Pub Date : 2024-09-01DOI: 10.1016/j.pccm.2024.05.002
Yin Zhu , Hui Shen , Andrew D Lerner , Qin Li , Si Chen , Lingxiao Zhou , Jiaqi Zhou , Yang Xia , Kopen Wang
Transbronchial needle aspiration (TBNA) is a commonly used sampling approach in the diagnosis of hilar and mediastinal lymphadenopathy as well as peripheral lesions. As a very important tool, the continued innovation of TBNA needles is a vital driving force for the development of the technique. Although TBNA plays an important role in interventional pulmonology, there are no clear standards guiding operators to choose an appropriate needle for their operation. In recent decades, with the advent of endobronchial ultrasound-guided TBNA (EBUS-TBNA), the real-time visualization of TBNA has been enabled. These modern TBNA needles, such as ViziShot2, FLEX 19G, Acquire FNB, and EchoTip ProCore, have made significant progress in specimen collection, convenience, and safety, though still remain grounded in the basic premise and initial upgrades to the original conventional TBNA (cTBNA) needles. This review introduced the developmental history of WANG cTBNA needles, and summarized the lessons of success and failure and the enlightenments for currently used EBUS- and other emerging TBNA needles, aiming to provide a significant reference for pulmonologists who lived through the cTBNA era and for junior physicians who start working in the EBUS-TBNA era. Despite its long history, TBNA is still playing significant roles in the diagnosis of pulmonary diseases. A deeper understanding from the historical perspectives would facilitate continued innovations in the field of TBNA and beyond.
{"title":"Evolution of transbronchial needle aspiration needles: Over the last half century","authors":"Yin Zhu , Hui Shen , Andrew D Lerner , Qin Li , Si Chen , Lingxiao Zhou , Jiaqi Zhou , Yang Xia , Kopen Wang","doi":"10.1016/j.pccm.2024.05.002","DOIUrl":"10.1016/j.pccm.2024.05.002","url":null,"abstract":"<div><div>Transbronchial needle aspiration (TBNA) is a commonly used sampling approach in the diagnosis of hilar and mediastinal lymphadenopathy as well as peripheral lesions. As a very important tool, the continued innovation of TBNA needles is a vital driving force for the development of the technique. Although TBNA plays an important role in interventional pulmonology, there are no clear standards guiding operators to choose an appropriate needle for their operation. In recent decades, with the advent of endobronchial ultrasound-guided TBNA (EBUS-TBNA), the real-time visualization of TBNA has been enabled. These modern TBNA needles, such as ViziShot2, FLEX 19G, Acquire FNB, and EchoTip ProCore, have made significant progress in specimen collection, convenience, and safety, though still remain grounded in the basic premise and initial upgrades to the original conventional TBNA (cTBNA) needles. This review introduced the developmental history of WANG cTBNA needles, and summarized the lessons of success and failure and the enlightenments for currently used EBUS- and other emerging TBNA needles, aiming to provide a significant reference for pulmonologists who lived through the cTBNA era and for junior physicians who start working in the EBUS-TBNA era. Despite its long history, TBNA is still playing significant roles in the diagnosis of pulmonary diseases. A deeper understanding from the historical perspectives would facilitate continued innovations in the field of TBNA and beyond.</div></div>","PeriodicalId":72583,"journal":{"name":"Chinese medical journal pulmonary and critical care medicine","volume":"2 3","pages":"Pages 162-170"},"PeriodicalIF":0.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142324179","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-01DOI: 10.1016/j.pccm.2024.08.002
Jinsong Zhang , Natalie Vokes , Man Li , Jiachen Xu , Hua Bai , Jie Wang , Zhijie Wang , Jianjun Zhang
Targeted therapy has ushered in a new era of precision medicine for non-small cell lung cancer (NSCLC). Currently, epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKIs) stand as the recommended first-line therapy for advanced NSCLC harboring sensitive EGFR mutations. Nevertheless, most patients inevitably confront the challenge of drug resistance. This phenomenon arises not solely from intrinsic alterations within cancer cells but also from the intricate dynamics of the tumor microenvironment and the complex interactions that occur between cancer cells and their immediate surroundings. This review consolidates the current knowledge regarding EGFR-TKI resistance mechanisms, with a specific emphasis on unraveling the role played by the tumor microenvironment. In addition, the review delineates strategic approaches to surmount TKI resistance, thereby enriching the understanding of the interplay between therapeutic agents and the intricate milieu surrounding cancer cells.
{"title":"Overcoming EGFR-TKI resistance by targeting the tumor microenvironment","authors":"Jinsong Zhang , Natalie Vokes , Man Li , Jiachen Xu , Hua Bai , Jie Wang , Zhijie Wang , Jianjun Zhang","doi":"10.1016/j.pccm.2024.08.002","DOIUrl":"10.1016/j.pccm.2024.08.002","url":null,"abstract":"<div><div>Targeted therapy has ushered in a new era of precision medicine for non-small cell lung cancer (NSCLC). Currently, epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKIs) stand as the recommended first-line therapy for advanced NSCLC harboring sensitive <em>EGFR</em> mutations. Nevertheless, most patients inevitably confront the challenge of drug resistance. This phenomenon arises not solely from intrinsic alterations within cancer cells but also from the intricate dynamics of the tumor microenvironment and the complex interactions that occur between cancer cells and their immediate surroundings. This review consolidates the current knowledge regarding EGFR-TKI resistance mechanisms, with a specific emphasis on unraveling the role played by the tumor microenvironment. In addition, the review delineates strategic approaches to surmount TKI resistance, thereby enriching the understanding of the interplay between therapeutic agents and the intricate milieu surrounding cancer cells.</div></div>","PeriodicalId":72583,"journal":{"name":"Chinese medical journal pulmonary and critical care medicine","volume":"2 3","pages":"Pages 151-161"},"PeriodicalIF":0.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142323543","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-01DOI: 10.1016/j.pccm.2024.08.001
Han Yang , Si Chen , Jiayuan Sun , Felix J.F. Herth
Chronic inflammatory airway diseases, such as chronic bronchitis, chronic obstructive pulmonary disease, emphysema, and bronchial asthma, pose significant healthcare challenges. Interventional treatments offer promise as valuable complements to the optimal medical therapy recommended by the Global Initiative for Chronic Obstructive Lung Disease guideline and the Global Initiative for Asthma guideline. By directly accessing the airways, these minimally invasive procedures enable precise interventions. They encompass a wide range of techniques including bronchial thermoplasty and targeted lung denervation for both chronic obstructive pulmonary disease and severe asthma, bronchoscopic lung volume reduction (including the use of endobronchial valves, coils, and bronchoscopic thermal vapor ablation), airway bypass and peripheral stent placement for emphysema, bronchial rheoplasty and spray cryotherapy for chronic bronchitis, and other emerging methods. These interventional treatments aim to improve patients’ symptoms by reducing lung volume, alleviating hyperinflation, eliminating vagal innervation, disrupting hyperplastic goblet cells and thus reducing excessive mucus secretion, and weakening submucosal smooth muscles. This review highlights the potential advantages of interventional treatments for chronic inflammatory airway diseases and discusses relevant techniques tailored to specific disease subtypes. The overall aim is to assist interventional pulmonologists in selecting the most appropriate techniques for individual patients.
{"title":"Interventional pulmonology for chronic inflammatory airway diseases","authors":"Han Yang , Si Chen , Jiayuan Sun , Felix J.F. Herth","doi":"10.1016/j.pccm.2024.08.001","DOIUrl":"10.1016/j.pccm.2024.08.001","url":null,"abstract":"<div><div>Chronic inflammatory airway diseases, such as chronic bronchitis, chronic obstructive pulmonary disease, emphysema, and bronchial asthma, pose significant healthcare challenges. Interventional treatments offer promise as valuable complements to the optimal medical therapy recommended by the Global Initiative for Chronic Obstructive Lung Disease guideline and the Global Initiative for Asthma guideline. By directly accessing the airways, these minimally invasive procedures enable precise interventions. They encompass a wide range of techniques including bronchial thermoplasty and targeted lung denervation for both chronic obstructive pulmonary disease and severe asthma, bronchoscopic lung volume reduction (including the use of endobronchial valves, coils, and bronchoscopic thermal vapor ablation), airway bypass and peripheral stent placement for emphysema, bronchial rheoplasty and spray cryotherapy for chronic bronchitis, and other emerging methods. These interventional treatments aim to improve patients’ symptoms by reducing lung volume, alleviating hyperinflation, eliminating vagal innervation, disrupting hyperplastic goblet cells and thus reducing excessive mucus secretion, and weakening submucosal smooth muscles. This review highlights the potential advantages of interventional treatments for chronic inflammatory airway diseases and discusses relevant techniques tailored to specific disease subtypes. The overall aim is to assist interventional pulmonologists in selecting the most appropriate techniques for individual patients.</div></div>","PeriodicalId":72583,"journal":{"name":"Chinese medical journal pulmonary and critical care medicine","volume":"2 3","pages":"Pages 171-181"},"PeriodicalIF":0.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142324180","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-01DOI: 10.1016/j.pccm.2024.08.004
Yang Zheng , Lei Lan , Gan Lu , Ya-dong Gao
Background
The urbanization and industrialization of East and Southeast Asia in decades past has significantly altered living environment and lifestyles, which may have complicated effects on the burden of asthma. We aim to examine the patterns and trends of asthma incidence rates in six major East and Southeast Asian countries as well as five major Western countries, and predict the numbers of new cases attributed to various factors.
Methods
Data on annual asthma incident cases and corresponding population by age group were drawn from 6 major selected East and Southeast Asian countries available in the Global Burden of Disease database, including China, Japan, Korea, Singapore, Philippines, and Thailand. We also collected data of five major high-income Western countries for comparative purposes. Two separate Bayesian age–period–cohort models, representing pre-COVID (model 1) and post-COVID (model 2) scenarios, were constructed to predict the asthma incidence until 2030.
Results
In model 1, the age-standardized incidence rate of asthma will be the highest in the US (1970.07 per 100,000, 95% confidence interval [CI] 533.05–4455.03), while the lowest incidence rate will be found in Singapore (296.72 per 100,000, 95% CI 135.16–899.55) in 2030. Between 1990 and 2030, the incidence of asthma is projected to increase in China and Thailand, with average annual percentages changes (AAPC) ranging from 0.70% to 1.80%. The remaining four Asian countries show a declining trend, with AAPC ranging from -0.51% to -2.00%. In model 2, the US is estimated to have the highest age-standardized incidence rate (902.71 per 100,000, 95% CI 375.44–2277.24), while Korea will have the lowest incidence rate (176.46 per 100,000, 95% CI 58.77–512.09) in 2030. A decrease in asthma incidence was observed in all countries with the overall AAPC ranging from -3.42% to -0.42%. Notably, a turning point was found around 2020, after which the incidence rates dropped significantly.
Conclusions
Pandemic-related factors may temporarily lower the incidence of asthma. The expected increasing asthma incidence in pre-COVID scenario (model 1) should still warrant attention from public health practitioners and call for efforts to reduce the burden of asthma.
{"title":"Patterns and trends in asthma incidence rates in main Asian and Western countries and their prediction to 2030","authors":"Yang Zheng , Lei Lan , Gan Lu , Ya-dong Gao","doi":"10.1016/j.pccm.2024.08.004","DOIUrl":"10.1016/j.pccm.2024.08.004","url":null,"abstract":"<div><h3>Background</h3><div>The urbanization and industrialization of East and Southeast Asia in decades past has significantly altered living environment and lifestyles, which may have complicated effects on the burden of asthma. We aim to examine the patterns and trends of asthma incidence rates in six major East and Southeast Asian countries as well as five major Western countries, and predict the numbers of new cases attributed to various factors.</div></div><div><h3>Methods</h3><div>Data on annual asthma incident cases and corresponding population by age group were drawn from 6 major selected East and Southeast Asian countries available in the Global Burden of Disease database, including China, Japan, Korea, Singapore, Philippines, and Thailand. We also collected data of five major high-income Western countries for comparative purposes. Two separate Bayesian age–period–cohort models, representing pre-COVID (model 1) and post-COVID (model 2) scenarios, were constructed to predict the asthma incidence until 2030.</div></div><div><h3>Results</h3><div>In model 1, the age-standardized incidence rate of asthma will be the highest in the US (1970.07 per 100,000, 95% confidence interval [CI] 533.05–4455.03), while the lowest incidence rate will be found in Singapore (296.72 per 100,000, 95% CI 135.16–899.55) in 2030. Between 1990 and 2030, the incidence of asthma is projected to increase in China and Thailand, with average annual percentages changes (AAPC) ranging from 0.70% to 1.80%. The remaining four Asian countries show a declining trend, with AAPC ranging from -0.51% to -2.00%. In model 2, the US is estimated to have the highest age-standardized incidence rate (902.71 per 100,000, 95% CI 375.44–2277.24), while Korea will have the lowest incidence rate (176.46 per 100,000, 95% CI 58.77–512.09) in 2030. A decrease in asthma incidence was observed in all countries with the overall AAPC ranging from -3.42% to -0.42%. Notably, a turning point was found around 2020, after which the incidence rates dropped significantly.</div></div><div><h3>Conclusions</h3><div>Pandemic-related factors may temporarily lower the incidence of asthma. The expected increasing asthma incidence in pre-COVID scenario (model 1) should still warrant attention from public health practitioners and call for efforts to reduce the burden of asthma.</div></div>","PeriodicalId":72583,"journal":{"name":"Chinese medical journal pulmonary and critical care medicine","volume":"2 3","pages":"Pages 188-196"},"PeriodicalIF":0.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142324075","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-01DOI: 10.1016/S2772-5588(24)00080-X
{"title":"Guide for Authors","authors":"","doi":"10.1016/S2772-5588(24)00080-X","DOIUrl":"10.1016/S2772-5588(24)00080-X","url":null,"abstract":"","PeriodicalId":72583,"journal":{"name":"Chinese medical journal pulmonary and critical care medicine","volume":"2 3","pages":"Pages 200-210"},"PeriodicalIF":0.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142324077","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Idiopathic pulmonary fibrosis (IPF) is characterized by accumulation of myofibroblasts (MYFs) and extracellular matrix components, which leads to severe distortion and scarring of the gas exchange units of the lung, the alveoli, and ultimately respiratory failure. Fibrosis-associated MYFs are therefore widely regarded as the culprits that compromise the architectural makeup of the lung in fibrotic disease. During the past decade, the cellular source of MYFs has been intensely investigated. The rationale for such studies is that identifying the origin of these cells might help identify novel therapeutic targets and candidates to treat IPF patients. Recent advances in basic and translational research employing lineage tracing and multi-omics approaches have helped address the identity of MYF precursors, highlight the underlying heterogeneity, and to a less extent investigate MYF fate during fibrosis resolution. In this review, we discuss the current understanding of such important aspects of MYF biology as well as recent developments in the treatment of IPF.
{"title":"Understanding myofibroblast origin in the fibrotic lung","authors":"Mahsa Zabihi , Mahtab Shahriari Felordi , Arun Lingampally , Saverio Bellusci , Xuran Chu , Elie El Agha","doi":"10.1016/j.pccm.2024.08.003","DOIUrl":"10.1016/j.pccm.2024.08.003","url":null,"abstract":"<div><div>Idiopathic pulmonary fibrosis (IPF) is characterized by accumulation of myofibroblasts (MYFs) and extracellular matrix components, which leads to severe distortion and scarring of the gas exchange units of the lung, the alveoli, and ultimately respiratory failure. Fibrosis-associated MYFs are therefore widely regarded as the culprits that compromise the architectural makeup of the lung in fibrotic disease. During the past decade, the cellular source of MYFs has been intensely investigated. The rationale for such studies is that identifying the origin of these cells might help identify novel therapeutic targets and candidates to treat IPF patients. Recent advances in basic and translational research employing lineage tracing and multi-omics approaches have helped address the identity of MYF precursors, highlight the underlying heterogeneity, and to a less extent investigate MYF fate during fibrosis resolution. In this review, we discuss the current understanding of such important aspects of MYF biology as well as recent developments in the treatment of IPF.</div></div>","PeriodicalId":72583,"journal":{"name":"Chinese medical journal pulmonary and critical care medicine","volume":"2 3","pages":"Pages 142-150"},"PeriodicalIF":0.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142324178","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-01DOI: 10.1016/j.pccm.2024.08.007
Justine V. Devulder
Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory lung disease characterized by airflow limitation and changes in airway structures that can lead to chronic bronchitis, small airway diseases, and emphysema. COPD is the 3rd leading cause of death worldwide and despite current research, there are no curative disease treatments for COPD. As the prevalence of COPD is higher in people over 60 years old than in younger age groups, COPD is considered a condition of accelerated lung aging. Natural lung aging is associated with molecular, cellular, and physiological changes that cause alteration in lung structure, in lung function and regeneration, and decreased immune system response that could lead to lung disease like COPD. Mechanisms of accelerated lung aging are complex and composed by increased oxidative stress induced by exposure to cigarette smoke, by chronic inflammatory processes, and increased number of senescent cells within the airways. Cellular senescence is the cessation of cell division after a finite number of proliferation cycles or in response to cell stressors, such as oxidative stress. Senescent cells show activation of the cell cycle regulators p21CIP1 (cyclin-dependent kinase inhibitor-1), p16INK4 (cyclin-dependent kinase inhibitor-2A), and p53 (cellular tumor antigen p53) that lead to cell cycle arrest. Senescent cells exhibit a change in their phenotype and their metabolic activity, along with the production of proinflammatory proteins collectively known as senescence-associated secretory phenotype (SASP). This review aims to describe recent developments in our understanding of aging mechanisms and how the acceleration of lung aging participates in COPD pathophysiology and comorbidities. Understanding and targeting aging mechanisms may result in the development of new therapeutics that could be effective for COPD and also for other age-related diseases.
{"title":"Unveiling mechanisms of lung aging in COPD: A promising target for therapeutics development","authors":"Justine V. Devulder","doi":"10.1016/j.pccm.2024.08.007","DOIUrl":"10.1016/j.pccm.2024.08.007","url":null,"abstract":"<div><div>Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory lung disease characterized by airflow limitation and changes in airway structures that can lead to chronic bronchitis, small airway diseases, and emphysema. COPD is the 3<sup>rd</sup> leading cause of death worldwide and despite current research, there are no curative disease treatments for COPD. As the prevalence of COPD is higher in people over 60 years old than in younger age groups, COPD is considered a condition of accelerated lung aging. Natural lung aging is associated with molecular, cellular, and physiological changes that cause alteration in lung structure, in lung function and regeneration, and decreased immune system response that could lead to lung disease like COPD. Mechanisms of accelerated lung aging are complex and composed by increased oxidative stress induced by exposure to cigarette smoke, by chronic inflammatory processes, and increased number of senescent cells within the airways. Cellular senescence is the cessation of cell division after a finite number of proliferation cycles or in response to cell stressors, such as oxidative stress. Senescent cells show activation of the cell cycle regulators p21<sup>CIP1</sup> (cyclin-dependent kinase inhibitor-1), p16<sup>INK4</sup> (cyclin-dependent kinase inhibitor-2A), and p53 (cellular tumor antigen p53) that lead to cell cycle arrest. Senescent cells exhibit a change in their phenotype and their metabolic activity, along with the production of proinflammatory proteins collectively known as senescence-associated secretory phenotype (SASP). This review aims to describe recent developments in our understanding of aging mechanisms and how the acceleration of lung aging participates in COPD pathophysiology and comorbidities. Understanding and targeting aging mechanisms may result in the development of new therapeutics that could be effective for COPD and also for other age-related diseases.</div></div>","PeriodicalId":72583,"journal":{"name":"Chinese medical journal pulmonary and critical care medicine","volume":"2 3","pages":"Pages 133-141"},"PeriodicalIF":0.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142324177","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-01DOI: 10.1016/j.pccm.2024.08.006
Taoyu Li , Heping Fang , Xiangyu Liu , Yu Deng , Na Zang , Jun Xie , Xiaohong Xie , Zhengxiu Luo , Jian Luo , Yulin Liu , Zhou Fu , Luo Ren , Enmei Liu
Objectives
Respiratory syncytial virus (RSV) is a leading cause of lower respiratory tract infection (LRTI). However, few comprehensive descriptions of the disease burden, medical resource utilization (MRU), and costs of RSV are available for China. This study aimed to provide the basis for the development of RSV prevention strategies by analyzing the burden of RSV among inpatients with lower respiratory tract infection under 5 years of age.
Methods
We conducted a retrospective hospital-based study from June 2009 to May 2019 in Chongqing. Inpatients with LRTI were tested for eight viruses. We analyzed the RSV disease burden, MRU, and direct hospitalization costs by using non-parametric Mann‒Whitney U test, Chi-squared test or Fisher's exact test and logistic regression.
Results
A total of 6991 children under 5 years of age with LRTI were included in this study. The overall RSV-positive rate was 34.5% (2410/6991). Prior to admission, 81.9% (1973/2410) of these RSV-positive cases were otherwise healthy. Compared with children aged 24–59 months, the odds ratio (OR) and 95% confidence interval (CI) for RSV infection were 2.509 (2.139–2.945), 1.882 (1.549–2.222), and 1.479 (1.240–1.765) for those aged 1–5 months, 6–11 months, and 12–23 months, respectively. The proportions of patients treated with invasive ventilation and continuous positive airway pressure (CPAP) were significantly higher among RSV-positive cases (1.1% [27/2410] and 3.9% [93/2410]) than RSV-negative cases (0.9% [43/4581] and 2.7% [124/4581]) (P = 0.023). Compared with RSV-negative cases, RSV-positive cases had significantly longer hospital length of stay (6 [5, 8] days vs. 6 [5, 8] days, P < 0.001) and higher hospitalization costs (963.0 [757.9, 1298.5] USD vs. 935.6 [719.7, 1296.3] USD, P = 0.022).
Conclusions
Most RSV infections occurred during early childhood and among individuals in the otherwise healthy group. Younger age was associated with a higher RSV-positive rate. Effective prevention measures are needed in the earliest stages to reduce the RSV burden.
{"title":"Burden of RSV among inpatients with lower respiratory tract infection under 5 years of age: A 10-year retrospective study in Southwest China from 2009 to 2019","authors":"Taoyu Li , Heping Fang , Xiangyu Liu , Yu Deng , Na Zang , Jun Xie , Xiaohong Xie , Zhengxiu Luo , Jian Luo , Yulin Liu , Zhou Fu , Luo Ren , Enmei Liu","doi":"10.1016/j.pccm.2024.08.006","DOIUrl":"10.1016/j.pccm.2024.08.006","url":null,"abstract":"<div><h3>Objectives</h3><div>Respiratory syncytial virus (RSV) is a leading cause of lower respiratory tract infection (LRTI). However, few comprehensive descriptions of the disease burden, medical resource utilization (MRU), and costs of RSV are available for China. This study aimed to provide the basis for the development of RSV prevention strategies by analyzing the burden of RSV among inpatients with lower respiratory tract infection under 5 years of age.</div></div><div><h3>Methods</h3><div>We conducted a retrospective hospital-based study from June 2009 to May 2019 in Chongqing. Inpatients with LRTI were tested for eight viruses. We analyzed the RSV disease burden, MRU, and direct hospitalization costs by using non-parametric Mann‒Whitney <em>U</em> test, Chi-squared test or Fisher's exact test and logistic regression.</div></div><div><h3>Results</h3><div>A total of 6991 children under 5 years of age with LRTI were included in this study. The overall RSV-positive rate was 34.5% (2410/6991). Prior to admission, 81.9% (1973/2410) of these RSV-positive cases were otherwise healthy. Compared with children aged 24–59 months, the odds ratio (OR) and 95% confidence interval (CI) for RSV infection were 2.509 (2.139–2.945), 1.882 (1.549–2.222), and 1.479 (1.240–1.765) for those aged 1–5 months, 6–11 months, and 12–23 months, respectively. The proportions of patients treated with invasive ventilation and continuous positive airway pressure (CPAP) were significantly higher among RSV-positive cases (1.1% [27/2410] and 3.9% [93/2410]) than RSV-negative cases (0.9% [43/4581] and 2.7% [124/4581]) (<em>P</em> = 0.023). Compared with RSV-negative cases, RSV-positive cases had significantly longer hospital length of stay (6 [5, 8] days <em>vs.</em> 6 [5, 8] days, <em>P</em> < 0.001) and higher hospitalization costs (963.0 [757.9, 1298.5] USD <em>vs.</em> 935.6 [719.7, 1296.3] USD, <em>P</em> = 0.022).</div></div><div><h3>Conclusions</h3><div>Most RSV infections occurred during early childhood and among individuals in the otherwise healthy group. Younger age was associated with a higher RSV-positive rate. Effective prevention measures are needed in the earliest stages to reduce the RSV burden.</div></div>","PeriodicalId":72583,"journal":{"name":"Chinese medical journal pulmonary and critical care medicine","volume":"2 3","pages":"Pages 182-187"},"PeriodicalIF":0.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142324181","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-01DOI: 10.1016/j.pccm.2024.05.001
Zhuxing Chen , Peng Liang , Haoxiang Xu , Shengli Yang , Jilong Liu , Shifu Chen , Ran Zhong , Akira Sugimoto , Wenhua Liang , Jianxing He , Tomoya Kawaguchi
{"title":"Screening for viruses in lung adenocarcinoma in China","authors":"Zhuxing Chen , Peng Liang , Haoxiang Xu , Shengli Yang , Jilong Liu , Shifu Chen , Ran Zhong , Akira Sugimoto , Wenhua Liang , Jianxing He , Tomoya Kawaguchi","doi":"10.1016/j.pccm.2024.05.001","DOIUrl":"10.1016/j.pccm.2024.05.001","url":null,"abstract":"","PeriodicalId":72583,"journal":{"name":"Chinese medical journal pulmonary and critical care medicine","volume":"2 3","pages":"Pages 197-199"},"PeriodicalIF":0.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142324076","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-06-01DOI: 10.1016/j.pccm.2024.04.002
Yunchao Su , Rudolf Lucas , David J.R. Fulton , Alexander D. Verin
Endothelial cells (ECs) form a semi-permeable barrier between the interior space of blood vessels and the underlying tissues. Pulmonary endothelial barrier integrity is maintained through coordinated cellular processes involving receptors, signaling molecules, junctional complexes, and protein-regulated cytoskeletal reorganization. In acute lung injury (ALI) or its more severe form acute respiratory distress syndrome (ARDS), the loss of endothelial barrier integrity secondary to endothelial dysfunction caused by severe pulmonary inflammation and/or infection leads to pulmonary edema and hypoxemia. Pro-inflammatory agonists such as histamine, thrombin, bradykinin, interleukin 1β, tumor necrosis factor α, vascular endothelial growth factor, angiopoietin-2, and platelet-activating factor, as well as bacterial toxins and reactive oxygen species, cause dynamic changes in cytoskeletal structure, adherens junction disorganization, and detachment of vascular endothelial cadherin (VE-cadherin) from the actin cytoskeleton, leading to an increase in endothelial permeability. Endothelial interactions with leukocytes, platelets, and coagulation enhance the inflammatory response. Moreover, inflammatory infiltration and the associated generation of pro-inflammatory cytokines during infection cause EC death, resulting in further compromise of the structural integrity of lung endothelial barrier. Despite the use of potent antibiotics and aggressive intensive care support, the mortality of ALI is still high, because the mechanisms of pulmonary EC barrier disruption are not fully understood. In this review, we summarized recent advances in the studies of endothelial cytoskeletal reorganization, inter-endothelial junctions, endothelial inflammation, EC death, and endothelial repair in ALI and ARDS, intending to shed some light on the potential diagnostic and therapeutic targets in the clinical management of the disease.
内皮细胞（EC）在血管内部空间和下层组织之间形成了一道半透性屏障。肺内皮屏障的完整性是通过涉及受体、信号分子、连接复合体和蛋白质调控的细胞骨架重组的协调细胞过程来维持的。在急性肺损伤（ALI）或更严重的急性呼吸窘迫综合征（ARDS）中，由于严重的肺部炎症和/或感染导致内皮功能障碍，继发内皮屏障完整性丧失，从而导致肺水肿和低氧血症。组胺、凝血酶、缓激肽、白细胞介素 1β、肿瘤坏死因子 α、血管内皮生长因子、血管生成素-2 和血小板活化因子等促炎激动剂，以及细菌毒素和活性氧、引起细胞骨架结构的动态变化、粘连接头的紊乱和血管内皮粘连蛋白（VE-cadherin）与肌动蛋白细胞骨架的分离，从而导致内皮通透性增加。内皮与白细胞、血小板和凝血的相互作用增强了炎症反应。此外，感染期间的炎症浸润和相关的促炎症细胞因子的产生会导致内皮细胞死亡，从而进一步损害肺内皮屏障的结构完整性。尽管使用了强效抗生素和积极的重症监护支持，ALI 的死亡率仍然很高，因为肺内皮屏障破坏的机制尚未完全清楚。在这篇综述中，我们总结了 ALI 和 ARDS 中内皮细胞骨架重组、内皮间连接、内皮炎症、内皮细胞死亡和内皮修复的最新研究进展，旨在为临床治疗该疾病的潜在诊断和治疗靶点提供一些启示。
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