   #copyright

Asthma

2007 Schools Wikipedia Selection. Related subjects: Health and medicine

   CAPTION: Bronchial Asthma
   Classifications and external resources

                      Image:Inhaler girl.png
   Young asthmatic girl using an inhaler attached to a spacer.
     ICD- 10   J 45.
     ICD- 9    493
      OMIM     600807
   DiseasesDB  1006
   MedlinePlus 000141
    eMedicine  med/177  emerg/43
   MeSH        C08.127.108

   Asthma is a disease of the respiratory system in which the airways
   constrict, become inflamed, and are lined with excessive amounts of
   mucus, often in response to one or more "triggers," such as exposure to
   an environmental stimulant (or allergen), cold air, exercise, or
   emotional stress. In children, the most common triggers are viral
   illnesses such as those that cause the common cold. This airway
   narrowing causes symptoms such as wheezing, shortness of breath, chest
   tightness, and coughing, which respond to bronchodilators. Between
   episodes, most patients feel fine.

   The disorder is a chronic or recurring inflammatory condition in which
   the airways develop increased responsiveness to various stimuli,
   characterized by bronchial hyper-responsiveness, inflammation,
   increased mucus production, and intermittent airway obstruction. 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. Susceptibility to asthma can be explained in part
   by genetic factors, but no clear pattern of inheritance has been found.
   Asthma is a complex disease that is influenced by multiple genetic,
   developmental, and environmental factors, which interact to produce the
   overall condition.

History

   The word asthma is derived from the Greek aazein, meaning "sharp
   breath." The word first appears in Homer's Iliad; Hippocrates was the
   first to use it in reference to the medical condition. Hippocrates
   thought that the spasms associated with asthma were more likely to
   occur in tailors, anglers, and metalworkers. Six centuries later, Galen
   wrote much about asthma, noting that it was caused by partial or
   complete bronchial obstruction. Moses Maimonides, an influential
   medieval rabbi, philosopher, and physician, wrote a treatise on asthma,
   describing its prevention, diagnosis, and treatment. In the 17th
   century, Bernardino Ramazzini noted a connection between asthma and
   organic dust. The use of bronchodilators started in 1901, but it was
   not until the 1960s that the inflammatory component of asthma was
   recognized, and anti-inflammatory medications were added to the
   regimen.

Signs and symptoms

   In some individuals asthma is characterized by chronic respiratory
   impairment. In others it is an intermittent illness marked by episodic
   symptoms that may result from a number of triggering events, including
   upper respiratory infection, airborne allergens, and exercise.

   An acute exacerbation of asthma is referred to as an asthma attack. The
   clinical hallmarks of an attack are shortness of breath ( dyspnea) and
   either wheezing or stridor. Although the latter is "often regarded as
   the sine qua non of asthma," some victims 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 or asthma attack are either stridor or
   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.
   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.

Diagnosis

   In most 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.

Differential diagnosis

   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.

   Only a minority of asthma sufferers have an identifiable allergy
   trigger. 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 pulmonary function has been measured, 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.

Pathophysiology

Bronchoconstriction

   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.
   Enlarge
   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.

   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 several categories of stimuli:
     * allergenic air pollution, from nature, typically inhaled, which
       include waste from common household insects, such as the house dust
       mite and cockroach, grass pollen, mould spores and pet epithelial
       cells;
     * medications, including aspirin and β-adrenergic antagonists (beta
       blockers);
     * Use of fossil fuel related allergenic air pollution, such as ozone,
       Smog, Summer smog, nitrogen dioxide, and sulfur dioxide, which is
       thought to be one of the major reasons for the high prevalence of
       asthma in urban areas;
     * various industrial compounds and other chemicals, notably sulfites;
       chlorinated swimming pools generate chloramines—monochloramine
       (NH[2]Cl), dichloramine (NHCl[2]) and trichloramine (NCl[3])—in the
       air around them, which are known to induce asthma.
     * early childhood infections, especially viral respiratory
       infections. However, persons of any age can have asthma triggered
       by colds and other respiratory infections even though their normal
       stimuli might be from another category (e.g. pollen) and absent at
       the time of infection. 80% of asthma attacks in adults and 60% in
       children are caused by respiratory viruses.
     * exercise, the effects of which differ somewhat from those of the
       other triggers;
     * (in some countries) - allergenic indoor air pollution from
       Newsprint & other literature such as, junk mail leaflets & glossy
       magazines.
     * emotional stress which is poorly understood as a trigger. Perhaps
       because crying might be a form of exercise or because being given
       an asthma attack may be distressing.

Bronchial inflammation

   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 ( T[H]0 cells) "check" and usually
   ignore the allergen molecules. In asthmatics, however, these cells
   transform into a different type of cell (T[H]2), for reasons that are
   not well understood. The resultant T[H]2 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.

Pathogenesis

   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. Szentivanyi's Beta Adrenergic Theory is a
   citation classic 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. Since overproduction of IgE is central to all atopic
   diseases, this was a watershed moment in the world of Allergy.

   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), Charles Reed
   (Chief of Allergy at Mayo Medical School), and Craig Venter (Human
   Genome Project).

   One 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 T[H]1 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 T[H]2 cells predominate,
   and asthma and other allergic diseases may develop. This " hygiene
   hypothesis" may explain the increase in asthma in affluent populations.
   The T[H]2 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.

   Another theory is based on the correlation of air pollution and the
   incidence of asthma. Although it is well known that substantial
   exposures to certain industrial chemicals can cause acute asthmatic
   episodes, it has not been proven that air pollution is responsible for
   the development of asthma. In Western Europe, most atmospheric
   pollutants have fallen significantly over the last 40 years, while the
   prevalence of asthma has risen.

   Finally, it has been postulated that some forms of asthma may be
   related to infection, in particular by Chlamydia pneumoniae. This issue
   remains controversial, as the relationship is not borne out by
   meta-analysis of the research. 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. One possible explanation is that some
   asthmatics may have altered immune response that facilitates long-term
   chlamydia pneumonia infection. 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.

Asthma and 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. CPAP is not
   effective in patients with nocturnal asthma only.

Asthma and gastro-esophageal reflux disease

   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. GERD may be common in
   difficult-to-control asthma, but generally speaking, treating it does
   not seem to affect the asthma.

Treatment

   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.

   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. Asthmatics who smoke typically require
   additional medications to help control their disease. Furthermore,
   exposure of both nonsmokers and smokers to secondhand smoke is
   detrimental, resulting in more severe asthma, more emergency room
   visits, and more asthma-related hospital admissions. Smoking cessation
   and avoidance of secondhand smoke is strongly encouraged in asthmatics.

   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) of the
   U.S. National Asthma Education and Prevention Program, and the British
   guideline on the management of asthma are broadly used and supported by
   many doctors. 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.

   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.

   A novel therapeutic target currently under investigation is the A[2B]
   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 A[2B] antagonists in
   pulmonary inflammation, fibrosis and airway remodelling.

Relief medication

   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 beta[2]-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, are available over the counter
       in the US. Cardiac side effects occur with these agents at either
       similar or lesser rates to albuterol. When used solely as a relief
       medication, inhaled epinephrine has been shown to be an effective
       agent to terminate an acute asthmatic exacerbation. 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
       β[2]-adrenoreceptor agonists.

Prevention medication

   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 ( ciclesonide, fluticasone, budesonide,
       beclomethasone, mometasone, flunisolide, and triamcinolone).
     * 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.

Long-acting β[2]-agonists

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

   Long-acting bronchodilators (LABD) give a 12-hour effect, and are used
   to give a smoothed symptomatic effect (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 β[2]-agonists could lead to a
   worsening of symptoms, and in some cases death.

   Currently available long-acting beta[2]-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 UK).

   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 Cornel 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 U.S. asthma-related deaths
   per year and should be taken off the market".

Emergency treatment

   When an asthma attack is unresponsive to a patient's usual medication,
   other treatments are available to the physician or hospital:
     * oxygen to alleviate the hypoxia (but not the asthma per se) that
       results from extreme asthma attacks;
     * nebulized salbutamol or terbutaline (short-acting beta-2-agonists),
       often combined with ipratropium (an anticholinergic);
     * systemic steroids, oral or intravenous ( prednisone, prednisolone,
       methylprednisolone, dexamethasone, or hydrocortisone)
     * other bronchodilators that are occasionally effective when the
       usual drugs fail:
          + nonspecific beta-agonists, injected or inhaled ( epinephrine,
            isoetharine, isoproterenol, metaproterenol);
          + anticholinergics, IV or nebulized, with systemic effects (
            glycopyrrolate, atropine);
          + methylxanthines ( theophylline, aminophylline);
          + inhalation anesthetics that have a bronchodilatory effect (
            isoflurane, halothane, enflurane);
          + the dissociative anaesthetic ketamine, often used in
            endotracheal tube induction
          + magnesium sulfate, intravenous; and
     * intubation and mechanical ventilation, for patients in or
       approaching respiratory arrest.

Alternative and complementary medicine

   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. 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. 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. A study of "manual therapies"
   for asthma, including osteopathic, chiropractic, physiotherapeutic and
   respiratory therapeutic maneuvers, found no evidence to support their
   use in treating asthma; these maneuvers 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; however, the number of patients involved in the analysis was
   small, and subsequent studies have not supported this finding. Several
   small trials have suggested some benefit from various yoga practices,
   ranging from integrated yoga programs —"yogasanas, Pranayama,
   meditation, and kriyas"—to sahaja yoga, a form of meditation.

   The Buteyko method, a Russian therapy based on breathing exercises, has
   been investigated with mixed degrees of effect shown. A randomized,
   controlled trial of just 39 patients in 1998, suggested that it may
   moderately reduce the need for beta-agonists among asthmatics, but
   found no objective improvement in lung function. Whilst a trial in New
   Zealand, 2003, showed reduced beta-agonist medication by 94% and
   inhaled steroid by 34% after just six weeks.

   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.

   See also Complementary and alternative medicine.

Prognosis

   The prognosis for asthmatics is good, especially for children with mild
   disease. For asthmatics diagnosed during childhood, 54% will no longer
   carry the diagnosis after a decade. The extent of permanent lung damage
   in asthmatics is unclear. Airway remodelling is observed, but it is
   unknown whether these represent harmful or beneficial changes. 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. 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. Better control of the condition may help prevent
   some of these deaths.

Epidemiology

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

   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

   The incidence of asthma is higher among low-income populations within a
   society (even though it is more common in developed countries than
   developing countries), 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 neighbourhoods.

   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.

Asthma and athletics

   Asthma appears to be more prevalent in athletes than in the general
   population. One survey of participants in the 1996 Summer Olympic Games
   showed that 15% had been diagnosed with asthma, and that 10% were on
   asthma medication. These statistics have been questioned on at least
   two bases. Persons with mild asthma may be more likely to be diagnosed
   with the condition than others 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.

   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.

   Retrieved from " http://en.wikipedia.org/wiki/Asthma"
   This reference article is mainly selected from the English Wikipedia
   with only minor checks and changes (see www.wikipedia.org for details
   of authors and sources) and is available under the GNU Free
   Documentation License. See also our Disclaimer.
