Course Content
Ideal in Brief
Asthma is a chronic respiratory disease that has an extensive history and today affects millions of Americans. Although there is still no cure, there has been much advancement in research and treatment. This program will address asthma pathophysiology and treatment options that manage the complications of asthma.
Asthma described by several asthmatics:1
Feel as though they could not get enough air into or out of their lungs as if breathing through a straw
Suffocating, choking or drowning
Struggling or ‘fighting’ for air
Feel as though there is a lost of half the lungs, as though the air is only going down half way, and only getting half the air that is needed
Not being able to breathe out, feeling as if the air had ‘nowhere to go’ or was ‘stuck’ or ‘closed off’
The feeling of a ‘tight’ chest
Feel as though a person was gripping them around the chest or sitting on them and squashing them so hard they could not breathe
Asthma is by no means a recent disease, nor recently discovered. The word asthma comes from the Greek verb aazein, which means to exhale with open mouth, pant, sharp breath or short of breath (anyone with breathlessness was asthmatic). 2,3 Eberle, a Philadelphia physician defined asthma in 1830 as: “paroxysmal affection of the respiratory organs, characterized by great difficulty of breathing, tightness across the breast, and a sense of impeding suffocation, without fever or local inflammation.”4
During the latter part of the 19th Century with the publication (scholarly work) of a treatise by Henry Hyde Salter entitled “On Asthma and its Treatment,” Salter defined asthma as: “paroxysmal dyspnoea of a peculiar character with intervals of healthy respiration between attacks,” describing his concept of a disease by narrowing airways due to contraction of the smooth muscle.3 Therefore, by the late 19th Century, physicians accepted the perspective that asthma was a distinct disease, which consist of specific set of causes, clinical inferences, and treatment requirements.3
The history of asthma reveals an interesting and progressive story. Treatment of asthma dates back to ancient times, tracing back to early “prescriptions” written in hieroglyphics meant to treat an enigmatic breathing disease. Ancient Chinese remedies have also been found, including inhaling the fumes produced by heating certain herbs on bricks. 5 Below is a time-line of events: 2,4
(460-360 BCE.): The Corpus Hippocraticum, an earliest text by Hippocrates is where the word asthma is found as a medical term. It is not certain whether Hippocrates meant asthma as a clinical concept or merely as a symptom. Hippocrates believed spasm linked to asthma were more likely to occur among tailors, anglers, and metalworkers.
(100 ACE): an ancient Greek master clinician named Aretaeus of Cappadocia, wrote a clinical description of asthma.
(130-200 ACE): Galen, an ancient Greek physician, generally agreed with the Hippocratic texts and to some extent those of Aretaeus of Cappadocia based on several mentions of asthma. Galen described asthma as bronchial obstructions and treated it with owl’s blood in wine.
(1135-1204 ACE): Moses Maimonides, a physician who practiced medicine in the court of Sultan Saladin of Egypt and Syri declared that his patient’s symptoms often started as a common cold during wet months and eventually the patient gasped for air and coughed until phlegm was expelled. Maimonides wrote Treatise of Asthma (among many medical texts) for Prince Al-Afdal (a patient). Also, Maimonides noted that dry months in Egypt helped asthmatics.
(1579-1644 ACE): Jean Baptiste Van Helmont, a Belgium physician, chemist and physiologist, indicated that asthma originates in the pipes of the lungs.
(1633-1714 ACE): Bernardino Ramazzini, known as the “Father of Sports Medicine,” ascertained a connection between asthma and organic dusts; thus, recognizing exercise-induced asthma.
(1830 ACE): asthma was defined (as discussed earlier).
In the year 1900, very little was known about asthma, and nothing about allergies.6 In 1901, epinephrine was discovered, and it was known to quickly abate asthma episodes.6 In Ancient Rome, (50 ACE), it was recommended to treat a person with herbs containing a predecessor of epinephrine (a beta2-agonist). 2 By 1910, Dr. Samuel Meltzer suggested that asthma was a symptom of allergies, and treating asthma was as simple as injecting the right protein into the asthmatic.6
Also, asthma at the beginning of the 20th Century was recognized as a psychosomatic disease.2 Asthma was thought to be a nervous condition that provoked a narrowing of the airways that caused shortness of breath when exposed to an emotional trigger, like stress.
Asthma during the 1930’s to the 1950’s, was known as one of the “holy seven” psychosomatic illnesses.2 Psychoanalysts believed that patients with asthma should be treated for depression; however, this psychiatric theory was eventually disproved, and asthma became known as a physical condition.2 It was not until the 1960’s that asthma was recognized as an inflammatory disease when anti-inflammatory medications were initially used.2
The Beta-Adrenergic Theory of Asthma (blockage of the Beta-2 receptors of pulmonary smooth muscle cells causes asthma) was first described by Andor Szentivanyi in 1968.7
In 1995, there was a monumental moment regarding allergies. Szentivanyi and colleagues demonstrated that IgE blocks beta-2 receptors, since overproduction of IgE is significant to all atopic diseases.7
Even with asthma’s known extensive history; there is still no cure, but it can be managed with proper treatment and prevention.
More Americans than ever before have asthma, and its prevalence has been increasing. The reason(s) for the rise is not clearly known; however, there are some hypotheses that are supported by some evidence, including the “hygiene hypothesis” (excessive cleanliness). It has been suggested that exposure to an environment enriched in microbial organisms as an infant is beneficial as they provide a sort of “resistance” that makes it less likely for an individual to develop asthma, allergies, and autoimmune diseases as they age.8,9
According to Doug Brugg (a professor of public health and community medicine at Tufts), comprehending the increase in asthma, particularly in children, is the important key to unlocking the limitation in what science can do to prevent children from developing the disease.8 Other hypotheses for the rise in asthma include:8,10
Health care providers diagnosing more asthma today, than in the past, due to awareness of milder cases of asthma, which were ignored a few decades ago. Diagnoses now get proper attention and treatment.
Sedentary lifestyle.A less active or physical lifestyle could affect lung strength, which could be exacerbated by comorbidity with obesity, increasing inflammation throughout the body.
Asthma and obesity have been an associated together as shown in many studies, but asthma is complex and there could be many reasons for the link.11 Obesity is defined as having a body mass index (BMI) of 30 or greater.11 Obesity is not just a problem for adults, but children as well. An estimated 21% of children between the ages of 12 and 19 years are diagnosed with obesity.12 Obesity can cause symptoms of asthma, such as shortness of breath due to the mechanical changes caused by having more abdominal fat on the lungs.11 Fat tissue produces inflammatory substances that may affect the lungs, and several studies have shown that these substances affect asthma.12 This certainly impacts obese asthmatics response to chronic and acute treatments. Inhaled corticosteroids, and theophylline are less effective in controlling obese asthmatics than non-obese.11,12
Although not proven that obesity may cause asthma, women with obesity were more likely to have asthma than those in lower weight categories. Between 2011-2014, asthma was more common among adults with obesity (11.1%) compared with adults overweight (7.8%) and in normal weight (7.1%) categories.13
In the United states, asthma is the most common chronic disease that can impede a person’s quality of life. Also, it is one of the country’s most costly.
Approximately 25 million Americans (1 in 12 people) have asthma, including six million children.14,15 Worldwide, there is an estimated 334 million people with asthma.16 Asthma is more common in children than adults and is the leading chronic disease in children.14 Also, it is the third-ranking cause of hospitalization among children younger than 15 years of age.14 However, adults are four times more likely to die from asthma than children.14 An estimated 3,400 people die each year in the United States.16 Asthma economical cost in America is more than $81.9 billion, including medical cost, loss of work and school days, and asthma-related mortality.14
Today to say asthma is a general term. Recently, researchers have started to define different types of asthma, identify several types or forms of the disease. The definition of asthma is based on the following:17
Medical history and physical examination
Results of lung function tests
Results of allergy tests
Lung and tissue characteristics
The type of cells involved in inflammation
Response to medications tried in the past
Age of onset
Asthma subtypes include:17,18,19
Child-onset asthma
Adult-onset asthma
Asthma with fixed airflow obstruction
Asthma with obesity
Aspirin-induced asthma
Exercise-induced bronchoconstriction (EIB) asthma
Cough-variant asthma
Nocturnal asthma (nighttime asthma)
Occupational (work-related) asthma
Steroid-resistant asthma (severe asthma)
Non-allergic asthma
Allergic bronchopulmonary mycosis
Allergic asthma
Allergic asthma, or extrinsic asthma, is the most common subtype of asthma.20 Of the 334 million asthmatics worldwide, approximately 75% have allergic asthma, which include approximately 90% of child asthmatics and 50% of adults.20
Allergic asthma is a type of asthma that involves an abnormal immune response to allergens (foreign substances). Allergens are harmless to people without allergies. Common allergens include:20
animal dander
plant pollen
dust mites
cockroach urine
mold spores
nuts/peanuts
eggs
milk
wheat
soy
fish/shellfish
Those with a genetic predisposition to developing asthma have an immune system that responds to allergens as harmful, and releases chemicals into the bloodstream.20 These chemicals trigger the release of a certain white blood cell (WBC) called T-cells, which release chemicals to instruct another type of WBC called B-cells to produce antibodies called immunoglobin E (IgE).19,20
IgE antibodies are designed to recognize allergens and can remain in the body for many years. 20 Some stay in the bloodstream, while others attach to another type of WBC called Mast cells. Mast cells are found throughout connective tissue, such as the skin, conjunctiva of the eyes, and respiratory tract (airways, nose, throat).20
With allergies, after exposure, allergen type (for example, animal dander) IgE antibodies recognize and instantly bind to the allergen. Mast cells now release mediators of inflammation (cause inflammation of certain cells to trap harmful substances) into the bloodstream.20 These mediators of inflammation include histamine, leukotrienes, and cytokines (discussed later) and cause allergy symptoms, such as, sneezing, watery eyes, nasal congestion, itchy skin, and coughing. 20
Therefore, allergic asthma is provoked by inhaling or ingesting allergens from “without the body” mainly from chronic exposure to anything that may cause the inflammatory response.6,20
Etiology/Risk Factors of Asthma
Anyone can develop asthma. The etiology of asthma is not conclusively known; however, there is a strong implication that the cause is due to a combination of genetic (heredity) and environmental factors (exposure) or gene-by-environment interactions.21,22 Genetic contributions in the development of asthma remains a complex and incomplete deduction of its etiology.22 Although it is common to find a family history of asthma; it is neither enough nor a precursor for the development of asthma.21 However, the probability increases with a familial linkage. A person’s risk of having asthma is 25% if one parent has asthma, 50% if there is both parents and 5% if there is no family history of asthma.23 By the end of 2005, 25 genes were associated with asthma, and by 2006, over 100 genes were associated with asthma.24 There are several genes or gene complexes, among others that have been identified by positional cloning (“a process of systematic disease gene identification that begins by finding genetic regions co-inherited with disease”): ADAM33, CTLA-4, GSTM1, lL10, lL4R. LTC4S, PHF11, DPP10, GRPA, and SPINK5.9,24 Asthma gene identification is incomplete, but genetic findings have already changed the prevailing view of asthma pathogenesis.9 Other risk factors or environmental factors for developing asthma may affect asthmatics differently at different times of a person’s life, and the risk factors may change over time. Risk factors include:25
allergies – anomaly of the immune system (discussed earlier).
air pollution – living in urban regions increases risk, exposure to smog (ozone).
obesity (discussed earlier)
occupational exposure – exposure to certain dusts (industrial or wood), chemical fumes/vapors, and molds.
smoking – irritant to the airways, including smoke by secondhand.
viral respiratory infections – some children who experience viral respiratory infections may continue to develop chronic asthma.
Asthma Pathophysiology
Asthma is a complex disease and involves many pathophysiological factors. The knowledge of asthma pathogenesis has changed significantly with the last 25 years.26
Asthma affects the trachea, bronchi, and bronchioles.26 The pathophysiology of asthma involves: airway inflammation, intermittent airflow obstruction (limitation), bronchial (airway) hyperresponsiveness.22,26,27
Airway inflammation – inflammation can be present even when there may be no obvious signs or symptoms of asthma. Inflammation can be acute, subacute (between acute and chronic) or chronic.26,27 Inflammation has a primary role in the pathophysiology of asthma and involves inflammatory cells and inflammatory mediators. Inflammatory cells consist of:22,27
Lymphocytes – T-lymphocytes regulate airway inflammation through the release of cytokines (IL-4, IL-5, IL-6, IL-9, and IL-13), which can mediate allergic inflammation. (IL = Interleukin)
Mast Cells – release bronchoconstrictor mediators: histamine, cysteinyl-leukotrienes, prostaglandin D2. Increased mast cells in airway smooth muscle may have an association with airway hyperresponsiveness. Also, mast cells can release an increased number of cytokines to modify the airway environment and promote inflammation, even though allergen exposure is limited.
Eosinophils – certain type of white blood cell that contain inflammatory enzymes that generate leukotrienes and express a variety of pro-inflammatory cytokines. Increased number of eosinophils exist in the airways of most, but not all persons who are asthmatic; however, increases in eosinophils often correlate with greater asthma severity.
Macrophages – most abundant cells in the airways. They can be activated by allergens through IgE receptors to release inflammatory mediators and cytokines that intensify the inflammatory response.
Epithelial cells – airway lining cell dramatically involved in asthma. Inflammatory mediators, inflammatory cells, and respiratory viral infections can cause epithelial cells to generate more inflammatory mediators or to injure the epithelium itself. Thus, the repair process to the epithelium may be abnormal in asthma, which may result in extreme airway impairment. Also, loss of the epithelium’s barrier function allows allergens to penetrate, which can cause the airways to become hyperresponsive.
Inflammatory mediators consist of:
Chemokines – important in the allowing inflammatory cells into the airways and are primarily expressed in airway epithelial cells.
Cytokines – direct and modify the inflammatory response in asthma and most likely determine its severity.
Cysteinyl-leukotrienes – bioactive lipid that act as a potent bronchoconstrictor that is derived from mast cells.
Nitric oxide (NO) – a potent vasodilator. Produced from NO synthase in airway epithelial cells.
Intermittent airflow obstruction (limitation) – bronchoconstriction is the prominent physiological factor that causes clinical symptoms in asthmatics; airway narrowing, following interference in airflow.22 Acute bronchoconstriction is the result of IgE released upon exposure to an allergen, which results in bronchial smooth muscle contraction, thus narrows the airways.22 Bronchospasm, edema, excessive mucus, epithelial and muscle damage may result in bronchoconstriction. Edema from microvascular leakage contributes to airway narrowing.26 Airway capillaries may dilate and leak, increasing secretions, which causes edema and impairs mucus clearance.26 Increase mucus secretion causes thick mucus plugs that block the airway, or cause obstruction.22,26
Bronchial (airway) hyperresponsiveness – chronic inflammation to the airway (bronchi and bronchioles) is associated with bronchial hyperresponsiveness, which subsequently results in increased contractibility of the smooth muscles.24 This contractibility along with other factors causes narrowing of the airways, which result in classic asthmatic symptoms.24,27
Active Learning
Name the drug classifications to treat asthma, and list the medications used in each class. How does your listing compare to the information provided in the program?
So, with an asthma attack (exacerbation), “smooth muscles that surround the airway spasm; this results in tightening of the airways, swelling and inflammation of the inner airway space (lumen) due to fluid buildup and infiltration by immune cells, and excessive secretion of mucous into the airways. Consequently, air is obstructed from circulating freely in the lungs and cannot be expired.”28 Figure 1 depicts the anatomy of an asthma attack and Figure 2 depicts the pathogenesis of asthma.27,28
Asthma Symptoms
Asthma symptoms are not the same for everyone, there is no set pattern. Symptoms can vary from person to person. Symptoms can be mild, moderate or severe, which can flare up occasionally and then be unnoticeable for long periods of time.29 Also, there can be variations from one episode to the next.
There are four classifications of asthma that medical professionals use to rank asthma, which are determined by the frequency and severity of symptoms – from mild (requiring little to no medical treatment) to severe (life-threatening). These classifications include:30
Mild intermittent asthma – symptoms are mild and last up to two days per week or two nights per month. This type usually does not interfere in any activities and can include exercise-induced asthma.
Mild persistent asthma – symptoms are still mild, but occur more than twice per week; however, no symptoms more than once per day.
Moderate persistent asthma – symptoms once each day, or most days. Also, there are symptoms at least one night each week.
Severe persistent asthma – symptoms several times during the day, which occurs almost every day. Also, there are symptoms many nights each week. This asthma does not respond well to medications, even with regular use.
Classic symptoms of asthma are wheezing, shortness of breath, coughing, and chest tightness, pain or pressure.31 There may be early warning signs of asthma (occur at the very start of an asthma episode), worsening symptoms of asthma (if not recognized and treated, can progress and symptoms may worsen), and late, severe symptoms (unable to perform regular activities). Early warning signs/symptoms include:31
Wheezing/coughing during or after exercise
Feeling very tired or weak when exercising
Frequent cough, particularly at night
Trouble sleeping
Losing your breath easily/shortness of breath
Signs of cold, upper respiratory infection, or allergies
Decreases or changes in a peak expiratory flow
Worsening symptoms of asthma include:31
Wheezing
Chest tightness
Persistent cough (day and night)
Shortness of breath
Poor response to inhaled bronchodilators (rescue medication)
Severe (late) symptoms include:31
Severe wheezing when inhaling and exhaling
Chest pain/pressure
Tachypnea (very rapid breathing)
Shortness of breath
Unable to fully exhale
Continuous persistent coughing
Difficulty speaking
Cyanosis (blue color) of the lips or fingertips
Pale, sweaty face
Feelings of panic or anxiety
Asthma symptoms can be provoked by what is known as triggers (any substance or thing that can cause asthma symptoms). Triggers can come from indoors or outdoors. Some indoor triggers include:32,33
Tobacco smoke (including secondhand) from cigarettes, pipes, or cigars. Tobacco smoke contains more than 250 different chemicals that may irritate airways.
Dust mites – microscopic insects that live on skin flakes shed by humans and animals. they are found on bedding products, carpets and upholstery.
Cockroaches – the insects waste products and body parts contain specific proteins.
Pets – allergens from dander, waste products, and saliva.
Mold (both inside and outside) – spores
Outdoor triggers include:32,33
Pollen – small, powdery, granules essential for plant fertilization that generally last from February to October. Found in different grasses, plants, trees and weeds.
Weather – extreme weather, very cold or high humidity. Also, changes in the seasons.
Other triggers include:32,33
Exercise
Foods
Work-related exposures
Colds and infections
Strong odors and sprays – talcum powder, hairspray, and room deodorizers
Pollutants and irritants – unvented gas stoves or heaters, cleaning agents, and volatile organic compounds (VOC), such as new carpeting, paint, and glues.
Emotions or strong feelings – stress, anxiety, and for some people, laughing, crying or yelling.
Heartburn or gastroesophageal reflux disease (GERD) – acid reflux an irritant not only to the esophagus, but the lungs as well.
Certain medications – aspirin (ASA), non-steroidal anti-inflammatory drugs (NSAIDs), beta-blockers, and ace inhibitors.
Diagnosing asthma is important for proper management of the disease, but also to determine what type of asthma. Currently, there is no precise test for diagnosis, which is typically based on symptoms and response to therapy over time.24 Asthma should be suspected if there is recurrent wheezing, coughing or breathing difficulties, and these symptoms occur or are exacerbated by exercise, viral infections or allergens.24
Diagnosis consist of the healthcare provider obtaining personal and medical history, physical exam, and lung function tests (breathing tests). Lung functions tests include:34
Peak airflow – how well air moves out of the lungs using a peak flow air meter, a handheld device. Device is very sensitive to changes in the airways and can alert one to breathing issues.
Spirometry – blow into a mouthpiece connected to a spirometer, or a laptop and the provider can measure how much air is inhaled, exhaled or how fast one can exhale.
FeNO tests (exhaled nitric oxide) – measures the amount of nitric oxide in the breath. FeNO is the acronym for fractional exhaled nitric oxide. When exhaling, the breath can show if there are inflamed airways. This test assists the provider by demonstrating how much inflammation is in one’s lungs.
Provocation tests – also known as challenge or trigger tests; demonstrates how sensitive the lungs are. This test may be chosen by a provider to confirm asthma diagnosis or to rule out asthma if other tests or exams are obscure or non-conclusive. The most common types of provocation tests are: irritant challenge, exercise challenge and methacholine challenge.
Once a diagnosis of asthma is conclusive, treatment is based on age, symptoms and the severity.35 This information determines the types and doses of medication(s) needed, as well as, medication side effects. Asthma can change over time; therefore, it is important for the asthmatic to work closely with their provider who can monitor symptoms and adjust medications, if needed.
Medications that are used to manage asthma symptoms are available in various dosage forms, such as tablets, inhalers, nebulizer solutions, and injectables. See Table 1 for a list of medications and associated class.35,36,37,38
Bronchodilators open the airways by relaxing the smooth muscles around the airways. This helps alleviate coughing and shortness of breath and makes breathing easier. Bronchodilators are available as short-acting beta agonists (SABA), long-acting beta agonist (LABA), and anticholinergics (short- and long- acting). Inhaled LABAs open airways and reduce swelling for at least 12 hours. They are used as a maintenance (regular schedule) medication to control moderate to severe asthma and to prevent nighttime symptoms. Although they are efficacious, there is a caution: they have been associated with known severe asthma attacks. Due to this association, LABAs are taken only in combination with inhaled corticosteroids.
Corticosteroids reduce inflammation in the airways, making airflow easier to the lungs by preventing and reducing airway swelling. Also, by reducing mucus in the lungs. Inhaled corticosteroids may need to be used for several months before maximum benefits are noticed.
Leukotriene modifiers, or receptor antagonists, block either the production or the effects of leukotrienes, which are immune chemicals that can cause asthma symptoms. This class of medication can help prevent symptoms for up to 24 hours.
Methylxanthines help relax and open airways and decreases the lungs’ response to irritants. Also, this class can be helpful for nighttime asthma symptoms.
Combination inhalers include both corticosteroids and LABA or anticholinergics.
Other medications/treatments for asthma are:24,37,38
Oral corticosteroids are used to reduce airway inflammation when other medications don’t adequately prevent asthma attacks, and to treat certain cases of severe asthma. Examples include: Prednisone, Methylprednisolone.
Mast Cell Stabilizer (Cromolyn sodium) is an inhaled non-steroid medication. It prevents airway swelling when encountered with an asthma trigger.
Biologics: monoclonal antibody
Fasrena (Benralizumab) is a monoclonal antibody (IgG1, kappa) that causes apoptosis (cell death or suicide) of eosinophils and basophils through antibody-dependent cell-mediated cytotoxicity. Administered as subcutaneous (under the skin) injection once every eight weeks after the first two months.
Xolair (Omalizumab) is a recombinant human monoclonal antibody directed against IgE. In allergic asthma, it inhibits the binding of IgE to the IgE receptor on the surface of mast cells and basophils, which limits the degree of release of mediators of the allergic response. Administered as subcutaneous injection every two to four weeks to prevent the body from reacting to allergenic triggers.
Dupixent (Dupilumab) is a human monoclonal IgG4 antibody that inhibits interleukin-4, and interleukin-13 cytokine-induced responses. As well as, cytokines, chemokines, and IgE. Note: sed for moderate to severe asthma, adjunct; eosinophilic or oral corticosteroid-dependent. Administered as subcutaneous injection. Dose will depend on whether treating eosinophilic or corticosteroid-dependent asthma.
Mepolizumab (orphan drug designation)is an interleukin-5 (IL-5) antagonist monoclonal antibody that reduces the production and survival of eosinophils by blocking the binding of IL-5. Note: used for severe asthma, add-on maintenance in asthmatics with eosinophilic type.
Immunotherapy (allergy shots) refer to a series of injections containing small doses of allergens (determined by skin test allergen triggers results) to develop desensitization. Injections are administered once weekly for a few weeks, then once monthly for three to five years until sensitivity to allergens are diminished.35
SABA | LABA | Anticholinergics | Corticosteroid | Leukotriene Receptor modifier | Methylxanthine | Combined Inhaler | |
Proventil | Serevent | Atrovent | Prednisone | Accolate | Theo-24 | Advair Diskus | |
Ventolin | Spiriva | Flovent | Singulair | Elixophyllin (elixir) | Breo Ellipta | ||
Alupent | Turodoza Pressair | Pulmicort | Zyflo | Dulera | |||
Xopenex | Asmanex Twisthaler | Symbicort | |||||
Brethine | Qvar | AirDuo Respiclick | |||||
Alvesco | |||||||
ArmonAir Respiclick | |||||||
Arnuity Ellipta |
Every asthmatic should have an Asthma Action Plan (Figure 3.) which is used as an aid for using asthma medications.34 Peak flow numbers are put into a chart with zones that are set up like a traffic light. Target zones should be added to the Asthma Action Plan; this helps the asthmatic know what to do when the peak flow number changes.34
What does living with asthma means for the asthmatic? The prognosis of adult asthma is not well defined. Although complete remission is possible, rates are low and limited to milder cases.39 Permanent lung function impairment exists in some asthmatics and those with severe asthma have a poorer prognosis, regarding development of permanent lung impairment, hospitalization and mortality.39 However, studies have shown that early and continuous treatment with inhaled steroids have beneficial effects, not only with asthma symptoms, but lung function as well.39
The prognosis for children with mild symptoms is generally good. Of children diagnosed with asthma, half of cases, will no longer be considered asthmatic after a decade.24
What does the near future hold for this long-known disease? Understanding the possible etiology of the disease and how it is best treated is due to extensive asthma research.40 Without the life-long dedication of lung association research, important and much needed discoveries would not be possible. Significant contributions to the field of asthma research continue, and include some current projects being funded by the American Lung Association: 40
Deepening Our Understanding of Immune System’s Role in Asthma
Understanding Role Receptor Involved in Lung Inflammation Plays in Asthma
Protein Holds Clue to Allergic Airway Inflammation
Harnessing Power of a Protein to Improve Lung Repair Following Injury
Researchers have discovered that calcium-sensing receptors (protein molecules) play a significant role in asthma.41 These proteins lead to further inflammation of the airways. The drug calcitriol, used to treat osteoporosis, is known to inhibit the actions of the receptors, as shown by reducing inflammation of the airways when used in mice.41 However, it is not conclusive that calcitriol is a “cure” for asthma, as the initial inflammation response by the immune system would still occur.41 The research is still ongoing. but exciting nevertheless. This drug may provide a new treatment for asthma, and possibly a soon “cure”.
Until there is a “cure,” pharmacy professionals have a pivotal role in asthma care. As awareness of population risk factors increases, so will the need for pharmacy technician to be aware of the importance and significance of asthma trigger prevention, as well as understanding available treatment options to better assist pharmacists in continuously providing the best quality of c.a.r.e (counteracting airway hyper-responsiveness experiences).