Canadian Respiratory Journal
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Acceptance rate9%
Submission to final decision163 days
Acceptance to publication16 days
CiteScore3.200
Journal Citation Indicator0.460
Impact Factor2.2

Changes of Serum Adiponectin Level in Patients with Obstructive Sleep Apnea Hypopnea Syndrome and Its Relationship with Sleep Monitoring Indexes

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 Journal profile

Canadian Respiratory Journal provides a multidisciplinary forum for research in all areas of respiratory medicine. The journal publishes research related to asthma, allergy, COPD, non-invasive ventilation, therapeutic intervention etc.

 Editor spotlight

Chief Editor, Dr Alice M Turner, is based at the University of Birmingham, UK. Her main research interests are the clinical aspects of alpha 1 antitrypsin deficiency and chronic obstructive pulmonary disease.

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Research Article

Use of the Serum Level of Cholinesterase as a Prognostic Marker of Nonfatal Clinical Outcomes in Patients Hospitalized with Acute Exacerbations of Chronic Obstructive Pulmonary Disease

Introduction. Acute exacerbation of chronic obstructive pulmonary disease (AECOPD) contributes to a poor prognosis. Reliable biomarkers to predict adverse outcomes during hospitalization are important. Aim. To investigate the relationship between the serum cholinesterase (ChE) level and adverse clinical outcomes, including hypoxemia severity, hypercapnia, duration of hospital stay (DoHS), and noninvasive ventilation (NIV) requirement, in patients with AECOPD. Methods. Patients hospitalized with AECOPD in the Wuhu Hospital of Traditional Chinese Medicine between January 2017 and December 2021 were included. Results. A total of 429 patients were enrolled. The serum ChE level was significantly lower in patients with hypercapnia, who required NIV during hospitalization and who had a DoHS of >10 days, with an oxygenation index < 300. The ChE level was correlated negatively with the C-reactive protein level and neutrophil-to-lymphocyte ratio and correlated positively with the serum albumin level. Multivariate logistic regression analysis indicated that a serum ChE level of ≤4116 U/L (OR = 2.857, 95% CI = 1.46–5.58, ) was associated significantly with NIV requirement. Conclusions. The serum ChE level was correlated significantly with complicating severe hypoxemia, hypercapnia, prolonged DoHS, and the need for NIV in patients hospitalized with AECOPD. The serum ChE level is a clinically important risk-stratification biomarker in patients hospitalized with AECOPD.

Research Article

Efficacy of Definitive Radiotherapy for Patients with Clinical Stage IIIB or IIIC Lung Adenocarcinoma and Epidermal Growth Factor Receptor (EGFR) Mutations Treated Using First- or Second-Generation EGFR Tyrosine Kinase Inhibitors

Background. The effectiveness of definitive radiotherapy (RT) for patients with clinical stage IIIB or IIIC lung adenocarcinoma and epidermal growth factor receptor (EGFR) mutations who received first- or second-generation EGFR tyrosine kinase inhibitors (TKIs) is unclear. Methods. Taiwan Cancer Registry data were used in this retrospective cohort study to identify adult patients diagnosed with EGFR-mutated stage IIIB or IIIC lung adenocarcinoma between 2011 and 2020. Patients treated with first- or second-generation EGFR TKIs were classified into RT and non-RT groups. Propensity score (PS) weighting was applied to balance covariates between groups. The primary outcome was overall survival (OS), and the incidence of lung cancer mortality (ILCM) was considered as a supplementary outcome. Additional supplementary analyses were conducted to assess the robustness of the findings. Results. Among 270 eligible patients, 41 received RT and 229 did not. After a median follow-up of 46 months, PS-weighted analysis showed the PS-weighted hazard ratio of death for the RT group compared to the non-RT group was 0.94 (95% CI: 0.61–1.45, ). ILCM rates did not differ significantly between the two groups. Supplementary analyses yielded consistent results. Conclusion. The addition of definitive RT to first- or second-generation EGFR TKI treatment does not significantly improve OS of patients with EGFR-mutated stage IIIB or IIIC lung adenocarcinoma. NCT03521154NCT05167851.

Research Article

Anlotinib Inhibits Cisplatin Resistance in Non-Small-Cell Lung Cancer Cells by Inhibiting MCL-1 Expression via MET/STAT3/Akt Pathway

Background. Anlotinib is an effective targeted therapy for advanced non-small-cell lung cancer (NSCLC) and has been found to mediate chemoresistance in many cancers. However, the underlying molecular mechanism of anlotinib mediates cisplatin (DDP) resistance in NSCLC remains unclear. Methods. Cell viability was assessed by the cell counting kit 8 assay. Cell proliferation, migration, and invasion were determined using the colony formation assay and transwell assay. The mRNA expression levels of mesenchymal-epithelial transition factor (MET) and myeloid cell leukemia-1 (MCL-1) were measured by quantitative real-time PCR. Protein expression levels of MET, MCL-1, and STAT3/Akt pathway-related markers were examined using western blot analysis. Results. Our data showed that anlotinib inhibited the DDP resistance of NSCLC cells by regulating cell proliferation and metastasis. Moreover, MET and MCL-1 expression could be decreased by anlotinib treatment. Silencing of MET suppressed the activity of the STAT3/Akt pathway and MCL-1 expression. Furthermore, MET overexpression reversed the inhibitory effect of anlotinib on the DDP resistance of NSCLC cells, and this effect could be eliminated by MCL-1 knockdown or ACT001 (an inhibitor for STAT3/Akt pathway). Conclusion. Our results confirmed that anlotinib inhibited DDP resistance in NSCLC cells, which might decrease MCL-1 expression via mediating the MET/STAT3/Akt pathway.

Research Article

Clustered Cystic Changes in Long-Term Follow-Up Thin-Section Computed Tomographic Findings in Fibrotic Nonspecific Interstitial Pneumonia

Objectives. The purpose of this study was to retrospectively assess cystic changes in findings on follow-up CT scans of patients with fibrotic nonspecific interstitial pneumonia (NSIP). Methods. The initial and last high-resolution CT scans of 58 patients with pathologically proven fibrotic NSIP were evaluated retrospectively. The median follow-up periods were 48 months (range, 12–183 months). The pattern, extent, and distribution of abnormal CT findings were compared with findings in the same region on previous and subsequent CT scans with a focus on cystic lesions. Results. Cystic lesions in a cluster were shown in 16 patients (28%) with fibrotic NSIP on the last CT scans. Focal clustered cysts were found in 5 cases and diffuse clustered cysts were seen in 11 cases. Focal clustered cysts mimicked honeycombing seen in usual interstitial pneumonia (UIP). Diffuse cysts were uniform in size in 7 of the 11 cases. Traction bronchiectasis in a cluster was seen in 3 of the 7 cases. The clustered cystic changes on CT during the course of NSIP mainly consisted of traction bronchiectasis and bronchiolectasis. Conclusions. Long-standing NSIP did not form honeycombing. The clustered cysts in patients with fibrotic NSIP were mainly remodeling of bronchiectasis.

Review Article

Hypersensitivity Pneumonitis: Challenges of a Complex Disease

Hypersensitivity pneumonitis (HP) is a complex interstitial lung disease caused by chronic inhalation of a wide variety of antigens in susceptible and sensitized individuals, commonly associated with an occupational exposure. An impressive number of inciting antigens causing hypersensitivity pneumonitis have been found to cover a wide range of occupations. As working practices have changed over time, especially in industrialized countries, new names for occupational HP have emerged. This review emphasizes the main diagnostic issues arising from the high variability of clinical presentation and the broad spectrum of causal antigens. Furthermore, it provides an overview of current methods to unveil possible causes of hypersensitivity pneumonitis, highlights HP’s current diagnostic and treatment challenges and the remaining areas of uncertainty, and presents prevention strategies.

Research Article

A Novel Scale to Assess Humidification during Noninvasive Ventilation: A Prospective Observational Study

Objective. To develop a novel scale to assess humidification during noninvasive ventilation (NIV). Methods. This study was performed in an ICU of a teaching hospital. Three ICU practitioners with more than 10 years of clinical experience developed an oral humidification scale with a range of 1–4 points. Each studied the current literature on humidification and examined 50 images of mouths of NIV patients with different levels of humidification. Then, through discussion, a consensus scale was developed. Next, 10 practitioners and 33 NIV patients were recruited to validate the scale. Finally, the patients rated the dryness of their mouths using the 1–4 visual scale just after the practitioners’ assessment. Talking and discussion were forbidden during the assessment, and the scorers were blinded to each other. Results. We performed 36 assessments in 33 NIV patients. Three patients were assessed twice each more than 2 days apart. The interitem correlation coefficients between the 10 practitioners ranged from 0.748 to 0.917. Fleiss’s kappa statistic was 0.516, indicating moderate agreement among practitioners. Of the 33 patients, 5 (15%) were unable to make an assessment using the 1–4 visual scale. Among the remainder, 55.7% provided scores that matched those given by the practitioners; 13.7% of scores were 1 point higher than that rated by the practitioners, and 20.7% were 1 point lower. Only 10% were beyond a 1-point difference. The kappa coefficient was 0.483 between patients and practitioners. Conclusions. The oral humidification scale showed moderate agreement between practitioners. It was also highly accurate in reflecting the level of humidification assessed by patients.

Canadian Respiratory Journal
 Journal metrics
See full report
Acceptance rate9%
Submission to final decision163 days
Acceptance to publication16 days
CiteScore3.200
Journal Citation Indicator0.460
Impact Factor2.2
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