name | description | evidence | review_notes |
---|---|---|---|
Allergic Asthma | Triggered by allergens such as pollen, pet dander, or dust mites. | TRUNCATED | None |
Non-Allergic Asthma | Triggered by factors such as stress, exercise, cold air, or respiratory infections. | TRUNCATED | None |
Adult-Onset Asthma | Develops later in adult life and often triggered by environmental factors. | TRUNCATED | None |
Asthma-COPD Overlap | Features of both chronic obstructive pulmonary disease and asthma. | TRUNCATED | None |
Exercise-Induced Asthma | Often triggered by physical exertion. | TRUNCATED | Added Exercise-Induced Asthma for a more comprehensive list of subtypes. |
reference | supports | snippet | explanation |
---|---|---|---|
PMID:18503727 | SUPPORT | The pathogenesis of allergic airway inflammation is complex, involving multiple cell types such as T helper 2 cells, regulatory T cells, eosinophils, dendritic cells, mast cells, and parenchymal cells of the lung. | This reference indicates the involvement of multiple cell types, including mast cells, eosinophils, and T lymphocytes in allergic airway inflammation, which supports the statement. |
PMID:8324396 | SUPPORT | The numbers of eosinophils and neutrophils are increased 4 h after challenge with allergen in the broncho-alveolar lavage fluid (BAL) of asthmatics who show an LPR. | This reference mentions eosinophils and neutrophils as part of the chronic inflammatory response in asthma, supporting the statement. |
PMID:9753516 | SUPPORT | Accumulation of basophils and mast cells in airway tissues during allergic and allergic-type inflammatory responses, including asthma, is one of the hallmarks of these disease processes. | This reference highlights the involvement of basophils and mast cells in airway inflammation in asthma, supporting the statement. |
PMID:38395082 | SUPPORT | Airway hyperresponsiveness (AHR) is a key clinical feature of asthma. The presence of AHR in people with asthma provides the substrate for bronchoconstriction in response to numerous diverse stimuli, contributing to airflow limitation and symptoms including breathlessness, wheeze, and chest tightness. | This reference supports the clinical manifestations of asthma as described in the statement. |
PMID:23234454 | PARTIAL | Pulmonary edema and pulmonary vascular congestion have been thought to be the primary causes of cardiac asthma but most patients have a poor response to diuretics... Evidence suggests that circulating inflammatory factors and tissue growth factors also lead to airway obstruction suggesting the possibility of developing novel therapies. | While this reference focuses on cardiac asthma, it acknowledges the involvement of inflammatory factors leading to airway obstruction, which partially supports the inflammatory aspect mentioned. |
PMID:1571812 | SUPPORT | Asthmatics can have a blood eosinophilia which in some studies correlates with the severity of the disease... The eosinophils that contribute to asthma will be those in the lung. | Specifically talks about the role of eosinophils in asthma, supporting the statement. |
PMID:28687463 | SUPPORT | Non-asthmatic eosinophilic bronchitis (NAEB) shares similar eosinophilic inflammation of the airway and response to corticosteroids with asthma. | This supports the role of eosinophils in airway inflammation in asthma, consistent with the statement. |
PMID:6101920 | NO_EVIDENCE | Exercise-induced asthma can appear as one of many forms of airway hyperreactivity or as a unique clinical entity. | Does not provide specific information about the role of the cell types mentioned in the statement. |
reference | supports | snippet | explanation |
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PMID:24914235 | SUPPORT | The other main cause of airway obstruction is contraction of airway smooth muscle. | The reference points out that contraction of airway smooth muscle is a main cause of airway obstruction, thus supporting the statement. |
PMID:22011234 | SUPPORT | Breathing difficulties are caused by excessive narrowing of the pulmonary airways, which is instigated by shortening of the airway smooth muscle (ASM). | This reference explains that the narrowing of the airways, caused by the contraction of airway smooth muscle, leads to breathing difficulties, thus supporting the statement. |
PMID:27603525 | SUPPORT | In acute and chronic allergen driven animal models of asthma, statins reduce airway hyper-responsiveness, inflammation and remodeling. | The use of statins to reduce airway hyper-responsiveness implies the involvement of smooth muscle cells, supporting the statement. |
PMID:16543052 | SUPPORT | ASM plays an important role in regulating bronchomotor tone, in perpetuating airway inflammation, and in remodeling of the airways. | This reference highlights multiple functions of airway smooth muscle in asthma, which supports the statement regarding the role of smooth muscle cells in bronchoconstriction. |
PMID:18669785 | SUPPORT | Airway smooth muscle cells are known to be the main effector cells of airway narrowing. | This reference clearly identifies airway smooth muscle cells as key players in the narrowing of airways (bronchoconstriction), thus supporting the statement. |
reference | supports | snippet | explanation |
---|---|---|---|
PMID:19689269 | PARTIAL | Goblet cells are major mucus-producing cells, and goblet cell hyperplasia (GCH) is one feature of airway remodeling, defined as structural changes occurring in the airway. | The reference confirms Goblet cell involvement in asthma and mucus production but does not mention Mucosal Epithelial Cell specifically. |
PMID:24914235 | PARTIAL | Airway epithelial cells, which are the first line of defense against inhaled pathogens and particles, initiate airway inflammation and produce mucus, an important contributor to airway obstruction. | The reference supports that Bronchial Epithelial Cells play a role in mucus production but does not discuss Mucosal Epithelial Cells specifically. |
PMID:37520564 | PARTIAL | Basal cells... goblet cell hyperplasia and increased epithelial mesenchymal transition, which contribute to impaired mucociliary clearance and airway remodelling. | The reference confirms Goblet cell hyperplasia and the contribution of epithelial cells in asthma but does not detail Mucosal Epithelial Cells. |
PMID:23638644 | PARTIAL | Goblet cell differentiation and mucus production are subject to extensive control. An emerging concept is that not all goblet cells are phenotypically identical suggesting that specific molecular pathways orchestrate mucin overproduction. | The reference supports Goblet cells' role in mucus production but lacks information on Mucosal Epithelial Cells. |
PMID:16101538 | PARTIAL | Bronchial epithelial cells (BEC) are known to play an integral role in the airway defense mechanism via mucociliary system as well as mechanical barriers. | The reference confirms the involvement of Bronchial Epithelial Cells but does not mention Mucosal Epithelial Cells. |
PMID:12190646 | NO_EVIDENCE | None. | The abstract does not provide evidence to support or refute the involvement of the specified cell types. |
PMID:8324396 | NO_EVIDENCE | None. | The abstract focuses on early-phase and late-phase reactions in asthma without mentioning the specific cell types. |
reference | supports | snippet | explanation |
---|---|---|---|
PMID:20500603 | SUPPORT | In asthma, it includes alterations of the epithelial cell layer with goblet cell hyperplasia, thickening of basement membranes, peri-bronchial and peri-bronchoalveolar fibrosis. | The reference acknowledges that airway remodeling in asthma involves changes to the epithelial cell layer, fibroblasts, and smooth muscle cells. |
PMID:10907591 | SUPPORT | In the long-term, asthma may become moderately to fully irreversible. Severe, irreversible airflow obstruction may develop despite apparently appropriate therapy. | The reference supports the idea that long-standing inflammation can result in irreversible structural changes affecting lung function. |
PMID:15896192 | SUPPORT | Structural changes reported in the airways of asthmatics include epithelial fragility, goblet cell hyperplasia, enlarged submucosal mucus glands, angiogenesis, increased matrix deposition in the airway wall, increased airway smooth muscle mass, wall thickening and abnormalities in elastin. | The reference details structural changes involving various cell types, including epithelial cells, smooth muscle cells, and other airway structures resulting from long-term inflammation in asthma. |
PMID:12405265 | SUPPORT | Asthma is a chronic inflammatory disorder of the airways interacting with altered structure and function of the formed elements including smooth muscle. | The reference confirms that chronic inflammation in asthma involves structural alterations involving smooth muscle cells and other components, supporting airway remodeling. |
PMID:24914235 | SUPPORT | Two airway cell types are critical for asthma pathogenesis: epithelial cells and smooth muscle cells. | The reference highlights the importance of epithelial cells and smooth muscle cells in asthma pathogenesis, supporting the role of these cell types in airway remodeling. |
reference | supports | snippet | explanation |
---|---|---|---|
PMID:20545704 | SUPPORT | It has been suggested that there are several distinct phenotypes of childhood asthma or childhood wheezing. Here, we review the research relating to these phenotypes, with a focus on the methods used to define and validate them. | The reference supports the existence and classification of asthma phenotypes, including wheezing as a common characteristic. |
PMID:8620967 | SUPPORT | Wheezes are usual clinical signs in patients with obstructive airway diseases and particularly during acute episodes of asthma. | The reference describes wheezing as a common symptom associated with asthma, supporting the statement's claim that wheezing is a common phenotype and respiratory diagnostic of asthma. |
PMID:1788358 | SUPPORT | Exercise-induced asthma is a common but frequently undiagnosed problem. The patient may not wheeze, but rather have shortness of breath, chest tightening, and coughing. | This reference mentions exercise-induced asthma and details its symptoms, including wheezing, though noting that wheezing may not always be present. |
PMID:26606077 | SUPPORT | The syndrome of asthma contains a number of different phenotypes that offer the possibility of personalized medicine based on the respective asthma phenotype. | Confirms the existence of multiple phenotypes within asthma, including wheezing, supporting the statement's categorization of wheezing as a phenotype of asthma. |
PMID:21722845 | SUPPORT | Oral corticosteroids are the cornerstone of management of acute moderate or severe asthma whilst preventive inhaled corticosteroids are the mainstay of the preventive management of children with asthma. Yet, variation in the magnitude of response to corticosteroids has been observed. | Supports the statement indirectly by acknowledging variations in asthma phenotypes, which includes wheezing as a common symptom. |
PMID:38716537 | SUPPORT | We want to highlight the presentation of a 75-year-old female who was initially managed as asthma and subsequently diagnosed with concurrent excessive dynamic airway collapse (EDAC). | Although the snippet discusses a different case, it implies that wheezing is commonly associated with asthma management. |
reference | supports | snippet | explanation |
---|---|---|---|
PMID:36096782 | SUPPORT | Asthma is a heterogeneous disease with variable symptoms, which presents with cough either as the sole or predominant symptom with or without wheezing. | The reference states that cough is a common phenotype in asthma, aligning with the statement's claim that coughing is a common respiratory phenotype in asthma. |
PMID:31662445 | SUPPORT | Asthma severity was dependent on variety of symptoms, consisting mostly of wheezing, breathlessness, chest tightness, and cough. | The reference indicates that coughing is one of the primary symptoms associated with asthma, supporting the claim that it is a common respiratory phenotype. |
PMID:36543577 | SUPPORT | Chronic cough is associated with poor quality of life and can negatively affect quality of life. Diseases causing chronic cough are most commonly asthma, eosinophilic bronchitis, gastroesophageal reflux, post-nasal drip syndrome, rhinosinusitis, chronic obstructive pulmonary disease, pulmonary fibrosis, and bronchiectasis. | The reference supports the association of chronic cough with asthma, aligning with the statement that coughing is a common phenotype in asthma. |
reference | supports | snippet | explanation |
---|---|---|---|
PMID:34610625 | SUPPORT | Respiratory diseases were the main underlying condition (40-57%), of which asthma was the most common (approx. 25%), and chronic obstructive pulmonary disease was particularly strongly associated with breathlessness. | The reference indicates that respiratory diseases, including asthma, are a common underlying condition for breathlessness. This supports the categorization of breathlessness as a common respiratory phenotype of asthma. |
reference | supports | snippet | explanation |
---|---|---|---|
PMID:31662445 | SUPPORT | CONCLUSIONS: Asthma severity was dependent on variety of symptoms, consisting mostly of wheezing, breathlessness, chest tightness, and cough. | The literature indicates that chest tightness is among the most common symptoms of asthma, supporting the statement that chest tightness is a frequent phenotype of respiratory symptoms in asthma patients. |
PMID:36292755 | SUPPORT | Asthma is a chronic disease of the airways characterized by inflammation, tightened muscles, and thickened airway walls leading to symptoms such as shortness of breath, chest tightness, and cough in patients. | This article confirms that chest tightness is a common symptom of asthma, supporting the statement. |
PMID:3595047 | SUPPORT | IMPLICATIONS: exercise-induced asthma should be considered in pediatric patients with symptoms of chest pain or dyspnea on exertion. | Exercise-induced asthma includes symptoms like chest pain, which is related to chest tightness, supporting the statement. |
PMID:19463209 | SUPPORT | We present the case of a 42-year-old man with a 2-year history of wheezing, chest tightness, and upper respiratory symptoms. | This case study highlights chest tightness as a symptom, supporting the statement as it shows chest tightness is a common feature in asthma triggered by recreational activities. |
name | presence | evidence | context | subtype |
---|---|---|---|---|
Eosinophils | Elevated | TRUNCATED | allergic asthma | Allergic Asthma |
Neutrophils | Elevated | TRUNCATED | non-allergic asthma | Non-Allergic Asthma |
IgE Antibodies | Elevated | TRUNCATED | allergic reactions | None |
reference | supports | snippet | explanation |
---|---|---|---|
PMID:23070918 | SUPPORT | The results indicated that there were an association between the IL-4 C-33T (P = 0.006) and C-589T (P = 0.04) ... and susceptibility to asthma. | This meta-analysis found a significant association between IL-4 polymorphisms (C-33T and C-589T) and asthma susceptibility. |
PMID:25786151 | NO_EVIDENCE | Title only: Anchored to asthma. | The title does not provide sufficient information to support or refute the statement. |
PMID:10073323 | SUPPORT | Using both the candidate gene and the positional cloning approaches, there is evidence that predisposing factors, if not the disease itself, are genetically transferred. | This reference generally supports the idea of genetic associations in asthma, including those likely involving IL-4. |
PMID:21325943 | PARTIAL | Genotype combinations of IL-4 receptor-alpha and CD14 single nucleotide polymorphisms (SNPs) were significantly associated with diisocyanate asthma. | This study refers to IL-4 receptor-alpha and not IL-4 directly, and its context is specific to occupational asthma caused by diisocyanate exposure. |
reference | supports | snippet | explanation |
---|---|---|---|
PMID:23996716 | SUPPORT | Interleukin-13 (IL-13) is known to be a key regulator in immunoglobulin E (IgE) synthesis, mucus hypersecretion and airway hyperresponsiveness... A statistically significant association of the A-1512C polymorphism in IL13 gene was observed with atopy. | The study provides evidence that the IL13 gene polymorphism A-1512C is significantly associated with asthma. |
PMID:30539779 | PARTIAL | An efficient memory Th2 cell response is dependent on IL-13 produced by ILC2s, causing allergic lung inflammation and elevated serum levels of immunoglobulin E. | The study indicates that IL-13 is involved in allergic lung inflammation which is relevant to asthma, but it primarily discusses IL-13's role in mediating immune responses rather than directly associating IL-13 genetic polymorphisms with asthma. |
PMID:23380221 | PARTIAL | Very recently, a novel population of IL-33-responsive innate immune cells, the type 2 innate lymphoid cells, was found to produce hallmark TH2 cytokines, such as IL-5 and IL-13. | The review highlights the role of IL-13 in the pathway involved in asthma pathogenesis but does not directly establish a genetic association between IL-13 and asthma. |
PMID:21681015 | NO_EVIDENCE | Genome-wide association studies identified genes and pathways underlying asthma... | The abstract discusses GWAS studies related to asthma but does not specifically mention IL13. |
reference | supports | snippet | explanation |
---|---|---|---|
PMID:26666372 | SUPPORT | A disintegrin and metalloproteinase 33 (ADAM33) gene has been considered as an asthma susceptibility gene due to its possible role in airway remodeling, abnormal cell proliferation, and differentiation. Association of this gene with asthma has been reported in several genetic studies on various populations. | This study and its findings directly support the statement about the association between the ADAM33 gene and asthma. |
PMID:19481925 | SUPPORT | Despite this, the field has identified 43 replicated genes from association studies. The most frequently replicated are: TNF alpha, IL4, FCERB, Adam 33, and GSTP1. | This study acknowledges the genetic association between ADAM33 and asthma among other genes, further supporting the statement. |
reference | supports | snippet | explanation |
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PMID:33963941 | SUPPORT | Our results revealed that polymorphic variants rs7216389, rs2290400 and rs2305480 are associated with the development of allergic diseases as well as with asthma and asthma combined with allergic rhinitis. | This reference specifically mentions GSDMB polymorphisms and their association with asthma. |
reference | supports | snippet | explanation |
---|---|---|---|
PMID:23181788 | SUPPORT | Overall, our findings further replicate the HLA-DQ region in the pathogenesis of asthma. | The study highlights the association of HLA-DQ genes, specifically HLA-DQA1, with asthma in adults, corroborating previous findings linking HLA-DQ to asthma susceptibility. |
reference | supports | snippet | explanation |
---|---|---|---|
PMID:25167772 | SUPPORT | The results of this meta-analysis firmly established that genetic variation at the rs7216389 locus, which controls the expression of the ORMDL3, may be a major, independent predisposing factor for asthma in ethnically diverse populations. | The meta-analysis confirms the association between the ORMDL3 gene and asthma susceptibility. |
PMID:18754760 | PARTIAL | It is far from being clear which gene caused the association signal, as it is derived from a large linkage disequilibrium (LD) block. | The study suggests an association signal that includes ORMDL3 but indicates uncertainty about the specific gene responsible due to a large LD block. |
PMID:21276132 | SUPPORT | The first GWAS for asthma discovered a novel associated locus on chromosome 17q21 encompassing the genes ORMDL3, GSDMB and ZPBP2. | This GWAS identifies ORMDL3 as part of a locus associated with asthma. |
reference | supports | snippet | explanation |
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PMID:26788835 | PARTIAL | Persons with asthma and multiple diagnoses reported odorous/pungent and building-related environmental factors to trigger symptoms to a larger extent than did the reference group, mainly due to perfume and odors from flowers. | This supports the role of environmental factors in triggering symptoms in people with asthma but does not specifically address allergens as a triggering factor. |
PMID:29732974 | SUPPORT | The link between asthma and food allergy has been well researched over the years; although the exact interplay between the two atopic conditions is yet to be fully described. Research suggests that children who have both asthma and food allergy are at greater risk of more severe asthmatic episodes. | This supports the idea that allergens (specifically food allergies) can trigger severe asthma attacks. |
PMID:20406590 | SUPPORT | A complex interplay of genetic predisposition and environmental influences results in the clinical picture of allergic asthma. | This supports the role of environmental influences, which includes allergens, in allergic asthma. |
PMID:29310764 | SUPPORT | The implementation of policies to reduce environmental allergic triggers can be an important adjunct to optimal patient care for allergic rhinitis and allergic asthma. | It supports that allergic asthma can be triggered by environmental allergens. |
PMID:29345235 | SUPPORT | The rising frequency of obstructive respiratory diseases during recent years, in particular allergic asthma, can be partially explained by changes in the environment, with the increasing presence in the atmosphere of chemical triggers (particulate matter and gaseous components such as nitrogen dioxide and ozone) and biologic triggers (aeroallergens). | This directly supports the role of environmental allergens as triggers for allergic asthma. |
PMID:23574397 | SUPPORT | For patients with asthma, exacerbations and poor control can result from exposure to environmental triggers, such as allergens and air particulates. | This supports the idea of allergens being environmental triggers for asthma. |
PMID:31187658 | SUPPORT | Environmental exposures varied across the year and demonstrated seasonal patterns. Metro health region regression models showed positive associations between increases in mold and particulate matter <10 microns in diameter (PM(10)) and outpatient asthma claims. | This supports the role of environmental allergens like mold in triggering asthma. |
PMID:21277508 | SUPPORT | Extrinsic factors include environmental exposure to temperature, humidity, aeroallergens, irritants, and pollution. | This supports the role of environmental allergens in asthma. |
PMID:37480203 | SUPPORT | Pollen is a key source of aeroallergens responsible for allergic rhinitis, conjunctivitis, and asthma. | This supports the role of environmental allergens like pollen in triggering allergic asthma. |
reference | supports | snippet | explanation |
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PMID:10518814 | SUPPORT | Air pollution is convincingly associated with many signs of asthma aggravation. | The article states that air pollution is associated with various signs and symptoms of asthma aggravation, supporting the statement that air pollution exacerbates asthma symptoms. |
PMID:21277508 | SUPPORT | Extrinsic factors include environmental exposure to temperature, humidity, aeroallergens, irritants, and pollution. | The article discusses how environmental factors, including pollution, can result in impaired function of the airways of athletes, which supports the statement. |
PMID:31187658 | SUPPORT | Increases in mold and PM(10) were associated with increases in asthma claims. | The study found associations between particulate pollution and increased asthma claims, supporting the statement. |
PMID:31239087 | SUPPORT | Days with historically high associations between pollution and asthma attacks were identified as supplemental warning days. | The framework identifies days with high pollution as high-risk days for asthma attacks, supporting the statement. |
PMID:31765853 | SUPPORT | Exacerbations are largely driven by environmental exposures including pollutants, stress, and viral and bacterial pathogens. | The text supports the notion that pollutants, including air pollution, drive exacerbations of asthma symptoms. |
PMID:35307034 | SUPPORT | The risk ratio for asthma patients to be hospitalised on the same day of NO(2) exposure was 1.101 per 10 microg/m(3) NO(2) increase. | The study observed a significant increase in hospitalization risk for asthma patients due to NO2 exposure, supporting the statement. |
reference | supports | snippet | explanation |
---|---|---|---|
PMID:25584912 | SUPPORT | Exposure to passive smoke as a risk factor for asthma onset in childhood. | The study highlights how environmental tobacco smoke (ETS) is a significant indoor pollutant and a likely cause for asthma onset and severity in childhood. |
PMID:29292313 | SUPPORT | Exposure to environmental tobacco smoke increases pediatric asthma severity. | The study found that higher state tax grades on tobacco were associated with reduced asthma severity, indicating the detrimental impact of tobacco smoke on asthma severity. |
PMID:31558249 | NO_EVIDENCE | Abstract not provided. | The provided content does not discuss asthma severity in relation to environmental tobacco smoke. |
PMID:35236762 | NO_EVIDENCE | This study aimed to consider associations between particulate matter, black carbon, nitrogen dioxide, and asthma in adults. | The study focuses on various air pollutants but does not specifically address tobacco smoke as an environmental factor affecting asthma severity. |
PMID:32493146 | NO_EVIDENCE | In the multivariate regression models, poorly controlled asthma was associated with obesity, late-onset disease, and comorbidities of sleep apnea and depression. | This study does not discuss tobacco smoke specifically as an environmental risk factor for asthma severity. |
PMID:37973258 | NO_EVIDENCE | The objective of this article is to review recent literature on the implications of extreme weather events such as thunderstorms, wildfires, tropical cyclones, freshwater flooding, and temperature extremes in relationship to asthma symptoms. | The study reviews the impact of extreme weather events on asthma but does not mention tobacco smoke. |
reference | supports | snippet | explanation |
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PMID:15579371 | SUPPORT | The prevalence of occupational asthma is rising, possibly due to the introduction of different chemicals and substances in the workplace. Etiologic agents include organic and inorganic compounds that are encountered in a variety of industries. | This reference explicitly states that occupational exposures to chemicals and substances in the workplace can trigger asthma. |
PMID:33104273 | SUPPORT | Dentists are exposed to a variety of airborne chemicals that can act as irritants and sensitizers and may give rise to work-related respiratory symptoms. | This supports the statement by indicating that occupational exposure to airborne chemicals can lead to respiratory symptoms including asthma. |
PMID:37971937 | SUPPORT | Multiple respiratory hazards have been identified in the cannabis cultivation and production industry, in which occupational asthma and work-related exacerbation of preexisting asthma have been reported. | This reference highlights occupational asthma caused by exposure to respiratory hazards in the cannabis industry. |
PMID:19463209 | SUPPORT | Common asthma triggers during recreational activities include allergen exposure, concomitant viral infection, and exercise. | Although this reference discusses recreational triggers, the exposure to allergens also supports the idea that similar environmental triggers in occupational settings can lead to asthma. |
PMID:36938642 | SUPPORT | Environmental and occupational exposures contribute to its causation. WTC-related or aggravated asthma is considered a World Trace Center (WTC) Health Program certifiable disease. | This supports the statement by acknowledging that occupational exposures can contribute to asthma. |
PMID:29427981 | SUPPORT | Low-molecular-weight chemical sensitizers, causes of occupational asthma, also cause asthma in a manner analogous to allergen. | This reference supports that occupational exposures to chemical sensitizers can trigger asthma. |
reference | supports | snippet | explanation |
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PMID:22559870 | SUPPORT | Current guidelines recommend long-term treatment with inhaled corticosteroids (ICS) because of their superior effectiveness in managing the chronic airway inflammation that characterizes persistent asthma. | This literature supports the statement that inhaled corticosteroids reduce inflammation in asthma. |
PMID:9817746 | SUPPORT | Glucocorticoids are highly effective in the control of asthma and suppression of airway inflammation. | This reference supports the role of glucocorticoids, which includes inhaled corticosteroids, in reducing airway inflammation in asthma. |
PMID:32868307 | SUPPORT | The 2019 Global Initiative for Asthma (GINA) guidelines recommend that all asthma patients be treated with inhaled corticosteroids taken daily or as needed; this improves symptoms and outcomes, even in those with mild disease. | This guideline indicates that inhaled corticosteroids are recommended for improving asthma outcomes, supporting their role in preventing flare-ups. |
PMID:37182593 | SUPPORT | Early treatment with inhaled corticosteroids not only diminishes lung inflammation and airway hyper-responsiveness, but also has a protective effect against the reduction of breathing pattern complexity due to asthma. | The findings indicate that early treatment with inhaled corticosteroids reduces lung inflammation and helps prevent further complications, such as reduced breathing pattern complexity, supporting their role in preventive care. |
reference | supports | snippet | explanation |
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PMID:34753370 | SUPPORT | Long-acting beta(2)-agonists (LABAs) with efficacy to bronchodilate, and prolonged lung function betterment. | The literature supports that LABAs help in relaxing the muscles around the airways, thereby improving lung function and providing symptomatic relief in asthma management. |
PMID:37489386 | SUPPORT | Long-acting muscarinic antagonists (LAMAs) are a class of inhalers that has recently been included as add-on therapy in the GINA guidelines, either in a single inhaler device with inhaled corticosteroids plus long-acting beta2-agonists (ICS + LABA). | Although primarily about LAMAs, the literature acknowledges that LABAs are part of the recommended treatment regimen for asthma, which implies their role in relaxing airway muscles. |
PMID:32306788 | SUPPORT | Contemporary mainstay therapies (inhaled corticosteroids and bronchodilators), prescribed empirically, control symptoms resulting from airways obstruction tolerably well in many patients... | The literature indicates that LABAs, as bronchodilators, help control symptoms related to airway obstruction by relaxing the airway muscles. |
reference | supports | snippet |
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PMID:14720013 | SUPPORT | Leukotriene modifiers increase the therapeutic options for patients with asthma and, based on recent data, it is expected that future guidelines will describe expanded uses for these agents in clinical circumstances where these drugs are effective. |
PMID:11085767 | SUPPORT | Their unique mechanism of action results in a combination of both bronchodilator and anti-inflammatory effects. |
PMID:19180262 | SUPPORT | Cysteinyl leukotrienes, which are derivatives of the 5-lipoxygenase pathway of arachidonic acid metabolism, are important mediators of airway allergic inflammation and have a role in the pathogenetic mechanism of EIB. Montelukast sodium (Singulair, Merck & Co.) is a selective and orally active leukotriene receptor antagonist with demonstrated activity for treating asthma and allergic rhinitis. |
reference | supports | snippet | explanation |
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PMID:29427989 | SUPPORT | Severe allergic asthma and severe eosinophilic asthma are two defined phenotypes for which there are efficacious targeted biologic therapies currently available, namely anti-immunoglobulin E (IgE) and anti-interleukin (IL)-5 antibodies, respectively. | This reference confirms that anti-IgE therapy is used to treat severe allergic asthma. |
PMID:20799475 | SUPPORT | Among these is anti-IgE, which directly targets IgE serum antibodies, thus inhibiting the central mechanism of immediate type hypersensitivity reactions. Application of anti-IgE antibodies effectively reduces IgE serum levels regardless of allergen specificity. | This reference supports that anti-IgE therapy is used in allergic asthma by targeting and reducing IgE. |
PMID:28635659 | SUPPORT | Blocking IgE with monoclonal antibodies such as omalizumab have demonstrated their efficacy, effectiveness, and safety in treating allergic asthma. | This reference confirms that anti-IgE therapy, specifically using omalizumab, is effective in treating allergic asthma. |
PMID:21114196 | SUPPORT | Omalizumab improves quality of life of patients with severe persistent allergic asthma that is inadequately controlled by currently available asthma medications. This therapy is well tolerated and significantly improves symptoms, disease control, reducing asthma exacerbations and the need to use high dosage of inhaled corticosteroids. | This reference further supports the efficacy of anti-IgE therapy (omalizumab) in treating severe allergic asthma by improving symptoms and reducing exacerbations. |
reference | supports | snippet | explanation |
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PMID:34369231 | SUPPORT | Albuterol is the most common fast acting medication for asthma, and it exists in multiple forms, including metered-dose inhaler and nebulized therapy. | Albuterol, a commonly used short-acting beta agonist, is indicated as a fast-acting medication for the relief of asthma symptoms. |
PMID:30297688 | SUPPORT | Initial therapy in the stepwise approach for asthma management is short-acting beta(2)-agonist (SABA) therapy as needed for symptom control. | Short-acting beta agonists are recommended as initial therapy for the control of asthma symptoms, indicating their rapid relief properties. |
PMID:27588581 | SUPPORT | Results demonstrate the efficacy of short-acting beta-agonist (SABA) delivered by metered-dose inhaler as first-line therapy for younger and older children. | The efficacy of SABAs as a first-line therapy in emergency asthma management highlights their role in providing rapid relief from acute asthma symptoms. |
PMID:32482150 | SUPPORT | A majority of patients uses daily quick-relief medication, with the belief that it is the most important treatment because of its rapid onset of action. | The use of quick-relief medication, such as SABAs, by a majority of patients for asthma management is based on their rapid onset of action. |
PMID:11253864 | SUPPORT | Clinical studies comparing the effectiveness of (R)-albuterol (levalbuterol) with racemic albuterol established a strong rationale for using single-isomer beta-agonists in place of the racemic mixture: reduced dosages provide equivalent bronchodilatory effects with fewer beta-mediated side effects. | Levalbuterol, a single-isomer beta-agonist, is shown to provide effective rapid bronchodilation for asthma management. |