Recently, many researchers paid more attentions to the association between air pollution and chronic obstructive pulmonary disease (COPD). Haze, a severe form of outdoor air pollution, affected most parts of northern and eastern China in the past winter. In China, studies have been performed to evaluate the impact of outdoor air pollution and biomass smoke exposure on COPD; and most studies have focused on the role of air pollution in acutely triggering symptoms and exacerbations. Few studies have examined the role of air pollution in inducing pathophysiological changes that characterise COPD. Evidence showed that outdoor air pollution affects lung function in both children and adults and triggers exacerbations of COPD symptoms. Hence outdoor air pollution may be considered a risk factor for COPD mortality. However, evidence to date has been suggestive (not conclusive) that chronic exposure to outdoor air pollution increases the prevalence and incidence of COPD. Cross-sectional studies showed biomass smoke exposure is a risk factor for COPD. A long-term retrospective study and a long-term prospective cohort study showed that biomass smoke exposure reductions were associated with a reduced decline in forced expiratory volume in 1 second (FEV1) and with a decreased risk of COPD. To fully understand the effect of air pollution on COPD, we recommend future studies with longer follow-up periods, more standardized definitions of COPD and more refined and source-specific exposure assessments.
Objective Sedation and/or analgesia is often applied during noninvasive positive pressure ventilation (NIPPV) to make patients comfortable, and thus improve the synchronization between patients and ventilator. Nevertheless, the effect of sedation and/or analgesia on the clinical outcome of the patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD) after extubation remains controversial. Methods A retrospective study was conducted on patients with AECOPD who received NIPPV after extubation in seven intensive care units in West China Hospital, Sichuan University between December 2013 and December 2017 . A logistic regression model was used to analyze the association between the use of sedation and/or analgesia and clinical outcomes including rate of NIPPV failure (defined as the need for reintubation and mechanical ventilation), hospital mortality, and length of intensive care unit stay after extubation. Results A total of 193 patients were included in the analysis, and 62 cases of these patients received sedation and/or analgesia during NIPPV. The usage of sedation and/or analgesia could result in failure of NIPPV (adjusted odd ratio [OR] 0.10, 95% confidence interval [CI] 0.02 - 0.52, P=0.006) and death (adjusted OR=0.13, 95%CI 0.04 - 0.42, P=0.001). Additionally, intensive care unit stay after extubation was longer in the patients who did not receive sedation and/or analgesia than those who did (11.02 d vs. 6.10 d, P< 0.01). Conclusion The usage of sedation and/or analgesia during NIPPV can decrease both the rate of NIPPV failure and hospital mortality in AECOPD patients after extubation.
Objective
To investigate the changes and clinical significance of cytokines and inflammatory species in exhaled breath condensate (EBC) in patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD).
Methods
Thirty AECOPD patients admitted in the Department of Respiratory Medicine from March 2015 to August 2016 (smokers and passive smokers) and 21 healthy volunteers (non-smokers) were recruited in this prospective study. General information and EBC were collected from each subject. The concentrations of interleukin-17 (IL-17), IL-10, and 8-isoprestane (8-iso-PG) in EBC were measured by enzyme-linked immunosorbent assay, meanwhile lung function test was performed in the AECOPD patients.
Results
Both IL-17 (ng/L) and 8-iso-PG (ng/L) levels increased significantly in the AECOPD patients before and after treatment compared with the healthy controls (10.74±1.02 and 5.65±0.88 vs. 3.36±0.61, 12.35±2.25 and 9.65±1.22 vs. 6.93±1.15, P<0.05). However, IL-10 level significantly decreased in the AECOPD patients before and after treatment compared with the healthy controls (1.68±0.17 and 2.59±0.31 vs. 2.85±0.43, P<0.05). Both IL-17 and 8-iso-PG levels in the AECOPD patients were significantly lower after treatment than those before treatment (5.65±0.88 vs. 10.74±1.02, 9.65±1.22 vs. 12.35±2.25, P<0.05), but IL-10 level were significantly higher aftertreatment than those before treatment (2.59±0.31 vs. 1.68±0.17, P<0.05). FEV1, FVC, and FEV1%pred improved significantly after treatment (P<0.01). FEV1, FEV1/FVC and FEV1%pred were not significantly correlated with IL-17, IL-10 or 8-is-PG levels.
Conclusion
IL-17, IL-10 and 8-iso-PG may be involved in the pathogenesis of COPD, and may be important biomarkers in monitoring airway inflammation and oxide stress during the treatment of AECOPD patients.
ObjectiveTo analyze the effect of different nebulization methods in patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD) requiring non-invasive ventilators (NIV). MethodsOne hundred and two patients with AECOPD were selected according to the standard, and randomly divided into a control group, a trial group I, and a trial group II according to the random number table. The patients in the control group received NIV intermittent oxygen-driven nebulization; the patients in the trial group I received NIV simultaneous oxygen-driven nebulization; and the patients in the trial group II received NIV simultaneous air-driven nebulization. The dynamic fluctuations of transcutaneous partial pressure of carbon dioxide (PtCO2), arterial blood gas indexes (PaCO2, PaO2, pH), vital signs and pulse oxygen saturation (SpO2) fluctuations were compared. ResultsPtCO2 at 15min of nebulization in the trial group II were lower than the other groups (P<0.05). PtCO2 at 15min of nebulization was higher than the other time points in the control group (P<0.05); there was no statistical difference of PtCO2 at different time points in the trial group I (P>0.05); PtCO2 gradually decreased with time in the trial group II (P<0.05). The difference before and after nebulization of PtCO2 (dPtCO2) was larger in trial group II than the other groups (P<0.05). PtCO2 at 0min and 5min after the end of nebulization in trial group II were lower than the other groups (P<0.05); there were no statistical differences of PtCO2 at 10min and 15min after the end of nebulization among three groups (P>0.05). There were statistical differences of the PtCO2 at each time point in the control group except for the PtCO2 at 10 min and 15min after the end of nebulization, all of which decreased with time; PtCO2 at each time points of nebulization decreased with time in the trial group I (P<0.05). PtCO2 only at 5min after the end of nebulization was lower than that at 0min after the end of nebulization in trial group II (P< 0.05), there were no statistical differences in other times (P>0.05). PaCO2, pH at the 4th day of treatment was lower than the pre-treatment in the control group (P<0.01); there were statistical differences of PaCO2 between the pre-treatment and the rest time points in the trial group I and group II (P<0.05). The number of abnormal fluctuations in vital signs and SpO2 during nebulization in three groups was not statistically different (P>0.05). ConclusionsThree groups can achieve good therapeutic effects. NIV intermittent oxygen-driven nebulization can make PtCO2 rise during nebulization; NIV simultaneous oxygen-driven nebulization can make PtCO2 remain stable during nebulization; NIV simultaneous air-driven nebulization can make PtCO2 fall during nebulization.
ObjectiveTo systematically review the clinical efficacy of low molecular weight heparin (LMWH) in treating patients with acute exacerbation of chronic obstructive pulmonary disease (COPD).
MethodsDatabases including PubMed, The Cochrane Library (Issue 10, 2013), EMbase, CBM, CNKI, VIP and WanFang Data were searched for the randomized controlled trials (RCTs) about LMWH in treating acute exacerbation of COPD from the establishment to October 2013. Two reviewers independently screened literature according to the inclusion and exclusion criteria, extracted data, and assessed methodological quality of the included studies. Meta-analysis was then performed using RevMan 5.2 software.
ResultsA total of 6 RCTs involving 501 patients were finally included. The results of meta-analysis showed that:compared with the control group, LMWH significantly improved levels of D-dimmer (MD=-0.28, 95%CI-0.50 to-0.05, P=0.02), reduced carbon dioxide partial pressure (PaCO2) (MD=-3.42, 95%CI-6.66 to-0.18, P=0.04), improved coagulation (PT) (MD=1.85, 95%CI 1.29 to 2.42, P < 0.000 01), and improved clinical symptoms and signs (RR=1.33, 95%CI 1.12 to 1.58, P=0.001), but it did not improve oxygen partial pressure (PaO2) (MD=0.28, 95%CI-3.04 to 3.61, P=0.87). During treatment, no severe adverse reaction occurred in both groups.
ConclusionLMWH could significantly improve symptoms caused by acute exacerbation of COPD. Due to limited quantity and quality of the included studies, the above conclusion needs to be confirmed by conducting more high quality RCTs with larger sample size.
Objective To explore the expression levels and clinical significance of serum long noncoding RNA myocardial infarction associated transcript (lncRNA MIAT) and microRNA-515-5p (miR-515-5p) in elderly patients with chronic obstructive pulmonary disease (COPD) at different periods. Methods From April 2021 to June 2023, 90 elderly patients with acute exacerbation of COPD treated in Huaibei People’s Hospital were selected as a COPD acute exacerbation group, 88 elderly patients with stable COPD as a COPD stable group, and 90 healthy elderly individuals undergoing physical examination as a control group. The white blood cell count (WBC) and serum lncRNA MIAT and miR-515-5p expression levels were detected in all subjects, blood gas analysis and pulmonary function indexes [oxygenation index (PaO2/FiO2), arterial blood carbon dioxide partial pressure (PaCO2), ratio of forced expiratory volume in the first second to forced vital capacity (FEV1/FVC), and FEV1 as a percentage of predicted value (FEV1%pred)] were detected in the patients with COPD. The correlation between serum lncRNA MIAT, miR-515-5p and smoking, WBC, blood gas analysis and pulmonary function indexes were analyzed in the elderly patients with acute exacerbation of COPD. The influencing factors of acute exacerbation of COPD, and the value of serum lncRNA MIAT, miR-515-5p in predicting the occurrence of acute exacerbation of COPD were also analyzed. Results The smoking proportion, WBC, serum lncRNA MIAT expression levels of the control group, the COPD stable group and the COPD acute exacerbation group were increased in turn, serum miR-515-5p expression levels were decreased in turn (P<0.05). Compared with the COPD stable group, PaCO2 was significantly increased in the COPD acute exacerbation group, while PaO2/FiO2, FEV1/FVC and FEV1%pred were significantly decreased (P<0.05); serum lncRNA MIAT in the elderly patients with acute exacerbation of COPD was positively correlated with smoking, WBC, PaCO2 (P<0.05), and negatively correlated with PaO2/FiO2, FEV1/FVC, FEV1%pred, miR-515-5p (P<0.05); serum miR-515-5p was negatively correlated with smoking, WBC, PaCO2 (P<0.05), and positively correlated with PaO2/FiO2, FEV1/FVC, FEV1%pred (P<0.05). Smoking, WBC, PaCO2, and lncRNA MIAT were risk factors affecting the acute exacerbation of COPD patients, PaO2/FiO2, FEV1/FVC, FEV1%pred, miR-515-5p were protective factors affecting the acute exacerbation of elderly COPD patients (P<0.05). The area under the ROC curve (AUC) of serum lncRNA MIAT, miR-515-5p and their combination in predicting acute exacerbation in elderly COPD patients were 0.823, 0.862 and 0.919, respectively, higher than the AUC predicted by serum lncRNA MIAT and miR-515-5p separately (P<0.05). Conclusions Serum lncRNA MIAT expression was high in elderly patients with COPD, and serum miR-515-5p expression was low, and the changes of both were more obvious in patients with acute exacerbation. Both were correlated with blood gas analysis and pulmonary function indexes in patients with acute exacerbation, and have high value in predicting the occurrence of acute exacerbation in elderly patients with COPD.
Lung injury could be classified as acute and chronic injuries, such as acute respiratory distress syndrome and chronic obstructive pulmonary disease. Lung function recovery mainly depends on inflammation adjusting, lung and airway remodeling, endogenous stem cell proliferation and differentiation, and tissue repair. The principles of clinical therapy include inhibition of inflammation, balancing coagulation and fibrinolysis, and protective lung ventilation for acute lung injury; while reduction of hyper-secretion, bronchodilation, adjusting airway mucosal inflammation and immunity, as well as improving airway remodeling for chronic obstructive pulmonary disease. The functional recovery of lung and airway depends on endogenous stem cell proliferation and repair. The purpose of clinical treatment is to provide assistance for lung and airway repair besides pathophysiological improvement.
Objective
To investigate the clinical significance of lateral position ventilation in the treatment of invasive ventilation in patients with acute exacerbations of chronic obstructive pulmonary disease (AECOPD).
Methods
From October 2014 to December 2016, 60 eligible patients with AECOPD who meeting the inclusion criteria were randomly assigned to an intervention group (n=30) or a control group (n=30). Expectorant, antiasthmatic, anti-infective, invasive ventilation, bronchoscopy, analgesic sedation, invasive-noninvasive sequential ventilation, nutritional support, intensive care and other treatment were conducted in two groups, but lateral position ventilation was subsequently performed in the intervention group and the control group used half lateral position. Outcome measurements included pH, PaO2/FiO2, arterial partial pressure of carbon dioxide (PaCO2), heart rate (HR), respiratory rate (R) and air way resistance (Raw) before and one day after invasive ventilation, and duration of control of pulmonary infection (PIC), invasive mechanic ventilation (IMV), mechanic ventilation (MV) and intensive care unit (ICU) stay.
Results
Compared with before ventilation, the levels of PaO2/FiO2, PaCO2, HR, R and Raw were significantly changed in two groups after ventilation (P<0.05). One day later after ventilation, pH [interventionvs. control: (7.43±0.07) vs. (7.37±0.11)], PaO2/FiO2[(253.52±65.33) mm Hg (1 mm Hg=0.133 kPa) vs. (215.46±58.72) mm Hg] and PaCO2 [(52.45±7.15) mm Hg vs. (59.39±8.44) mm Hg] were statistically significant (P<0.05), but no significant difference was found in HR, R or Raw between two groups (P>0.05). Compared with the control group, PIC [(3.7±1.4) daysvs. (5.3±2.2) days], IMV [(4.0±1.5) days vs. (6.1±3.0) days], MV [(4.7±2.0) days vs. (7.3±3.7) days] and ICU stay [(6.2±2.1) days vs. (8.5±4.2) days] were significantly decreased (P<0.05) in the intervention group.
Conclusions
In AECOPD patients, invasive ventilation using lateral position ventilation can significantly improve arterial blood gas index, decrease Raw, shorten the time of PIC, IMV, MV and ICU stay.
Objective To investigate the expression of dipeptidyl peptidase 4 (DPP4) and angiotensin-converting enzyme 2 (ACE2) in lung tissues of patients with four different diseases including coronavirus disease 2019 (COVID-19), chronic obstructive pulmonary disease (COPD), pulmonary sarcoidosis and pulmonary bullae, and to find out the potential risk factors affecting COVID-19. Methods This study retrospectively analyzed the clinical data of 40 patients admitted to Renmin Hospital of Wuhan University with COVID-19 (COVID-19 group), COPD (COPD group), pulmonary sarcoidosis (pulmonary sarcoidosis group) and pulmonary bullae (pulmonary bullae group) and surgically resected paraffin-embedded pathological lung tissues were obtained from their lung tissue pathological specimens after surgery and paraffin embedding. The GEO database (https://www.ncbi.nlm.nih.gov/geo/) was used for bioinformatics analysis to explore the expression difference of DPP4 and ACE2 mRNA in COVID-19, COPD, pulmonary sarcoidosis and normal lung tissues. Immunohistochemistry method was used to detect the expression of DPP4 and ACE2 protein in lung tissues of each group and the average optical density was measured by image analysis software. Results The results of GEO database analysis showed that compared with pulmonary bullae group, the expression level of DPP4 mRNA had no significant difference in the COPD group and pulmonary sarcoidosis group (both P>0.05), but it was increased in the COVID-19 group (P<0.05); There was no significant difference in the expression level of ACE mRNA in the pulmonary sarcoidosis group (P>0.05), but it was increased in the lung tissue of COVID-19 group and COPD group (both P<0.05). The results of immunohistochemistry showed that DPP4 and ACE2 proteins were lowly expressed in the pulmonary sarcoidosis group and pulmonary bullae group, while their expression level was high in COVID-19 and COPD groups without significant difference (P>0.05). The expression of DPP4 and ACE2 proteins in COVID-19 group was not related to the patient’s gender and age (P>0.05), but was related to smoking and long smoking duration (P<0.05), and there was a positive correlation between DPP4 and ACE2 expression (P<0.05). Conclusions DPP4 and ACE2 proteins are lowly expressed in the pulmonary sarcoidosis group and pulmonary bullae group, while their expression level is high in COVID-19 and COPD groups. There is no significant difference in the expression level of DPP4 and ACE2 protein in the COVID-19 and COPD lung tissues. There may be a positive correlation between DPP4 and ACE2 proteins expression in lung tissue, and smoking may be a potential risk factor for COVID-19.
ObjectiveTo investigate the value of neutrophil/lymphocyte ratio (NLR) in acute exacerbation of chronic obstructive pulmonary disease (AECOPD) by detecting the relationship between NLR and other well-known inflammatory biomarkers.MethodsRetrospective study of 610 AECOPD cases was performed. In order to analyze the influence of NLR level on disease condition, treatment plan and prognosis, the clinical data with acute exacerbation were collected and the value of NLR in AECOPD were analyzed.ResultsThe level of NLR was higher in the group with pneumonia than that in the non-pneumonia group (P<0.05), and the more severe the pulmonary inflammation, the higher the NLR level (P<0.05). The level of NLR was higher in the group with heart failure and the group treated with ventilator and glucocorticoid (P<0.05). The NLR level was higher in the group of hospital stay over 14 days than the group of hospital stay less than 14 days (P<0.05). The NLR value of the death group was higher than that of the survival group (P<0.05). With the increase of NLR value, the mortality rate in hospital increased gradually. Compared with C-reactive protein and interleukin-6, NLR had the highest odds ratio by binary regression analysis. Cutoff value of NLR was 5.92 by analysis of receiver-operating characteristic curve with a sensitivity of 88% and a specificity of 51%, and the area under the curve in predicting in-hospital death was 0.727 (OR=4.112, 95% confidence interval 0.609 - 0.849, P=0.02).ConclusionsNLR can be used as an inflammatory marker to evaluate the severity of AECOPD and to predict the prognosis.
