Pub Date : 2024-05-16DOI: 10.1183/23120541.00104-2024
Bertrand Renaud, R. Chocron, Guillaume Reverdito, Anne Blanchard, Thong Hua-Huy, J. Diehl, M. Livrozet, Marielle Subileau, Cédric Lemogne, Salma El-Batti, Edouard Auclin, A. Jannot, B. Rance, Elie Mousseaux, David Smadja, D. Lebeaux, J. Hulot, O. Sanchez, Sven Günther
Limited data are available on long-term respiratory disabilities in patients following acute COVID-19.This prospective, monocentric, observational cohort study included patients admitted to our hospital with acute COVID-19 between March 3 and April 24, 2020. Clinical, functional, and radiological data were collected up to 28 months after hospital discharge.Among 715 patients hospitalized for COVID-19, 493 (69.0%) were discharged alive. We could access complete medical records for 268/493 patients (54.4%); 138/268 (51.5%) exhibited persistent respiratory symptoms and agreed with the data collection and follow-up. Patients were predominantly male (64.5%), with a mean (±sd) age of 58.9±15.3 years. At the last follow-up, the leading symptoms were asthenia (31.5%), dyspnoea (29.8%), and neuropsychological symptoms (17.7%). Lung function improved up to the last visit. Mean diffusing capacity of the lung for carbon monoxide (DLCO) was 77.8% of predicted value, total lung capacity (TLC) 83.5%, and O2desaturation during exercise (O2desaturation) −2.3%. While DLCO improved over the entire period, TLC improved in the early phase and O2desaturation in the late phase. Except for those with lung comorbidities, only one patient presented with minor functional and chest radiological alterations at 28-months.Patients with acute COVID-19 discharged alive showed improved clinical symptoms, lung function parameters and radiological signs up to 28 months post infection. Persistent symptoms consisted mainly of asthenia and dyspnoea, with lung function returning to normal. One patient without prior respiratory issues exhibited moderate pulmonary fibrosis.
{"title":"Persistent disabilities 28 months after COVID-19 hospitalization, a prospective cohort study","authors":"Bertrand Renaud, R. Chocron, Guillaume Reverdito, Anne Blanchard, Thong Hua-Huy, J. Diehl, M. Livrozet, Marielle Subileau, Cédric Lemogne, Salma El-Batti, Edouard Auclin, A. Jannot, B. Rance, Elie Mousseaux, David Smadja, D. Lebeaux, J. Hulot, O. Sanchez, Sven Günther","doi":"10.1183/23120541.00104-2024","DOIUrl":"https://doi.org/10.1183/23120541.00104-2024","url":null,"abstract":"Limited data are available on long-term respiratory disabilities in patients following acute COVID-19.This prospective, monocentric, observational cohort study included patients admitted to our hospital with acute COVID-19 between March 3 and April 24, 2020. Clinical, functional, and radiological data were collected up to 28 months after hospital discharge.Among 715 patients hospitalized for COVID-19, 493 (69.0%) were discharged alive. We could access complete medical records for 268/493 patients (54.4%); 138/268 (51.5%) exhibited persistent respiratory symptoms and agreed with the data collection and follow-up. Patients were predominantly male (64.5%), with a mean (±sd) age of 58.9±15.3 years. At the last follow-up, the leading symptoms were asthenia (31.5%), dyspnoea (29.8%), and neuropsychological symptoms (17.7%). Lung function improved up to the last visit. Mean diffusing capacity of the lung for carbon monoxide (DLCO) was 77.8% of predicted value, total lung capacity (TLC) 83.5%, and O2desaturation during exercise (O2desaturation) −2.3%. While DLCO improved over the entire period, TLC improved in the early phase and O2desaturation in the late phase. Except for those with lung comorbidities, only one patient presented with minor functional and chest radiological alterations at 28-months.Patients with acute COVID-19 discharged alive showed improved clinical symptoms, lung function parameters and radiological signs up to 28 months post infection. Persistent symptoms consisted mainly of asthenia and dyspnoea, with lung function returning to normal. One patient without prior respiratory issues exhibited moderate pulmonary fibrosis.","PeriodicalId":11739,"journal":{"name":"ERJ Open Research","volume":null,"pages":null},"PeriodicalIF":4.6,"publicationDate":"2024-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140969760","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-05-13eCollection Date: 2024-05-01DOI: 10.1183/23120541.00919-2023
Steven P Cass, Dan V Nicolau, Jonathan R Baker, Christine Mwasuku, Sanjay Ramakrishnan, Mahdi Mahdi, Peter J Barnes, Louise E Donnelly, Rocio T Martinez-Nunez, Richard E K Russell, Mona Bafadhel
Introduction: Understanding the interplay of immune mediators in relation to clinical outcomes during acute infection has the potential to highlight immune networks critical to symptom recovery. The objective of the present study was to elucidate the immune networks critical to early symptom resolution following severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection.
Methods: In a community-based randomised clinical trial comparing inhaled budesonide against usual care in 139 participants with early onset SARS-CoV-2 (the STOIC study; clinicaltrials.gov identifier NCT04416399), significant clinical deterioration (reported need for urgent care, emergency department visit, hospitalisation: the primary outcome), self-reported symptom severity (Influenza Patient-Reported Outcome questionnaire) and immune mediator networks were assessed. Immune mediator networks were determined using pre-defined mathematical modelling of immune mediators, determined by the Meso Scale Discovery U-Plex platform, within the first 7 days of SARS-CoV-2 infection compared to 22 healthy controls.
Results: Interferon- and chemokine-dominant networks were associated with high viral burden. Elevated levels of the mucosal network (chemokine (C-C motif) ligand (CCL)13, CCL17, interleukin (IL)-33, IL-5, IL-4, CCL26, IL-2, IL-12 and granulocyte-macrophage colony-stimulating factor) was associated with a mean 3.7-day quicker recovery time, with no primary outcome events, irrespective of treatment arm. This mucosal network was associated with initial nasal and throat symptoms at day 0.
Conclusion: A nasal immune network is critical to accelerated recovery and improved patient outcomes in community-acquired viral infections. Overall, early prognostication and treatments aimed at inducing epithelial responses may prove clinically beneficial in enhancing early host response to virus.
{"title":"Coordinated nasal mucosa-mediated immunity accelerates recovery from COVID-19.","authors":"Steven P Cass, Dan V Nicolau, Jonathan R Baker, Christine Mwasuku, Sanjay Ramakrishnan, Mahdi Mahdi, Peter J Barnes, Louise E Donnelly, Rocio T Martinez-Nunez, Richard E K Russell, Mona Bafadhel","doi":"10.1183/23120541.00919-2023","DOIUrl":"10.1183/23120541.00919-2023","url":null,"abstract":"<p><strong>Introduction: </strong>Understanding the interplay of immune mediators in relation to clinical outcomes during acute infection has the potential to highlight immune networks critical to symptom recovery. The objective of the present study was to elucidate the immune networks critical to early symptom resolution following severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection.</p><p><strong>Methods: </strong>In a community-based randomised clinical trial comparing inhaled budesonide against usual care in 139 participants with early onset SARS-CoV-2 (the STOIC study; clinicaltrials.gov identifier NCT04416399), significant clinical deterioration (reported need for urgent care, emergency department visit, hospitalisation: the primary outcome), self-reported symptom severity (Influenza Patient-Reported Outcome questionnaire) and immune mediator networks were assessed. Immune mediator networks were determined using pre-defined mathematical modelling of immune mediators, determined by the Meso Scale Discovery U-Plex platform, within the first 7 days of SARS-CoV-2 infection compared to 22 healthy controls.</p><p><strong>Results: </strong>Interferon- and chemokine-dominant networks were associated with high viral burden. Elevated levels of the mucosal network (chemokine (C-C motif) ligand (CCL)13, CCL17, interleukin (IL)-33, IL-5, IL-4, CCL26, IL-2, IL-12 and granulocyte-macrophage colony-stimulating factor) was associated with a mean 3.7-day quicker recovery time, with no primary outcome events, irrespective of treatment arm. This mucosal network was associated with initial nasal and throat symptoms at day 0.</p><p><strong>Conclusion: </strong>A nasal immune network is critical to accelerated recovery and improved patient outcomes in community-acquired viral infections. Overall, early prognostication and treatments aimed at inducing epithelial responses may prove clinically beneficial in enhancing early host response to virus.</p>","PeriodicalId":11739,"journal":{"name":"ERJ Open Research","volume":null,"pages":null},"PeriodicalIF":4.6,"publicationDate":"2024-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11089385/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140921765","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-05-09DOI: 10.1183/23120541.00089-2024
E. Daynes, Molly M Baldwin, M. Annals, N. Gardiner, E. Chaplin, S. Ward, N. J. Greening, Rachael A Evans, Sally J Singh
There is evidence to support COVID-19 rehabilitation programmes improving persistent COVID-19 symptoms; however, there is concern that therapies that include an exercise component may increase fatigue and post-exertional symptom exacerbation (PESE).To determine the effect of a 6 week COVID-19 rehabilitation programme on fatigue and PESE in individuals with on-going COVID-19 symptoms.After a routine medical assessment, individuals with persistent COVID-19 symptoms were enrolled on a 6-week COVID-19 specific rehabilitation programme. The programme included symptom-titrated exercise, education, and self-management advice. Fatigue was assessed pre- and post-programme using the Functional Assessment Chronic Illness Therapy-Fatigue questionnaire (FACIT). Exercise capacity (Incremental and Endurance Shuttle Walking Test; ISWT/ESWT) and PESE (DePaul Symptom Questionnaire; DSQ) were also assessed pre- and post-programme. Composite scores were calculated for the frequency and severity domains of the DSQ.148 patients (median [IQR] age 59[49–72] years, 82 (60%) female, 81(54%) hospitalised) completed the COVID-19 rehabilitation programme. FACIT score reduced pre- to post-programme by a mean[CI] change of −5[−7, −4];p<0.01. Exercise capacity increased by 82[65, 99] m for the ISWT and 398[333, 462]seconds for the ESWT (n=148). PESE was assessed in 44 patients. The DSQ frequency and severity composite score improved by 20[13, 28] and 19[13, 26] points, respectively (p<0.01, n=44).This data demonstrates the potential benefits of a COVID-19 rehabilitation programme on improving fatigue, exercise capacity, and symptom exacerbation, in those with persistent COVID-19 symptoms.
{"title":"Changes in fatigue symptoms following an exercise-based rehabilitation programme for patients with Long-COVID","authors":"E. Daynes, Molly M Baldwin, M. Annals, N. Gardiner, E. Chaplin, S. Ward, N. J. Greening, Rachael A Evans, Sally J Singh","doi":"10.1183/23120541.00089-2024","DOIUrl":"https://doi.org/10.1183/23120541.00089-2024","url":null,"abstract":"There is evidence to support COVID-19 rehabilitation programmes improving persistent COVID-19 symptoms; however, there is concern that therapies that include an exercise component may increase fatigue and post-exertional symptom exacerbation (PESE).To determine the effect of a 6 week COVID-19 rehabilitation programme on fatigue and PESE in individuals with on-going COVID-19 symptoms.After a routine medical assessment, individuals with persistent COVID-19 symptoms were enrolled on a 6-week COVID-19 specific rehabilitation programme. The programme included symptom-titrated exercise, education, and self-management advice. Fatigue was assessed pre- and post-programme using the Functional Assessment Chronic Illness Therapy-Fatigue questionnaire (FACIT). Exercise capacity (Incremental and Endurance Shuttle Walking Test; ISWT/ESWT) and PESE (DePaul Symptom Questionnaire; DSQ) were also assessed pre- and post-programme. Composite scores were calculated for the frequency and severity domains of the DSQ.148 patients (median [IQR] age 59[49–72] years, 82 (60%) female, 81(54%) hospitalised) completed the COVID-19 rehabilitation programme. FACIT score reduced pre- to post-programme by a mean[CI] change of −5[−7, −4];p<0.01. Exercise capacity increased by 82[65, 99] m for the ISWT and 398[333, 462]seconds for the ESWT (n=148). PESE was assessed in 44 patients. The DSQ frequency and severity composite score improved by 20[13, 28] and 19[13, 26] points, respectively (p<0.01, n=44).This data demonstrates the potential benefits of a COVID-19 rehabilitation programme on improving fatigue, exercise capacity, and symptom exacerbation, in those with persistent COVID-19 symptoms.","PeriodicalId":11739,"journal":{"name":"ERJ Open Research","volume":null,"pages":null},"PeriodicalIF":4.6,"publicationDate":"2024-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140995241","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-05-09DOI: 10.1183/23120541.01010-2023
L. A. Cimini, Dieuwke Luijten, Stefano Barco, Waleed Ghanima, Ø. Jervan, Susan R. Kahn, Stavros Konstantinides, Daniel Lachante, Yoshihisa Nakano, Maarten Ninaber, Josien van Es, T. V. van Mens, Anton Vonk Noordegraaf, Cecilia Becattini, F.A. Klok
Up to 50% of pulmonary embolism (PE) patients has perfusion defects or residual vascular obstruction during follow-up despite adequate anticoagulant treatment and a similar percentage experience chronic functional limitations and/or dyspnea post-PE. We aimed to evaluate the association between pulmonary perfusion defects or residual vascular obstruction and functional recovery after PE.We performed a systematic review and meta-analysis including studies assessing both the presence of perfusion defects or residual vascular obstruction and functional recovery (i.e.persistent symptoms, quality of life, exercise endurance). An odds-ratio (OR) was pooled for perfusion defects or residual vascular obstruction and persistent symptoms using a random-effect model.12 studies were included totaling 1888 PE patients; at a median of 6 months after PE (range 2–72), 34% had perfusion defects or residual vascular obstruction and 37% reported persistent symptoms. Among patients with perfusion defects or residual vascular obstruction, 48% (95%CI 37–60, I2=82%) remained symptomatic during follow-up, compared to 34% (95%CI 20–51, I2=96%) of patients without such defects. Presence of perfusion defects or residual vascular obstruction was associated with persistent symptoms (OR 2.15, 95%CI 1.66–2.78; I2=0%, τ=0). Notably, there was no association between these defects and quality of life or cardiopulmonary exercise test parameters.While the odds of having persistent symptoms was higher in patients with perfusion defects or residual vascular obstruction after acute PE, a significant proportion of these patients reported no limitations. A possible causality between perfusion defects or residual vascular obstruction and residual functional limitation therefore remains to be proven.
尽管进行了充分的抗凝治疗，但仍有多达 50% 的肺栓塞（PE）患者在随访期间出现灌注缺陷或残余血管阻塞，还有类似比例的患者在 PE 后出现慢性功能受限和/或呼吸困难。我们进行了一项系统回顾和荟萃分析，其中包括评估灌注缺陷或残余血管阻塞的存在与功能恢复（即持续症状、生活质量、运动耐力）的研究。12 项研究共纳入了 1888 名 PE 患者；在 PE 后 6 个月的中位数（2-72 个月）中，34% 的患者有灌注缺损或残余血管阻塞，37% 的患者有持续症状。在有灌注缺损或残余血管阻塞的患者中，48%（95%CI 37-60，I2=82%）在随访期间仍有症状，而在无此类缺损的患者中，34%（95%CI 20-51，I2=96%）仍有症状。灌注缺损或残余血管阻塞与持续症状相关（OR 2.15，95%CI 1.66-2.78；I2=0%，τ=0）。值得注意的是，这些缺陷与生活质量或心肺运动测试参数之间没有关联。虽然急性 PE 后有灌注缺陷或残留血管阻塞的患者出现持续症状的几率更高，但这些患者中有相当一部分报告称没有任何限制。因此，灌注缺陷或残余血管阻塞与残余功能限制之间可能存在的因果关系仍有待证实。
{"title":"Pulmonary perfusion defects or residual vascular obstruction and persistent symptoms after pulmonary embolism: a systematic review and meta-analysis","authors":"L. A. Cimini, Dieuwke Luijten, Stefano Barco, Waleed Ghanima, Ø. Jervan, Susan R. Kahn, Stavros Konstantinides, Daniel Lachante, Yoshihisa Nakano, Maarten Ninaber, Josien van Es, T. V. van Mens, Anton Vonk Noordegraaf, Cecilia Becattini, F.A. Klok","doi":"10.1183/23120541.01010-2023","DOIUrl":"https://doi.org/10.1183/23120541.01010-2023","url":null,"abstract":"Up to 50% of pulmonary embolism (PE) patients has perfusion defects or residual vascular obstruction during follow-up despite adequate anticoagulant treatment and a similar percentage experience chronic functional limitations and/or dyspnea post-PE. We aimed to evaluate the association between pulmonary perfusion defects or residual vascular obstruction and functional recovery after PE.We performed a systematic review and meta-analysis including studies assessing both the presence of perfusion defects or residual vascular obstruction and functional recovery (i.e.persistent symptoms, quality of life, exercise endurance). An odds-ratio (OR) was pooled for perfusion defects or residual vascular obstruction and persistent symptoms using a random-effect model.12 studies were included totaling 1888 PE patients; at a median of 6 months after PE (range 2–72), 34% had perfusion defects or residual vascular obstruction and 37% reported persistent symptoms. Among patients with perfusion defects or residual vascular obstruction, 48% (95%CI 37–60, I2=82%) remained symptomatic during follow-up, compared to 34% (95%CI 20–51, I2=96%) of patients without such defects. Presence of perfusion defects or residual vascular obstruction was associated with persistent symptoms (OR 2.15, 95%CI 1.66–2.78; I2=0%, τ=0). Notably, there was no association between these defects and quality of life or cardiopulmonary exercise test parameters.While the odds of having persistent symptoms was higher in patients with perfusion defects or residual vascular obstruction after acute PE, a significant proportion of these patients reported no limitations. A possible causality between perfusion defects or residual vascular obstruction and residual functional limitation therefore remains to be proven.","PeriodicalId":11739,"journal":{"name":"ERJ Open Research","volume":null,"pages":null},"PeriodicalIF":4.6,"publicationDate":"2024-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140996218","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-05-09DOI: 10.1183/23120541.01006-2023
K. Cunnion, J. Goss, Pamela Hair, L. Dell, Destrey Roberson, U. Thienel, Meike Mϋller, Saskia Carstensen-Aurèche, P. Badorrek, Olaf Holz, Jens M Hohlfeld
This study was a randomised, double-blind, placebo-controlled study intended to establish the translatability of the RLS-0071 mechanisms of action from animal disease models to humans by inhibiting neutrophil-mediated inflammation at the tissue level and major inflammatory biomarkers. We hypothesized that RLS-0071 inhibits a temporary neutrophil-mediated inflammation in the lungs induced by inhalation of low-dose LPS in healthy participants.Participants were randomised to one of three arms to receive inhaled LPS followed by three doses of either low-dose (10 mg·kg−1) or high-dose (120 mg·kg−1loading dose followed by 2 doses of 40 mg·kg−1) RLS-0071 IV or placebo (saline) every 8 h (Q8H). Biomarkers evaluating inflammatory responses, with absolute neutrophil counts in induced sputum as the primary endpoint, were collected before and at 6 and 24 h after LPS challenge.Active treatment with RLS-0071 showed a similar safety profile to participants receiving placebo. RLS-0071 significantly decreased the numbers of neutrophils in sputum at 6 h post LPS by approximately half (p=0.04). Neutrophil effectors myeloperoxidase, neutrophil elastase, and Interleukin-1β in sputum were also significantly decreased at 6 h for RLS-0071 compared with placebo. Several biomarkers showed trends suggesting sustained decreases for RLS-0071versusplacebo at 24 h.This clinical trial demonstrated that RLS-0071 was safe and well tolerated and modulated neutrophil-mediated inflammation in humans after inhaled LPS challenge, consistent with results from prior animal model studies.
{"title":"RLS-0071, a novel anti-inflammatory agent, significantly reduced inflammatory biomarkers in a randomised human evaluation of mechanisms and safety study","authors":"K. Cunnion, J. Goss, Pamela Hair, L. Dell, Destrey Roberson, U. Thienel, Meike Mϋller, Saskia Carstensen-Aurèche, P. Badorrek, Olaf Holz, Jens M Hohlfeld","doi":"10.1183/23120541.01006-2023","DOIUrl":"https://doi.org/10.1183/23120541.01006-2023","url":null,"abstract":"This study was a randomised, double-blind, placebo-controlled study intended to establish the translatability of the RLS-0071 mechanisms of action from animal disease models to humans by inhibiting neutrophil-mediated inflammation at the tissue level and major inflammatory biomarkers. We hypothesized that RLS-0071 inhibits a temporary neutrophil-mediated inflammation in the lungs induced by inhalation of low-dose LPS in healthy participants.Participants were randomised to one of three arms to receive inhaled LPS followed by three doses of either low-dose (10 mg·kg−1) or high-dose (120 mg·kg−1loading dose followed by 2 doses of 40 mg·kg−1) RLS-0071 IV or placebo (saline) every 8 h (Q8H). Biomarkers evaluating inflammatory responses, with absolute neutrophil counts in induced sputum as the primary endpoint, were collected before and at 6 and 24 h after LPS challenge.Active treatment with RLS-0071 showed a similar safety profile to participants receiving placebo. RLS-0071 significantly decreased the numbers of neutrophils in sputum at 6 h post LPS by approximately half (p=0.04). Neutrophil effectors myeloperoxidase, neutrophil elastase, and Interleukin-1β in sputum were also significantly decreased at 6 h for RLS-0071 compared with placebo. Several biomarkers showed trends suggesting sustained decreases for RLS-0071versusplacebo at 24 h.This clinical trial demonstrated that RLS-0071 was safe and well tolerated and modulated neutrophil-mediated inflammation in humans after inhaled LPS challenge, consistent with results from prior animal model studies.","PeriodicalId":11739,"journal":{"name":"ERJ Open Research","volume":null,"pages":null},"PeriodicalIF":4.6,"publicationDate":"2024-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140996972","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-05-09DOI: 10.1183/23120541.00139-2024
R. Stockley, D. Parr
The past 60 years has seen multiple publications related to lung disease in Alph-1 Antitrypsin deficiency largelyreflectingthe pathophysiology, biochemical effect and outcomes of augmentation therapy. However, the complexity of disease phenotype and the impact of the natural history presents problems of patient management, study design and hence interpretation of outcome. Although many National and some International registries exist the lack of consistent in-depth assessment and importantly, the impact of augmentation therapylikelyinfluences our perception of the true natural history.Development of new therapeutic strategies, and even assessment of the role and efficacy of augmentation remain a challenge as powering such studies for conventional COPD outcomes is impractical due to relative rarity of the genetic condition and the presence ofclinicalphenotypic variation.The current review approaches these issues, discusses the nature and complexity of assessing patient variability, and provides guidance on further studies required to address them.
{"title":"Antitrypsin deficiency; still more to learn about the lung after 60 years","authors":"R. Stockley, D. Parr","doi":"10.1183/23120541.00139-2024","DOIUrl":"https://doi.org/10.1183/23120541.00139-2024","url":null,"abstract":"The past 60 years has seen multiple publications related to lung disease in Alph-1 Antitrypsin deficiency largelyreflectingthe pathophysiology, biochemical effect and outcomes of augmentation therapy. However, the complexity of disease phenotype and the impact of the natural history presents problems of patient management, study design and hence interpretation of outcome. Although many National and some International registries exist the lack of consistent in-depth assessment and importantly, the impact of augmentation therapylikelyinfluences our perception of the true natural history.Development of new therapeutic strategies, and even assessment of the role and efficacy of augmentation remain a challenge as powering such studies for conventional COPD outcomes is impractical due to relative rarity of the genetic condition and the presence ofclinicalphenotypic variation.The current review approaches these issues, discusses the nature and complexity of assessing patient variability, and provides guidance on further studies required to address them.","PeriodicalId":11739,"journal":{"name":"ERJ Open Research","volume":null,"pages":null},"PeriodicalIF":4.6,"publicationDate":"2024-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140995485","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-05-09DOI: 10.1183/23120541.00930-2023
A. Briançon-Marjollet, M. Joyeux-faure, R. Ben Messaoud, S. Bailly, V. Ngo, Sabrina Colombet, Jonathan Gaucher, S. Baillieul, R. Tamisier, Jean Louis Pépin
{"title":"Long-term incident hard outcomes in a prospective cohort of non-obese obstructive sleep apnoea patients free of comorbidities at inclusion","authors":"A. Briançon-Marjollet, M. Joyeux-faure, R. Ben Messaoud, S. Bailly, V. Ngo, Sabrina Colombet, Jonathan Gaucher, S. Baillieul, R. Tamisier, Jean Louis Pépin","doi":"10.1183/23120541.00930-2023","DOIUrl":"https://doi.org/10.1183/23120541.00930-2023","url":null,"abstract":"","PeriodicalId":11739,"journal":{"name":"ERJ Open Research","volume":null,"pages":null},"PeriodicalIF":4.6,"publicationDate":"2024-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140995960","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-05-09DOI: 10.1183/23120541.00167-2024
Maurizio Balbi, F. Sabia, R. Ledda, L. Rolli, G. Milanese, M. Ruggirello, Camilla Valsecchi, A. Marchianò, N. Sverzellati, U. Pastorino
The management of sub-solid nodules (SSNs) in lung cancer screening (LCS) is still a topic of debate, with no current uniform strategy to deal with these lesions at risk of overdiagnosis and overtreatment.The BioMILD LCS trial has implemented a prospective conservative approach for SSNs, managing with annual low-dose CT nonsolid nodules (NSNs) and part-solid nodules (PSNs) with a solid component <5 mm, regardless of the size of the nonsolid component. The present study aims to determine the lung cancer (LC) detection and survival in BioMILD volunteers with SSNs.Eligible participants were 758 out of 4071 (18.6%) BioMILD volunteers without baseline LC and at least one SSN detected at the baseline or further LDCT rounds. The outcomes of the study were LC detection and long-term survival.A total of 844 NSNs and 241 PSNs were included. LC detection was 3.7% (31/844) in NSNs and 7.1% (17/241) in PSNs, being significantly greater in prevalent than incident nodules (8.4%versus1.3% in NSNs; 14.1%versus2.1% in PSNs; p-value for both nodule types<0.01). Most LCs from SSNs were stage I (42/48, 87.5%), resectable (47/48, 97.9%), and caused no deaths. The 8-year cumulative survival of volunteers with LC derived from SSNs and not derived from SSNs was 93.8% and 74.9%, respectively.Conservative management of SSNs in LCS enables timely diagnosis and treatment of LCs arising from SSNs while ensuring the resection of more aggressive LCs detected away from SSNs.
{"title":"Surveillance of subsolid nodules avoids unnecessary resections in lung cancer screening: Long-term results of the prospective BioMILD trial","authors":"Maurizio Balbi, F. Sabia, R. Ledda, L. Rolli, G. Milanese, M. Ruggirello, Camilla Valsecchi, A. Marchianò, N. Sverzellati, U. Pastorino","doi":"10.1183/23120541.00167-2024","DOIUrl":"https://doi.org/10.1183/23120541.00167-2024","url":null,"abstract":"The management of sub-solid nodules (SSNs) in lung cancer screening (LCS) is still a topic of debate, with no current uniform strategy to deal with these lesions at risk of overdiagnosis and overtreatment.The BioMILD LCS trial has implemented a prospective conservative approach for SSNs, managing with annual low-dose CT nonsolid nodules (NSNs) and part-solid nodules (PSNs) with a solid component <5 mm, regardless of the size of the nonsolid component. The present study aims to determine the lung cancer (LC) detection and survival in BioMILD volunteers with SSNs.Eligible participants were 758 out of 4071 (18.6%) BioMILD volunteers without baseline LC and at least one SSN detected at the baseline or further LDCT rounds. The outcomes of the study were LC detection and long-term survival.A total of 844 NSNs and 241 PSNs were included. LC detection was 3.7% (31/844) in NSNs and 7.1% (17/241) in PSNs, being significantly greater in prevalent than incident nodules (8.4%versus1.3% in NSNs; 14.1%versus2.1% in PSNs; p-value for both nodule types<0.01). Most LCs from SSNs were stage I (42/48, 87.5%), resectable (47/48, 97.9%), and caused no deaths. The 8-year cumulative survival of volunteers with LC derived from SSNs and not derived from SSNs was 93.8% and 74.9%, respectively.Conservative management of SSNs in LCS enables timely diagnosis and treatment of LCs arising from SSNs while ensuring the resection of more aggressive LCs detected away from SSNs.","PeriodicalId":11739,"journal":{"name":"ERJ Open Research","volume":null,"pages":null},"PeriodicalIF":4.6,"publicationDate":"2024-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140994742","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-05-09DOI: 10.1183/23120541.00177-2024
Michael E Wechsler, J. M. Wells
Inflammation drives chronic obstructive pulmonary disease (COPD) pathogenesis and exacerbations. Although the conceptual framework and major players in the inflammatory milieu of COPD have been long established, the nuances of cellular interactions and the etiologic differences that create heterogeneity in inflammatory profiles and treatment response continue to be revealed. This wealth of data and understanding is not only a boon to the researcher but also provides guidance to the clinician, moving the field closer to precision medicine. It is through this lens that this review seeks to describe the inflammatory processes at play in COPD, relating inflammation to pathologic and functional changes, identifying patient-specific and disease-related factors that may influence clinical observations, and providing current insights on existing and emerging anti-inflammatory treatments and treatment targets, including biologic therapies and phosphodiesterase inhibitors.
{"title":"What Every Clinician Should Know About Inflammation in COPD","authors":"Michael E Wechsler, J. M. Wells","doi":"10.1183/23120541.00177-2024","DOIUrl":"https://doi.org/10.1183/23120541.00177-2024","url":null,"abstract":"Inflammation drives chronic obstructive pulmonary disease (COPD) pathogenesis and exacerbations. Although the conceptual framework and major players in the inflammatory milieu of COPD have been long established, the nuances of cellular interactions and the etiologic differences that create heterogeneity in inflammatory profiles and treatment response continue to be revealed. This wealth of data and understanding is not only a boon to the researcher but also provides guidance to the clinician, moving the field closer to precision medicine. It is through this lens that this review seeks to describe the inflammatory processes at play in COPD, relating inflammation to pathologic and functional changes, identifying patient-specific and disease-related factors that may influence clinical observations, and providing current insights on existing and emerging anti-inflammatory treatments and treatment targets, including biologic therapies and phosphodiesterase inhibitors.","PeriodicalId":11739,"journal":{"name":"ERJ Open Research","volume":null,"pages":null},"PeriodicalIF":4.6,"publicationDate":"2024-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140995200","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-05-09DOI: 10.1183/23120541.00142-2024
Heikki Olavi Koskela, Johanna Tuulikki Kaulamo, Anne Marika Lätti
{"title":"Severity grading of the Leicester Cough Questionnaire in chronic cough","authors":"Heikki Olavi Koskela, Johanna Tuulikki Kaulamo, Anne Marika Lätti","doi":"10.1183/23120541.00142-2024","DOIUrl":"https://doi.org/10.1183/23120541.00142-2024","url":null,"abstract":"","PeriodicalId":11739,"journal":{"name":"ERJ Open Research","volume":null,"pages":null},"PeriodicalIF":4.6,"publicationDate":"2024-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140997941","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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