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:: BPCO
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Epidemiology, clinical and economic burden, and natural history of chronic obstructive pulmonary disease and asthma
Skrepnek GH, Skrepnek SV
- Department of Pharmaceutical Sciences, and Center for Health Outcomes and Pharmacoeconomics Research, University of Arizonia, College of Pharmacy, Tucson, USA
Chronic obstructive pulmonary disease (COPD) and asthma are conditions that exact a tremendous toll on patients, providers, and society. The substantial increase in the prevalence of both conditions in recent decades has generated sizable concern from both domestic and global perspectives. The underlying characteristics of both conditions involve inflammation of the respiratory tract, although the specific nature and reversibility of these processes differ according to each illness. Within the context of disease management, acute exacerbations are important clinical events that contribute to an increase in morbidity and mortality, and may occur in any patient suffering from the disease. Because these conditions are highly important to clinical practice and healthcare systems, this article will highlight key aspects of epidemiology, burden of illness, and clinical presentation of COPD and asthma. A review of the definition, classification, and natural history is also offered, emphasizing the role of acute exacerbations. In general, the natural history of both COPD and asthma is highly variable and not precisely defined because of their heterogeneous clinical courses. Continued inquiry concerning the epidemiology, etiology, classification, and prognosis of each condition and related exacerbations may offer clinicians improved decision-making information to optimize interventions for affected patient populations.
PMID: 15354678 [PubMed - in process]
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Differences in airway remodeling between asthma and chronic obstructive pulmonary disease
Aoshiba K, Nagai A
- First Department of Medicine, Tokyo Women's Medical University
The functional consequence of asthma and chronic obstructive pulmonary disease (COPD)is airflow limitation, which is mostly reversible in asthma and not fully reversible in COPD. Inboth diseases, inflammatory conditions are associated with cellular and structural changes,referred to as remodeling, and these structural changes may lead to thickening of the airwaywall, thereby promoting airway narrowing and airflow limitation. However, the pattern ofinfiltrated cells and the pattern of structural changes occur differently in the two diseases. Inasthma, CD4+, T lymphocytes, eosinophils, and mast cells are the predominant cells involved,whereas in COPD, CD8+, T lymphocytes, and macrophages are predominantly involved. Insevere cases of asthma and COPD, neutrophil infiltration becomes evident. Regarding structuralchanges, epithelial injury and early thickening of reticular basement membrane are highlycharacteristic of the airway wall of asthmatics. Increases in airway smooth muscle mass occurin large airways of severe asthmatics and in small airways of patients with COPD. Thickeningof the airway wall, goblet cell hyperplasia, mucous gland hypertrophy, and the luminalobstruction caused by inflammatory exudates and mucous are features of both asthma andCOPD. Squamous epithelial metaplasia and airway wall fibrosis are commonly observed characteristicsof COPD. Destruction and fibrosis of the alveolar wall occur in COPD but not inasthma. The remodeling processes accompanied by chronic inflammatory infiltrates interactin a complex fashion and contribute to the development of airflow limitation in both asthmaand COPD.PMID: 15347849 [PubMed - in process]
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Transcription factors in asthma and COPD
Caramori G, Ito K, Adcock IM
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Dipartimento di Medicina Clinica e Sperimentale, Centro di Ricerca su Asma e BPCO, Universita di Ferrara, Via Savonarola 9, Italy. crm@unife.it
Inflammation is a central feature of asthma and chronic obstructive pulmonary disease (COPD) and both are characterized by an increased transcription of pro-inflammatory proteins (eg, cytokines, chemokines, growth factors and enzymes). Changes in inflammatory gene transcription are regulated by transcription factors that may therefore play a key role in the pathogenesis of asthma and COPD by amplifying and perpetuating the inflammatory process, and thereby contributing to disease severity and responsiveness to treatment. Several new compounds based on interactions with specific transcription factors or their activation pathways are now in development for the treatment of asthma and COPD.
PMID: 15334310 [PubMed - in process]
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Therapeutic responses in asthma and COPD: corticosteroids
Larj MJ, Bleecker ER
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Center for Human Genomics, Division of Pulmonary and Critical Care Medicine, Wake Forest University School of Medicine, Winston-Salem, NC 27157-1008, USA
The effects of inhaled corticosteroids (ICSs) in asthma include reduced severity of symptoms, improved pulmonary function, diminished bronchial hyperresponsiveness (BHR), prevention of exacerbations, and possible prevention of airway wall remodeling. Compared with an inhaled beta(2)-agonist, ICSs improve airway function and BHR, reduce bronchial-epithelium abnormalities, decrease bronchial inflammation, and reduce inflammatory-cell infiltration into the bronchial lamina propria; thus, they may prevent airway remodeling. In children, early use of ICSs may result in improved airway function over time. ICSs reduce use of prednisone, asthma medications, hospitalizations, and urgent-care visits. The primary side effects of ICSs in children are limited to transient reduction in growth. Compared with a leukotriene receptor antagonist (LTRA), ICSs produced a greater change from baseline in FEV(1) and greater reductions in symptoms. A long-acting beta(2)-agonist (LABA) combined with an ICS produced greater improvements than does therapy with ICSs even at higher doses. In COPD, the therapeutic value of ICSs is not as clear. While clinical trials in patients with mild COPD have not shown a reduction in decline in FEV(1) over time, other studies have shown that ICS therapy reduces exacerbations in patients with more severe COPD. Combination therapy with both ICS and LABA has recently been shown to be effective in COPD, where studies have documented additive improvement in FEV(1). Overall, the same therapeutic approaches show clinical effectiveness in both asthma and COPD. This supports the hypothesis that there are some similarities in these obstructive airway diseases. Future approaches should further define phenotypes, perhaps based in part on pharmacogenetic factors that will guide anti-inflammatory therapy in asthma and COPD
PMID: 15302774 [PubMed - in process]
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Therapeutic responses in asthma and COPD: bronchodilators
Donohue JF
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Division of Pulmonary/Critical Care Medicine, University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA. jdonohue@med.unc.edu
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The presence of acute reversibility to bronchodilators does not distinguish asthma from COPD. Patients with either condition can benefit from bronchodilators, and should be given a trial to assess their response. Some respond with a change in lung volume with less hyperinflation; others improve their forced inspiratory flow and become much more comfortable. The combination of long-acting beta-agonists (LABAs) and inhaled steroids is useful in both conditions. While anticholinergics seem to yield the best results in COPD, some patients with asthma benefit from their use. Tiotropium may be the most effective agent as monotherapy in COPD, but the combination of an inhaled steroid and a LABA may produce similar results in improving lung function. Long-acting bronchodilators are effective agents as monotherapy in COPD, but in asthma should be combined with a controller medication. Short-acting beta-agonists should be used intermittently in asthma, but may be used regularly or combined with an anticholinergic in COPD. The roles of stereoisomers, leukotriene receptor antagonists, and type 4 phosphodiesterase inhibitors in asthma and COPD remain uncertain at this time.
PMID: 15302773 [PubMed - in process]
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Physiologic similarities and differences between COPD and asthma
Sciurba FC
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Division of Pulmonary, Allergy and Critical Care Medicine, University of Pittsburgh, 1211 Kaufmann Bldg, Pittsburgh, PA 15213, USA. sciurbafc@upmc.edu
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The structural and physiologic findings in asthma and COPD appear, on average, and in the extremes of presentation, to be easily distinguished. A closer inspection of the literature reveals that significant overlap exists in individual patients with respect to airway wall thickening and low-attenuation parenchymal regions on CT scans, and in reversibility, airway hyperresponsiveness, lung diffusion, resting and dynamic hyperinflation, lung elastic recoil, exercise response, and a "pharmaceutical volume reduction" effect following therapy with bronchodilators. In particular, the subgroup of COPD patients having an airway-dominant phenotype becomes indistinguishable from asthmatic subjects with reversible disease that evolves into an incompletely reversible pattern.
PMID: 15302772 [PubMed - in process]
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Physiologic similarities and differences between COPD and asthma
Elias J
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Section of Pulmonary and Critical Care Medicine, Yale University School of Medicine, 333 Cedar St, New Haven, CT 06520, USA. jack.elias@yale.edu
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Asthma is characterized by eosinophilic and mononuclear cell infiltration, mucous metaplasia, airway remodeling, reversible airflow obstruction, and airway hyperresponsiveness. COPD is typified by nonreversible or incompletely reversible airway obstruction, often accompanied by mucous metaplasia and alveolar destruction. There is considerable overlap in pathogenesis and clinical features between the conditions. However, asthma and COPD may be distinguished by their respective cytokine profiles. Studies in transgenic mice have illuminated the roles of the T helper (Th) 1-mediated cytokine interferon-gamma in COPD, supporting the British hypothesis, and the Th2-mediated cytokine interleukin-13 in asthma, supporting the Dutch hypothesis. COPD and asthma may represent disease states along a continuum, with varying degrees of each disease often present in the same patient.
PMID: 15302771 [PubMed - in process]
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Genetics of asthma and COPD: similar results for different phenotypes
Meyers DA, Larj MJ, Lange L
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Center for Human Genomics, Wake Forest University School of Medicine, Medical Center Blvd, Winston-Salem, NC 27157, USA
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Asthma and COPD are common respiratory diseases that are caused by the interaction of genetic susceptibility with environmental factors. Environmental influences are important in both diseases, and although there are differences in genetic susceptibilities, there are also similarities. Three examples of interest for both asthma and COPD patients are discussed. The first is the results of family studies, which have shown evidence for susceptibility loci for both asthma-related and COPD-related phenotypes in the same chromosomal region. Second, evidence for a gene-environment interaction with passive smoking for asthma patients compared with individual smoking for COPD patients will be covered. The third is an example of one candidate gene (interleukin-13), in which similar results have been observed for both asthma and COPD.
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PMID: 15302770 [PubMed - in process]
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Rationale for the Dutch hypothesis: allergy and airway hyperresponsiveness as genetic factors and their interaction with environment in the development of asthma and COPD
Postma DS, Boezen HM
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Department of Pulmonology, University Hospital, University of Groningen, Postbus 30001, Hanseplein 1, 9700 RB Groningen, the Netherlands.
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The Dutch hypothesis, formulated in the 1960s, holds that the various forms of airway obstruction are different expressions of a single disease entity. It suggests that genetic factors (eg, airway hyperresponsiveness [AHR] and atopy), endogenous factors (eg, sex and age), and exogenous factors (eg, allergens, infections, and smoking) all play a role in the pathogenesis of chronic nonspecific lung disease. This review finds evidence that AHR and smoking are common risk factors for asthma and COPD. To prove the Dutch hypothesis definitively, however, genetic studies, preferably longitudinal, must be performed. Such studies must include subjects who have airway obstruction that does not necessarily meet the current strict definitions of asthma or COPD (ie, the extremes of these conditions) that are used in clinical studies.
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PMID: 15302769 [PubMed - in process]
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Similarities and differences in asthma and COPD: the Dutch hypothesis
Bleecker ER
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Center for Human Genomics, WakeForestUniversity, Medical Center Blvd, Winston-Salem, NC27157, USA. ebleeck@wfubmc.edu
PMID: 15302768 [PubMed - in process]
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Differentiating asthma and COPD patients
El-Kassimi FA
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Publication Types:
• Comment
• Letter
PMID: 15302761 [PubMed - indexed for MEDLINE]
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Dutch hypothesis: revisited?
Jindal SK
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Publication Types:
• Comment
• Editorial
PMID: 15302709 [PubMed - indexed for MEDLINE]
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Cardiovascular effects of beta-agonists in patients with asthma and COPD: a meta-analysis
Salpeter SR, Ormiston TM, Salpeter EE
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Santa ClaraValleyMedicalCenter, San Jose, CA, USA. salpeter@stanford.edu
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BACKGROUND: beta-Adrenergic agonists exert physiologic effects that are the opposite of those of beta-blockers. beta-Blockers are known to reduce morbidity and mortality in patients with cardiac disease. beta(2)-Agonist use in patients with obstructive airway disease has been associated with an increased risk for myocardial infarction, congestive heart failure, cardiac arrest, and acute cardiac death. OBJECTIVES: To assess the cardiovascular safety of beta(2)-agonist use in patients with obstructive airway disease, defined as asthma or COPD. METHODS: A meta-analysis of randomized placebo-controlled trials of beta(2)-agonist treatment in patients with obstructive airway disease was performed, to evaluate the short-term effect on heart rate and potassium concentrations, and the long-term effect on adverse cardiovascular events. Longer duration trials were included in the analysis if they reported at least one adverse event. Adverse events included sinus and ventricular tachycardia, syncope, atrial fibrillation, congestive heart failure, myocardial infarction, cardiac arrest, or sudden death. RESULTS: Thirteen single-dose trials and 20 longer duration trials were included in the study. A single dose of beta(2)-agonist increased the heart rate by 9.12 beats/min (95% confidence interval [CI], 5.32 to 12.92) and reduced the potassium concentration by 0.36 mmol/L (95% CI, 0.18 to 0.54), compared to placebo. For trials lasting from 3 days to 1 year, beta(2)-agonist treatment significantly increased the risk for a cardiovascular event (relative risk [RR], 2.54; 95% CI, 1.59 to 4.05) compared to placebo. The RR for sinus tachycardia alone was 3.06 (95% CI, 1.70 to 5.50), and for all other events it was 1.66 (95% CI, 0.76 to 3.6). CONCLUSION: beta(2)-Agonist use in patients with obstructive airway disease increases the risk for adverse cardiovascular events. The initiation of treatment increases heart rate and reduces potassium concentrations compared to placebo. It could be through these mechanisms, and other effects of beta-adrenergic stimulation, that beta(2)-agonists may precipitate ischemia, congestive heart failure, arrhythmias, and sudden death.
Publication Types:
• Meta-Analysis
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PMID: 15189956 [PubMed - indexed for MEDLINE]
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Can endobronchial biopsy analysis be recommended to discriminate between asthma and COPD in routine practice?
Bourdin A, Serre I, Flamme H, Vic P, Neveu D, Aubas P, Godard P, Chanez P
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Service des Maladies Respiratoires, Hopital Arnaud de Villeneuve, CHU de Montpellier, Montpellier, France
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BACKGROUND: International guidelines stress the importance of accurately discriminating between asthma and chronic obstructive pulmonary disease (COPD). Although characteristic pathological features have been described for both conditions, their discriminatory power has never been systematically assessed. METHODS: Endobronchial biopsy (EBB) specimens from patients with a clear clinical diagnosis of asthma and COPD (50 per group) were examined by three pathologists in a double blind manner. They were asked to propose a pathological diagnosis of either asthma or COPD and to analyse qualitatively the most frequent abnormalities reported in the literature. RESULTS: The sensitivity and specificity of EBB ranged from 36% to 48% and from 56% to 79%, respectively. Eosinophils strongly biased the pathological diagnoses in favour of asthma, whereas their estimated prevalence was similar (11-37% in asthma and 13-41% in COPD). Metaplasia (11-39% in COPD, 1-18% in asthma) and epithelial inflammation (28-61% in COPD, 11-38% in asthma) tended to be specific to COPD, whereas epithelial desquamation (80-98% in asthma, 61-88% in COPD) and basement membrane thickening (71-94% in asthma, 53-88% in COPD) tended to be associated with asthma. There was acceptable intra- and inter-observer agreement only for metaplasia and epithelial eosinophils. CONCLUSIONS: Specific histopathological features of asthma and COPD probably exist, but current routine analysis procedures to assess EBB specimens are not sufficiently discriminatory. This might be rectified by improving pathological definitions.
Publication Types:
• Clinical Trial
• Randomized Controlled Trial
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PMID: 15170031 [PubMed - indexed for MEDLINE]
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Airway inflammation in chronic obstructive pulmonary disease: comparisons with asthma.
Sutherland ER, Martin RJ
- Department of Medicine, National Jewish Medical and Research Center and the University of Colorado Health Sciences Center, Denver, Colo, USA
Chronic obstructive pulmonary disease (COPD) is a progressive syndrome of expiratory airflow limitation caused by chronic inflammation of the airways and lung parenchyma. The airway inflammatory response in COPD is initiated by smoking in the overwhelming majority of cases, and chronic exposure to cigarette smoke initiates a series of events that causes damage to central airways, peripheral airways, and terminal airspaces, leading to physiologic and clinical abnormalities. Although COPD shares some clinical features with asthma, another prevalent airway inflammatory disease, there are distinct differences in the phenotypic characteristics of airway inflammation between COPD and asthma. The eosinophil is the most prominent inflammatory cell in asthma, with mast cells, lymphocytes, and macrophages playing important but less prominent roles. In COPD the cellular composition of the airway inflammatory infiltrate differs, with neutrophils, macrophages, and lymphocytes assuming prominence and the eosinophil playing a minor role, except in the setting of exacerbations. The contrasting inflammatory phenotypes of asthma and COPD have important implications for clinical and physiologic manifestations of disease, as well as for therapy.
PMID: 14610463 [PubMed - indexed for MEDLINE]
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| Eur Respir J Suppl 2003 Jan;39:30s-35s |
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Similarities and differences between asthma and chronic obstructive pulmonary disease: treatment and early outcomes.
Buist AS.
- Pulmonary and Critical Care Medicine, Oregon Health and Science University, 3181 SW Sam Jackson Park Road, UHN 67 Portland, OR 97239-3098, USA. buists@ohsu.edu
There are now many guidelines that provide direction for the diagnosis and management
of asthma and chronic obstructive pulmonary disease (COPD). However, both diseases are
still underdiagnosed (or misdiagnosed) and undertreated. There is considerable evidence that
treatment with anti-inflammatory drugs reduces morbidity and mortality in asthma.
The evidence is growing regarding their effect on slowing the remodelling that occurs in subsets of asthmatics.
COPD is more challenging. There are no disease-modifying drugs available yet that will change the natural history
of COPD. However, there is overwhelming evidence that smoking cessation will slow the progression of disease.
Until better drugs are available for the treatment of COPD, emphasis must be placed on primary and secondary
prevention by reducing exposure to noxious agents (cigarette smoke in particular).
Inhaled corticosteroids appear to have a place in the management of severe chronic obstructive pulmonary disease,
perhaps by decreasing the frequency of exacerbations.
PMID: 12572699 [PubMed - in process]
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Differences in airway inflammation
in patients with fixed airflow obstruction due to
asthma or chronic obstructive pulmonary disease.
Fabbri LM, Romagnoli M, Corbetta
L, Casoni G, Busljetic K, Turato G, Ligabue G, Ciaccia
A, Saetta M, Papi A.
- Research Center on Asthma and COPD, University of
Ferrara, Italy. fabbri.leonardo@unimo.it
To determine whether patients with fixed airflow
obstruction have distinct pathologic and functional
characteristics depending on a history of either
asthma or chronic obstructive pulmonary disease
(COPD), we characterized 46 consecutive outpatients
presenting with fixed airflow obstruction by clinical
history, pulmonary function tests, exhaled nitric
oxide, sputum analysis, bronchoalveolar lavage,
bronchial biopsy, and high-resolution computed tomography
chest scans. Subjects with a history of COPD (n
= 27) and subjects with a history of asthma (n =
19) had a similar degree of fixed airflow obstruction
(FEV1: 56 +/- 2 versus 56 +/- 3% predicted) and
airway hyperresponsiveness (PC20FEV1: 2.81 [3.1]
versus 1.17 [3.3]). Subjects with a history of asthma
had significantly more eosinophils in peripheral
blood, sputum, bronchoalveolar lavage, and airway
mucosa; fewer neutrophils in sputum and bronchoalveolar
lavage fluid; a higher CD4+/CD8+ ratio of T cells
infiltrating the airway mucosa; and a thicker reticular
layer of the epithelial basement membrane. They
also had significantly lower residual volume, higher
diffusing capacity, higher exhaled nitric oxide,
lower high-resolution computed tomography scan emphysema
score, and greater reversibility to bronchodilator
and steroids. In conclusion, despite similar fixed
airflow obstruction, subjects with a history of
asthma have distinct characteristics compared with
subjects with a history of COPD and should be properly
identified and treated.
PMID: 12426229 [PubMed - in process]
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Comparison of the structural and
inflammatory features of COPD and asthma. Giles F.
Filley Lecture.
Jeffery PK.
- Imperial College School of Medicine at the Royal
Brompton Hospital, London, UK. p.jeffrey@ic.ac.uk
At least three conditions contribute to COPD. (1)
Chronic bronchitis (mucous hypersecretion) is an
inflammatory condition in which CD8+ T-lymphocytes,
neutrophils, and CD68+ monocytes/macrophages predominate.
The condition is defined clinically by the presence
of chronic cough and recurrent increases in bronchial
secretions sufficient to cause expectoration. There
is enlargement of mucus-secreting glands and goblet
cell hyperplasia, which can occur in the absence
of airflow limitation. (2) Adult chronic bronchiolitis
(small or peripheral airways disease) is an inflammatory
condition of small bronchi and bronchioli in which
there are predominantly CD8+ and pigmented macrophages.
The functional defect is difficult to detect clinically
but may be recognized by sophisticated tests of
small airway function. There is mucous metaplasia,
enlargement of the mass of bronchiolar smooth muscle,
and loss of alveolar attachments. (3) Emphysema
is an inflammatory condition of the alveoli in which
T-lymphocytes, neutrophils, and pigmented alveolar
macrophages are involved, associated with the release
of excessive amounts of elastases. It is defined
anatomically by permanent, destructive enlargement
of airspaces distal to terminal bronchioli without
obvious fibrosis. In contrast, asthma is a clinical
syndrome characterized by allergic inflammation
of bronchi and bronchioli in which CD4+ (helper)
T-lymphocytes and eosinophils predominate. There
is increased production and release of interleukin
(IL)-4 and IL-5, which is referred to as a Th2-type
response. There is usually increased tracheobronchial
responsiveness to a variety of stimuli, and the
condition is usually manifest as variable airflow
obstruction. While differences between COPD and
asthma have been highlighted, new data are emerging
that indicate there may also be similarities.
Publication Types:
* Lectures
PMID: 10843939 [PubMed - indexed for MEDLINE]
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Clinical, physiological and
radiological features of asthma with incomplete reversibility
of airflow obstruction compared with those of COPD.
Boulet LP, Turcotte H, Hudon C, Carrier G,
Maltais F.
- Universite Laval, Sainte-Foy, Canada. medlpb@hermes.ulaval.ca
OBJECTIVES: To compare clinical features, pulmonary
function and high-resolution computed chest tomography
(HRCT) findings of asthmatic patients with a component
of incomplete reversibility of airflow obstruction
(AIRAO) with those of patients with smoking-induced
chronic obstructive pulmonary disease (COPD). METHODS:
Thirteen patients with COPD (six males and seven
females, mean age 59 years, mean smoking 50.5 pack-years)
and 14 patients with AIRAO (six males and eight
females, mean age 52 years) despite optimal treatment,
with no significant smoking history (mean 1.5 pack-years)
and no significant environmental exposure or any
other respiratory disease, were studied. Patients
had respiratory questionnaires, pulmonary function
tests, allergy skin-prick tests and an HRCT to evaluate
possible parenchymal or bronchial abnormalities.
Eight patients in each group also had exercise tests.
All patients were stable at the time of the study.
RESULTS: As expected, atopy was more prevalent in
AIRAO (n=13) than in COPD (n=1) patients. Mean forced
expiratory volume in 1 s (FEV1) and forced vital
capacity (percentage of predicted value) were 39%
and 61%, respectively, in COPD patients and 49%
and 71%, respectively, in AIRAO patients; FEV1 improved
by 18% in COPD patients and and by 22% in AIRAO
patients after use of inhaled salbutamol. Mean functional
residual capacity was greater in COPD patients than
in AIRAO patients (178% versus 144% of the predicted
value), while the mean carbon monoxide diffusing
capacity of the lungs (DLCO) was lower in COPD patients
than in AIRAO patients (62% versus 89% of the predicted
value). Exercise tolerance was similar in both groups,
as were postexercise changes in arterial oxygen
pressure (PaO2). Emphysematous changes were observed
in COPD patients and AIRAO patients who had evaluable
HRCTs (10 versus two patients, although very mild
in asthma), bronchial dilations (zero versus six
patients), bronchial wall thickening (two versus
eight patients) and an acinar pattern (one versus
five patients). Mean thickness of the large airway
wall to outer diameter (intermediary bronchus) ratio
was 0.176 in COPD and 0.183 in AIRAO (P>0.05).
CONCLUSIONS: Asthma may lead to physiological features
similar to COPD but may be distinguished by demonstrating
a preserved DLCO and a higher ratio of airway to
parenchymal abnormalities on HRCT scan.
PMID: 9753528 [PubMed - indexed for MEDLINE]
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