Stable Chronic Obstructive Pulmonary Disease Group Research Articles

Diagnostic Value of Galectin-3 in Exacerbations of Chronic Obstructive Pulmonary Disease.

Background and Objectives: Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disease characterized by acute exacerbations. Systemic inflammation and oxidative stress play an important role in the pathogenesis of COPD. Exacerbations in COPD reduce the quality of life and are associated with rapid disease progression. Galectin-3 is a beta-galactoside-binding lectin of approximately 30 kDa with pro-inflammatory and pro-fibrotic properties. This study aims to analyze the efficacy of serum galectin-3 in predicting exacerbations in COPD patients. Materials and Methods: Baseline demographic and clinical characteristics of all patients were recorded and blood samples were collected. A total of 58 consecutive COPD patients, including 28 patients (19 male and 9 female) with stable COPD and 30 patients (23 male and 7 female) with acute exacerbation of COPD (AECOPD), were included in the study. Results: Serum galectin-3 levels were significantly higher in the AECOPD group compared to the stable COPD group. A logistic regression analysis revealed that increased galectin-3 levels and disease duration were independent predictors of COPD exacerbation (OR = 5.322, 95% CI: 1.178-24.052, p = 0.03; and OR = 1.297, 95% CI: 1.028-1.635, p = 0.028; respectively). Conclusions: The results of our study demonstrated that Galectin-3 was a strong and independent predictor of exacerbations in COPD patients.

Correlation of Coagulation Dysfunction with Infection and Hypercapnia in Acute Exacerbation of COPD Patients.

This study aims to explore the factors influencing the coagulation function of patients with chronic obstructive pulmonary disease (COPD) and its effects on thrombosis. A total of 155 COPD patients, including 118 patients with acute exacerbation of COPD (AECOPD) and 37 patients with stable COPD (SCOPD), were enrolled in this study. Meanwhile, 50 patients with gastrointestinal polyps found during physical examination and treated with surgery in the same period were enrolled as the control group. The basic data, routine blood tests, C-reactive protein (CRP), procalcitonin (PCT), and coagulation indexes of the three groups were collected, as well as arterial blood gas indexes of AECOPD patients. The differences in erythrocyte count and hemoglobin among groups were not statistically significant. Compared with the SCOPD group and control group, white blood cell (WBC), neutrophil percentage, PCT, CRP, prothrombin time (PT), and fibrinogen (FIB) in the AECOPD group increased significantly, while the international normalized ratio (INR) decreased (P < 0.05). The differences in activated partial thromboplastin time (APTT) and D-dimer among groups were not statistically significant (P > 0.05). Thrombin time (TT) in the AECOPD group was shorter than that of the control group, and PT was longer than that of the SCOPD group (P < 0.05). Five patients with AECOPD and one patient with SCOPD had venous thrombosis. The abnormal coagulation function in AECOPD patients is related to the degree of infection and hypercapnia, which may be a risk factor for thrombosis.

Association Between IL-17 and Chronic Obstructive Pulmonary Disease: A Systematic Review and Meta-Analysis.

Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disease characterized by neutrophils airway infiltration. It is currently known that Interleukin-17 (IL-17) is an important pro-inflammatory factor. It can promote the accumulation of neutrophils and participate in the chronic inflammatory process of COPD. However, the value of IL-17 levels in the diagnosis and assessment of COPD remains controversial. In view of this, we conducted a systematic review and meta-analysis to assess its relevance. We searched databases such as PubMed, Web of Science, Cochrane Library and Embase to extract original research. A total of 10 studies with 2268 participants were included in this meta-analysis. The results showed that the level of serum IL-17 in patients with stable COPD was significantly higher than that in healthy controls (standard mean difference SMD, 1.59, 95% CI 0.84-2.34; p<0.001). Compared with the stable COPD group, the serum IL-17 level in acute exacerbation (AECOPD) was significantly higher (SMD, 1.78, 95% CI 1.22-2.33; p<0.001). The level of IL-17 in sputum of COPD patients was also higher than that of healthy controls (SMD, 2.03, 95% CI 0.74-3.31; p<0.001). Our results showed that IL-17 levels were elevated in serum and sputum in COPD patients compared with healthy controls, and IL-17 levels increased with disease progression. IL-17 serves as a potential biomarker to indicate the persistence of neutrophilic inflammation and exacerbation of COPD.

The Diagnostic and Assessment Value of Plasma Pentraxin 3 in Acute Exacerbation of Chronic Obstructive Pulmonary Disease.

Pentraxin 3 (PTX3) is an acute-phase protein and an important inflammatory mediator. We hypothesized plasma PTX3 could be a valuable diagnostic biomarker in acute exacerbation of chronic obstructive pulmonary disease (AECOPD). In this prospective controlled study, 458 COPD patients and 71 healthy controls from May 2019 to December 2020 in two hospitals were enrolled. COPD patients were divided into AECOPD group (n = 173) and stable COPD group (n = 285). AECOPD patients were subdivided into mild or moderate group (n = 43) and severe group (n = 130) based on severity. Plasma PTX3 levels were detected by ELISA. Plasma PTX3 levels were significantly higher in AECOPD (2.8 ng/mL) compared to stable COPD (0.87 ng/mL) and healthy controls (0.83 ng/mL). In the analysis of AECOPD subgroups, plasma PTX3 level of severe group (4.51 ng/mL) was significantly higher than that of mild or moderate group (1.25 ng/mL). Patients with respiratory failure had higher PTX3 than those without respiratory failure. No difference was observed between stable COPD patients and healthy controls. ROC analysis showed that plasma PTX3 had a considerable ability to distinguish AECOPD from stable COPD [AUC: 0.85, 95% CI (0.81-0.88), P < 0.0001; cut-off 1.25 ng/mL, sensitivity 77.5%, specificity 74%]. AUC of PTX3 was better than CRP regarding diagnosis of AECOPD. Combination of PTX3 and CRP was superior to either of them in diagnosing AECOPD. Plasma PTX3 levels were significantly higher in AECOPD than stable COPD. The level was associated with the severity of exacerbation. Plasma PTX3 has potential value as a biomarker to diagnose and evaluate AECOPD.

N6-methyladenosine-methylomic landscape of lung tissues of mice with chronic obstructive pulmonary disease.

Chronic obstructive pulmonary disease (COPD), a common respiratory disease, can be divided into stable phase and acute exacerbation phase (AECOPD) and is characterized by inflammation and hyper-immunity. Methylation of N6-methyladenosine (m6A) is an epigenetic modification that regulates the expression and functions of genes by influencing post-transcriptional RNA modifications. Its influence on the immune regulation mechanism has attracted great attention. Herein, we present the m6Amethylomic landscape and observe how the methylation of m6A participates in the pathological process of COPD. The m6A modification of 430 genes increased and that of 3995 genes decreased in the lung tissues of mice with stable COPD. The lung tissues of mice with AECOPD exhibited 740 genes with hypermethylated m6A peak and 1373 genes with low m6A peak. These differentially methylated genes participated in signaling pathways related to immune functions. To further clarify the expression levels of differentially methylated genes, RNA immunoprecipitation sequencing (MeRIP-seq) and RNA-sequencing data were jointly analyzed. In the stable COPD group, 119 hypermethylated mRNAs (82 upregulated and 37 downregulated mRNAs) and 867 hypomethylated mRNAs (419 upregulated and 448 downregulated mRNAs) were differentially expressed. In the AECOPD group, 87 hypermethylated mRNAs (71 upregulated and 16 downregulated mRNAs) and 358 hypomethylated mRNAs (115 upregulated and 243 downregulated mRNAs) showed differential expression. Many mRNAs were related to immune function and inflammation. Together, this study provides important evidence on the role of RNA methylation of m6A in COPD.

Neutrophil-Lymphocyte Ratio as a Section Predictor of COPD Exacerbations: A Cross-sectional Study

Introduction: Chronic Obstructive Pulmonary Disease (COPD) is characterised by a modified inflammatory response to chronic irritants which is often associated with some degree of systemic inflammation. Exacerbations in COPD are characterized by exaggeration of the ongoing inflammation. A number of inflammatory mediators are found to be raised in COPD exacerbations but most of them are expensive and not readily available. The Neutrophil-lymphocyte Ratio (NLR) is a rapid, easy and cheap biomarker that has been shown to be raised in patients of COPD. Aim: To evaluate the role of NLR in patients of stable and acute exacerbation of COPD. Materials and Methods: This cross-sectional observational study was conducted in Department of Pulmonary Medicine at Government Medical College, Patiala, Punjab, India. Study included 150 patients of stable COPD, 150 patients of Acute Exacerbation COPD (AECOPD) and 100 subjects as controls. NLR was calculated from a peripheral blood sample of the study participants. Continuous variables were summarised as mean with standard deviation and compared between groups using Unpaired t-test. A p-value &lt;0.05 was considered statistically significant. Results: The mean age in AECOPD group was 61.7±10.4 years, in stable COPD group was 63.1±8.9 years and 63.2±7.8 years in controls. Mean NLR was found to be highest in AECOPD group (4.0±1.7) followed by stable COPD (2.9±0.8) and then control (1.8±0.4).NLR showed good predictive value for predicting exacerbations in stable COPD patients with sensitivity and specificity of 75.3% and 70.7% respectively (cut-off 3.4 and AUC=0.806). Conclusion: NLR is an easily available biomarker of inflammation and can be used as a predictor of exacerbation in patients of COPD.

Evaluating the clinical role of fibrinogen, D-dimer, mean platelet volume in patients with acute exacerbation of COPD

BackgroundThere is limited research on clinical indicators for clinicians to judge the hypercoagulability of COPD patients. ObjectiveThe aim in this study was to evaluate the level changes of fibrinogen (FIB), d-dimer (D-D), and mean platelet volume (MPV) in plasma during the stable phase of chronic obstructive pulmonary disease (COPD), as compared with acute exacerbation of COPD (AECOPD). MethodsA total of 240 patients admitted with COPD in our hospital and 60 healthy people were enrolled in this prospective study using data from August 2016 to August 2017. Patients were allocated to AECOPD or stable COPD group. The levels of white blood cell (WBC) count, absolute neutrophil counts (NEU%), activated partial thromboplastin time (APTT), prothrombin time (PT), and hypoxia inducible factor-1(HIF-1) were detected. The MPV, D-D, and the FIB level were also determined and compared between groups. ResultsThe WBC count, NEU%, FIB, and D-D were significantly higher in the AECOPD group than in the stable COPD group and the healthy group (P < 0.05), while the MPV, APTT and PT was significantly lower in the AECOPD group than in the stable COPD group and the healthy group (P < 0.05). Additionally, MPV was significantly negatively correlated with WBC count (r=-0.798) and NEU% (r=-0.749) in the AECOPD group (P < 0.05); and the percentage of forced expiratory volume in one second (FEV1) in the predicted value was significantly negatively correlated with D-D (r=-0.891) and FIB (r=-0.656) (P <0.05). ConclusionWe demonstrated that, for patients hospitalized for exacerbation of COPD, MPV may indeed be a valid indicator of inflammation and a marker of thrombosis.

Inducible Costimulator-C-X-C Motif Chemokine Receptor 3 Signaling is Involved in Chronic Obstructive Pulmonary Disease Pathogenesis.

BackgroundThe role of inducible costimulator (ICOS) signaling in chronic obstructive pulmonary disease (COPD) has not been fully elucidated.MethodsWe compared the percentages of ICOS+ T cells and ICOS+ regulatory T (Treg) cells in CD4+ T cells and CD4+CD25+FOXP3+ Tregs, respectively, in the peripheral blood of smokers with or without COPD to those in healthy controls. We further characterized their phenotypes using flow cytometry. To investigate the influence of ICOS signaling on C-X-C motif chemokine receptor 3 (CXCR3) expression in COPD, we evaluated the expression levels of ICOS and CXCR3 in vivo and in vitro.ResultsICOS expression was elevated on peripheral CD4+ T cells and CD4+ Tregs of COPD patients, which positively correlated with the severity of lung function impairment in patients with stable COPD (SCOPD), but not in patients with acute exacerbation of COPD (AECOPD). ICOS+CD4+ Tregs in patients with SCOPD expressed higher levels of coinhibitors, programmed cell death protein 1 (PD-1) and T-cell immunoreceptor with Ig and ITIM domains (TIGIT), than ICOS−CD4+ Tregs, whereas ICOS+CD4+ T cells mostly exhibited a central memory (CD45RA−CCR7+) or effector memory (CD45RA−CCR7−) phenotype, ensuring their superior potential to respond potently and quickly to pathogen invasion. Furthermore, increased percentages of CXCR3+CD4+ T cells and CXCR3+CD4+ Tregs were observed in the peripheral blood of patients with SCOPD, and the expression level of CXCR3 was higher in ICOS+CD4+ T cells than in ICOS−CD4+ T cells. The percentage of CXCR3+CD4+ T cells was even higher in the bronchoalveolar lavage fluid than in matched peripheral blood in SCOPD group. Lastly, in vitro experiments showed that ICOS induced CXCR3 expression on CD4+ T cells.ConclusionsICOS signaling is upregulated in COPD, which induces CXCR3 expression. This may contribute to increased numbers of CXCR3+ Th1 cells in the lungs of patients with COPD, causing inflammation and tissue damage.

Efficacy of silymarin in treatment of COPD via P47phox signaling pathway

Chronic obstructive pulmonary disease (COPD) is the third leading cause of death worldwide. To investigate effect of silymarin on chronic obstructive pulmonary disease (COPD). The serum samples of 20 healthy controls, 20 patients with acute exacerbation of COPD and 20 patients with stable COPD were collected. LPS and smoking were used to induce COPD mouse model. Our results showed that in patients with acute exacerbation of COPD, O2-level release from peripheral blood neutrophils were negatively correlated with forced expiratory volume in the first second (FEV1), FEV1 in predicted value, FEV1/forced vital capacity (FVC), and arterial partial pressure (PaO2). (r=-0.898, -0.878, -874, -0.890, all P<0.01). Compared with that in the control group, the phosphorylation of NADPH oxidase p47phox factor and peripheral blood neutrophil membrane protein in the stable COPD group and the acute exacerbation COPD group were significantly stronger. Silymarin can inhibit the inflammatory response and oxidative stress. In conclusion, silymarin reduces oxidative stress in phagocytic and non-phagocytic cells, thus decreasing the oxidative stress in COPD patients

Comparing cardiac function and structure and their relationship with exercise capacity between patients with stable COPD and recent acute exacerbation: a cross-sectional study.

Patients with COPD are prone to cardiac remodeling; however, little is known about cardiac function in patients recovering from an acute exacerbation of COPD (AECOPD) and its association with exercise capacity. The aim of this study was to evaluate the cardiac function and structure and to compare their relationship with exercise capacity in patients with a recent AECOPD and patients with clinically stable COPD. This was a cross-sectional study including 40 COPD patients equally divided into two groups: recent AECOPD group (AEG) and clinically stable COPD group (STG). Echocardiography was performed to assess cardiac function and chamber structure. The six-minute walk distance (6MWD) and the Duke Activity Status Index (estimated Vo2) were used in order to assess exercise capacity. No significant differences in cardiac function and structure were found between the groups. The 6MWD was associated with early/late diastolic mitral filling velocity ratio (r = 0.50; p < 0.01), left ventricular posterior wall thickness (r = -0.33; p = 0.03), and right atrium volume index (r = -0.34; p = 0.04), whereas Vo2 was associated with right atrium volume index (r = -0.40; p = 0.02). Regardless of the clinical condition (recent AECOPD vs. stable COPD), the cardiac function and structure were similar between the groups, and exercise capacity (determined by the 6MWD and Vo2) was associated with cardiac features.

Application Value of Blood Heparin-Binding Protein in the Diagnosis of Acute Exacerbation of Chronic Obstructive Pulmonary Disease.

Objective To investigate the expression and clinical significance of serum heparin-binding protein (HBP), C-reactive protein (CRP), and white blood cell count (WBC) in an acute exacerbation of chronic obstructive pulmonary disease (COPD). Methods A prospective research model was used to select 63 patients with acute exacerbation of chronic obstructive pulmonary disease who were hospitalized in Xuzhou First People's Hospital from January 2020 to June 2020, and among the chronic obstructive pulmonary disease patients who were followed up in our hospital during the same period, 18 patients were in the stable phase, and 43 healthy patients in our hospital during the same period were selected as the healthy control group. 18 patients with stable chronic obstructive pulmonary disease were selected as the observation group, and 43 healthy people who underwent examination at the same time as the control group. For patients with acute COPD recombination, 5 ml of venous blood was collected according to whether the condition of COPD patients with acute exacerbation was stable or not. 5 ml of venous blood was collected for acute exacerbation. According to their clinical symptoms (such as cough, sputum, and asthma), dyspnea score (MRC score), and pulmonary function (FEV1 and FEV1/FVC), it is determined whether the patient's condition is stable. Patients in the stable COPD group will collect 5 ml of venous blood during the outpatient follow-up, and those in the healthy physical examination group will collect veins on the day of the physical examination. In 5 ml of blood, the levels of HBP and CRP in the blood were measured by the enzyme-linked immunosorbent method and the immunoturbidimetric method, respectively, and the peripheral blood WBC was measured by a blood cell analyzer and its supporting reagents. The differences of the three indicators in each group were statistically analyzed. Normally distributed measurement data were compared using t-test, homogeneity of variance of nonnormally distributed measurement data were compared using one-way analysis of variance, uneven variance of nonnormally distributed measurement data were compared using a rank-sum test, and Pearson linear analysis was used for correlation test. Subject working characteristic curve (ROC) was drawn, P < 0.05 means the difference is statistically significant, the receiver working characteristic curve was established, and the area under the curve (AUC) was calculated to analyze blood HBP. The value of blood CRP and peripheral blood WBC counts alone or in combination in the diagnosis of acute exacerbations of chronic obstructive pulmonary disease. Results The level of blood heparin-binding protein in the acute exacerbation phase was significantly higher than that in the stable phase and healthy controls (P < 0.05). In the acute exacerbation stage and stable stage group, the blood heparin binding protein, the percentage of leukocytes, neutrophils, and CRP were detected. There is a correlation between (P < 0.05) and a correlation with lung function (FEV1) (P < 0.05). The predictive value of heparin-binding protein, white blood cells, neutrophil percentage, CRP, etc. for the acute exacerbation of chronic obstructive pulmonary disease, with the area under the heparin-binding protein curve, is the largest, and compared with the stable phase, the comparison of heparin-binding protein, white blood cells, and CRP is statistically significant (P < 0.05). Conclusion Heparin-binding protein increases in the stable phase and acute exacerbation phase and is related to other inflammatory factors. It is one of the important inflammatory factors in chronic obstructive pulmonary disease. Heparin-binding protein, white blood cells, CRP, etc. have diagnostic and predictive value for acute exacerbation of chronic obstructive pulmonary disease. Heparin-binding protein has the best predictive result, and the combined index test has a better diagnostic predictive value, which is better than single index detection.

NT-pro BNP in AECOPD-PH: old biomarker, new insights-based on a large retrospective case-controlled study

BackgroundPulmonary hypertension (PH) is one of the common complications in chronic obstructive pulmonary disease (COPD). The study aimed to evaluate the predicting ability of N-terminal pro brain natriuretic peptide (NT-pro BNP) in patients with AECOPD-PH and its relationship with the severity of PH.MethodsA large retrospective case-controlled study (n = 1072) was performed in the First Affiliated Hospital of Xinjiang Medical University from January 2018 to December 2020, and patients were divided into stable COPD (n = 178), AECOPD (n = 688) and AECOPD-PH group (n = 206). Different statistical models were used to screen for reliable and stable biomarkers.ResultsIn unadjusted analysis and PSM (model 1, 2, 3), red cell distribution width (RDW), total bilirubin (TBIL), and NT-pro BNP were higher in patients with AECOPD-PH than those in AECOPD group. Logistic regression analysis showed, when the range of NT-proBNP was 271–1165 pg/mL (OR: 0.293; 95%CI: 0.184–0.467; P < 0.001) and NT-proBNP > 1165 pg/mL (OR: 0.559; 95%CI: 0.338–0.926; P = 0.024), the morbidity risk of PH in AECOPD patients was increased, so did TBIL. In receiver operating characteristic (ROC) curves, at the cut-off value of NT-proBNP was 175.14 pg/mL, AUC was 0.651 (P < 0.001), which was better than TBIL (AUC: 0.590, P < 0.001). As for the results of rank correlation analysis, NT-proBNP had a weak correlation with severity of PH with AECOPD (rs = 0.299, P = 0.001) and its relative relevance with other biomarkers (RDW was 0.359 and TBIL was 0.238, P < 0.001).ConclusionsOur findings suggest that NT-proBNP has a diagnostic efficacy in AECOPD-PH and NT-proBNP has a weak correlation with severity of PH with AECOPD.

Association of the Tight Junction Protein Claudin-4 with Lung Function and Exacerbations in Chronic Obstructive Pulmonary Disease.

PurposeChronic obstructive pulmonary disease (COPD) imposes a major healthcare burden. A tight junction protein, claudin-4 (CLDN4), may play a protective role in acute lung injury, but its role in COPD is unclear. To investigate the relationship between CLDN4 and COPD, we evaluated the association of CLDN4 with the clinical parameters of COPD, including exacerbations.Patients and MethodsWe analyzed a cohort of 30 patients with COPD and 25 healthy controls and evaluated their clinical parameters, including lung function. The plasma CLDN4 level in stable and exacerbated COPD was measured.ResultsThe COPD patients were all males and predominantly smokers; their initial lung function was poorer than the healthy controls. The mean CLDN4 plasma level was 0.0219 ± 0.0205 ng/mg in the control group, 0.0086 ± 0.0158 ng/mg in the stable COPD group (COPD-ST) and 0.0917 ± 0.0871 ng/mg in the exacerbated COPD (COPD-EXA) group. The plasma CLDN4 level was significantly lower in the COPD-ST than the control group, but was significantly elevated in the COPD-EXA group. The plasma CLDN4 level was inversely correlated with forced vital capacity and forced expiratory volume in 1 second in the COPD-EXA group (r=0.506, P=0.001 and r=0.527, P<0.001, respectively).ConclusionThe plasma CLDN4 level is closely correlated with COPD exacerbations and decreased lung function. This suggests that CLDN4 has potential as a severity marker for COPD.

Chronic non-invasive ventilation for chronic obstructive pulmonary disease.

Chronic non-invasive ventilation for chronic obstructive pulmonary disease.

Fibrinogen: A Feasible Biomarker in Identifying the Severity and Acute Exacerbation of Chronic Obstructive Pulmonary Disease.

BackgroundChronic obstructive pulmonary disease (COPD) is no longer considered a disease exclusive to the respiratory system. It is a multipronged disease with both lung and systemic involvement. Although the forced expiratory volume (FEV) in one second is one of the most commonly used markers to assess disease severity, in recent years, biomarkers such as interleukin-1 beta, serum C-X-C motif chemokine ligand 10, fibrinogen, soluble receptor for advanced glycation, surfactant protein D, and club cell secretory protein have been proven to be effective markers to assess disease severity.ObjectiveThe current study aimed to test the association of fibrinogen levels with increased exacerbation of COPD per year and lower lung function and to discuss its potential utility as a biomarker.MethodologyA total of 105 participants were enrolled in the study. The study participants included 35 stable COPD patients, 35 COPD patients with acute exacerbation, and 35 non-COPD healthy controls (matched for age and gender). All patients above 18 years of age who were diagnosed with COPD as per the Global Initiative for Chronic Obstructive Disease (GOLD) guidelines were considered for inclusion in the study. The patients were divided into stable COPD group and acute exacerbations of COPD (AECOPD) group based on the Anthonisen criteria. Sociodemographic factors, six-minute walk test, Medical Research Council Dyspnea Scale, and COPD Assessment Test scale were computed. Spirometry according to the American Thoracic Society guidelines and hematological investigations including serum fibrinogen were performed. Additionally, GOLD staging and severity indices were used to determine the clinical phenotyping of COPD, namely, ADO (age, dyspnea, airflow obstruction) index, BODE (body mass index, airflow obstruction, dyspnea, and exercise capacity) index, and DOSE (dyspnea, obstruction, smoking, exacerbation) index.ResultsPlasma fibrinogen level was significantly higher in the COPD groups compared to the control group. Plasma fibrinogen level was elevated in AECOPD compared to stable COPD patients. In addition, fibrinogen levels showed a positive correlation with important functional indices and prognostic markers such as BODE, ADO, and DOSE indices and a negative correlation with lung function. The odds of predicting an acute exacerbation of COPD for patients with FEV of <50% and FEV of >50% were 17.2 (area under the curve [AUC] = 0.825; sensitivity = 90.4%; specificity = 62.79%) and 15.1 (AUC = 0.791; sensitivity = 57.7%; specificity = 92.5%), respectively.ConclusionsPlasma fibrinogen has the potential to be an important biomarker in the management of COPD and its exacerbation due to its ability to be responsive to the COPD disease statuses such as the severity of COPD and AECOPD.

The relationship between serum uric acid level and uric acid/creatinine ratio with chronic obstructive pulmonary disease severity (stable or acute exacerbation) and the development of cor pulmonale.

There are studies reporting that uric acid elevation is a marker for hypoxemia and pulmonary hypertension secondary to some diseases. The aim of this study is to investigate the relationship between serum uric acid level and uric acid/creatinine ratio with chronic obstructive pulmonary disease (COPD) exacerbation, hypoxemia in exacerbation and development of cor pulmonale. A total of 96 COPD patients who were admitted to Ondokuz Mayıs University Faculty of Medicine emergency department and Chest Diseases outpatient clinic and whose written consent was obtained were included in our study. Forty-three of these patients were in the period of exacerbation (Group 1), and 53 were in the stable period (Group 2). Complete blood count, blood biochemistry (including serum uric acid level) and arterial blood gas analysis were performed in our patients. In addition, spirometry and echocardiography findings were examined. Serum uric acid level of patients in the period of exacerbation group (Group 1) was 6.97±1.34 and in stable COPD group (Group 2) was 4.30±1.01 (P<.05). Uric acid/creatinine ratios in Group 1 was 8.00±2.06; in Group 2, it was 5.52±1.57 (P<.05). In patients with hypoxemia, serum uric acid level and uric acid/creatinine ratio were significantly higher than nonhypoxemic patients (P<.05). Serum uric acid level and serum uric acid/creatinine ratio of Group 1 were significantly higher than Group 2 (P<.001). Serum uric acid level and serum uric acid/creatinine ratio of patients who developed cor pulmonale were significantly higher than patients without cor pulmonale (P<.05). Serum uric acid level and uric acid/creatinine ratio were found to be higher in patients with exacerbation of COPD and those developing cor pulmonale. Consequently, it suggests that serum uric acid level and serum uric acid/creatinine ratio may be a stimulating laboratory test for the severity of COPD and the development of COPD induced cor pulmonale.

Endocan as a potential biomarker of disease severity and exacerbations in COPD.

Endocan is a proteoglycan that is regarded as a novel marker of endothelial dysfunction. Endothelial dysfunction in pulmonary vascular bed is known to play an important role for the pathogenesis of COPD. This study aimed to determine serum endocan levels in patients with stable COPD and acute exacerbation of COPD (AECOPD) and to test the relationship between serum endocan levels and exacerbations. This study enrolled a total of 55 COPD patients, 24 of which had AECOPD and 31 had stable COPD. All patients' basic demographic and clinical data were recorded and blood samples were collected. Serum endocan levels were significantly higher in the AECOPD group compared to the stable COPD and control groups (for both p<0.001) and stable COPD group had higher levels than the control group (p<0.005). Additionally, serum endocan levels were negatively correlated with FVC, FEV1, partial oxygen pressure and oxygen saturation (r=-0.30, p=0.03; r=-0.34, p=0.01; r=-0.34, p=0.01 and r=-0.36, p=0.007 respectively), and positively correlated with disease duration and systolic pulmonary artery pressure (r=0.47, p<0.001; r=0.31, p=0.02 respectively). A cut-off value of 434.29pg/ml for endocan predicted exacerbation with a sensitivity of 79% and a specificity of 84% (AUC: 0.778, 95% Cl 0.648-0.909; p<0.001). Logistic regression analysis revealed that increased endocan levels was independent predictor of COPD exacerbation (OR=9.32, 95%CI, 1.64-52.95; p=0.01). Endocan may be a novel biomarker for detection of endothelial dysfunction and prediction of exacerbations in patients with COPD.

The Predictive Value of microRNA-134 and microRNA-1233 for the Early Diagnosis of Acute Exacerbation of Chronic Obstructive Pulmonary Disease with Acute Pulmonary Embolism.

BackgroundThe differential diagnosis of acute exacerbation of chronic obstructive pulmonary disease (AECOPD) with acute pulmonary embolism (APE) complications are difficult because of the variability of clinical presentations and the shortage of an unfailing screening biomarkers or instruments.ObjectiveAimed to detect and compare the expression of serum microRNAs (miR-1233, miR-134) in AECOPD patients complicated with APE.Patients/MethodsBlood samples were collected from 52 AECOPD patients (13 patients with APE complications, 39 patients without APE) and 10 patients with stable COPD. Serum miRNAs expression was detected with real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR). The levels of plasma D-dimers were determined by detection with an enzyme-linked immunosorbent assay (ELISA). The receiver-operator characteristic (ROC) curve was used for evaluating the diagnostic accuracy of the studied miRNAs.ResultsAccording to the Wells score, 42 of the 52 AECOPD patients were unlikely to have APE (≤4 points), whereas the remaining 10 (>4 points) were likely to have APE. There were 4 cases (4/13 30.8%) in the AECOPD combined with APE group with a Wells score of >4 points. The expression levels of miR-1233 and miR-134 in the serum were considerably upregulated in the AECOPD+APE group compared with the AECOPD group and the stable COPD group (P<0.05). The areas under the curve (AUCs) for miR-134 and miR-1233 were, respectively, 0.931 (95% CI 0.863–0.999) (P<0.05) and 0.884 (95% CI 0.79–0.978) (P<0.05) and were higher compared with the AUC for D-dimer of 0.628 (95% CI 0.447–0.809), the AUC for age-adjusted D-dimer of 0.705 (95% CI 0.525–0.885) and the AUC for Wells score of 0.577 (95% CI 0.389–0.765).ConclusionOur study indicated that serum miR-1233 and miR-134 have high clinical value in the early diagnosis of AECOPD patients combined with APE, or could be used as potential biomarkers for clinical identification of AECOPD with or without APE complication.

Correlation of serum fatty acid binding protein-4 and interleukin-6 with airflow limitation and quality of life in stable and acute exacerbation of COPD

Background/aim The serum fatty acid binding protein 4 (FABP-4) level increases in chronic inflammatory diseases. The present study aimed to examine serum FABP-4 and interleukin (IL)-6 levels in patients with stable and acute exacerbation of chronic obstructive pulmonary disease (COPD) and the correlation of these markers with airflow limitation.Materials and methods We measured serum FABP-4 and IL-6 levels in 60 COPD patients [30 stable COPD (SCOPD), and 30 acute exacerbation of COPD (AECOPD)], and 30 healthy subjects and compared them with airflow limitation according to the COPD stage in the Global Initiative for Chronic Obstructive Pulmonary Disease (GOLD) criteria, peripheral O2 saturation (SpO2), and COPD Assessment Test (CAT) score. We also tested the association between serum FABP-4 levels and some characteristics of study parameters. Results Both serum FABP-4 and IL-6 levels increased with increasing severity of GOLD grades in SCOPD (P < 0.01 for both) and AECOPD groups (P < 0.001 and P < 0.01, respectively). It also increased in patients with AECOPD group compared with SCOPD group in GOLD grades I-II (P < 0.01) and GOLD grades III-IV (P < 0.05). In addition, there was a significant positive correlation between serum FABP-4 level with IL-6, CAT score, and smoking history and inversely with FEV1 and SpO2. Conclusion The study revealed that serum FABP-4 level was elevated with increasing GOLD grades in COPD patients, markedly in acute exacerbation phase. The increase was associated with elevated serum levels of IL-6 and severity of hypoxia. Thus, it seems that FABP-4 may be involved in the pathogenesis of COPD.

Correlations Between Serum Decoy Receptor 3 and Airflow Limitation and Quality of Life in Male Patients with Stable Stage and Acute Exacerbation of COPD.

Serum decoy receptor 3 (DcR3) level increases in chronic inflammatory diseases. The present study aimed to examine serum DcR3 and IL-6 levels in male patients with stable chronic obstructive pulmonary disease (COPD) and acute exacerbation of the disease and correlations between these markers and airflow limitation. We measured serum DcR3 and IL-6 levels in 60 COPD patients [30 stable COPD (SCOPD), and 30 acute exacerbation of COPD (AECOPD)], and 30 control subjects and assessed their correlations with airflow limitation according to the COPD stage indicated by the global initiative for chronic obstructive pulmonary disease (GOLD) criteria, peripheral O2 saturation (SpO2), and COPD assessment test (CAT) score. We also tested associations between serum DcR3 levels and COPD patients' clinical parameters. Both serum DcR3 and IL-6 levels increased with increasing severity of airflow limitation in SCOPD and AECOPD groups (P < 0.01 to 0.001). These markers also increased in patients with AECOPD compared with subjects in SCOPD group in GOLD stages III-IV (P < 0.05 to 0.001). In addition, there was a significant positive correlation between serum DcR3 level and IL-6, CAT score and smoking history (per year). The study revealed that serum DcR3 level elevated with increasing severity of airflow limitation in male COPD patients, particularly in acute exacerbation phase. This increase was associated with a reduced quality of life and increased severity of hypoxia. These results suggest that DcR3 may be associated with the underlying pathophysiology of COPD in male patients.