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What is known about the precise molecular mechanisms involved in asthma? For instance, is it known why the bronchi tissue alteration cannot be reversed? Were any new mechanisms discovered in the last decade or so?
Airway pathology in asthma
This review focuses on the major cellular and structural changes present in the airways and lung parenchyma in asthma in comparison with chronic obstructive pulmonary disease (COPD) in an attempt to underline the possible mechanisms contributing to airflow limitation in these two diseases.
Both asthma and COPD are characterized by a thickening of the airway wall and by the presence of an inflammatory process, but the inflammatory cells infiltrating the airway wall differ between the two diseases.
In asthma, the most striking feature is the eosinophilic infiltration, whereas, in COPD, it is the CD8 T‐lymphocytic infiltration of the airway wall. In the lung parenchyma, both diseases are characterized by an inflammatory process, whereas destruction and fibrosis of the alveolar walls occur in COPD but not in asthma.
These cellular and structural changes may contribute to the development of airflow limitation (that characterizes both asthma and chronic obstructive pulmonary disease) by inducing either an increase in resistance or a decrease in driving pressure.
Asthma and chronic obstructive pulmonary disease (COPD) are two diseases characterized by airflow limitation. The airflow limitation is mostly reversible in asthma and mostly irreversible in COPD, at least in the majority of patients. Since flow is the result of a driving pressure that promotes flow and of an opposing resistance that counters flow, a reduction in flow can be due to either a reduced driving pressure (loss of elastic recoil of the lung parenchyma) or an increased resistance (airway obstruction) 1. This review, therefore, focuses on the major cellular and structural changes present in the airways and lung parenchyma in asthma in comparison with what is known to occur in COPD in an attempt to underline the possible mechanisms contributing to airflow limitation in these two diseases.
Pathological Mechanisms- What does it mean?
I've been set an essay with the title: Discuss the pathological mechanisms leading to the development of foetal (fetal) alcohol syndrome.
The only problem is, I'm not sure I understand what it means by Pathological Mechanisms.
The understanding that I get from it, is it's asking how the alcohol affects the foetus, but every journal article I read says that it's unknown how it affects the foetus, so I'm a tad confused.
I was just wondering if anybody could help me figure out what they mean by Pathological Mechanisms,
Not what you're looking for? Try&hellip
They are the series of processes/events involved by which the resulting condition occurs.
e.g. the cartilage losing its smoothness/flexibility in osteoarthritis.
Hope it helps
(Original post by JJMick)
They are the series of processes/events involved by which the resulting condition occurs.
e.g. the cartilage losing its smoothness/flexibility in osteoarthritis.
Hope it helpsSee that makes sense, but apart from: Mother drinks alcohol, alcohol enters blood stream, alcohol diffuses across placenta, baby gets FAS I dunno what else lol :P Thanks for your help
Concentrate on what happens in each step and why. How alcohol gets from the mother to the foetus in the first place. Are there any defence mechanisms to protect against the build up of alcohol, but which get overcome? Are there factors which protect against FAS and the factors which exacerbate the condition? How does it affect proteins or cells or hormones etc. and how does that scale up to the foetus as a whole? Look at each of the symptoms of FAS and trace them back to their physiological causes so there's a clear pathway of cause & effect. There'll probably be a lot of biochemistry and cellular biology involved. If it's unknown then there should still be various supposed theories in journals to talk about.
The three main processes responsible for the clinical features of asthma are well recognized: bronchoconstriction, mucus hypersecretion, and airway inflammation. However, the underlying pathophysiology responsible for these processes is complex and nuanced, involving multiple cell types and cytokines (1). Furthermore, the activity and clinical impact of each cellular and subcellular component varies considerably between individuals and can change over time, as well as in response to drug therapy and environmental/lifestyle influences.
Among these myriad cellular interactions and this extremely heterogeneous patient group, it is possible to identify certain key cells that are commonly involved—of which, arguably, the eosinophil is the most important.
Eosinophil precursors originate in the bone marrow and following differentiation traffic to the lungs (among other sites) via the bloodstream (2). While high concentrations of circulating eosinophils are often measured in asthmatic patients, of more clinical relevance is the lung tissue eosinophilia that is also frequently present.
The phenotype of “severe eosinophilic asthma” refers to a subgroup of asthmatic patients with evidence of eosinophilia that often require high maintenance doses of oral corticosteroids to maintain reasonable disease control. The notoriously non-specific mechanisms of action of corticosteroid therapy give rise to numerous well-documented adverse effects (3), which have driven decades of research focused on the development of targeted anti-eosinophil drug therapies. In order to understand how to better assist this group of patients, who currently have an unmet clinical need, it is helpful to understand the eosinophil itself, and the role that it plays in asthma. Targeted anti-eosinophil therapies will be touched upon but will be covered in greater detail by other reviews in this Research Topic.
Asthma diagnosis goes beyond symptoms, such as coughing, chest tightness, wheezing, and dyspnea—and even beyond signs and symptoms that worsen at night and improve after treatment. Diagnosis may require pulmonary function tests (PFTs) and peak expiratory flow (PEF) measurements. With asthma, the ratio of forced expiratory volume in 1 second (FEV1) to forced vital capacity (FVC, also called FEV1%) typically declines.
Asthma symptoms can be reversed by a rapid-acting beta2-agonist, such as albuterol, as measured by spirometry. The generally acceptable response to beta2-agonists is a 12% or 200-mL increase in FEV1 or FVC. PEF measurements not only aid diagnosis but also help clinicians monitor the disease.
Some patients with asthma signs and symptoms may have normal PFT results. They may need further diagnostic testing, such as airway response testing using a bronchial challenge. (See Bronchial challenge.)
Clinicians must rule out other conditions that may decrease FEV1 and cause signs and symptoms that mimic asthma. These conditions include vocal cord dysfunction, gastroesophageal reflux disease, ischemic cardiac pain, chronic obstructive pulmonary disease, heart failure, upper-airway obstruction, cystic fibrosis, hyperventilation, and foreign-body aspiration. Viral respiratory infections may lead to asthma exacerbations or contribute to eventual development of the disorder.
Causes and inciting factors of asthmatic episodes
Asthmatic episodes may begin suddenly or may take days to develop. Although an initial episode can occur at any age, about half of all cases occur in persons younger than 10 years of age, boys being affected more often than girls. Among adults, however, women are affected more often than men.
When asthma develops in childhood, it is often associated with an inherited susceptibility to allergens—substances, such as pollen, dust mites, or animal dander, that may induce an allergic reaction. In adults, asthma may develop in response to allergens, but viral infections, aspirin, weather conditions, and exercise may cause it as well. In addition, stress may exacerbate symptoms. Adults who develop asthma may also have chronic rhinitis, nasal polyps, or sinusitis. Adult asthma is sometimes linked to exposure to certain materials in the workplace, such as chemicals, wood dusts, and grains. These substances provoke both allergic and nonallergic forms of the disease. In most of these cases, symptoms will subside if the causative agent is removed from the workplace.
Asthma is classified based on the degree of symptom severity, which can be divided into four categories: mild intermittent, mild persistent, moderate persistent, and severe persistent. Although the mechanisms underlying an asthmatic episode are not fully understood, in general it is known that exposure to an inciting factor stimulates the release of chemicals from the immune system. These chemicals can cause spasmodic contraction of the smooth muscle surrounding the bronchi, swelling and inflammation of the bronchial tubes, and excessive secretion of mucus into the airways. The inflamed, mucus-clogged airways act as a one-way valve—i.e., air is inspired but cannot be expired. The obstruction of airflow may resolve spontaneously or with treatment.
1 Biophysical basis of airway smooth muscle contraction and hyperresponsiveness in asthma 1
Steven S. An and Jeffrey J. Fredberg
1.2 Airway hyperresponsiveness 2
1.3 Classical behaviour of airway smooth muscle and the balance of static forces 6
1.4 Shortening velocity and other manifestations of muscle dynamics 8
1.5 Biophysical characterization of airway smooth muscle: bronchospasm in culture? 10
1.6 Mechanical plasticity: a nonclassical feature of airway smooth muscle 14
1.7 Recent observations 18
2 Dynamics of cytoskeletal and contractile protein organization: an emerging paradigm for airway smooth muscle contraction 31
Wenwu Zhang and Susan J. Gunst
2.2 Molecular structure and organization of contractile and cytoskeletal filaments in the airway smooth muscle cell 33
2.3 Cytoskeletal dynamics and airway smooth muscle contraction 38
3 Airway smooth muscle: role in airway constrictor hyperresponsiveness 53
Melanie Brown and Julian Solway
3.1 What is airway constrictor hyperresponsiveness (AHR)? 53
3.3 Potential mechanisms leading to airflow obstruction 55
3.4 Potential abnormalities of airway smooth muscle (ASM) 60
3.5 If ASM is dysfunctional, how did it get that way? 63
4 Airway smooth muscle phenotypic and functional plasticity 71
Andrew J. Halayko, Reinoud Gosens and Thai Tran
4.2 Historical perspective: smooth muscle phenotype plasticity 72
4.3 Features of phenotype plasticity 74
4.4 Mechanisms for phenotypic plasticity 76
4.5 Functional plasticity of airway smooth muscle: role in asthma pathogenesis 80
5 Airway smooth muscle proliferation: insights into mechanisms regulating airway smooth muscle mass 89
Reynold A. Panettieri, Jr.
5.1 Increases in airway smooth muscle (ASM) mass and the functional consequences 89
5.2 Growth factors, inflammatory mediators and cytokines modulate ASM proliferation 91
6 Airway smooth muscle bidirectional interactions with extracellular matrix 105
Jane E. Ward and Stuart J. Hirst
6.3 Airway extracellular matrix (ECM) in health and disease 108
6.5 Airway smooth muscle (ASM) as a modulator of airway ECM 111
6.6 Airway ECM as modulator of ASM function 113
6.7 Impact of anti-asthma therapy on ASM&ndashECM interactions 118
7 Airway smooth muscle interaction with mast cells 127
Roger Marthan, Patrick Berger, Pierre-Olivier Girodet and J. Manuel Tunon-de-Lara
7.2 Mast cell mediators alter smooth muscle function 129
7.3 Smooth muscle cells induce mast cell chemotaxis 132
7.4 Mast cells can adhere to airway smooth muscle 134
8 Airway smooth muscle synthesis of inflammatory mediators 141
Alison E. John, Deborah L. Clarke, Alan J. Knox and Karl Deacon
8.4 Growth and remodelling factors 149
9 Airway smooth muscle in experimental models 159
Anne-Marie Lauzon and James G. Martin
9.2 Methods of assessment of airway smooth muscle (ASM) function 160
9.3 Potential mechanisms by which ASM properties may contribute to airway responsiveness 161
9.4 Experimental models 164
10 Altered properties of airway smooth muscle in asthma 181
Judith Black, Janette Burgess, Brian Oliver and Lyn Moir
10.2 The extracellular matrix (ECM) and the airway smooth muscle (ASM) 182
10.3 ASM and integrins 190
10.4 The ASM cell and inflammation 191
10.5 The ASM cell and infection 193
11 The airway smooth muscle in chronic obstructive pulmonary disease (COPD) 201
Maria B. Sukkar and Kian Fan Chung
11.2 Definition and assessment of COPD 202
11.3 Pathological features of COPD 203
12 Glucocorticoid actions on airway smooth muscle 235
Ian M. Adcock, Loukia Tsaprouni and Pank Bhavsar
12.2 Airway smooth muscle (ASM) in airways disease 236
12.3 Gene induction by glucocorticoid receptors (GR) 240
12.4 Actions of &beta2-agonists and glucocorticoids on growth, proliferation, and migration of ASM 245
12.5 Summary and conclusions 248
13 &beta2-Adrenergic receptors: effects on airway smooth muscle 255
13.1 The &beta2-adrenoceptor 255
13.2 &beta2-Receptor activation 257
13.3 &beta2-Receptor signalling pathways 257
13.4 Effects in airway smooth muscle (ASM) 258
13.5 &beta2-Receptor desensitization 260
13.6 Influence of polymorphisms of the &beta2-adrenoceptor in ASM 262
13.7 Non-bronchodilator effects of &beta2-agonists in ASM 264
14 Asthma treatments: effects on the airway smooth muscle 277
Kian Fan Chung
14.2 Role and abnormalities of airway smooth muscle (ASM) in asthma and COPD 279
Clinical and Pathologic Factors Predicting Future Asthma in Wheezing Children. A Longitudinal Study
Wheeze is a common symptom in infants, but not all wheezers develop asthma. Indeed, up to 50% of wheezing children outgrow their symptoms by school age. How to predict if early wheeze will become asthma is still a matter of vivid debate. In this work, we sought to assess the clinical and pathological factors that might predict the future development of asthma in children. Eighty children (mean age 3.8 ± 1 yr) who underwent a clinically indicated bronchoscopy were followed prospectively for a median of 5 years. At baseline, clinical characteristics with a particular focus on wheezing and its presentation (episodic or multitrigger) were collected, and structural and inflammatory changes were quantified in bronchial biopsies. Follow-up data were available for 74 of the 80 children. Children who presented with multitrigger wheeze were more likely to have asthma at follow-up than those with episodic wheeze (P = 0.04) or without wheeze (P < 0.0001). Children with asthma also had lower birth weights (P = 0.02), a lower prevalence of breastfeeding (P = 0.02), and a trend for increased IgE (P = 0.07) at baseline than those with no asthma. Basement membrane thickness and airway eosinophils at baseline were increased in children who developed asthma at follow-up (P = 0.001 and P = 0.026, respectively). Multivariate analysis showed that among all clinical and pathological factors, multitrigger wheezing, basement membrane thickening, and reduced birth weight were predictive of future asthma development. We conclude that multitrigger wheeze and reduced birth weight are clinical predictors of asthma development. Basement membrane thickening in early childhood is closely associated with asthma development, highlighting the importance of airway remodeling in early life as a risk factor for future asthma.
Clinical and pathological factors that could predict the future development of asthma in wheezing children have not been clearly identified. Our study shows that multitrigger wheeze in early childhood and reduced birth weight are clinical predictors of asthma development later in life. Thickening of the basement membrane in early childhood is a pathological finding that is closely associated with the development of asthma, highlighting the importance of airway remodeling in early life as a risk factor for future asthma development.
Asthma is a disease with a highly variable clinical spectrum, in which wheezing is a cardinal symptom (1). Although it is known that asthma is influenced by age, sex, genetic background, and environmental exposure, the natural history of the disease is still poorly understood. The current knowledge about the evolution from wheeze in early childhood to asthma later on in life originates mainly from epidemiological studies (2–8). However, our understanding of the underlying pathophysiological mechanisms, particularly in the transition from childhood to adolescence, remains incomplete.
Wheezing in infants is a common worrying event for families and pediatricians because it may herald the development of asthma. Indeed, up to 50% of children experience at least one wheezing episode before the age of 3 however, recurrent wheeze in early childhood is not always asthma, and about one-half of wheezing preschool children will outgrow their symptoms by school age (3, 4, 8). The relationship between early wheeze and the future development of asthma is still a matter of vivid debate. A possible way to understand this relationship would be to conduct a prospective study of wheezing children to determine whether wheezing (and, if so, which kind of wheezing—multitrigger or episodic) can predict the future development of asthma. Furthermore, it would be important to know which, if any, airway pathological changes are associated with a particular type of wheezing. Although the pathology of asthma is well established, the airway pathology in wheezing children and its potential to predict future development of asthma are less known.
Our aim in this study was to investigate the clinical characteristics (with a particular focus on the presence and type of wheezing) and airway pathological features present in early childhood that could herald the development of asthma later on in life. For this purpose, we evaluated clinically and pathologically a cohort of 80 children (mean age 3.8 yr) who had bronchial biopsies while undergoing a clinically indicated bronchoscopy at baseline, and reassessed them clinically after a median follow-up of 5 years. Some of the results of this study have been reported in abstract form (9, 10).
Children were recruited at the Department of Women’s and Children’s Health, University of Padova, Italy, from 2002 to 2014. All of the children underwent bronchoscopy for the appropriate clinical indications according to European Respiratory Society guidelines (11), as summarized in Table 1. Fiberoptic bronchoscopy was well tolerated by all of the children.
Table 1. Clinical Indications for Bronchoscopy*
*According to European Respiratory Society Guidelines (Reference 11).
† Six out of 80 children were lost during the follow-up.
Respiratory symptoms (particularly wheezing and its pattern [multitrigger or episodic]) were diagnosed at baseline by a respiratory pediatrician. He/she collected a detailed clinical history, visited the child, and administered parental interviews focused on the presence of respiratory symptoms, the treatment during the previous 12 months, and the presence of allergic manifestations (Table E1 in the data supplement).
Episodic wheeze and multitrigger wheeze were defined according to the European Respiratory Society 2008 Task Force: episodic wheeze is wheezing during discrete time periods, often in association with clinical evidence of a viral cold, with absence of wheeze between episodes, whereas multitrigger wheeze is wheezing that shows discrete exacerbations, but also symptoms between episodes (12). The severity of wheezing was graded on a scale from 0 to 3 (0: no symptoms 1: mild 2: moderate 3: severe), and the frequency of wheezing was graded on a scale from 0 to 6 (0: no episodes 1: less than one episode/month 2: one episode/month 3: two to three episodes/month 4: one episode/week 5: more than one episode/week 6: daily episodes).
At baseline, all children underwent routine blood tests, including complete blood cell counts and total and specific IgE levels The presence of atopy was defined by an increase in total and specific IgE levels (IMMunoCAp Phadia) (Table E2 in the data supplement). Spirometry was performed only in children who were able to cooperate with the test.
At the follow-up visit, a respiratory pediatrician interviewed the children’s parents or the study subjects and conducted a detailed clinical investigation to confirm or exclude asthma diagnosis. The asthma diagnosis was obtained by the respiratory pediatrician who regularly followed the children during the follow-up and was made according to clinical and lung-function criteria as recommended by current guidelines (1, 13) in children with a history of repeated episodes of wheezing, breathlessness, or cough—particularly at night or in the early morning—that were present even apart from colds, and were responsive to prescribed bronchodilators. At the follow-up visit, the typical symptoms (wheezing, shortness of breath, and cough) were to be associated with at least one of the following conditions: 1) treatment with regular or as-needed asthma medications, and 2) the presence of airflow obstruction that was reversible with bronchodilators. At the follow-up visit, pulmonary function tests (Superspiro Micro Medical) and fractional exhaled nitric oxide (F e NO) measurements (NIOX VERO Aerocrine) were performed.
Full details regarding the bronchoscopy and bronchial biopsy procedures have been previously described (14, 15). Briefly, the biopsies were formalin fixed and paraffin embedded, and then 5-μm-thick sections were stained with hematoxylin-and-eosin to quantify epithelial loss and basement membrane (BM) thickness. Immunohistochemical techniques were used to quantify inflammatory cells (eosinophils, neutrophils, mast cells, CD4 + T lymphocytes, and macrophages see the data supplement). To avoid observer bias, all cases were coded and measurements made without knowledge of the clinical data. Coefficients of variation for repeated measurements reflecting inter- and intraobserver variability ranged from 4% to 7% for epithelial loss and BM thickness, and from 5% to 10% for inflammatory cells. Written consent was obtained from the children’s parents. The study was performed according to the Declaration of Helsinki and was approved by the Ethics Committee of the Padova City Hospital.
The children’s characteristics were expressed using the mean ± SD or median (range) for continuous variables, and counts and percentages for categorical variables. For continuous variables, normal distributions were tested using the Shapiro-Wilk test. Comparisons among groups were evaluated with either Student’s t test or the Mann-Whitney U test as appropriate. Distributions of categorical variables were compared using the χ 2 test or Fisher’s exact test when the sample size was small (n < 5). Correlation coefficients were calculated using the nonparametric Spearman’s rank method. Univariate logistic analyses, followed by a multivariate logistic regression, were performed to detect the strongest predictors of asthma at follow-up. The covariates included in the final models were those that were significantly different between children with and without asthma at follow-up in univariate analyses. All analyses were performed using R (version ×64 3.3.3 for Windows) as detailed in the data supplement. Statistical significance was assumed for P value < 0.05.
Our cohort included 80 children, all ≤5 years of age (mean 3.8 ± 1 yr). The median follow-up duration was 5 years (range 1–13 yr). Figure 1 summarizes the outcomes of the study. Follow-up data were available for 74 children: 54 out of 80 attended a follow-up visit, and 20 children who lived far away from our hospital completed a questionnaire by telephone and provided available clinical records. The clinical characteristics at baseline of the six children lost at follow-up were not different from those of the remaining 74. At baseline, 38% of the children had multitrigger wheezing, 15% had episodic wheezing, and 47% had no wheezing.
Figure 1. Flow diagram of the children included in our study stratified according to the presence and type of wheezing (multitrigger/episodic/no wheeze) at baseline. The overall attendance rate was 92.5%.
Table 2 illustrates the clinical characteristics of all of the children at baseline according to their asthma status at follow-up. At follow-up, 31 children in our cohort had confirmed asthma (42%), and 43 did not (58%). Children with asthma at follow-up did not differ from those without asthma in sex distribution, age at baseline, age at symptom onset, and follow-up duration. Subjects who had asthma at follow-up were more likely to have wheezing at baseline (P = 0.0002). When the pattern of wheezing (multitrigger or episodic) was examined, it was found that children with multitrigger wheezing at baseline were more likely to have asthma at follow-up (71%) than children with episodic wheezing (36%) or without wheezing (20%) (P = 0.04, P < 0.0001 Figure 1 ). Both the frequency and severity of wheezing at baseline were higher in children who developed asthma at follow-up (P = 0.001, P = 0.0008). There was a trend for children who developed asthma at follow-up to have increased IgE levels at baseline (P = 0.07) compared with children who did not. Similarly, when we analyzed separately children with only one or two sensitizations (n = 15) and those with multiple sensitizations (n = 20), we found that the percentage of children who developed asthma at follow-up was higher in multisensitized children (>2 allergens 53%) than in children with 2 or less sensitizations (35%) but the difference was not significant. Of interest, children with asthma at follow-up had lower birth weight and less breastfeeding than those without asthma (both P = 0.02). The two groups did not differ with regard to pulmonary function parameters, blood eosinophils, history of previous bronchiolitis, or parental smoking exposure.
Table 2. Clinical Characteristics at Baseline in Relation to Asthma at Follow-up
Definition of abbreviations: FEV1 = forced expiratory volume in 1 second FVC = forced vital capacity n.s. = not significant.
Data are expressed as counts (percentages) mean ± SD or median (range). P values refer to the comparison between children with asthma and those with no asthma at follow-up.
*Data at baseline were available for a subset of children (17/74).
† Data at baseline were available for a subset of children (46/74).
‡ Data at baseline were available for a subset of children (59/74).
§ Data at baseline were available for a subset of children (53/74).
|| Data at baseline were available for a subset of children (40/74).
Seventeen out of 74 children (23%) were treated with inhaled corticosteroids at baseline, with a higher proportion among children who developed asthma at follow-up (42%) than in those who did not (9%, P < 0.0001). No difference was observed between the two groups in the proportion of children treated with oral corticosteroids (6% vs. 5%) (Table E1 in the data supplement).
Figure 2 illustrates the distribution of body weights at birth, showing that children who developed asthma at follow-up had lower birth weights than those who did not, even if the median birth weight values were in the physiological range ( Figure 2A ). When stratified by the type of wheezing at baseline ( Figure 2B ), the effect of low birth weight on the asthma outcome was mostly evident in children with episodic wheezing or no wheezing. Indeed, all children who developed asthma at follow-up in these two groups were among those subjects with the lowest weight at birth. No such effect was seen in children with multitrigger wheeze ( Figure 2B ).
Figure 2. (A) Frequency distribution curves for the values of birth weight in children with asthma (orange) and without asthma (blue) at follow-up. (B) Scatterplot reporting birth weights in children of our cohort stratified according to the presence and type of wheezing at baseline (multitrigger/episodic/no wheeze). The dashed line represents the median birth weight value for children with asthma, and the dotted line represents the median birth weight value for children without asthma. Data for this analysis were available for 46 out of 74 children.
The clinical characteristics of children with asthma or no asthma at follow-up are reported in Table 3. Ages at follow-up were similar between children who developed asthma (8.9 ± 2.9 yr) and those who did not (9.5 ± 2.7 yr). As expected, subjects with asthma at follow-up had increased frequency of wheezing and increased use of as-needed bronchodilators compared with those who did not develop asthma. Overall, asthma was well controlled in the majority of subjects with asthma at follow-up: 77% were treated with inhaled corticosteroids and used as-needed bronchodilators a median of twice per month. Only one subject had severe asthma and needed treatment with oral steroids. Of note, subjects with asthma were prescribed more courses of antibiotics and had more lower-respiratory-tract infections (bronchitis and pneumonia) in the previous year.
Table 3. Clinical Characteristics at Follow-up in Relation to Asthma at Follow-up
Definition of abbreviations: AB = antibiotics BD = bronchodilator F e NO = fractional exhaled nitric oxide FEV1 = forced expiratory volume in 1 second FVC = forced vital capacity ICS = inhaled corticosteroids LRI = lower respiratory infection n.s. = not significant ppm = parts per million.
Data are expressed as counts (percentages) mean ± SD or median (range). P values refer to the comparison between children with asthma and those with no asthma at follow-up.
*Data were available for a subset of children (53/74).
† Data were available for a subset of children (49/74).
In our cohort, most subjects had lung-function tests (FEV1 and FEV1/FVC) within the normal range, and no difference was observed between subjects with and without asthma at follow-up. Of note, children with asthma at follow-up had significantly increased F e NO values compared with those without asthma (P = 0.04). When we performed a F e NO analysis in children with asthma using the previously reported cutoff of 20 ppb (16, 17), we found that 47% of the children with asthma had F e NO > 20 ppb, and 53% had F e NO < 20 ppb. When we compared children with asthma and F e NO > 20 ppb with those with F e NO < 20 ppb, we observed no differences in symptoms, FEV1, FEV1/FVC, or bronchodilator need at follow-up. Similarly, no differences were observed in the pathological measurements at baseline.
The results of the quantitative pathology in bronchial biopsies and BAL analysis performed at baseline according to the asthma status at follow-up are shown in Table 4. Of all parameters evaluated, only BM thickening (P = 0.001) and eosinophils in bronchial tissue (P = 0.026) were higher at baseline in children who developed asthma at follow-up compared with those who did not. The percentage of damaged epithelium and the number of neutrophils, macrophages, mast cells, and CD4 + lymphocytes in bronchial biopsies did not differ between the two groups of children, and neither did inflammatory cells and mediators in BAL (Table 4). Figure 3 illustrates the distribution of BM thicknesses at baseline, showing that children who developed asthma at follow-up had thicker BMs than those who did not ( Figures 3A and 3B ). This finding was confirmed even when only children who were ≤3 years of age were considered (n = 24 Table E3). Children with a history of wheezing (mainly multitrigger wheezing) at baseline had significantly thicker BMs than nonwheezing children ( Figure 3C ). BM thickness was positively correlated with the frequency (r = 0.49 P < 0.0001) and severity of wheezing (r = 0.4 P = 0.0005) at baseline, and with the frequency of wheezing (r = 0.41 P = 0.0005) and use of bronchodilators (r = 0.26 P = 0.03) at follow-up. Because well-preserved airway smooth muscle was present in a minority of subjects in our study (n = 10), we could not perform a complete analysis for this parameter. Results of the stereological quantification of smooth muscle volume fraction in this small subset of subjects are reported in the data supplement.
Table 4. Pathological Characteristics at Baseline in Relation to Asthma at Follow-up
Definition of abbreviations: BM = basement membrane ECP = eosinophilic cationic protein n.s. = not significant.
Data are expressed as median (range).
Figure 3. (A) Frequency distribution curves for the values of basement membrane (BM) thickness in children with asthma (orange) and without asthma (blue) at follow-up. (B) Scatterplot reporting BM thickness in children with asthma (orange) and without asthma (blue) at follow-up. (C) Scatterplot reporting BM thickness in children of our cohort stratified according to the presence and type of wheezing at baseline (multitrigger/episodic/no wheeze). The dashed line represents the median BM value for children with asthma, and the dotted line represents the median BM value for children without asthma. Data for this analysis were available for all children (n = 74).
Figure 4 shows the distribution of tissue eosinophils at baseline, indicating that children who developed asthma at follow-up had higher eosinophil numbers than children with no asthma at follow-up ( Figure 4A ). When stratified by the pattern of wheezing at baseline, children with multitrigger wheeze, but not children with episodic wheeze, had an increased airway eosinophilia compared with nonwheezing children ( Figure 4B ). Of interest, children with episodic wheezing at baseline had increased epithelial damage and increased numbers of mast cells in bronchial biopsies compared with nonwheezing children (Table E4).
Figure 4. (A) Scatterplot reporting eosinophils in bronchial biopsies from children with asthma (orange) or without asthma (blue) at follow-up. (B) Scatterplot reporting eosinophils in bronchial biopsies from children of our cohort stratified according to the presence and type of wheezing at baseline (multitrigger/episodic/no wheeze). The dashed line represents the median eosinophil value for children with asthma, and the dotted line represents the median eosinophil value for children without asthma. Data for this analysis were available for 68 out of 74 children.
When we examined the relationship between the number of eosinophils in airway tissue and the number of eosinophils in blood, we found a weak, albeit significant, correlation (r = 0.24, corresponding to r 2 = 0.06), indicating that blood eosinophils cannot be considered representative of tissue eosinophils in our population ( Figure 5 ). No correlations between blood and tissue eosinophils were observed when only values above or below the normal limits (18) were considered (Figure E1 in the data supplement).
Figure 5. Relationship between eosinophils in blood and eosinophils in tissue (bronchial biopsies) at baseline in all of the children in the cohort. Spearman’s rank correlation coefficient P = 0.046 r = 0.24 (r 2 = 0.06). The red line represents the cutoff for normal values of eosinophils in tissue (23 cells/mm 2 ) and in blood (400 cells/μl). No correlations between blood and tissue eosinophils were observed when only values above (P = 0.7 r = 0.09) or below (P = 0.7 r = 0.06) the normal limits were considered.
A subset of children included in our study (n = 17 23%) were treated at baseline with inhaled steroids, which could have influenced the relationship between pathological changes and asthma outcome. When we restricted our analysis to children who were not treated with inhaled steroids (n = 57), the main findings were confirmed (baseline BM thickness and airway eosinophilia were increased in subjects with asthma at follow-up P < 0.05 for both).
We performed a logistic regression analysis of our data at baseline to determine which of the variables were related to the development of asthma at follow-up (Table 5). Then, a multivariate analysis showed that the clinical factors multitrigger wheeze and low birth weight, and the pathological factor BM thickening were the factors at baseline that could predict the eventual development of asthma in our cohort (Table 5).
Table 5. Logistic Regression Analysis in Relation to Asthma at Follow-up
Definition of abbreviations: BM = basement membrane CI = confidence interval OR = odds ratio n.s. = not significant.
Wheezing in early childhood is a common worrying event for families and pediatricians alike, because it might herald the development of asthma. However, there is the possibility that the wheezing is benign and not a sign of early asthma presentation.
In an attempt to clarify the meaning of childhood wheezing, we prospectively studied a cohort of children who had undergone bronchial biopsies, and assessed their clinical characteristics (with a particular focus on wheezing), airway pathology, and eventual asthma development. Our results showed that multitrigger wheezing, BM thickening, and reduced birth weight were significantly associated with the development of asthma at follow-up.
We defined the wheezing pattern in our cohort using the two symptom-based phenotypes of wheeze: episodic (triggered mostly by viral respiratory infections, with affected children being symptom-free between episodes) and multitrigger (triggered by viruses and other causes such as allergens, characterized by the presence of symptoms between episodes) (12). Once we had defined the wheezing pattern and obtained bronchial biopsies, we followed our cohort for a median of 5 years after the first evaluation, and found that 71% of the multitrigger wheezers had asthma at follow-up, whereas only 36% of the episodic wheezers did. These data, obtained in a prospective evaluation of our cohort, highlight the importance of recognizing this symptom early in childhood and confirm previous evidence that episodic wheeze frequently undergoes remission, whereas multitrigger wheeze is more likely to be persistent (19). Furthermore, there are differences in airway function (i.e., conductive airways ventilation inhomogeneity) between multitrigger and episodic wheezers (20), which may indicate that they reflect different disease entities.
Although it has been suggested that the episodic/multitrigger classification is not stable over time (21, 22), recent evidence from two large longitudinal cohorts suggests that multitrigger and, to a lesser extent, episodic wheeze tend to persist longitudinally regardless of wheezing severity (23). Our results, which were based on clinical information (including both the type and severity of wheezing) that was carefully collected during a single visit, demonstrate that wheezing information can be valuable and predictive of the future development of asthma.
Among the other clinical factors examined, we observed that low birth weight and reduced breastfeeding were associated with established asthma at follow-up in our study cohort. Children who developed asthma at follow-up had both a significantly lower birth weight (∼500 g lower) and significantly less breastfeeding than children with no asthma at follow-up. A number of other studies have shown similar associations, although this had not been consistently replicated (24–28). The findings in our study underline the important contribution of birth weight to the mechanism of asthma development, especially in children with episodic wheeze or no wheeze ( Figure 2 ). The mechanisms underlying the association between low birth weight and asthma outcomes are not completely understood. Low birth weight as a consequence of low gestational age might have a long-lasting impact on the structure of the airways and the lung, which could predispose, along with other factors, to the development of increased airway reactivity and asthma.
Children who developed asthma also tended to have higher IgE levels than those who did not develop asthma. This confirms the role of atopy as a predictor of asthma persistence throughout childhood and adolescence (3, 29), directly through early allergen sensitization and indirectly by impairing the immune response to viral infections (30, 31).
To determine whether wheezing and asthma development at follow-up were linked to airway pathology at baseline, we prospectively investigated children who had to undergo diagnostic bronchoscopies. All of the children in our cohort, who had a mean age of 3.8 years, had bronchoscopies performed for the appropriate clinical indications, according to international guidelines (11). The bronchial biopsies (obtained with approval of the local ethics committee and with consent) provided a pathological basis for the clinical and wheezing characteristics and their association with future asthma outcomes.
BM thickening at baseline was significantly increased in children who developed asthma at follow-up compared with children who did not. Importantly, when our cohort was stratified by age, BM thickness was the only factor that was associated with asthma at follow-up in children who were ≤3 years of age at baseline. The multivariate analysis of our data showed that BM thickening, along with multitrigger wheezing and low birth weight, was a predictor of asthma development later in life.
Our results differ substantially from previous studies (32–34) in which bronchial biopsies in children with asthma were also performed, but BM thickening was not found to predict asthma development. These differences may be due to the dissimilar populations studied. The children in those studies were younger, had severe airway obstruction, and had all been treated with high-dose corticosteroids at the time of bronchoscopy (32–34). By contrast, the children in our study were older, their asthma was not severe, and most had not been treated with corticosteroids at the time of bronchoscopy. When we reanalyzed our data excluding the few children who were on corticosteroids, our results did not change.
The number of eosinophils in bronchial tissue at baseline was also significantly higher in children who developed asthma than in children who did not. When we examined the relationship between tissue and blood eosinophilia in the whole group of children, although the correlation reached the level of significance, its coefficient was very low (r = 0.24, r 2 = 0.06) to reliably predict tissue eosinophilia from blood eosinophils. Our findings are in agreement with other studies correlating blood and airway inflammation (35, 36), and indicate that attempts to infer the presence of airway eosinophilia from blood eosinophil numbers to guide therapy should be contemplated with caution.
In our study, we could also compare the airway pathology of multitrigger and episodic wheezing. It has been questioned whether multitrigger wheezing and episodic wheezing are truly different conditions, with different pathogenetic mechanisms, or simply different severity classes of the same underlying conditions (21, 37–39). Our results from a similar pathology substrate in the two forms of wheezing support the latter conclusion.
A possible limitation of our study is that the cohort of children who underwent a clinically indicated bronchoscopy may not be representative of wheezing children in general, as the concomitant diseases could have influenced the results. However, these concomitant conditions were evenly distributed among the study groups (Table 1) and most likely did not affect the observed differences.
Unfortunately, at variance with previous studies (32), we were unable to provide a complete assessment of smooth muscle mass, a crucial component of airway remodeling in asthma. The lack of smooth muscle in the majority of the biopsies might be due to the limited depth of the bronchial wall sampled, but also to the mild severity of asthma in our cohort. Indeed, studies in adult asthma have shown that in severe asthma, but not in milder disease, airway smooth muscle gets close to the BM, and can be more easily sampled by endobronchial biopsies (40).
It should be acknowledged that even if the differences in BM thickness (P = 0.001) and tissue eosinophils (P = 0.026) between children with asthma and those without asthma were statistically significant, there was a considerable overlap at the individual level between the two groups ( Figures 3B and 4A ), as can be expected for any credible biological measurements. Therefore, these measurements should not be used as predictors at the individual level, but they can be of pathological importance in comparisons between groups, and can help to further elucidate the early mechanisms of asthma. Finally, a potential limitation of this study is that we did not perform any mechanistic analyses of BAL, as the study was focused mainly on bronchial biopsies and on measurements of airway pathology.
In conclusion, our study shows that multitrigger wheeze in early childhood and reduced birth weight are clinical predictors of asthma development later in life. Thickening of the BM in early childhood is a pathological finding that is closely associated with the development of asthma, highlighting the importance of airway remodeling in early life as a risk factor for future asthma development.
Hyaluronan and heavy chains
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Despite our increased understanding of the pathobiology of airways inflammation and the development of biologics as a therapeutic tool in the treatment of severe asthma, we still have much to learn regarding the movement of inflammatory cells within the lung and the long-term consequences of chronic inflammation within the lung. Part of the answer may lie in the extracellular matrix.
Much of our understanding of inflammatory cell movement is based on the established roles of selectins, integrins and chemokines in trafficking cells from blood vessels to sites of inflammation. Though we know how these cells are moved, we don’t fully understand what happens when they do.
Hyaluronan: more than just goo
Hyaluronan (HA) is a glucosaminoglycan in which the disaccharide (glucuronic acid-beta-1,3-N-acetylglucosamine-beta-1,4-) is repeated several thousand times. HA is a major constituent of the extracellular matrix. Due to its very simple composition, physical properties and near ubiquitous distribution, for many years HA was considered to be inert scaffolding, having only a mechanical role in supporting and maintaining tissue structure — essentially a goo. However, findings over the last decade indicate that the role of HA is much broader than previously thought.
HA was first noted in the secretions of asthmatics in 1978, and HA levels in the bronchoalveolar lavage (BAL) of asthmatics have since been associated with severity of disease. Additionally, HA can be covalently modified during inflammation with the heavy chains (HCs) of inter-alpha-inhibitor (IαI) to form an HC-HA complex. We and others have shown that HC substitution of HA significantly increases leukocyte adhesion to HA, thereby potentially defining a mechanism through which HC-HA could direct inflammatory events in the asthmatic lung.
Our group’s research has revealed the importance of HA in inflammation and provided strong evidence for HA’s major role in providing the preliminary matrix necessary for collagen synthesis and fibrosis noted in asthmatic airways. We have shown that HA deposition is an early event in the lung, with detectable levels within 12 hours of the first antigen exposure. Our data also reveal that inflammatory cells colocalize in areas of HA deposition, suggesting a role for HA in maintaining and localizing inflammatory cells to sites of danger.
Translating the data to human asthma
Although we completed much of this work in murine models of asthma, we also wanted to confirm that these findings and pathways are present in human asthma. We used immunofluorescent microscopy to examine the distribution of leukocytes within HC-HA matrices in lung tissue from three patients with acute severe asthma. (Figure). The airways of these patients displayed significant smooth muscle proliferation, epithelial metaplasia, mucus gland hypertrophy and airway obstruction due to mucus plugging (E,F). HA was distributed throughout the submucosa region and distributed around, but not within, serous mucus glands (A). Furthermore, HA was largely absent within the mucus of the airway lumen. IαI (i.e., HC) distribution was almost exclusively present in the submucosa region, displaying a striking colocalization with HA indicative of pathological HC-HA matrices (B). Using the common leukocyte antigen CD45 as a generic marker of inflammatory cells, we found large numbers of leukocytes in the submucosa region of these lungs colocalizing with and embedded within pathological HC-HA matrices.
Colocalization of leukocytes within HA matrices modified with heavy chains in asthmatic airways. A paraffin lung section of a patient with acute severe asthma was probed with a hyaluronan binding protein (green A), an antibody against IαI (red panel B) and the common leukocyte antigen CD45 (panel C magenta). DAPI stained nuclei are shown in blue. Overlay is shown in panel D. H&E and trichrome staining from the same region shown in panels A-D are shown in panels E and F, respectively. Magnification is 10x. A magnification bar is portrayed as a white line in panel A (150 μm). The airway epithelium is identified by an E, airway smooth muscle by SM, submucosal glands by G and a mucus plug by an asterisk in panels A-D. These images were representative of three asthmatic replicates. Figure and legend originally appeared in J Biol Chem. 2015290(38):23124-34. © American Society for Biochemistry and Molecular Biology.]
In summary, we believe that the extracellular matrix, an often ignored component in many diseases, is an active and direct participant in inflammatory processes including asthma, and a better understanding of these mechanisms may lead not only to insights into these processes but also to novel treatment pathways.
Dr. Aronica is staff in the departments of Pulmonary Medicine, Allergy and Clinical Immunology, and Pathobiology
Types, causes, and diagnosis of asthma
Asthma is a chronic condition that affects the airways. It causes wheezing and can make it hard to breathe. Some triggers include exposure to an allergen or irritant, viruses, exercise, emotional stress, and other factors.
Asthma causes the inside walls of the airways, or the bronchial tubes, to become swollen and inflamed.
During an asthma attack, the airways will swell, the muscles around them will tighten, and it becomes difficult for air to move in and out of the lungs.
Around 7.9% of people in the United States had asthma in 2017. There are many types of asthma, and several factors can cause asthma or trigger an acute attack.
This article looks at the types, causes, and triggers of asthma, as well as how a doctor diagnoses it.
Learn more about managing asthma here.
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Asthma is a long-term condition affecting the airways. It involves inflammation and narrowing inside the lungs, which restricts air supply.
A person with asthma may experience:
- tightness in the chest
- increased mucus production
An asthma attack occurs when the symptoms become severe. Attacks can begin suddenly and range from mild to life threatening.
In some cases, swelling in the airways can prevent oxygen from reaching the lungs. This means that oxygen cannot enter the bloodstream or reach vital organs. Therefore, people who experience severe symptoms need urgent medical attention.
A doctor can prescribe suitable treatments and advise a person on the best ways to manage their asthma symptoms.
Learn more about the signs and symptoms of asthma here.
Asthma can occur in many different ways and for many different reasons, but the triggers are often the same. They include airborne pollutants, viruses, pet dander, mold, and cigarette smoke.
The sections below list some common types of asthma.
Asthma is the most common chronic condition in children. It can develop at any age, but it is slightly more common in children than in adults.
In 2017, children aged 5–14 years were most likely to experience asthma. In this age group, the condition affected 9.7% of people. It also affected 4.4% of children aged 0–4 years.
In the same year, asthma affected 7.7% of people aged 18 years and over.
According to the American Lung Association, some common triggers of childhood asthma include:
- respiratory infections and colds
- cigarette smoke, including secondhand tobacco smoke
- air pollutants, including ozone and particle pollution, both indoors and outside
- exposure to cold air
- sudden changes in temperature
It is vital to seek medical attention if a child starts to experience asthma, as it can be life threatening. A doctor can advise on some of the best ways to manage the condition.
In some cases, asthma may improve as the child reaches adulthood. For many people, however, it is a lifelong condition.
Asthma can develop at any age, including during adulthood. According to one 2013 study, adults are more likely than children to have persistent symptoms.
Some factors that affect the risk of developing asthma in adulthood include:
- respiratory illness
- allergies and exposure to allergens
- hormonal factors
Learn more about adult-onset asthma here.
Occupational asthma results from exposure to an allergen or irritant present in the workplace.
In the following workplaces, allergens may cause asthma in those with a sensitivity or allergy:
- bakeries, flour mills, and kitchens
- hospitals and other healthcare settings
- pet shops, zoos, and laboratories where animals are present
- farms and other agricultural settings
In the following occupations, irritants can trigger asthma symptoms:
- car repairs and manufacturing
- engineering and metalwork
- woodwork and carpentry
- electronics and assembly industries
- hairdressing salons
- indoor swimming pools
Those with a higher risk include people who:
A person’s work environment can trigger a return of childhood asthma or the start of adult-onset asthma.
Difficult-to-control and severe asthma
Research suggests that around 5–10% of people with asthma have severe asthma.
Some people have severe symptoms for reasons that do not relate directly to asthma. For example, they may not yet have learned the correct way to use an inhaler.
Others have severe refractory asthma. In these cases, the asthma does not respond to treatment — even with high dosages of medication or the correct use of inhalers. This type of asthma may affect 3.6% of people with the condition, according to one 2015 study.
Eosinophilic asthma is another type of asthma that, in severe cases, may not respond to the usual medications. Although some people with eosinophilic asthma manage with standard asthma medications, others may benefit from specific “biologic” therapies. One type of biologic medication reduces the numbers of eosinophils, which are a type of blood cell involved in an allergic reaction that can trigger asthma.
Learn more about severe asthma here.
This type of asthma occurs in response to allergens that are only in the surrounding environment at certain times of year. For example, cold air in the winter or pollen in the spring or summer may trigger symptoms of seasonal asthma.
People with seasonal asthma still have the condition for the rest of the year, but they usually do not experience symptoms.
Asthma does not always stem from an allergy, however. Learn more about the difference between allergic and nonallergic asthma here.
Health professionals do not know exactly what causes asthma, but genetic and environmental factors both seem to play significant roles.
Some factors, such as sensitization to an allergen, may be both causes and triggers. The sections below list some others.
According to one study , smoking during pregnancy appears to increase the risk of the fetus developing asthma later in life. Some women also experience an aggravation of asthma symptoms while pregnant.
One article from 2014 suggested that there seem to be higher levels of asthma in people with obesity than those without it. The authors note that, in one study, children with obesity who lost weight also saw improvements in their asthma symptoms.
There is now a growing body of evidence suggesting that both conditions involve a chronic inflammatory response, and this could explain the link.
Allergies develop when a person’s body becomes sensitized to a specific substance. Once the sensitization has taken place, the person will be susceptible to an allergic reaction each time they come into contact with the substance.
Not every person with asthma has an allergy, but there is often a link. In people with allergic disease, exposure to specific allergens can trigger symptoms.
One 2013 study found that 60–80% of children and young adults with asthma are sensitive to at least one allergen.
Learn more about allergic asthma here.
Cigarette smoking can trigger asthma symptoms, according to the American Lung Association.
Asthma, even without smoking, can cause damage to the lungs. This can increase the risk of developing various tobacco-related lung conditions, such as chronic obstructive pulmonary disease, and it can make symptoms more severe.
Air pollution, both inside the home and outside of it, can affect the development and triggers of asthma.
Some allergens inside the home include:
- animal hair and dander
- fumes from household cleaners and paints
Other triggers in the home and outdoors include:
Stress can give rise to asthma symptoms, but so can several other emotions. Joy, anger, excitement, laughter, crying, and other emotional reactions can all trigger an asthma attack.
Scientists have also found evidence to suggest that asthma may be more likely in people with mental health conditions such as depression.
Others have suggested that long-term stress may lead to epigenetic changes that result in chronic asthma.
There is evidence to suggest that asthma runs in families. Recently, scientists have mapped out some of the genetic changes that may play a role in its development.
In some cases, epigenetic changes are responsible. These occur when an environmental factor causes a gene to change.
Around 5.5% of males and 9.7% of females have asthma. In addition, symptoms may vary according to a female’s reproductive stage and point in the menstrual cycle.
For example, during their reproductive years, symptoms may worsen during menstruation, compared with other times of the month. Doctors call this perimenstrual asthma. During menopause, however, asthma symptoms may improve.
Some scientists believe that hormonal activity may impact immune activity, resulting in hypersensitivity in the airways.
People with intermittent asthma may also have symptoms only some of the time. Learn more about intermittent asthma here.
A doctor will ask the person about their symptoms, their family medical history, and their personal medical history. They will also carry out a physical examination, and they may conduct some other tests.
When the doctor makes their diagnosis, they will also note whether the asthma is mild, intermittent, moderate, or severe. They will also try to identify the type.
People can keep a log of their symptoms and possible triggers to help the doctor make an accurate diagnosis. This should include information about potential irritants in the workplace.
The sections below discuss some other tests a doctor may conduct to help diagnose asthma.
The doctor will focus on the upper respiratory tract, the chest, and the skin. They will listen for signs of wheezing, which can indicate an obstructed airway and asthma.
They will also check the skin for signs of eczema or hives.
The doctor may also carry out a lung function test to assess how well the lungs are working.
A spirometry test is one example of a lung function test. The person will need to breathe in deeply and then breathe out forcefully into a tube. The tube links up to a machine called a spirometer, which shows how much air a person inhales and exhales and the speed at which they expel the air from the lungs.
The doctor will then compare these results with those of a person who is similarly aged but who does not have asthma.
To confirm the diagnosis, the doctor may then give the person a bronchodilator drug — to open the air passages — and repeat the test. If these second results are better, the person may have asthma.
This test may not be suitable for young children, however. Instead, the doctor may prescribe asthma medicines for 4–6 weeks and monitor any changes in their symptoms.
Other tests for diagnosis include:
A challenge test. This test allows a doctor to assess how cold air or exercise affect a person’s breathing.
A skin prick. A doctor can use this test to identify a specific allergy.
Tests to rule out other conditions. Sputum tests, X-rays, and other tests can help rule out sinusitis, bronchitis, and other conditions that can affect a person’s breathing.
Asthma is a chronic inflammatory condition that causes swelling in the airways. It can affect people of any age, and the symptoms can range from mild to severe.
In most cases, effective treatment is available that can help a person live a full and active life with asthma.