroids and long-acting bronchodilators are becoming more widespread; the most common combination currently in use is fluticasone/salmeterol (Advair in the United States, and Seretide in the United Kingdom).

A recent meta-analysis of the roles of long-acting beta-agonists may indicate a danger to asthma patients. "These agents can improve symptoms through bronchodilation at the same time as increasing underlying inflammation and bronchial hyper-responsiveness, thus worsening asthma control without any warning of increased symptoms," said Shelley Salpeter in a Cornell study. The study goes on to say that "Three common asthma inhalers containing the drugs salmeterol or formoterol may be causing four out of five US asthma-related deaths per year and should be taken off the market".[३८] This assertion has drawn criticism from many asthma specialists for being inaccurate. As Dr. Hal Nelson points out in a recent letter to the Annals of Internal Medicine,

"Salpeter and colleagues also assert that salmeterol may be responsible for 4000 of the 5000 asthma-related deaths that occur in the United States annually. However, when salmeterol was introduced in 1994, more than 5000 asthma-related deaths occurred per year. Since the peak of asthma deaths in 1996, salmeterol sales have increased about 5-fold, while overall asthma mortality rates have decreased by about 25%, despite a continued increase in asthma diagnoses. In fact, according to the most recent data from the National Center for Health Statistics, U.S. asthma mortality rates peaked in 1996 (with 5667 deaths) and have decreased steadily since. The last available data, from 2004, indicate that 3780 deaths occurred. Thus, the suggestion that a vast majority of asthma deaths could be attributable to LABA use is inconsistent with the facts."

Dr. Salpeter has since tempered her comments regarding LABAs

Emergency treatment[सम्पादन]

When an asthma attack is unresponsive to a patient's usual medication, other treatments are available to the physician or hospital:[३९]

Alternative and complementary medicine[सम्पादन]

Many asthmatics, like those who suffer from other chronic disorders, use alternative treatments; surveys show that roughly 50% of asthma patients use some form of unconventional therapy.[४१][४२] There are little data to support the effectiveness of most of these therapies. A Cochrane systematic review of acupuncture for asthma found no evidence of efficacy.[४३] A similar review of air ionisers found no evidence that they improve asthma symptoms or benefit lung function; this applied equally to positive and negative ion generators.[४४] A study of "manual therapies" for asthma, including osteopathic, chiropractic, physiotherapeutic and respiratory therapeutic manoeuvers, found there is insufficient evidence to support or refute their use in treating asthma;[४५] these manoeuvers include various osteopathic and chiropractic techniques to "increase movement in the rib cage and the spine to try and improve the working of the lungs and circulation"; chest tapping, shaking, vibration, and the use of "postures to help shift and cough up phlegm." On the other hand, one meta-analysis found that homeopathy has a potentially mild benefit in reducing symptom intensity;[४६] however, the number of patients involved in the analysis was small, and subsequent studies have not supported this finding.[४७] Several small trials have suggested some benefit from various yoga practices, ranging from integrated yoga programs[४८] —"yogasanas, Pranayama, meditation, and kriyas"—to sahaja yoga,[४९] a form of meditation. Ayurveda recommends use of herbs such as Ajwain, Harad, Hing, Ajamoda, Lavanga, Sunthi and others.[५०]

The Buteyko method, a Russian therapy based on breathing exercises, has been investigated. A randomized, controlled trial of just 39 patients in 1998 showed a substantial reduction in the need for beta-agonists and a 50% reduction in the need for inhaled steroids. Lung function remained the same despite the decrease in medication.[५१] A trial in New Zealand in 2003 showed an 85% reduction in the use of beta-agonist medication and a 50% reduction in inhaled steroid use after six months.[५२]

Given that some research has identified a negative association between helminth infection (hookworm) and asthma and hay fever, some have suggested that hookworm infestation, although not medically sanctioned, would cure asthma. There is anectdotal evidence to support this.[५३]

Guaifenesin, an expectorant available over the counter, may have a small effect in managing thickened bronchial mucus.

See also Complementary and alternative medicine.


आज्माया प्रोग्नोसिस बांला, विशेषयाना माइल्ड ल्वय् दुगु मचातेत। मचाबिले डायग्नोसिस जुगु आज्माय् ५४%य् थ्व डायग्नोसिस १०दं धुंका दैमखु। आज्मातिक्सय् extent of permanent lung damage गुलि दु धका बांलाक्क जानकारी मदुनि। Airway remodelling खनेदै तर थुकिलिं म्हयात द्याइ वा त्याइ धका आतक्क धाय्‌ मछिं।[९] Although conclusions from studies are mixed, most studies show that early treatment with glucocorticoids prevents or ameliorates decline in lung function as measured by several parameters.[५४] For those who continue to suffer from mild symptoms, corticosteroids can help most to live their lives with few disabilities. The mortality rate for asthma is low, with around 6000 deaths per year in a population of some 10 million patients in the United States.[५] Better control of the condition may help prevent some of these deaths.


The prevalence of childhood asthma has increased since 1980, especially in younger children.

More than 6% of children in the United States have been diagnosed with asthma, a 75% increase in recent decades. The rate soars to 40% among some populations of urban children. Asthma is usually diagnosed in childhood. The risk factors for asthma include:

  • a personal or family history of asthma or atopy;
  • triggers (see Pathophysiology above);
  • premature birth or low birth weight;
  • viral respiratory infection in early childhood;
  • maternal smoking;
  • being male, for asthma in prepubertal children; and
  • being female, for persistence of asthma into adulthood.

There is a reduced occurrence of asthma in people who were breast-fed as babies. Current research suggests that the prevalence of childhood asthma has been increasing. According to the Centers for Disease Control and Prevention's National Health Interview Surveys, some 9% of US children below 18 years of age had asthma in 2001, compared with just 3.6% in 1980 (see figure). The World Health Organization (WHO) reports that some 8% of the Swiss population suffers from asthma today, compared with just 2% some 25–30 years ago.[५५] Although asthma is more common in affluent countries, it is by no means a problem restricted to the affluent; the WHO estimate that there are between 15 and 20 million asthmatics in India. In the U.S., urban residents, Hispanics, and African Americans are affected more than the population as a whole. Globally, asthma is responsible for around 180,000 deaths annually.[५५]

On the remote South Atlantic island Tristan da Cunha, 50% of the population are asthmatics due to heredity transmission of a mutation in the gene CC16.

Socioeconomic factors[सम्पादन]

The incidence of asthma is higher among low-income populations within a society (it is not more common in developed countries than developing countries[३]), which in the western world are disproportionately minority, and more likely to live near industrial areas. Additionally, asthma has been strongly associated with the presence of cockroaches in living quarters, which is more likely in such neighborhoods.[५६]

The quality of asthma treatment varies along racial lines, likely because many low-income people cannot afford health insurance and because there is still a correlation between class and race. For example, black Americans are less likely to receive outpatient treatment for asthma despite having a higher prevalence of the disease. They are much more likely to have emergency room visits or hospitalization for asthma, and are three times as likely to die from an asthma attack compared to whites. The prevalence of "severe persistent" asthma is also greater in low-income communities compared with communities with better access to treatment.[५७][५८]

Asthma and athletics[सम्पादन]

Asthma appears to be more prevalent in athletes than in the general population. One survey of participants in the 1996 Summer Olympic Games, in Atlanta, Georgia, U.S., showed that 15% had been diagnosed with asthma, and that 10% were on asthma medication.[५९] These statistics have been questioned on at least two bases. Athletes with mild asthma may be more likely to be diagnosed with the condition than non-athletes, because even subtle symptoms may interfere with their performance and lead to pursuit of a diagnosis. It has also been suggested that some professional athletes who do not suffer from asthma claim to do so in order to obtain special permits to use certain performance-enhancing drugs.

There appears to be a relatively high incidence of asthma in sports such as cycling, mountain biking, and long-distance running, and a relatively lower incidence in weightlifting and diving. It is unclear how much of these disparities are from the effects of training in the sport, and from self-selection of sports that may appear to minimize the triggering of asthma.[५९][६०]

In addition, there exists a variant of asthma called exercise-induced asthma that shares many features with allergic asthma. It may occur either independently, or concurrent with the latter. Exercise studies may be helpful in diagnosing and assessing this condition.

स्वया दिसँ[सम्पादन]


  1. Zhao J, Takamura M, Yamaoka A, Odajima Y, Iikura Y. Altered eosinophil levels as a result of viral infection in asthma exacerbation in childhood. J Pediatr Allergy Immunol. 2002 Feb;13(1):47–50. PMID 12000498
  2. Lilly CM. Diversity of asthma: Evolving concepts of pathophysiology and lessons from genetics. J Allergy Clin Immunol. 2005;115 (4 Suppl):S526-31. PMID 15806035
  3. Marketos SG, Ballas CN. Bronchial asthma in the medical literature of Greek antiquity. J Asthma. 1982;19(4):263-9. PMID 6757243
  4. Rosner F. Moses Maimonides' treatise on asthma. Thorax. 1981;36:245–251. PMID 7025335
  5. ५.० ५.१ ५.२ McFadden ER, Jr. "Asthma". In Kasper DL, Fauci AS, Longo DL, et al (eds). Harrison's Principles of Internal Medicine, 16th ed., pp. 1508–1516. New York: McGraw-Hill;2004.
  6. Longmore, Murray et al (2007). Oxford Handbook of Clinical Medicine, 7th ed., Oxford University Press.
  7. Pinnock H, Shah R (2007). "Asthma". Br Med J 334 (7598): 847–50. DOI:10.1136/bmj.39140.634896.BE. 
  8. Vargas, PA (September 2004). "Characteristics of children with asthma who are enrolled in a Head Start program". J Allergy Clin Immunol: 499–504. PMID 15356547. 
  9. ९.० ९.१ Maddox L, Schwartz DA. The Pathophysiology of Asthma. Annu. Rev. Med. 2002, 53:477-98. PMID 11818486
  10. Jenkins C, Costello J, Hodge L. Systematic review of prevalence of aspirin induced asthma and its implications for clinical practice. BMJ 2004;328:434. PMID 14976098
  11. Nemery B, Hoet PH, Nowak D. Indoor swimming pools, water chlorination and respiratory health. Eur Respir J. 2002;19(5):790-3. PMID 12030714
  12. Szentivanyi, Andor (1968). "The Beta Adrenergic Theory of the Atopic Abnormality in Asthma". 
  13. Lockey, Richard, In lasting tribute: Andor Szentivanyi, MD. J. Allergy and Clinical Immunology, January, 2006
  14. Szentivanyi A., Ali K., Calderon EG., Brooks SM., Coffey RG., Lockey RF. (1993). "The in vitro effect of Imunnoglobulin E {IgE} on cyclic AMP concentrations in A549 human pulmonary epithelial cells with or without beta adrenergic stimulation". J. Allergy Clin Immunol. 91: 379.  - Part of Abstracts from:
    (1993) "50th Anniversary of the American Academy of Allergy and Immunology. 49th Annual Meeting. Chicago, Illinois, March 12–17, 1993. Abstracts.". J Allergy Clin Immunol 91 (1 Pt 2): 141–379. PMID 8421135. 
  15. (2001) Kowalak JP, Hughes AS et al (eds) Professional Guide To Diseases, 7th ed., Springhouse.
  16. Lockey, Richard F. (2006-04-28). Anaphylaxis: Synopsis. Allergic Diseases Resource Center. World Allergy Organization. September 23, 2006 कथं।
  17. Ouellette, J. J.; C. E. Reed (March 1967). "The effect of partial beta adrenergic blockade on the bronchial response of hay fever subjects to ragweed aerosol.". Journal of Allergy 39 (3): 160-6. PubMed. 
  18. Fraser, Claire M.; J. Craig Venter (May 14, 1980). "The synthesis of beta-adrenergic receptors in cultured human lung cells: induction by glucocorticoids." (PDF). Biochemical and Biophysical Research Communications 94 (1): 390–397. DOI:10.1016/S0006-291X(80)80233-6. PubMed. Retrieved on 2006-09-23. 
  19. Asthma and Air Quality.
  20. California Children's Health Study.
  21. Terttu HH, Leinonen M, Nokso-Koivisto J, Korhonen T, Raty R, He Q, Hovi T, Mertsola J, Bloigu A, Rytila P, Saikku P (2006). "Non-random distribution of pathogenic bacteria and viruses in induced sputum or pharyngeal secretions of adults with stable asthma". Thorax. PMID 16517571. 
  22. २२.० २२.१ Richeldi L, Ferrara G, Fabbri LM, Lasserson TJ, Gibson PG (2005). "Macrolides for chronic asthma". Cochrane Database Syst Rev (4): CD002997. PMID 16235309. 
  23. Pasternack R, Huhtala H, Karjalainen J (2005). "Chlamydophila (Chlamydia) pneumoniae serology and asthma in adults: a longitudinal analysis". J Allergy Clin Immunol 116 (5): 1123–8. PMID 16275386. 
  24. Ronchetti R, Biscione GL, Ronchetti F, Ronchetti MP, Martella S, Falasca C, Casini C, Barreto M, Villa MP (2005). "Why Chlamydia pneumoniae is associated with asthma and other chronic conditions? Suggestions from a survey in unselected 9 years old schoolchildren". Pediatr Allergy Immunol 16 (2): 145-50. PMID 15787872. 
  25. Breathing disorders during sleep are common among asthmatics, may help predict severe asthma, University of Michigan Health System, May 25, 2005, <http://www.med.umich.edu/opm/newspage/2005/asthmasleep.htm>. Retrieved on २३ सेप्टेम्बर २००६ 
  26. Basner, Robert C. (2006-07-25). Asthma and OSA. ASAA Resources > Publications. American Sleep Apnea Association. September 23, 2006 कथं।
  27. Leggett, Julian J.; Brian T. Johnston, Moyra Mills, Jackie Gamble, and Liam G. Heaney (April 2005). "Prevalence of Gastroesophageal Reflux in Difficult Asthma". Chest 127 (4): 1227–1231. PubMed. Retrieved on 2006-09-23. 
  28. American Journal of Respiratory and Critical Care Medicine 1995;151:969–74.
  29. Thomson NC, Spears M. The influence of smoking on the treatment response in patients with asthma. Curr Opin Allergy Clin Immunol. 2005;5(1):57–63. PMID 15643345
  30. Eisner MD, Yelin EH, Katz PP, et al. Exposure to indoor combustion and adult asthma outcomes: environmental tobacco smoke, gas stoves, and wood-smoke. Thorax. 2002;57(11):973-8. PMID 12403881
  31. ३१.० ३१.१ National Asthma Education and Prevention Program. Expert Panel Report: Guidelines for the Diagnosis and Management of Asthma. National Institutes of Health pub no 97–4051. Bethesda, MD, 1997. (PDF)
  32. British Thoracic Society & Scottish Intercollegiate Guidelines Network (SIGN). British Guideline on the Management of Asthma. Guideline No. 63. Edinburgh:SIGN; 2004. (HTML, Full PDF, Summary PDF)
  33. Cromie, William J.. "Researchers uncover cause of asthma", Harvard University Gazette, Harvard News Office, 2006-03-16. Retrieved on 2006-09-23.
  34. D. Zeng & R. Polosa (2006). A Novel Therapeutic Target in Asthma - The A2B Adenosine Agonist.
  35. ३५.० ३५.१ Hendeles L, Marshik PL, et al. Response to nonprescription epinephrine inhaler during nocturnal asthma. Ann Allergy Asthma Immunol. 2005 Dec;95(6):530-4. PMID 16400891
  36. Rodrigo GJ, Nannini LJ. Comparison between nebulized adrenaline and beta2 agonists for the treatment of acute asthma. A meta-analysis of randomized trials. Am J Emerg Med. 2006 Mar;24(2):217-22. PMID 16490653
  37. Serevent Diskus, Advair Diskus, and Foradil Information (Long Acting Beta Agonists) - Drug information. FDA (2006-03-03).
  38. Ramanujan, Krishna (2006-06-09). Common asthma inhalers cause up to 80 percent of asthma-related deaths, Cornell and Stanford researchers assert. Cornell Chronicle Online. Cornell News Service. 2006-09-23 कथं।
  39. Rodrigo GJ, Rodrigo C, Hall JB. Acute asthma in adults: a review. Chest. 2004;125(3):1081-102. PMID 15006973
  40. Rodrigo G (2005). "Comparison of inhaled fluticasone with intravenous hydrocortisone in the treatment of adult acute asthma". Am J Respir Crit Care Med 171 (11): 1231–6. PMID 15764724. 
  41. Blanc PD, Trupin L, Earnest G, et al. Alternative therapies among adults with a reported diagnosis of asthma or rhinosinusitis: data from a population-based survey. Chest. 2001;120(5):1461–7. PMID 11713120
  42. Shenfield G, Lim E, Allen H. Survey of the use of complementary medicines and therapies in children with asthma. J Paediatr Child Health. 2002;38(3):252-7. PMID 12047692
  43. McCarney RW, Brinkhaus B, Lasserson TJ, et al. Acupuncture for chronic asthma. Cochrane Database Syst Rev. 2004;(1):CD000008. PMID 14973944
  44. Blackhall K, Appleton S, Cates CJ. Ionisers for chronic asthma. Cochrane Database Syst Rev. 2003;(3):CD002986 PMID 12917939
  45. Hondras MA, Linde K, Jones AP. Manual therapy for asthma. Cochrane Database Syst Rev. 2005;(2):CD001002. PMID 15846609
  46. Reilly D, Taylor MA, Beattie NG, et al. Is evidence for homoeopathy reproducible? Lancet. 1994;344(8937):1601–6. PMID 7983994
  47. White A, Slade P, Hunt C, et al. Individualised homeopathy as an adjunct in the treatment of childhood asthma: a randomised placebo controlled trial. Thorax. 2003;58(4):317-21. PMID 12668794
  48. Nagendra HR, Nagarathna R. An integrated approach of yoga therapy for bronchial asthma: a 3-54-month prospective study. J Asthma. 1986;23(3):123-37. PMID 3745111
  49. Manocha R, Marks GB, Kenchington P, et al. Sahaja yoga in the management of moderate to severe asthma: a randomised controlled trial. Thorax. 2002;57(2):110-5. PMID 11828038
  50. Asthma Treatment
  51. Bowler SD, Green A, Mitchell CA. Buteyko breathing techniques in asthma: a blinded randomised controlled trial. Med J Aust. 1998;169(11-12):575-8. PMID 9887897. Free full text
  52. McHugh P, Aitcheson F, Duncan B, Houghton F. Buteyko Breathing Technique for asthma: an effective intervention. NZ Med J. 2003;116:1187 PMID 14752538. Free full text
  53. "Worm infestation 'beats asthma'", BBC News, 2001-11-02.
  54. Beckett PA, Howarth PH. Pharmacotherapy and airway remodelling in asthma? Thorax. 2003;58(2):163-74. PMID 12554904
  55. ५५.० ५५.१ World Health Organization. Bronchial asthma: scope of the problem. 2005-08-23 कथं।
  56. Patient/Public Education: Fast Facts - Asthma Demographics/Statistics. American Academy of Allergy Asthma & Immunology. 2006-05-02 कथं।
  57. National Heart, Lung, and Blood Institute (May 2004). Morbidity & Mortality: 2004 Chart Book On Cardiovascular, Lung, and Blood Diseases. National Institutes of Health.
  58. National Center for Health Statistics (07 April 2006). Asthma Prevalence, Health Care Use and Mortality, 2002. Centers for Disease Control and Prevention.
  59. ५९.० ५९.१ Weiler JM, Layton T, Hunt M. Asthma in United States Olympic athletes who participated in the 1996 Summer Games. J Allergy Clin Immunol. 1998;102(5):722-6. PMID 9819287
  60. Helenius I, Haahtela T. Allergy and asthma in elite summer sport athletes. J Allergy Clin Immunol. 2000;106(3):444-52 PMID 10984362

पिनेया स्वापूत[सम्पादन]