Transcutaneous PCO 2 ‐based dead space ventilation at submaximal exercise accurately discriminates healthy controls from patients with chronic obstructive pulmonary disease

2021 ◽  
Vol 41 (3) ◽  
pp. 253-261
Author(s):  
Thibault Leprat ◽  
Fabrice Ivanes ◽  
Anne Bernard ◽  
Sylvain Marchand‐Adam ◽  
Laurent Plantier

Antioxidants ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 1891
Author(s):  
Jun Watanabe ◽  
Kazuhiko Kotani ◽  
Alejandro Gugliucci

Oxidative stress is a driving factor in the pathophysiology of chronic obstructive pulmonary disease (COPD). While paraoxonase 1 (PON1) is an antioxidant enzyme and a potential biomarker of this disease, data regarding the status of PON-1 in COPD are inconclusive. In this regard, to shed light on this issue, we performed a meta-analysis of data on PON1 activity in COPD. Electronic databases (MEDLINE, Embase and CENTRAL) were searched for available studies on PON1 activity in patients with stable COPD published before October 2021. A meta-analysis was performed using random-effects models. Twelve studies (12 studies on paraoxonase and three on arylesterase) were identified. Patients with COPD had lower levels of paraoxonase activity (standard mean difference [SMD] −0.77, 95% confidence interval [CI] −1.35 to −0.18) and arylesterase activity (SMD −1.15, 95% CI −1.95 to −0.36) in comparison to healthy controls. In subgroup analyses, paraoxonase activity was lower in patients of studies as consisted of mainly non-severe COPD (SMD −1.42, 95% CI −2.04 to −0.79) and, by contrast, slightly higher in patients of studies including severe COPD (SMD 0.33, 95% CI 0.02 to 0.64) in comparison to healthy controls. Arylesterase activity showed a similar trend. Overall, PON1 activity was lower in patients with COPD, suggesting that PON1-related antioxidant defense is impaired in COPD. Future studies are warranted.



Author(s):  
Steven P Cass ◽  
Anna Dvorkin-Gheva ◽  
Yuqiong Yang ◽  
Joshua JC McGrath ◽  
Danya Thayaparan ◽  
...  

Chronic obstructive pulmonary disease (COPD) is a complex and progressive respiratory disease. Autoimmune processes have been hypothesised to contribute to disease progression; however, the presence of autoantibodies in the serum has been variable. Given that COPD is a lung disease, we sought to investigate whether autoantibodies in sputum supernatant would better define pulmonary autoimmune processes. Matched sputum and serum samples were obtained from the Airways Disease Endotyping for Personalised Therapeutics (ADEPT) study and at the Guangzhou Institute of Respiratory Health (GIRH). Samples were collected from patients with varying severity of COPD, asymptomatic smokers and healthy control subjects. IgG and IgM autoantibodies were detected in sputum and serum of all subjects in both cohorts using a broad-spectrum autoantigen array. No differences were observed in sputum autoantibodies between COPD and asymptomatic smokers in either cohort. In contrast, 16% of detectable sputum IgG autoantibodies were decreased in COPD subjects compared to healthy controls in the ADEPT cohort. Compared to asymptomatic smokers, approximately 13% of detectable serum IgG and 40% of detectable serum IgM autoantibodies were differentially expressed in GIRH COPD subjects. Of the differentially expressed specificities, anti-nuclear autoantibodies were predominately decreased. A weak correlation between increased serum IgM anti-tissue autoantibodies and a measure of airspace enlargement was observed. The differential expression of specificities varied between the cohorts. In closing, using a comprehensive autoantibody array, we demonstrate that autoantibodies are present in COPD subjects, asymptomatic smokers and healthy controls. Cohorts displayed high levels of heterogeneity, precluding the utilisation of autoantibodies for diagnostic purposes.



2020 ◽  
Author(s):  
Rizwan Qaisar ◽  
Mughal Qayyum ◽  
Tahir Muhammad

Abstract Background The potential contribution of chronic dysregulation of sarcoplasmic reticulum (SR) protein homeostasis (a condition called SR stress) to skeletal muscle loss is poorly understood. We investigated the degree of activation of SR stress in locomotor muscles of patients with chronic obstructive pulmonary disease (COPD), a respiratory disease with systemic manifestations. Methods We analyzed the markers of SR stress and associated pathologies in vastus lateralis muscles of 60-65 years old male healthy controls and patients with mild (COPD stages 1 & 2) and advanced (COPD stages 3 & 4) COPD (N = 6-8 / group). Results Skeletal muscle proteins expressions of GRP94, BiP, CHOP and ATF were significantly elevated in advanced COPD (≈53%, ≈3.6 fold, ≈3.5 fold and ≈3.2 fold, respectively) compared with healthy controls. The expression of downstream markers of SR stress including apoptosis, inflammation and autophagy was increased, while the maximal activity of SR Ca2+ ATPase (SERCA) enzyme was significantly reduced in advanced COPD (≈41%) than healthy controls. Single muscle fiber diameter and cytoplasmic domain per myonucleus were significantly smaller (≈14% and 13%, respectively) in patients with advanced COPD than healthy controls. These changes in SR dysfunction were accompanied by substantially elevated levels of global oxidative stress including lipid peroxidation and mitochondrial ROS production. Conclusion Taken together, our data suggests that the muscle weakness in advanced COPD is in part driven by elevated SR stress and its pathological consequences. The data provided can lead to potential therapeutic interventions of SR dysfunction for muscle detriment in COPD.



Author(s):  
Anna Lena Jung ◽  
Malene Møller Jørgensen ◽  
Rikke Bæk ◽  
Kathrin Griss ◽  
Maria Han ◽  
...  

Abstract Background Community-acquired pneumonia (CAP) and acute exacerbation of chronic obstructive pulmonary disease (AECOPD) represent a major burden of disease and death and their differential diagnosis is critical. A potential source of relevant accessible biomarkers are blood-borne small extracellular vesicles (sEVs). Methods We performed an extracellular vesicle array to find proteins on plasma sEVs that are differentially expressed and possibly allow the differential diagnosis between CAP and AECOPD. Plasma samples were analyzed from 21 healthy controls, 24 patients with CAP, and 10 with AECOPD . The array contained 40 antibodies to capture sEVs, which were then visualized with a cocktail of biotin-conjugated CD9, CD63, and CD81 antibodies. Results We detected significant differences in the protein decoration of sEVs between healthy controls and patients with CAP or AECOPD. We found CD45 and CD28 to be the best discrimination markers between CAP and AECOPD in receiver operating characteristic analyses, with an area under the curve >0.92. Additional ensemble feature selection revealed the possibility to distinguish between CAP and AECOPD even if the patient with CAP had COPD, with a panel of CD45, CD28, CTLA4 (cytotoxic T-lymphocyte-associated protein 4), tumor necrosis factor–R-II, and CD16. Conclusion The discrimination of sEV-associated proteins is a minimally invasive method with potential to discriminate between CAP and AECOPD.





2011 ◽  
Vol 36 (6) ◽  
pp. 821-830 ◽  
Author(s):  
Megan F.B. Sherman ◽  
Jeremy D. Road ◽  
Donald C. McKenzie ◽  
A. William Sheel

The objective of this study was to measure the magnitude of the muscle metaboreflex in people with chronic obstructive pulmonary disease (COPD) compared with healthy controls and to assess the relationships between disease severity, exercise capacity, and the magnitude of the muscle metaboreflex. Nine people with mild-to-severe COPD and 11 age- and gender-matched healthy controls performed isometric handgrip exercise (IHG), followed by postexercise circulatory occlusion (PECO) while hemodynamic changes were measured. Continuous measures of heart rate, arterial pressure, leg blood flow, leg vascular resistance, and total peripheral resistance were obtained. Participants then performed a cycle test to exhaustion. Heart rate, blood pressure, and blood flow responses during IHG and PECO were similar between the COPD group and healthy controls (p > 0.05). There was no association between disease severity or exercise capacity and the magnitude of the muscle metaboreflex. We observed a preserved muscle metaboreflex in mild-to-severe COPD, suggesting the metaboreflex is not a contributing factor to the development of exercise intolerance in this population.



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