Canadian respiratory journal最新文献

Objective: At present, there is a lack of studies on depression and the likelihood for mortality among those suffering from chronic obstructive pulmonary disease (COPD). This research explores the connection between depression and the risks of overall mortality as well as cardiovascular mortality in individuals with COPD. Methods: A total of 1336 COPD patients from seven cycles of the National Health and Nutrition Examination Survey (NHANES) conducted between 2005 and 2018 were selected. We created a multivariate Cox proportional hazards model and performed a subgroup analysis to investigate the connection between depression and both overall and cardiovascular mortality. Additionally, we used restricted cubic spline (RCS) curves to examine the relationship between depression and both overall and cardiovascular mortality to better reveal the association between the two. The Kaplan-Meier technique was employed to determine the likelihood of survival. Results: Over the course of a mean follow-up period of 91 months, 1336 COPD patients were studied, of which 340 patients experienced overall mortality, and 82 had cardiovascular-related deaths. Using RCSs, we found that depression was positively correlated with both all-cause and cardiovascular mortality in COPD patients. In the multivariable-adjusted model, individuals suffering from moderate to severe depression had a greater likelihood of overall and cardiovascular mortality compared to those without depression. The results were consistent in subgroup analyses based on age, gender, body mass index (BMI), and poverty income ratio (PIR), and there was no significant interaction between these traits and depression (p for interaction > 0.05). Conclusion: In COPD patients, depression is associated with higher risks of both cardiovascular and overall mortality. However, further validation of this finding is needed in large-scale prospective studies with sufficient follow-up time.

Pulmonary fibrosis (PF) is a terminal-stage lung change in interstitial lung disease. It is characterized by proliferation of fibroblasts and deposition of a large amount of extracellular matrix, accompanied by inflammatory damage and structural destruction, caused by various reasons. The prognosis of PF is poor, and the average survival time after diagnosis is 2.5-3.5 years. The pathogenesis of PF is not yet fully understood. Its main mechanisms are diverse and include damage to alveolar epithelial cells, aggregation and activation of inflammatory cells and chemokines, proliferation of fibroblasts, transformation of myofibroblasts, production and deposition of large amounts of collagen, autophagy, epithelial-mesenchymal transition (EMT), mitochondrial quality-control disorders, microRNA, and circular RNA. The diagnosis of PF is mainly based on the comprehensive evaluation of clinical manifestations, imaging characteristics, and histopathological examination. Medical and family history to determine all potential causes of PF. For PF of unknown etiology, one can refer to the Official Clinical Practice Guideline of idiopathic pulmonary fibrosis (IPF) for definitive diagnosis. In terms of treatment, modern medications such as pirfenidone and nintedanib can inhibit the progression of PF to some extent and improve lung function. However, there is no drug that can significantly improve PF, except for lung transplantation. In addition, many patients are forced to stop taking medication due to adverse reactions in clinical practice. Therefore, to better control the progression of disease, some new drugs have been developed based on the pathogenesis of PF. However, there is still controversy over their efficacy and widespread clinical application in PF, and the evidence is limited. The results of in vitro and in vivo experiments, as well as randomized clinical trials, indicate that traditional Chinese medicine (TCM) can improve PF by intervening in multiple pathways and targets. This study combines the pathogenesis and diagnosis of PF, focusing on the intervention mechanism and targets of TCM in the treatment of PF, so as to provide more options for clinical treatment and provide scientific basis for a new approach to better management of PF.

Venous thromboembolism (VTE) is widespread and poses significant risks of illness and death, making it a vital public health issue. Obstructive sleep apnea (OSA), which is the most prevalent sleep disorder, is connected to an increased possibility of cardiovascular diseases and VTE. The length of VTE treatment hinges mainly on the frequency of its recurrence in patients. Our data about VTE and its recurrence in OSA patients are limited. In this review, we aim to investigate the risk of VTE recurrence in OSA patients and evaluate the role of continuous positive airway pressure (CPAP) therapy in mitigating this risk. A literature search gathered information about VTE pathogenesis and its potential recurrence mechanism in OSA. The recurrent episodes of partial or complete obstruction of the upper airway in OSA lead to intermittent lack of oxygen. Hypoxemia acts as a central cornerstone of VTE incidence in OSA patients, leads to activating all the vertices of Virchow's triad, and creates the appropriate condition for the developmental and even recurrence of VTE. Intermittent hypoxia causes an increase in the inflammatory state and coagulation activity, leading to oxidative stress and endothelial dysfunction. Furthermore, it results in heightened viscosity and venous stasis. The results of previous studies on VTE recurrence in OSA patients are conflicting. Even though the use of CPAP leads to diminished proinflammatory cytokines and oxidative stress indicators, there is currently insufficient clinical evidence to support that this therapy can prevent recurrent VTE in patients with OSA. Further investigation is necessary to gain a better comprehension of the probability and frequency of relapse of VTE in OSA patients, as the present research has generated inconclusive outcomes.

Bronchiolitis obliterans is a rare form of chronic obstructive lung disease, with postinfectious bronchiolitis obliterans being particularly prevalent in pediatric populations. The pathogenic investigations of pediatric postinfectious bronchiolitis obliterans predominantly center on adenovirus and Mycoplasma pneumoniae. Following the illness, children's lung function is impacted to varying extents; however, a definitive diagnosis relies on lung biopsy, which is not conducive to early detection and timely intervention. Consequently, there remains a need for novel research methodologies. This article synthesizes the 2023 China Reformulation of the Expert Consensus on the Diagnosis and Treatment of Bronchiolitis Obliterans in Children along with recent studies, providing a comprehensive overview of early diagnosis, treatment modalities, and preventive strategies for postinfectious bronchiolitis obliterans in children. Additionally, it outlines future research directions aimed at enhancing pediatricians' understanding of this complex disease.

Introduction: The Canadian Cystic Fibrosis Registry (CCFR) was developed in the 1970s and has longitudinal demographic and clinical data on persons living with cystic fibrosis (CF) attending accredited clinics in Canada. We aimed to validate the data collection and identify potential limitations of the CCFR. Methods: Of 40 accredited CF clinics in Canada invited and based on an a priori sample size calculation, eight clinics were included. 15% of each CF clinic's population in 2019 were randomly selected. Data variables were selected based on their importance to care, epidemiologic trends, and data related to demography, clinic visits, and hospitalizations. The accuracy of the registry data was compared to the medical records as the gold standard. Each data element was categorized as correct, incorrect, or not able to be validated. The accuracy rate was calculated as the percent correct out of all records validated. Results: A total of 4382 individuals had data entered into the CCFR in 2019. The validation cohort consisted of 208 individuals from 8 clinics, which were representative across location, size of clinic (small/medium/large), and type of clinic (adult, pediatric, and combined). The 208 individuals were 52% male and 95% White, and with a median age of 26.3 years (IQR: 15.2-36.6). Approximately 95% of CCFR data on clinical measurements, infections, treatments, and hospitalizations validated were accurate as compared to the medical record. For demography, sex and date of birth had 100% accuracy. Conclusion: Our validation of the CCFR demonstrated high accuracy for clinical and demographic variables used in clinical research.

Systemic sclerosis (SSc) is predominantly characterized by an array of cutaneous manifestations including Raynaud's phenomenon, calcinosis, telangiectasias, and skin fibrosis contributing toward substantial morbidity and diminished quality of life. The monumental impact of the disease regarding mortality is due to its pulmonary involvement known as SSc-associated interstitial lung disease (SSc-ILD). Currently, treatment is chiefly directed toward impeding disease progression with the mainstay treatment approaches involving the utilization of cyclophosphamide, mycophenolate mofetil, rituximab, and tocilizumab. Recently, a tyrosine kinase inhibitor, nintedanib, has been approved for the treatment of SSc-ILD and thus became the first medication to be fully licensed for SSc-ILD. A systematic review based on the Preferred Reporting Items of Systematic Review with Meta-analysis (PRISMA) was conducted after successful registration in PROSPERO to evaluate the efficacy and safety of nintedanib in SSc-ILD. We searched PubMed, Scopus, and CENTRAL up to the first of September 2023 utilizing the following keywords: ((Diffuse Parenchymal Lung Disease) OR (Diffuse Parenchymal Lung Diseases) OR (Interstitial Lung Disease) OR (Interstitial Lung Diseases) OR (Interstitial Pneumonia) OR (Interstitial Pneumonitis) OR (Pulmonary Fibrosis)) AND ((Systemic Scleroderma) OR (Systemic Scleroderma)) AND ((BIBF 1120) OR (BIBF-1120) OR (BIBF1120) OR (Nintedanib esylate) OR (Ofev) OR (Vargatef)). The clinical safety profile of nintedanib was deemed more favorable than other therapeutic regimens currently utilized, in addition to adequate clinical efficacy toward SSc-ILD.

Introduction: Kallistatin is an enzyme with antioxidative and anti-inflammatory properties and has been shown to provide protection against pneumosepsis, acute respiratory distress syndrome (ARDS), and lung fibrosis. This study revealed the use of kallistatin in the clinical management of COPD. Materials and Methods: Forty-eight COPD patients were evaluated during both exacerbation and stable periods. A control group of 30 healthy individuals was also included. In addition to kallistatin, serum levels of TAS, TOS, OSI, VEGF, and TNF-α were measured. Data were statistically analyzed for the exacerbation and stable periods of COPD patients, as well as the control group. Correlation analysis of serum parameters was conducted, and regression analysis was performed on those with significant results. Results: Serum kallistatin levels were significantly lower in COPD patients compared to the normal population (p < 0.001). Additionally, kallistatin levels were lower during COPD exacerbations compared to the stable period (p < 0.001). Kallistatin levels measured during exacerbations were positively correlated with OSI and VEGF (r = 0.333, p=0.021; r = 0.301, p=0.037, respectively). The relationship between kallistatin and OSI was strongly supported by regression analysis (p=0.049, CI 16.889). Conclusion: Kallistatin is a promising biomarker for distinguishing COPD patients from the normal population and for identifying disease exacerbations.

[This corrects the article DOI: 10.1155/2021/4835536.].

Chronic obstructive pulmonary disease (COPD) is a lung condition characterized by persistent airway obstruction and is associated with various phenotypes and endotypes. While eosinophilic inflammation is typically seen in asthma, it also occurs in COPD, with known increases in eosinophil counts during exacerbations. However, the impact of cumulative tobacco exposure on eosinophil counts is not well understood. This study aims to investigate this relationship. Data for this prospective study were collected from three centers, involving patients diagnosed with COPD. Patients' demographic data and eosinophil levels were documented. They were categorized according to GOLD Stages A, B, and E, and each group was analyzed relative to the amount of cigarette smoking. The study enrolled 227 COPD patients, predominantly male (92.5%) with an average age of 64.6 years. Of the study population, 39.8% (n: 90) were current smokers, and 86.9% had a smoking history of more than 20 packs/year. The average smoking history of our patients was 52.38 ± 30.69 (mean ± SD) pack/year. Our patients had an average smoking history of 39.49 ± 12.56 years. No statistically significant results were found between the amount of cigarettes smoked and eosinophil counts. However, in the correlation between smoking history and eosinophil counts, higher eosinophil counts were found in those who had former smoking compared to current smokers or never smokers. While the number of pack-years and the duration of smoking increased from Stage A to Stage E, daily cigarette consumption remained constant, and eosinophil counts did not show a significant correlation with the quantity of tobacco. Eosinophil counts in COPD patients did not vary significantly with either the amount of tobacco exposure or the severity of COPD as categorized by GOLD stages. These findings suggest that factors other than tobacco exposure may influence eosinophil levels in COPD patients.

Objectives: Excess adipose tissue induces low-intensity inflammation, which is an important pathogenetic factor adversely affecting the course of bronchial asthma (BA) in overweight/obese patients. The key effector cells of this inflammation are monocytes and macrophages. However, there are currently no studies characterising the effect of body mass index (BMI) on peripheral blood monocyte levels in children and adolescents with BA and their relationship with spirometric parameters reflecting bronchial patency. The aim of this study was to investigate the effect of BMI on peripheral blood monocyte and eosinophil levels and their relationship with spirometric parameters in children and adolescents with asthma. Methods: A single-centre, observational cross-sectional study was conducted. A total of 212 patients with asthma aged 7-17 years were studied. Anthropometric and spirometric parameters and the cellular composition of peripheral blood were evaluated. The children were divided into two groups: Group 1: with normal body weight (BW) and Group 2: with overweight/obesity. Results: In overweight/obesity patients, the number of peripheral blood monocytes (0.62 ± 0.19) was significantly higher compared to the group of normal weight patients (0.54 ± 0.15, p < 0.001). In contrast, eosinophil levels were statistically lower in the overweight/obesity group (0.22 [0.12; 0.42]) than in the normal weight patients (0.30 [0.14; 0.56], p = 0.039). A statistically significant negative correlation was found between the absolute number of monocytes and z FEV1/FVC, z MMEF_25-75 in the overweight/obesity group (R = -0.32, p = 0.005, R = -0.30, p = 0.007, respectively) and a statistically significant negative correlation between eosinophil count and z FEV1/FVC, z MMEF25-75 in normal weight patients (R = -0.20, p = 0.021, R = -0.22, p = 0.010, respectively). Conclusions: The results obtained may indicate a modifying effect of overweight/obesity on inflammation endotypes in children and adolescents with BA.