Airways resistance and specific conductance for the diagnosis of obstructive airways diseases.
Ontology highlight
ABSTRACT:
SUBMITTER: Topalovic M
PROVIDER: S-EPMC4509748 | biostudies-literature | 2015 Jul
REPOSITORIES: biostudies-literature
Publications
Airways resistance and specific conductance for the diagnosis of obstructive airways diseases.
Topalovic Marko M Derom Eric E Osadnik Christian R CR Troosters Thierry T Decramer Marc M Janssens Wim W
Respiratory research 20150722
<h4>Background</h4>Airway resistance (RAW) and specific airway conductance (sGAW) are measures that reflect the patency of airways. Little is known of the variability of these measures between different lung diseases. This study investigated the contribution of RAW and sGAW to a diagnosis of obstructive airways disease and their role in differentiating asthma from COPD.<h4>Methods</h4>976 subjects admitted for the first time to a pulmonary practice in Belgium were included. Clinical diagnoses we ...[more]
Similar Datasets
Project description: Not available
| S-EPMC8626223 | biostudies-literature
Project description:A concomitant decrease in FEV1 and FVC with normal FEV1/FVC ratio and TLC defines small airways obstructive pattern (SAOP) and constitutes a classic pitfall of pulmonary-function-tests interpretation.To evaluate the prevalence of flow- (FEV1 increase≥12% and 200 mL), volume- (FVC or inspiratory capacity [IC] increase≥12% and 200 mL), flow and volume-, and non-response to bronchodilation in patients with SAOP. An additional objective was to assess whether impulse oscillometry (IOS) parameters allow the diagnosis of SAOP and its reversibility.Fifty consecutive adult patients with SAOP (FEV1 and FVC < lower limit of normal, FEV1/FVC and TLC > lower limit of normal) diagnosed on spirometry and plethysmography underwent the assessment of reversibility (400 µg salbutamol) on FEV1, FVC, IC and IOS parameters.The diseases most frequently associated with SAOP were COPD and asthma (26 and 15 patients, respectively). Six patients were flow-responders, 20 were volume-responders, 9 were flow and volume-responders and 15 patients were non-responders. Overall, 26 patients had a significant improvement of IC, and 35 / 50 (70%, 95%CI: 57-83) exhibited a significant bronchodilator response. The difference between Rrs5Hz and Rrs20Hz was increased in 28/50 patients (56%, 95%CI: 42-70 with value higher than upper limit of normal) and its decrease after bronchodilator significantly correlated to FEV1 increase only, suggesting proximal airway assessment.A significant reversibility, mainly assessed on IC increase, is frequent in Small Airways Obstructive Pattern. Impulse oscillometry is of limited value in this context because of its low sensitivity.
| S-EPMC5543622 | biostudies-other
Project description:Cigarette smoke and smoking-induced inflammation decrease cystic fibrosis transmembrane conductance regulator (CFTR) activity and mucociliary transport in the nasal airway and cultured bronchial epithelial cells. This raises the possibility that lower airway CFTR dysfunction may contribute to the pathophysiology of COPD. We compared lower airway CFTR activity in current and former smokers with COPD, current smokers without COPD, and lifelong nonsmokers to examine the relationships between clinical characteristics and CFTR expression and function.Demographic, spirometry, and symptom questionnaire data were collected. CFTR activity was determined by nasal potential difference (NPD) and lower airway potential difference (LAPD) assays. The primary measure of CFTR function was the total change in chloride transport (?chloride-free isoproterenol). CFTR protein expression in endobronchial biopsy specimens was measured by Western blot.Compared with healthy nonsmokers (n = 11), current smokers (n = 17) showed a significant reduction in LAPD CFTR activity (?chloride-free isoproterenol, -8.70 mV vs -15.9 mV; P = .003). Similar reductions were observed in smokers with and without COPD. Former smokers with COPD (n = 7) showed a nonsignificant reduction in chloride conductance (-12.7 mV). A similar pattern was observed for CFTR protein expression. Univariate analysis demonstrated correlations between LAPD CFTR activity and current smoking, the presence of chronic bronchitis, and dyspnea scores.Smokers with and without COPD have reduced lower airway CFTR activity compared with healthy nonsmokers, and this finding correlates with disease phenotype. Acquired CFTR dysfunction may contribute to COPD pathogenesis.
| S-EPMC3734887 | biostudies-literature
Project description:Practical relevanceAlthough gait disturbance is one of the most common neurological presentations in feline medicine, the clinical approach to the paralyzed cat can be challenging. After excluding orthopedic and cardiovascular diseases that may mimic a neurological condition, the clinician has to address a long list of different diseases that may affect the spinal cord and produce paresis.Clinical challengesIn many cases a definitive cause of spinal weakness in cats is difficult to prove. Even when treatable diseases are identified, the prognosis is very much dependent on the severity of the clinical signs and their chronicity. This review sets out to describe the specific approach, diagnosis and management of cats with spinal cord disease and to outline the most common diseases responsible.Patient groupPatients of either gender and all ages and breeds can be affected by spinal cord disease.Evidence baseMany diseases affecting the spinal cord of cats, which include fibrocartilaginous embolic myelopathy, intervertebral disc disease, exogenous spinal cord trauma, spinal cord lymphosarcoma and feline infectious peritonitis, are well described in the literature. Many of these descriptions, however, have been based on case reports or series. While there have been several retrospective studies that describe the characteristics and incidence of these diseases in cats, there are no long term treatment trials or outcome studies to assist with prognostic determinations.
| S-EPMC7128365 | biostudies-literature
Project description:The World Trade Center (WTC) collapse produced a massive exposure to respirable particulates in New York City Fire Department (FDNY) rescue workers. This group had spirometry examinations pre-September 11, 2001, and post-September 11, 2001, demonstrating declines in lung function with parallel declines in FEV(1) and FVC. To date, the underlying pathophysiologic cause for this has been open to question.Of 13,234 participants in the FDNY-WTC Monitoring Program, 1,720 (13%) were referred for pulmonary subspecialty evaluation at a single institution. Evaluation included 919 full pulmonary function tests, 1,219 methacholine challenge tests, and 982 high-resolution chest CT scans.At pulmonary evaluation (median 34 months post-September 11, 2001), median values were FEV(1) 93% predicted (interquartile range [IQR], 83%-101%), FVC 98% predicted (IQR, 89%-106%), and FEV(1)/FVC 0.78 (IQR, 0.72-0.82). The residual volume (RV) was 123% predicted (IQR, 106%-147%) with nearly all participants having normal total lung capacity, functional residual capacity, and diffusing capacity of carbon monoxide. Also, 1,051/1,720 (59%) had obstructive airways disease based on at least one of the following: FEV(1)/FVC, bronchodilator responsiveness, hyperreactivity, or elevated RV. After adjusting for age, gender, race, height and weight, and tobacco use, the decline in FEV(1) post-September 11, 2001, was significantly correlated with increased RV percent predicted (P < .0001), increased bronchodilator responsiveness (P < .0001), and increased hyperreactivity (P = .0056). CT scans demonstrated bronchial wall thickening that was significantly associated with the decline in FEV(1) post-September 11, 2001 (P = .024), increases in hyperreactivity (P < .0001), and increases in RV (P < .0001). Few had evidence for interstitial disease.Airways obstruction was the predominant physiologic finding underlying the reduction in lung function post-September 11, 2001, in FDNY WTC rescue workers presenting for pulmonary evaluation.
| S-EPMC2832867 | biostudies-other
Project description:Vitronectin, a multifunctional glycoprotein, is involved in coagulation, inhibition of the formation of the membrane attack complex (MAC), cell adhesion and migration, wound healing, and tissue remodeling. The primary cellular source of vitronectin is hepatocytes; it is not known whether resident cells of airways produce vitronectin, even though the glycoprotein has been found in exhaled breath condensate and bronchoalveolar lavage from healthy subjects and patients with interstitial lung disease. It is also not known whether vitronectin expression is altered in subjects with asthma and COPD. In this study, bronchial tissue from 7 asthmatic, 10 COPD and 14 control subjects was obtained at autopsy and analyzed by immunohistochemistry to determine the percent area of submucosal glands occupied by vitronectin. In a separate set of experiments, quantitative colocalization analysis was performed on tracheobronchial tissue sections obtained from donor lungs (6 asthmatics, 4 COPD and 7 controls). Vitronectin RNA and protein expressions in bronchial surface epithelium were examined in 12 subjects who undertook diagnostic bronchoscopy. Vitronectin was found in the tracheobronchial epithelium from asthmatic, COPD, and control subjects, although its expression was significantly lower in the asthmatic group. Colocalization analysis of 3D confocal images indicates that vitronectin is expressed in the glandular serous epithelial cells and in respiratory surface epithelial cells other than goblet cells. Expression of the 65-kDa vitronectin isoform was lower in bronchial surface epithelium from the diseased subjects. The cause for the decreased vitronectin expression in asthma is not clear, however, the reduced concentration of vitronectin in the epithelial/submucosal layer of airways may be linked to airway remodeling.
| S-EPMC4358944 | biostudies-literature
Project description:BACKGROUND:Although the use of e-cigarettes is increasing worldwide, their short and long-term effects remain undefined. We aimed to study the acute effect of short-term use of e-cigarettes containing nicotine on lung function and respiratory symptoms in smokers with airways obstructive disease (COPD, asthma), "healthy" smokers, and healthy never smokers. METHODS:Respiratory symptoms, vital signs, exhaled NO, airway temperature, airway resistance (Raw), specific airway conductance (sGaw) and single nitrogen breath test were assessed before and immediately after short term use of an e-cigarette containing 11mg of nicotine among adults with COPD, asthma, "healthy" smokers, and never-smokers. The effect of the use of nicotine-free e-cigarettes among "healthy" never smokers was also studied. RESULTS:The majority of participants reported acute cough. Short term use of nicotine e-cigarettes was associated: a) with increased heart rate in all subjects except in the COPD group, b) decreased oxygen saturation in "healthy" and COPD smokers, c) increased Raw in asthmatic smokers, "healthy" smokers, and healthy never smokers, d) decreased sGaw in healthy subjects, and e) changed slope of phase III curve in asthmatic smokers. Short-term use of nicotine-free e-cigarettes increased Raw and decreased sGaw among healthy never smokers. CONCLUSIONS:Short-term use of an e-cigarette has acute effects on airways physiology and respiratory symptoms in COPD smokers, asthmatic smokers, "healthy" smokers and healthy never smokers. E-cigarette use was associated with effects in "healthy" never smokers irrespectively of nicotine concentration. More studies are needed to investigate both short and long-term effects of e-cigarette use.
| S-EPMC7232825 | biostudies-literature
Project description:Chronic obstructive lung diseases are characterized by the inability to prevent bacterial infection and a gradual loss of lung function caused by recurrent inflammatory responses. In the past decade, numerous studies have demonstrated the importance of nucleotide-mediated bacterial clearance. Their interaction with P2 receptors on airway epithelia provides a rapid 'on-and-off' signal stimulating mucus secretion, cilia beating activity and surface hydration. On the other hand, abnormally high ATP levels resulting from damaged epithelia and bacterial lysis may cause lung edema and exacerbate inflammatory responses. Airway ATP concentrations are regulated by ecto nucleoside triphosphate diphosphohydrolases (E-NTPDases) which are expressed on the mucosal surface and catalyze the sequential dephosphorylation of nucleoside triphosphates to nucleoside monophosphates (ATP --> ADP --> AMP). The common bacterial product, Pseudomonas aeruginosa lipopolysaccharide (LPS), induces an acute reduction in azide-sensitive E-NTPDase activities, followed by a sustained increase in activity as well as NTPDase 1 and NTPDase 3 expression. Accordingly, chronic lung diseases, including cystic fibrosis (CF) and primary ciliary dyskinesia, are characterized by higher rates of nucleotide elimination, azide-sensitive E-NTPDase activities and expression. This review integrates the biphasic regulation of airway E-NTPDases with the function of purine signaling in lung diseases. During acute insults, a transient reduction in E-NTPDase activities may be beneficial to stimulate ATP-mediated bacterial clearance. In chronic lung diseases, elevating E-NTPDase activities may represent an attempt to prevent P2 receptor desensitization and nucleotide-mediated lung damage.
| S-EPMC2096640 | biostudies-other
Project description:Nontypeable Haemophilus influenzae (NTHi) exclusively colonize and infect humans and are critical to the pathogenesis of chronic obstructive pulmonary disease (COPD). In vitro and animal models do not accurately capture the complex environments encountered by NTHi during human infection. We conducted whole-genome sequencing of 269 longitudinally collected cleared and persistent NTHi from a 15-y prospective study of adults with COPD. Genome sequences were used to elucidate the phylogeny of NTHi isolates, identify genomic changes that occur with persistence in the human airways, and evaluate the effect of selective pressure on 12 candidate vaccine antigens. Strains persisted in individuals with COPD for as long as 1,422 d. Slipped-strand mispairing, mediated by changes in simple sequence repeats in multiple genes during persistence, regulates expression of critical virulence functions, including adherence, nutrient uptake, and modification of surface molecules, and is a major mechanism for survival in the hostile environment of the human airways. A subset of strains underwent a large 400-kb inversion during persistence. NTHi does not undergo significant gene gain or loss during persistence, in contrast to other persistent respiratory tract pathogens. Amino acid sequence changes occurred in 8 of 12 candidate vaccine antigens during persistence, an observation with important implications for vaccine development. These results indicate that NTHi alters its genome during persistence by regulation of critical virulence functions primarily by slipped-strand mispairing, advancing our understanding of how a bacterial pathogen that plays a critical role in COPD adapts to survival in the human respiratory tract.
| S-EPMC5889651 | biostudies-literature
Project description:Mucosal-associated invariant T (MAIT) cells are a novel class of innate-like T cells, expressing a semi-invariant T-cell receptor (TCR) and able to recognize small molecules presented on the non-polymorphic MHC-related protein 1. Their intrinsic effector-memory phenotype, enabling secretion of pro-inflammatory cytokines, and their relative abundance in humans imply a significant potential to contribute to autoimmune processes. However, as MAIT cells were unknown until recently and specific immunological tools were unavailable, little is known of their roles in disease. Here I review observations from clinical studies and animal models of autoimmune and immune-mediated diseases including the roles of MAIT cells in systemic lupus erythematosus, rheumatoid arthritis, multiple sclerosis, inflammatory bowel disease and airways diseases. MAIT cell deficiencies are frequently observed in peripheral blood, and at sites of disease such as the airways in asthma. However, MAIT cells have a specific sensitivity to suppression by therapeutic corticosteroids that may confound many of these observations, as may the tendency of the surface marker CD161 to activation-induced down-regulation. Nonetheless, the dependence on bacteria for the development of MAIT cells suggests a potentially important protective role linking the influences of early life microbial exposures and subsequent development of autoimmunity. Conversely, MAIT cells could contribute to chronic inflammation either through TCR-independent activation, or potentially by TCR recognition of as yet undiscovered ligands. Future research will be greatly facilitated by the immunological tools that are now available, including murine genetic models and human and murine specific tetramers.
| S-EPMC4819138 | biostudies-other