scholarly journals Plasma pro-surfactant protein B and lung function decline in smokers

2015 ◽  
Vol 45 (4) ◽  
pp. 1037-1045 ◽  
Author(s):  
Janice M. Leung ◽  
John Mayo ◽  
Wan Tan ◽  
C. Martin Tammemagi ◽  
Geoffrey Liu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Lung Function ◽  
Surfactant Protein ◽  
Airflow Limitation ◽  
Ct Scans ◽  
Rapid Decline ◽  
Chronic Obstructive ◽  
Lung Function Decline ◽  
Surfactant Protein B ◽  
Protein B

Plasma pro-surfactant protein B (pro-SFTPB) levels have recently been shown to predict the development of lung cancer in current and ex-smokers, but the ability of pro-SFTPB to predict measures of chronic obstructive pulmonary disease (COPD) severity is unknown. We evaluated the performance characteristics of pro-SFTPB as a biomarker of lung function decline in a population of current and ex-smokers.Plasma pro-SFTPB levels were measured in 2503 current and ex-smokers enrolled in the Pan-Canadian Early Detection of Lung Cancer Study. Linear regression was performed to determine the relationship of pro-SFTPB levels to changes in forced expiratory volume in 1 s (FEV1) over a 2-year period as well as to baseline FEV1 and the burden of emphysema observed in computed tomography (CT) scans.Plasma pro-SFTPB levels were inversely related to both FEV1 % predicted (p=0.024) and FEV1/forced vital capacity (FVC) (p<0.001), and were positively related to the burden of emphysema on CT scans (p<0.001). Higher plasma pro-SFTPB levels were also associated with a more rapid decline in FEV1 at 1 year (p=0.024) and over 2 years of follow-up (p=0.004).Higher plasma pro-SFTPB levels are associated with increased severity of airflow limitation and accelerated decline in lung function. Pro-SFTPB is a promising biomarker for COPD severity and progression.

scholarly journals Longitudinal decline in lung function: a community-based cohort study in Korea

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Ah Young Leem ◽  
Boram Park ◽  
Young Sam Kim ◽  
Joon Chang ◽  
Sungho Won ◽  
...  
Keyword(s):  
Smoking Cessation ◽  
Lung Function ◽  
Mixed Model ◽  
Smoking Status ◽  
Airflow Limitation ◽  
Chronic Obstructive ◽  
Lung Function Decline ◽  
Rate Of Decline ◽  
Never Smokers ◽  
Over Time

Abstract Progressive decline in lung function is the hallmark of chronic obstructive pulmonary disease (COPD). We aimed to assess the rate of decline in forced expiratory volume in 1 second (FEV1) in patients from a community cohort database in Korea. 5,865 subjects aged 40–69 years from the Ansung-Ansan cohort database I–III (2001–2006) were included in this study. We assessed the annual rate of decline in FEV1 over time in relation to smoking status, patient sex, and presence or absence of pre-bronchodilator airflow limitation using a generalized additive mixed model. The mean follow-up duration was 3.8 years. The annual mean decline in FEV1 in the entire cohort was significantly more rapid for men than women (31.3 mL vs 27.0 mL, P = 0.003). Among men without pre-bronchodilator airflow limitation, annual mean declines in FEV1 were 31.5, 35.5, and 40.1 mL for never smokers, former smokers (P = 0.09 vs. never smokers), and current smokers (P < 0.001 vs. never smokers), respectively; and 23.4, 19.7, and 33.9 mL, respectively, for men with pre-bronchodilator airflow limitation. Thus, among Korean males, smoking accelerates lung function decline over time whereas smoking cessation slows the rate of FEV1 decline regardless of pre-bronchodilator airflow limitation. This underscores the importance of smoking cessation in Koreans.

Asthma and COPD Overlap Syndrome (ACOS)

2015 ◽  
Vol 69 (1) ◽  
pp. 8-11
Author(s):  
Deska Dimitrievska ◽  
Marija Zdraveska ◽  
Dejan Todevski ◽  
Elena Janeva ◽  
Suzana Arbutina ◽  
...  
Keyword(s):  
Quality Of Life ◽  
Lung Function ◽  
Randomized Clinical Trials ◽  
Significant Proportion ◽  
Overlap Syndrome ◽  
Airflow Limitation ◽  
Rapid Decline ◽  
Chronic Obstructive ◽  
Acute Exacerbations

Abstract Asthma and chronic obstructive pulmonary disease (COPD) have traditionally been viewed as distinct clinical entities. Recently, however, much attention has been focused on patients with overlapping features of both asthma and COPD: those with asthma COPD overlap syndrome (ACOS). A significant proportion of patients who present with symptoms of a chronic airways disease have features of both asthma and COPD. Several diagnostic terms, most including the word “overlap”, have been applied to such patients, and the topic has been extensively reviewed. However, there is no generally agreed term or defining features for this category of chronic airflow limitation, although a definition based upon consensus has been published for overlap in patients with existing COPD. In spite of these uncertainties, there is broad agreement that patients with features of both asthma and COPD experience frequent exacerbations, have poor quality of life, a more rapid decline in lung function and high mortality, and consume a disproportionate amount of healthcare resources than asthma or COPD alone. ACOS accounts for approximately 15-25% of the obstructive airway diseases and patients experience worse outcomes compared to asthma or COPD alone. Patients with ACOS often have the combined risk factors of smoking and atopy, are generally younger than patients with COPD and experience acute exacerbations with higher frequency and greater severity than in COPD alone. Pharmacotherapeutic considerations require an integrated approach, first to identify the relevant clinical phenoltype( s), then to determine the best available therapy. The authors discuss the array of existing and emerging classes of drugs which patients with ACOS could benefit from and share their therapeutic approach. A consensus international definition of ACOS is needed to design prospective. Randomized clinical trials are necessary to evaluate specific influence of drug interventions on important outcomes such as lung function, acute exacerbations, quality of life and mortality.

Surfactant protein B gene variations and susceptibility to lung cancer in chromate workers

2006 ◽  
Vol 49 (5) ◽  
pp. 367-373 ◽  
Author(s):  
Ashraf A. Ewis ◽  
Kazuya Kondo ◽  
Fuquan Dang ◽  
Yutaka Nakahori ◽  
Yasuo Shinohara ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Surfactant Protein ◽  
Surfactant Protein B ◽  
Protein B

scholarly journals Fibrocyte accumulation in bronchi: a cellular hallmark of COPD

2018 ◽  
Author(s):  
Isabelle Dupin ◽  
Matthieu Thumerel ◽  
Elise Maurat ◽  
Florence Coste ◽  
Hugues Begueret ◽  
...  
Keyword(s):  
Lung Function ◽  
Ct Scan ◽  
Wall Thickness ◽  
High Density ◽  
Airflow Limitation ◽  
Normal Lung ◽  
Chronic Obstructive ◽  
Lung Function Decline ◽  
Control Subjects ◽  
Copd Patients

AbstractBackgroundThe remodeling mechanism and cellular players causing persistent airflow limitation in chronic obstructive pulmonary disease (COPD) remain largely elusive. We have recently demonstrated that circulating fibrocytes, a rare population of fibroblast-like cells produced by the bone marrow stroma, are increased in COPD patients during an exacerbation. It remains, however, unclear, whether fibrocytes are present in bronchial tissue of COPD patients.ObjectiveWe aimed to quantify fibrocytes density in bronchial specimens from both control subjects and COPD patients, and to define associations with clinical, functional and computed tomography relevant parameters.Methods17 COPD patients and 25 control subjects with normal lung function testing and no chronic symptoms, all of them requiring thoracic surgery, were recruited. LFT and CT-scan were performed before surgery. Using co-immunostaining and image analysis, we identify CD45+ FSP1+ cells as tissue fibrocytes and quantify their density in distal and proximal bronchial specimens from the whole series.ResultsHere, we demonstrate that fibrocytes are increased in both distal and proximal tissue specimens of COPD patients, compared to those of controls. The density of fibrocytes is negatively correlated with lung function parameters, such as FEV1 and FEV1/FVC, and positively with bronchial wall thickness assessed by CT scan. High density of distal bronchial fibrocytes predicts presence of COPD with a sensitivity of 83% and a specificity of 70%.ConclusionsOur results thus suggest that recruitment of fibrocytes in the bronchi may participate to lung function decline during COPD progression.Clinical ImplicationsHigh density of tissue fibrocytes is associated with a deteriorated lung function and an increase in airway wall thickness. A low density tissue fibrocytes virtually eliminates the presence of COPD.Capsule summaryBlood fibrocytes assessed during exacerbation is a predictor of mortality in COPD. This study shows an increase of bronchial fibrocytes, that is associated with lower lung function, increased bronchial thickness and air trapping in COPD.

scholarly journals Circulating Pro-Surfactant Protein B as a Risk Biomarker for Lung Cancer

2013 ◽  
Vol 22 (10) ◽  
pp. 1756-1761 ◽  
Author(s):  
Ayumu Taguchi ◽  
Samir Hanash ◽  
Andrew Rundle ◽  
Ian W. McKeague ◽  
Deliang Tang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Surfactant Protein ◽  
Surfactant Protein B ◽  
Protein B

scholarly journals Epigenome-wide association study on asthma and chronic obstructive pulmonary disease overlap reveals aberrant DNA methylations related to clinical phenotypes

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yung-Che Chen ◽  
◽  
Ying-Huang Tsai ◽  
Chin-Chou Wang ◽  
Shih-Feng Liu ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Lung Function ◽  
Pulmonary Disease ◽  
Airflow Limitation ◽  
Chronic Obstructive ◽  
Lung Function Decline ◽  
Obstructive Pulmonary Disease ◽  
Copd Patients ◽  
Dna Methylations

AbstractWe hypothesized that epigenetics is a link between smoking/allergen exposures and the development of Asthma and chronic obstructive pulmonary disease (ACO). A total of 75 of 228 COPD patients were identified as ACO, which was independently associated with increased exacerbations. Microarray analysis identified 404 differentially methylated loci (DML) in ACO patients, and 6575 DML in those with rapid lung function decline in a discovery cohort. In the validation cohort, ACO patients had hypermethylated PDE9A (+ 30,088)/ZNF323 (− 296), and hypomethylated SEPT8 (− 47) genes as compared with either pure COPD patients or healthy non-smokers. Hypermethylated TIGIT (− 173) gene and hypomethylated CYSLTR1 (+ 348)/CCDC88C (+ 125,722)/ADORA2B (+ 1339) were associated with severe airflow limitation, while hypomethylated IFRD1 (− 515) gene with frequent exacerbation in all the COPD patients. Hypermethylated ZNF323 (− 296) / MPV17L (+ 194) and hypomethylated PTPRN2 (+ 10,000) genes were associated with rapid lung function decline. In vitro cigarette smoke extract and ovalbumin concurrent exposure resulted in specific DNA methylation changes of the MPV17L / ZNF323 genes, while 5-aza-2′-deoxycytidine treatment reversed promoter hypermethylation-mediated MPV17L under-expression accompanied with reduced apoptosis and decreased generation of reactive oxygen species. Aberrant DNA methylations may constitute a determinant for ACO, and provide a biomarker of airflow limitation, exacerbation, and lung function decline.

Sign in / Sign up

Export Citation Format

Share Document