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Chuang Cai,1,&ast; Wentan Zeng,2,&ast; Hongwei Wang,3 Shuqi Ren2 1Cancer Research Institute of Zhongshan City, Zhongshan City People’s Hospital, Zhongshan City, Guangdong Province, People’s Republic of China; 2Department of Laboratory Medicine, Tanzhou People’s Hospital of Zhongshan, Zhongshan City Hospital of Integration of TCM & Western Medicine, Zhongshan City, Guangdong Province, People’s Republic of China; 3Department of Pediatrics, Tanzhou People’s Hospital of Zhongshan, Zhongshan City hospital of integration of TCM & western medicine, Zhongshan City, Guangdong Province, People’s Republic of China&ast;These authors contributed equally to this workCorrespondence: Shuqi Ren, Department of Laboratory Medicine, Tanzhou People’s Hospital of Zhongshan, Zhongshan City hospital of integration of TCM & western medicine, No. 10 Dexiu road, Zhongshan City, Guangdong Province, People’s Republic of China, Tel +8615521067602, Fax +860760-23639928, Email shuchijen@163.com Chuang Cai, Cancer Research Institute of Zhongshan City, Zhongshan City People’s Hospital, No. 2 Sunwen East Road, Zhongshan City, Guangdong Province, 528404, People’s Republic of China, Tel +86 18826431030, Fax +86 0760-88823566, Email caich6@foxmail.comPurpose: Hierarchical management is advocated in China to effectively manage chronic obstructive pulmonary disease (COPD) patients and reduce the incidence and mortality of acute exacerbation of COPD (AE-COPD). However, primary and community hospitals often have limited access to advanced equipment and technology. Complete blood count (CBC), which is commonly used in these hospitals, offers the advantages of being cost-effective and easily accessible. This study aims to evaluate the significance of routine blood indicators in aiding of diagnosing AE-COPD.Patients and Methods: In this research, we enrolled a total of 112 patients diagnosed with AE-COPD, 92 patients with stable COPD, and a control group comprising 60 healthy individuals. Clinical characteristics, CBC parameters, and serum CRP levels were collected within two hours. To assess the associations between NLR/PLR/MLR and CRP by Spearman correlation test. The diagnostic accuracy of NLR, PLR and MLR in AE-COPD was assessed using Receiver Operating Characteristic Curve (ROC) and the area under the curve (AUC). Binary Logistic Regression analysis was conducted for the indicators of NLR, PLR and MLR.Results: We found that patients with AE-COPD had significantly higher levels of NLR, PLR and MLR in contrast to patients with stable COPD. Additionally, the study revealed a noteworthy correlation between CRP and NLR (rs=0.5319, P< 0.001), PLR (rs=0.4424, P< 0.001), and MLR (rs=0.4628, P< 0.001). By utilizing specific cut-off values, the amalgamation of NLR, PLR and MLR augmented diagnostic sensitivity. Binary logistic regression analysis demonstrated that heightened NLR and MLR act as risk factors for the progression of AE-COPD.Conclusion: The increasing levels of NLR, PLR and MLR could function as biomarkers, akin to CRP, for diagnosis and assessment of acute exacerbations among COPD patients. Further research is required to validate this concept. Keywords: acute exacerbation of chronic obstructive pulmonary disease, AE-COPD, neutrophil-lymphocyte ratio, NLR, platelet-lymphocyte ratio, PLR, monocyte-lymphocyte ratio, MLR

Chronic obstructive pulmonary disease (COPD) is one of the top three causes of mortality worldwide. Vitamin D deficiency in COPD has been associated with poor lung function and decreased muscle power, which further increases the risk of exacerbations. The role of vitamin D in preventing acute exacerbations of COPD has conflicting results in the literature. Hence, we planned this study to assess the relationship between vitamin D3 levels and the risk of acute exacerbations among COPD patients in a tertiary care center in north India. This was a prospective randomized control trial that was performed on 100 consecutive stable COPD patients attending the Department of Respiratory Medicine at Maharishi Markandeshwar Medical College and Hospital, Solan, India. The patients with subnormal vitamin D3 levels (i.e., less than 30 ng/mL) were divided into the intervention and control groups. Baseline demographic profiles, lung function, COPD assessment test (CAT) score, modified Medical Research Council grade and chest radiology were performed and repeated after 12 months in all these patients. All these parameters were recorded and compared with the baseline values obtained at the beginning of the study. Out of 100 subjects, 96 had vitamin D deficiency, of which 48 were assigned to the intervention group and 48 to the control group. Among the 100 subjects, 74 (74%) were males and 26 (26%) were females, with a mean age of 66.9±9.4 years. The mean vitamin D level was 14.71±6.69 in these 96 patients. The vitamin D level improved after 3 months of supplementation to the mean level of 45.56±16.18 in the intervention group. Vitamin D supplementation was positively correlated with a decrease in the rate of acute exacerbations in the intervention group in terms of reduction in mean CAT score (4.17 in intervention and 1.43 in non-interventional group, p

Cigarette smoke (CS) poses a significant risk factor for respiratory, vascular, and organ diseases owing to its high content of harmful chemicals and reactive oxygen species (ROS). These substances are known to induce oxidative stress, inflammation, apoptosis, and senescence due to their exposure to environmental pollutants and the presence of oxidative enzymes. The lung is particularly susceptible to oxidative stress. Persistent oxidative stress caused by chronic exposure to CS can lead to respiratory diseases such as chronic obstructive pulmonary disease (COPD), pulmonary fibrosis (PF), and lung cancer. Avoiding exposure to environmental pollutants, like cigarette smoke and air pollution, can help mitigate oxidative stress. A comprehensive understanding of oxidative stress and its impact on the lungs requires future research. This includes identifying strategies for preventing and treating lung diseases as well as investigating the underlying mechanisms behind oxidative stress. Thus, this review aims to investigate the cellular processes induced by CS, specifically inflammation, apoptosis, senescence, and their associated biomarkers. Furthermore, this review will delve into the alveolar response provoked by CS, emphasizing the roles of potential therapeutic target markers and strategies in inflammation and oxidative stress. [ABSTRACT FROM AUTHOR]

Aim: The Objectives of our study were to study the clinical profile and microbiological etiology of AE-COPD. Methods: It was a hospital-based cross-sectional study, conducted in a tertiary care center and included patients hospitalized with a principal diagnosis of AE-COPD. Diagnosis of COPD was based on the GOLD guidelines. Detailed history, physical examination, sputum microbiology and blood investigations were recorded for all patients. All statistical analyses were done using Epi info 7.2. Results: Mean age of the patients was 66.9 years. Majority of the patients (66) were ex-smokers, 26 were current- and 8 were never-smokers. One-third of the patients were frequent exacerbators. Most common co-morbidity was hypertension (25%) followed by diabetes (10%). Increased dyspnea was seen in all the patients, followed by increased quantity of sputum in 56. The most common clinical findings were use of accessory muscles of respiration in 92 patients, followed by crackles (84) and decreased breath sound intensity (62). Majority of the exacerbations (55%) were non-infectious, followed by 33% bacterial and 12% viral exacerbations. The most common isolated bacteria were Streptococcus pneumoniae (31%), Pseudomonas (27%) and Klebsiella (12%). Conclusion: This study shows the common risk factors and clinical features presented by COPD patients hospitalized with severe exacerbation. Majority of the exacerbations were non-infectious, warranting further studies to determine the environmental factors. Although one-third of the exacerbations were bacterial, viruses were important etiological agents.

Background: Many studies have indicated that S100A8 and S100A9 may be involved in the development and progression of chronic obstructive pulmonary disease (COPD). However, there has been no clinical study analyzing the role of the serum S100A8/S100A9 heterodimer in COPD patients. The aim of this study was to analyze the correlation of the serum S100A8/S100A9 heterodimer with pulmonary function in COPD patients during acute exacerbation (AE-COPD) based on a cross-sectional study. Methods: A total of 131 AE-COPD patients and matched healthy subjects were recruited. Pulmonary function, arterial blood gas values, and serum inflammatory cytokines were measured. Results: Serum S100A8/S100A9 was increased in AE-COPD patients. AE-COPD patients were ranked into different grades based on FEV1%. Serum S100A8/S100A9 was higher in Grade 4 than in Grade 1–2 and Grade 3 patients with AE-COPD. Univariate regression analysis found that serum S100A8/S100A9 was negatively correlated with FEV1% in AE-COPD patients. Furthermore, serum S100A8/S100A9 was positively associated with MCP-1 in AE-COPD patients. Further stratified analysis revealed that serum S100A8/S100A9 was negatively associated with FEV1/FVC in Grade 3 (OR 0.629, P < 0.05) and in Grade 4 (OR 0.347, P < 0.05). In addition, there was a positive relationship between serum S100A8/S100A9 and PaCO2 in Grade 3 (OR 1.532, P < 0.05) and Grade 4 (OR 1.925, P < 0.01). Conclusion: S100A8/S100A9 was negatively associated with pulmonary function in AE-COPD patients, indicating that the serum S100A8/S100A9 heterodimer may be involved in the progression of AE-COPD, and may be a relevant serum biomarker in the diagnosis for AE-COPD. [ABSTRACT FROM AUTHOR]

Background and Objective Acute exacerbations of chronic obstructive pulmonary disease ( AE- COPD) are leading causes of mortality in hospital intensive care units. We sought to determine whether dental plaque biofilms might harbor pathogenic bacteria that can eventually cause lung infections in patients with severe AE- COPD. Material and Methods Paired samples of subgingival plaque biofilm and tracheal aspirate were collected from 53 patients with severe AE-COPD. Total bacterial DNA was extracted from each sample individually for polymerase chain reaction amplification and/or generation of bacterial 16S rDNA sequences and cDNA libraries. We used a metagenomic approach, based on bacterial 16S rDNA sequences, to compare the distribution of species present in dental plaque and lung. Results Analysis of 1060 sequences (20 clones per patient) revealed a wide range of aerobic, anaerobic, pathogenic, opportunistic, novel and uncultivable bacterial species. Species indistinguishable between the paired subgingival plaque and tracheal aspirate samples (97-100% similarity in 16S rDNA sequence) were dental plaque pathogens ( Aggregatibacter actinomycetemcomitans, Capnocytophaga sputigena, Porphyromonas gingivalis, Tannerella forsythia and Treponema denticola) and lung pathogens ( Acinetobacter baumannii, Klebsiella pneumoniae, Pseudomonas aeruginosa and Streptococcus pneumoniae). Real-time polymerase chain reaction of 16S rDNA indicated lower levels of Pseudomonas aeruginosa and Porphyromonas gingivalis colonizing the dental plaques compared with the paired tracheal aspirate samples. Conclusion These results support the hypothesis that dental bacteria may contribute to the pathology of severe AE- COPD. [ABSTRACT FROM AUTHOR]