Asthma

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Philip Marcus, M.D., M.P.H. [2] Associate Editor(s)-in-Chief:

Asthma was first mentioned in Homer’s Iliad. It was later studied by influential thinkers such as, Hippocrates, Galen, and Moses Maimonides. Asthma treatment methods emerged in the late 1800s.

• The word asthma is derived from the Ancient Greek word aazein, meaning sharp breath.
• The word first appeared in Homer’s Iliad.^[1]
• Hippocrates was the first to use it in reference to a medical condition, in 450 BC and thought 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.
• In 1190 AD, Moses Maimonides, an influential medieval rabbi, philosopher, and physician, wrote a treatise on asthma, describing its prevention, diagnosis, and treatment.^[2]
• In the 17th century, Bernardino Ramazzini noted a connection between asthma and organic dust.
• In the year 1880, Dr. J.B. Berkart used intravenous administration of pilocarpine to treat asthma.^[3][4]
• In the year 1886, F.H. Bosworth F.H. suspected an association between asthma and hay fever.^[5]
• Epinephrine was first referred to in the treatment of asthma in 1905,^[6] and for acute asthma in 1910.^[7]
• The use of bronchodilators for the treatment of asthma 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 regimens.
• During the 1930s–50s, asthma was considered to be one of the holy seven psychosomatic illnesses and suspected a psychological etiology. Among the first papers in modern medicine, the one published in 1873 explained the pathophysiology of the disease,^[8] and another paper published in 1872 discussed the treatment of asthma with the author concluding that rubbing the chest with chloroform liniment cured asthma.^[9]

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Lakshmi Gopalakrishnan, M.B.B.S. [2] Anum Ijaz M.B.B.S., M.D.[3]

Asthma is classified into atopic and non-atopic types based on the onset of symptoms. Atopic refers to early-onset whereas non-atopic refers to late-onset. Despite the differentiation, a significant degree of overlap exists between the two types. The severity of symptoms is further classified based on the GINA severity grades into mild intermittent, mild persistent, moderate persistent and severe persistent asthma.

• Early-age of onset
• Atopic individuals have an increased predisposition
• Environmental allergens play a strong role in the pathogenesis
• Positive personal and/or family history of atopic diseases such as allergic rhinitis, urticaria and eczema
• Laboratory tests may reveal increased serum IgE levels, positive skin test to specific aero-allergens and a positive bronchoprovocation test

• Late-age of onset
• Non- atopic individuals have an increased predisposition
• Indoor allergens play a strong role in the pathogenesis
• Negative personal and/or family history of allergic diseases
• Laboratory tests may reveal normal serum IgE levels and a negative bronchoprovocation test

Asthma is classified into four subgroups: mild intermittent, mild persistent, moderate persistent and severe persistent based on the Global Initiative for Asthma – GINA severity grades.^[1]

Severity Components	Intermittent	Persistent Asthma
		Mild	Moderate	Severe
Symptoms	Less than 1 day/week	More than 2 days/week Not daily	Daily	Daily Throughout the day
Nocturnal Symptoms	Less than 2 times/month	3 to 4 times/month	More than 1 time/week Not every night	Every night
Interference w/ Activity	Minimal to none	Minor limitation of activity	Some limitation of activity	Severe limitation of activity
Short-Acting Beta-Agonist Use	Less than 2 days/week	More than 2 days/week but not daily Not more than once/day	Daily	Several times/day
Pulmonary Function Test	Normal FEV1 between exacerbations FEV1 > 80% predicted FEV1/FVC normal	FEV1 > 80% predicted FEV1/FVC normal	FEV1 > 60% but < 80% predicted FEV1/FVC reduced by 5%	FEV1 < 60% predicted FEV1/FVC reduced by > 5%
Recommended Treatment Strategy	STEP 1 Preferred: Short-acting beta-agonist PRN	STEP 2 Preferred: Low-dose inhaled corticosteroids Alternative: Cromolyn, Leukotriene receptor antagonist, Nedocromil, or Theophylline	STEP 3 Preferred: Either low-dose inhaled corticosteroids + long-acting beta-agonist OR Medium-dose inhaled corticosteroid Alternative: Low-dose inhaled corticosteroid + either Leukotriene receptor antagonist, Theophylline, or Zileuton	STEP 4 Preferred: Medium-dose inhaled corticosteroid + long-acting beta-agonist Alternative: Medium-dose inhaled corticosteroids + either Leukotriene receptor antagonist, Theophylline, or Zileuton STEP 5 Preferred: High-dose inhaled corticosteroids + long-acting beta-agonist Consider adding Omalizumab for patients with allergies STEP 6 Preferred: High-dose inhaled corticosteroids + long-acting beta-agonist + oral corticosteroids Consider adding Omalizumab for patients with allergies
Step down if possible and asthma is controlled for at least 3 months Step-up if needed, but first check adherence, environmental control, and comorbidities
In each step, patient education, environmental control, and management of comorbidities are important. In STEP 2 – 4, consider subcutaneous allergen immunotherapy for patients with allergic asthma
Short-acting beta-agonist as needed for symptoms. Up to 3 treatments at 20 minute intervals as needed. A short course of oral systemic corticosteroids may be needed. Use of a short-acting beta agonist for >2 days a week for symptom control indicates inadequate control and the need to step up therapy.

^[3]

It is defined as asthma that remains uncontrolled despite treatment with high-dose inhaled corticosteroids (ICS) plus one or more additional controller therapies (such as long-acting β-agonists), in patients who are adherent to therapy, use correct inhaler technique, and receive treatment for comorbidities that may exacerbate asthma, including allergic rhinitis, chronic rhinosinusitis, and gastroesophageal reflux disease.

Patients with severe refractory asthma may experience accelerated loss of lung function and have higher mortality rates associated with exacerbations compared with individuals with milder asthma.

Severe refractory asthma affects approximately 1% to 5% of patients with asthma.

Most patients with severe refractory asthma in the United States are managed exclusively in primary care, and only 50.4% see an asthma specialist within a year following an asthma exacerbation requiring emergency department or hospital care.

Type 2 (T2)–high asthma is the most common subtype, characterized by elevations in IL‑4, IL‑5, IL‑13, eosinophils, and fractional exhaled nitric oxide (FeNO). This subtype carries a higher risk of exacerbations and is more responsive to biologic therapies, though access is limited because specialists prescribe more than 90% of biologics.

All patients with severe refractory asthma should undergo the following diagnostic evaluation:

• Pulmonary function testing (pre- and post-bronchodilator) to assess airflow obstruction, bronchodilator responsiveness, and monitor lung function decline associated with airway remodeling.

• Laboratory and biomarker testing, including complete blood count with differential to assess eosinophils, total serum IgE, and fractional exhaled nitric oxide (FeNO), available in many asthma clinics and some primary care practices.

• Environmental allergy testing using skin prick testing or allergen-specific IgE to identify sensitization to pollen, dust mites, mold, pet dander, and other allergens. These help identify allergic asthma, guide exposure reduction strategies, and determine eligibility for anti-IgE therapy (omalizumab). Allergy test interpretation should be performed by allergists, as positive predictive value may be as low as 50% unless supported by clinical history.

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Philip Marcus, M.D., M.P.H. [2]; Associate Editor(s)-in-Chief: Varun Kumar, M.B.B.S. [3]

Asthma is caused by a complex interaction of environmental and genetic factors that researchers do not yet fully understand.^[1] These factors can also influence how severe a person’s asthma is and how well they respond to medication.^[2] As with other complex diseases, many environmental and genetic factors have been suggested as causes of asthma, but not all studies posing such claims have been verified by further studies. In addition, as researchers detangle the complex causes of asthma, it is becoming more evident that certain environmental and genetic factors may affect asthma only when combined.^[3]

• Many environmental risk factors have been associated with asthma development and morbidity in children, but a few stand out as well-replicated or that have a meta-analysis of several studies to support their direct association.
• Environmental tobacco smoke, especially maternal cigarette smoking, is associated with high risk of asthma prevalence and asthma morbidity, wheeze, and respiratory infections.^[4]
• Poor air quality, from traffic pollution or high ozone levels, has been repeatedly associated with increased asthma morbidity and has a suggested association with asthma development that needs further research.^[4][5]
• Caesarean sections have been associated with asthma when compared with vaginal birth; a meta-analysis found a 20% increase in asthma prevalence in children delivered by Cesarean section compared to those who were not. It was proposed that this is due to modified bacterial exposure during Cesarean section compared with vaginal birth, which modifies the immune system (as described by the hygiene hypothesis).^[11]
• Psychological stress, has long been suspected of being an asthma trigger, but only in recent decades has convincing scientific evidence substantiated this hypothesis. Rather than stress directly causing the asthma symptoms, it is thought that stress modulates the immune system to increase the magnitude of the airway inflammatory response to allergens and irritants.^[4][9]
• Viral respiratory infections at an early age, along with siblings and day care exposure, may be protective against asthma, although there have been controversial results, and this protection may depend on genetic context.^[4][12][13]
• Antibioticuse early in life has been linked to development of asthma in several examples; it is thought that antibiotics make one susceptible to development of asthma because they modify gut flora, and thus the immune system (as described by the hygiene hypothesis).^[14]
• The hygiene hypothesis is an hypothesis about the cause of asthma and other allergic disease, and is supported by epidemiologic data for asthma. For example, asthma prevalence has been increasing in developed countries along with increased use of antibiotics, C-sections, and cleaning products.^[14][11][15] All of these things may negatively affect exposure to beneficial bacteria and other immune system modulators that are important during development, and thus may cause increased risk for asthma and allergy.

Over 100 genes have been associated with asthma in at least one genetic association study.^[16] However, such studies must be repeated to ensure the findings are not due to chance. Through the end of 2005, 25 genes had been associated with asthma in six or more separate populations:^[16]

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Philip Marcus, M.D., M.P.H. [2] Associate Editor(s)-in-Chief:

Asthma must be clinically differentiated from other conditions that cause recurrent cough and wheezing such as viral bronchiolitis, chronic obstructive pulmonary disease, congestive heart failure, vocal cord dysfunction, ACE inhibitors use and allergic rhinitis.^[1][2]

• Asthma must be differentiated from other respiratory and cardiac diseases that can cause the same clinical manifestations like cough and dyspnea. These diseases include Bronchiolitis, COPD, pneumonia, congestive heart failure, diffuse idiopathic neuroendocrine cell hyperplasia, tuberculosis, pertussis, foreign body aspiration, pulmonary embolism and Harmann-Rich syndrome.^{[1][3][4][5][6]}

• Although, many cases of recurrent cough and wheezing in children and adults are due to asthma, other conditions are often misdiagnosed as asthma.^{[1][6][5][4][3]}

• Chronic obstructive pulmonary disease (COPD)
• Hyperventilation syndrome and panic attacks
• Congestive heart failure
• Pulmonary embolism
• Laryngeal dysfunction
• Pulmonary aspiration
• Mechanical obstruction of the airways (benign and malignant tumors)
• Pulmonary infiltration with eosinophilia
• Diffuse parenchymal lung diseases
• Cough, secondary to drugs (ACE inhibitors)^[2]
• Vocal cord dysfunction^[6]
• Pharyngitis

• Allergic rhinitis and sinusitis^[6]

• Foreign body in trachea or bronchus
• Vocal cord dysfunction
• Vascular rings or laryngeal webs
• Laryngotracheomalacia, tracheal stenosis, or bronchostenosis
• Enlarged lymph nodes or tumor^[6]

• Viral bronchiolitis or obliterative bronchiolitis
• Cystic fibrosis
• Bronchopulmonary dysplasia^[6]

• Congenital heart diseases
• Recurrent cough not due to asthma
• Aspiration from swallowing mechanism
• Gastroesophageal reflux^[6]

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2]; Philip Marcus, M.D., M.P.H. [3]; Associate Editor(s)-in-Chief: Varun Kumar, M.B.B.S. [4]

Approximately 300 million people around the world currently have asthma^[1] and the number is estimated to increase by additional 100 million by the year 2025. Prevalence of asthma is high among children and females in industrialized nations. International Study of Asthma and Allergies in Childhood (ISAAC), which measured the global prevalence and severity of asthma symptoms in children, demonstrated that the high rates of asthma were noted in countries whose predominant language is English.^[2] Puerto Rican people have the highest prevalence of asthma in USA.^[3] Asthma accounts for 217,000 emergency room visits and 10.5 million physician office visits every year.^[4]

• Over 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.^[5]

• Males are affected more often during their childhood and the prevalence declines with age. On the contrary, prevalence rises among females steadily through childhood equaling that among males between ages 14-17 years.
• During adulthood, females report higher current asthma prevalence compared with men.^[3]

• Asthma incidence and quality of treatment varies among different racial groups, though this may be due to correlations with income (and thus affordability of health care) and geography. 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. They are also three times as likely to die from an asthma attack compared to whites.
• The prevalence of severe persistence asthma is also greater in low-income communities compared with communities with better access to treatment.^[6][7]

• 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.^[8]
• In the U.S., urban residents, Hispanics, and African Americans are affected more than the population as a whole. Globally, asthma is responsible for 180,000 deaths annually.^[8]
• According to the National Health Statistic Reports, 2009, there is higher prevalence of asthma among people residing in northeast (9.3%) and midwest (8.8%) regions of USA in comparison to those in south.^[3]

• 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, a country whose per capita income is just around $3,500 USD.
• 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.
• Studies suggest that, in developing countries, the rate of asthma increases as communities adopt western lifestyles and become urbanized.^[1]

• The incidence of asthma is higher among low-income populations within a society (it is not more common in developed countries than developing countries,^[9]) which in the western world are disproportionately ethnic minorities, and more likely to live near industrialized areas.
• Asthma has been strongly associated with the presence of cockroaches in living quarters, which is more likely in urban neighborhoods.^[10]
• It is estimated that 15 million disability-adjusted life years (DALYs) are lost worldwide due to asthma per year and is similar to that for diabetes, cirrhosis of the liver, or schizophrenia.^[1]
• Between 2002-2007, asthma cost the US roughly $3,300 USD per person affected with asthma in commoditizations/ quality of life measures such as medical expenses, missed school and work days, and early deaths.^[11]

• 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.^[12] 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.^[12][13]

• In addition, a variant of asthma called exercise-induced asthma 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.

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Philip Marcus, M.D., M.P.H. [2]; Associate Editor(s)-in-Chief: Lakshmi Gopalakrishnan, M.B.B.S. [3]

Asthma is usually diagnosed in childhood. Numerous risk factors such as gender, allergen exposure, airway hyper-reactivity have been identified to play a role in the development of asthma.^[1]

The risk factors for asthma include:

• Personal or family history of asthma or atopy.^[2][3][4][5]
• Allergic rhinitis is a significant risk factor for adult-onset asthma in both atopic and non- atopic individuals.^[6][7][8][9]
• Triggers such as: smoke, dust, pollen, emotional stress and consumption of milk, peanuts, or eggs.^{[10][11][12][13]}
• Exposure to indoor nitrogen dioxide at levels well below the Environmental Protection Agency outdoor standard (53 ppb) has been shown to be associated with respiratory symptoms among children with asthma in multifamily housing.^[14]
• Obesity has shown to be associated with increased severity of asthma.^{[15][16][17][18][19]}
• Male preponderance for asthma in prepubertal children.^[20]
• Female preponderance results in the persistence of asthma into adulthood.^[21]
• Maternal smoking^{[22][23][24][25]}
• Premature birth or low birth weight^[26][27][28]: Reduced lung function at birth has shown to be associated with an increased risk of development of asthma by 10 years of age.^[29]
• Upper respiratory viral infections are associated with an increased incidence of asthma exacerbations in childhood and in adults.^{[30][31][32][33]}
• The presence of bronchial hyperresponsiveness and concomitant atopic manifestations in childhood increase the risk of developing asthma in adulthood.^[34][35][36]
• There is a reduced occurrence of asthma in people who were breast-fed as babies.^[37][38][39]

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Usama Talib, BSc, MD [2]

The United States Preventive Services Task Force (USPSTF) has issued no guidelines for screening of asthma.

The United States Preventive Services Task Force (USPSTF) has issued no guidelines for screening of asthma.

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2]; Philip Marcus, M.D., M.P.H. [3]; Associate Editor(s)-in-Chief: Varun Kumar, M.B.B.S. [4]

Wheezing may occur early in childhood. But in majority of cases, it may not persist into adulthood unless severe or has predisposition to asthma. Asthma progression during childhood vary with gender and may sometimes regress completely unlike adult onset asthma. Prognosis of asthma in absence of other co- morbidities is generally good with treatment and life expectancy is similar to that of general population. Complications of asthma may include status asthmaticus, respiratory failure, candidiasis and cardiac dysfunction.

• Many children often develop one or more episodes of wheezing early in life. These episodes are often associated with respiratory viral infection.^[1] Tucson Children’s Respiratory Study, a longitudinal birth cohort study, demonstrated that the prevalence of wheezing in presence of lower respiratory tract illness was 32%, 17% and 12% at first, second and third year of life, respectively.^[2] Respiratory syncytial virus (RSV) followed by parainfluenza virus type 3 are the most common causative agents identified.^[3][4][2] At age of 6 years, 20% of children who had previous episodes of lower respiratory illness with wheezing during the first three years of life had no wheezing. 13.7% of children who had wheezing before three years of age continued to have wheezing. 15% of children were reported to have new onset wheezing at 6 years of age. The majority of children with wheeze were associated with transient conditions such as viral illness which were found not to increase the risk of asthma later in life.^[5] Lung function values among children with persistent wheezing were not different from those who never wheezed. However, their IgE levels were elevated^[2] suggesting allergic/ asthma predisposition. The late-onset wheezing and the persistent wheezing groups had more episodes of wheezing in late childhood and adolescence.^[6]
• The Melbourne Asthma Study, a longitudinal community based study (1964-1999), evaluated the natural course of asthma from childhood (7 years of age) into adult life (42 years of age) in patients not optimally treated according to present guidelines. The study demonstrated that the children with few episodes of wheezing associated with respiratory infection had a benign course, with many becoming asymptomatic by adult life. While, those with severe asthma during childhood continued to be symptomatic during adulthood and there was a progressive loss in pulmonary function noted as the patients approached 14 years of age but did not progress in adult life. Loss of lung function was not noted in patients with milder symptoms.^[7]
• In another birth cohort study in Dunedin, New Zealand 613 children were followed every 2 years between 3 and 15 years of age and then at 18, 21, and 26 years of age.^[8] By 26 years of age, approximately 50% of the cohort had reported wheezing at least once. Bronchodilator response (or a positive methacholine test) and a positive skin test result to mite or cat at 9 years of age, predicted the persistence of asthma at 26 years of age.^[9]
• Similar to above mentioned studies, the Childhood Asthma Management Program (CAMP) also reported a decline in pulmonary function with age if asthmatic onset is early on in childhood. Significant correlation between duration of asthma and decline in lung function, greater methacholine responsiveness, more asthma symptoms, and greater use of as-needed albuterol was noted from the baseline data of 1041 children. In addition it also reported that independent of baseline lung function, the airway responsiveness increased after puberty in girls, but decreased after puberty in boys.^[10]

Asthma in adults may be of new onset or persistent from childhood. Unlike asthma in children, among adults, asthma is seldom clinically progressive or undergo complete remission. However, rapid rate of decline in lung function may be observed among patients with severe asthma^[11][12] or those with new onset asthma. The Copenhagen City Heart Study demonstrated this observation where the decline in lung function was, on average, 39 ml/yr in men and 11 ml/yr in women, respectively, compared with that in non- asthmatic subjects. Among patients with chronic asthma, the rate of lung function decline did not increase compared with that in non- asthmatic subjects.^[13] Asthmatics who are smokers have higher rates of decline.^[14] Relapse rates among patients with past history of asthma tend to increase with age.^[15]

The complications of asthma can be severe. Some include:

• Acute severe exacerbation may progress to status asthmaticus in which asthma symptoms are refractory to initial bronchodilator therapy. Delayed treatment with systemic corticosteroids in such situations or presence of co-existing conditions such as restrictive lung disease or congestive heart failure increase the risk of death.
• Decreased ability to exercise and take part in other activities
• Lack of sleep due to nighttime symptoms
• Decrease in pulmonary function^[11] may be observed with age. This may lead to airway remodeling.^[16][17]
• Decline in pulmonary function and air way remodelling may increase the risk for airway obstruction, frequent respiratory infections and may ultimately lead to respiratory failure.
• Cardiac dysfunction may occur secondary to decrease in lung function or due to inflammatory response. Right ventricular diastolic and systolic dysfunction were noted in a study involving 64 children with varying degree of severity.^[18] However cardiac complications in asthmatics are usually related to treatment of asthma i.e. use of beta agonists or avoidance of beta blockers among patients with pre- existing cardiac conditions.
• Trouble breathing that requires breathing assistance (ventilator) which may cause complications such as pneumothorax and infections.
• Oral thrush may occur in patients using corticosteroid inhalers.
• Relapse of asthma among patients with past history of asthma tend to increase with age.^[15]
• Asthma in pregnancy can cause preterm labor^[19], pre-eclampsia^[20], intra uterine growth retardation^[21] or miscarriage^[22]. These complications are attributed to hypoxia.^[23]

The prognosis for asthmatics is good; especially for children with mild disease. Among those experiencing wheezing during childhood, majority would be symptom free after a decade.^[5] However, if the asthma is severe during childhood, it may persist to adulthood.^[7] In a birth cohort study in Dunedin, New Zealand, bronchodilator response (or a positive methacholine test) and a positive skin test result to mite or cat at 9 years of age, predicted the persistence of asthma at 26 years of age.^[9] 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.^[24] 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.^[25] For those who continue to suffer from mild symptoms, corticosteroids can help most to live their lives with few disabilities.

It is estimated that 15 million disability-adjusted life years (DALYs) are lost due to asthma worldwide per year and is similar to that for diabetes, cirrhosis of the liver, or schizophrenia.^[26]. Asthma cost the US about $3,300 per person with asthma each year from 2002 to 2007 in medical expenses, missed school and work days, and early deaths^[27].

Life expectancy is not generally affected by asthma and is not different from general population. However, elderly patients with asthma often die from other respiratory diseases than individuals in general population.^[28][29] 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.

Monitoring eosinophilic markers (exhaled nitric oxide or sputum eosinophils) may reduce exacerbation according to a systematic review<ref name=”pmid29858277″>Petsky HL, Cates CJ, Kew KM, Chang AB (2018). “Tailoring asthma treatment on eosinophilic markers (exhaled nitric oxide or sputum eosinophils): a systematic review and meta-analysis”. Thorax. doi:10.1136/thoraxjnl-2018-211540. PMID 29858277.CS1 maint: Multiple names: authors list (link) </.

Template:WH Template:WS