BACKGROUNDAbout half of patients with chronic obstructive pulmonary disease (COPD) have hypertension, which significantly worsens prognosis. Yet its critical environmental drivers and vulnerable phenotypes remain unclear.OBJECTIVESTo evaluate associations between size-fractionated particulate matter (PM) and blood pressure, assess differential effects by hypertension status and identify susceptible individuals by smoking and inflammatory phenotypes.METHODSIn this prospective panel study, 82 patients with COPD (42 with hypertension) completed 281 clinical visits. Personal exposure to ambient inhalable PM (PM10), fine PM (PM2.5) and ultrafine particles (UFPs) of 0-7 days was estimated using infiltration factors and time-activity patterns. Inflammatory phenotypes were defined by blood neutrophils and eosinophils. Linear mixed-effect models were applied to evaluate blood pressure changes associated with PM.RESULTSUFPs and PM2.5, rather than PM10, were significantly associated with increased systolic blood pressure (SBP), whereas diastolic blood pressure (DBP) and pulse pressure showed non-significant changes. The effects appeared earlier after UFP exposure (lag 03d) than PM2.5 exposure (lag 06d), with central responses exceeding brachial responses. Notably, hypertensive individuals exhibited stronger responses to UFPs and PM2.5 exposure, in whom significant elevations were observed in both SBP and DBP. Stratification by smoking status revealed no evidence of effect modification. Comparatively, individuals with an eosinophilic, instead of neutrophilic, phenotype showed heightened susceptibility to PM2.5-related and UFP-related blood pressure increases, particularly in those with hypertension.CONCLUSIONSSmall-sized PM is an important risk factor for blood pressure elevations in patients with COPD, especially among those with hypertension and an eosinophilic inflammatory phenotype.TRIAL REGISTRATION NUMBERNCT05076630.
{"title":"Short-term effects of size-fractioned particulate matter on blood pressure in patients with COPD: the key role of inflammatory phenotypes.","authors":"Baiqi Chen,Wenlou Zhang,Yahong Chen,Chen Zhao,Zhihong Zhang,Shurun Li,Lifang Zhao,Liqiong Guo,Masayuki Shima,Yoshiko Yoda,Shaowei Wu,Xinbiao Guo,Furong Deng","doi":"10.1136/thorax-2025-224085","DOIUrl":"https://doi.org/10.1136/thorax-2025-224085","url":null,"abstract":"BACKGROUNDAbout half of patients with chronic obstructive pulmonary disease (COPD) have hypertension, which significantly worsens prognosis. Yet its critical environmental drivers and vulnerable phenotypes remain unclear.OBJECTIVESTo evaluate associations between size-fractionated particulate matter (PM) and blood pressure, assess differential effects by hypertension status and identify susceptible individuals by smoking and inflammatory phenotypes.METHODSIn this prospective panel study, 82 patients with COPD (42 with hypertension) completed 281 clinical visits. Personal exposure to ambient inhalable PM (PM10), fine PM (PM2.5) and ultrafine particles (UFPs) of 0-7 days was estimated using infiltration factors and time-activity patterns. Inflammatory phenotypes were defined by blood neutrophils and eosinophils. Linear mixed-effect models were applied to evaluate blood pressure changes associated with PM.RESULTSUFPs and PM2.5, rather than PM10, were significantly associated with increased systolic blood pressure (SBP), whereas diastolic blood pressure (DBP) and pulse pressure showed non-significant changes. The effects appeared earlier after UFP exposure (lag 03d) than PM2.5 exposure (lag 06d), with central responses exceeding brachial responses. Notably, hypertensive individuals exhibited stronger responses to UFPs and PM2.5 exposure, in whom significant elevations were observed in both SBP and DBP. Stratification by smoking status revealed no evidence of effect modification. Comparatively, individuals with an eosinophilic, instead of neutrophilic, phenotype showed heightened susceptibility to PM2.5-related and UFP-related blood pressure increases, particularly in those with hypertension.CONCLUSIONSSmall-sized PM is an important risk factor for blood pressure elevations in patients with COPD, especially among those with hypertension and an eosinophilic inflammatory phenotype.TRIAL REGISTRATION NUMBERNCT05076630.","PeriodicalId":23284,"journal":{"name":"Thorax","volume":"127 1","pages":""},"PeriodicalIF":10.0,"publicationDate":"2026-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147447024","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-03-12DOI: 10.1136/thorax-2025-224093
Enrico Valerio,Daniele De Luca
{"title":"Omics approaches to bronchopulmonary dysplasia: a first step in the right direction?","authors":"Enrico Valerio,Daniele De Luca","doi":"10.1136/thorax-2025-224093","DOIUrl":"https://doi.org/10.1136/thorax-2025-224093","url":null,"abstract":"","PeriodicalId":23284,"journal":{"name":"Thorax","volume":"43 1","pages":""},"PeriodicalIF":10.0,"publicationDate":"2026-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147439210","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Refractory multisystem sarcoidosis on a long axial field of view (LAFOV) PET-CT system.","authors":"Kathryn Biddle,Manil Subesinghe,Katie Bechman,Anne Collett,James Galloway","doi":"10.1136/thorax-2025-224343","DOIUrl":"https://doi.org/10.1136/thorax-2025-224343","url":null,"abstract":"","PeriodicalId":23284,"journal":{"name":"Thorax","volume":"50 1","pages":""},"PeriodicalIF":10.0,"publicationDate":"2026-03-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147381185","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BACKGROUNDPulmonary fibrosis (PF) caused by interstitial lung diseases (ILDs) affects up to 0.1% of the global population. There is growing global interest in PF, evident from a nearly threefold increase in PF-related research publications over the last 15 years. Idiopathic PF, connective tissue disease-related ILD, sarcoidosis and hypersensitivity pneumonitis rank as the top four causes of ILD-related PF, in descending order of incidence. This article explores the variation in global incidence and prevalence, genetics, diagnostic pathways, treatment approach, care gaps and recent advances in PF management.FINDINGSThe global annual incidence of ILD-related PF has more than doubled between 1990 and 2019; conservative estimates suggest current incidence of about 15-20 cases per 100 000 population. The incidence, prevalence and spectrum of ILD-related PF vary greatly across regions based on genetics, environment, industries and diagnostic rigour. Diagnosis of PF hinges on chest imaging, lung histology and expert evaluation, which remain scarce in underserved regions. About 30-60% of patients with ILD-related PF develop progressive disease over 1-2 years. Annual PF care cost averages approximately US$30 000 in developed countries. Although significant gaps remain in PF care globally, recent progress is encouraging. Key steps to enhance PF care include ensuring universal health coverage via public systems or insurance, improving access to imaging and expert diagnostic teams, incorporating telehealth technologies, accelerating drug development and expanding the availability of pulmonary rehabilitation, palliative care and lung transplantation. Emerging techniques such as gene silencing, alveolar organoids, stem cells, lung-on-a-chip and nano-based drug delivery could transform PF care in the future.CONCLUSIONSPF is an important global healthcare challenge, especially due to its clinical heterogeneity and geographic variation. Gaps in care need to be addressed by prioritising new drug development and ensuring wider dissemination of PF-related awareness and services.
{"title":"Global perspective on pulmonary fibrosis: epidemiology, regional variations, gaps in care and future directions.","authors":"Sahajal Dhooria,Yoshikazu Inoue,Kritarth Rathi,Takayuki Takimoto","doi":"10.1136/thorax-2025-223392","DOIUrl":"https://doi.org/10.1136/thorax-2025-223392","url":null,"abstract":"BACKGROUNDPulmonary fibrosis (PF) caused by interstitial lung diseases (ILDs) affects up to 0.1% of the global population. There is growing global interest in PF, evident from a nearly threefold increase in PF-related research publications over the last 15 years. Idiopathic PF, connective tissue disease-related ILD, sarcoidosis and hypersensitivity pneumonitis rank as the top four causes of ILD-related PF, in descending order of incidence. This article explores the variation in global incidence and prevalence, genetics, diagnostic pathways, treatment approach, care gaps and recent advances in PF management.FINDINGSThe global annual incidence of ILD-related PF has more than doubled between 1990 and 2019; conservative estimates suggest current incidence of about 15-20 cases per 100 000 population. The incidence, prevalence and spectrum of ILD-related PF vary greatly across regions based on genetics, environment, industries and diagnostic rigour. Diagnosis of PF hinges on chest imaging, lung histology and expert evaluation, which remain scarce in underserved regions. About 30-60% of patients with ILD-related PF develop progressive disease over 1-2 years. Annual PF care cost averages approximately US$30 000 in developed countries. Although significant gaps remain in PF care globally, recent progress is encouraging. Key steps to enhance PF care include ensuring universal health coverage via public systems or insurance, improving access to imaging and expert diagnostic teams, incorporating telehealth technologies, accelerating drug development and expanding the availability of pulmonary rehabilitation, palliative care and lung transplantation. Emerging techniques such as gene silencing, alveolar organoids, stem cells, lung-on-a-chip and nano-based drug delivery could transform PF care in the future.CONCLUSIONSPF is an important global healthcare challenge, especially due to its clinical heterogeneity and geographic variation. Gaps in care need to be addressed by prioritising new drug development and ensuring wider dissemination of PF-related awareness and services.","PeriodicalId":23284,"journal":{"name":"Thorax","volume":"6 1","pages":""},"PeriodicalIF":10.0,"publicationDate":"2026-03-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147381183","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-03-05DOI: 10.1136/thorax-2025-224664
Parris Jade Williams
{"title":"Running away from the smoke, the role of physical activity in tobacco dependency treatment.","authors":"Parris Jade Williams","doi":"10.1136/thorax-2025-224664","DOIUrl":"https://doi.org/10.1136/thorax-2025-224664","url":null,"abstract":"","PeriodicalId":23284,"journal":{"name":"Thorax","volume":"70 1","pages":""},"PeriodicalIF":10.0,"publicationDate":"2026-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147359212","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
INTRODUCTIONThere is an unmet need for a validated qualitative and quantitative tool to assess environmental exposures in patients with interstitial lung disease (ILD). This study aimed to develop and validate a comprehensive tool to systematically identify exposures in patients with ILD.METHODSA systematic literature search was completed to identify exposures associated with more than five documented hypersensitivity pneumonitis (HP) cases. These exposures were evaluated through a two-round Delphi survey involving 39 pulmonologists from India, Sri Lanka, Pakistan and Nepal. The questionnaire was prospectively derived at one centre and validated across five centres in India and Sri Lanka. The HP South Asian Questionnaire for Exposure (HP-SAQE) was validated against the gold standard multidisciplinary discussion diagnosis, distinguishing HP from non-HP ILD.RESULTSThe literature search screened 5170 records and included 407 studies, identifying 24 exposures. A 50-item Delphi survey achieved expert consensus (>70%) on 17 qualitative and 4 quantitative items (six questions) by 39 pulmonologists. HP-SAQE score ranged from 0 to 14. After pilot testing, the questionnaire was translated into Hindi, Tamil and Sinhala. In the derivation cohort (n=40), the HP-SAQE score was significantly higher in patients with HP versus non-HP (mean: 10.2±1.6 vs 6.7±4.2; p=0.001). This finding was validated in a separate cohort (n=163; mean: 9.4±2.2 vs 4.13±4.28; p<0.001). Receiver operating characteristic curve analysis showed good diagnostic performance (area under the receiver operating characteristic curve, AUC: 0.791 derivation; 0.858 validation, centre-wise AUCs 0.705-0.967).CONCLUSIONThe HP-SAQE is the first qualitative and quantitative exposure assessment tool for patients with ILD that has a good diagnostic performance.
目前尚不需要一种有效的定性和定量工具来评估间质性肺疾病（ILD）患者的环境暴露。本研究旨在开发和验证一种全面的工具来系统地识别ILD患者的暴露。方法进行系统的文献检索，以确定与5例以上记录的超敏性肺炎（HP）病例相关的暴露。通过对来自印度、斯里兰卡、巴基斯坦和尼泊尔的39名肺病学家进行两轮德尔菲调查，对这些暴露情况进行了评估。问卷是在一个中心前瞻性地得出的，并在印度和斯里兰卡的五个中心得到验证。HP南亚暴露问卷（HP- saqe）与金标准多学科讨论诊断相对照，将HP与非HP ILD区分开来。结果文献检索筛选了5170份记录，包括407项研究，确定了24项暴露。对39名肺科医生进行了一项50项德尔菲调查，对17项定性和4项定量（6个问题）达成了专家共识（bbb70%）。HP-SAQE评分范围为0 ~ 14。经过初步测试，问卷被翻译成印地语、泰米尔语和僧伽罗语。在衍生队列中（n=40）， HP患者的HP- saqe评分明显高于非HP患者（平均值：10.2±1.6 vs 6.7±4.2;p=0.001）。这一发现在一个单独的队列中得到了验证（n=163；平均值：9.4±2.2 vs 4.13±4.28;p<0.001）。受试者工作特征曲线分析具有较好的诊断效果（受试者工作特征曲线下面积，推导AUC为0.791；验证AUC为0.858，中心AUC为0.705 ~ 0.967）。结论HP-SAQE是第一个用于ILD患者的定性和定量暴露评估工具，具有较好的诊断效果。
{"title":"Development and validation of the Hypersensitivity Pneumonitis South Asian Questionnaire for Exposure (HP-SAQE): a novel, qualitative and quantitative tool.","authors":"Sheetu Singh,Ambika Sharma,Khushboo Pilania,Prerna Singh,Arvind Kumar Sharma,Sahajal Dhooria,Vijay Hadda,Nitesh Gupta,Mansi Gupta,Amila Rathnapala,Arundhati Agarwal,Nishtha Singh,Madhur Joshi,Aniket Mondal,Jitendra Bairwa,Avishek Layek,Sanchit Mohan,Chhaya Goyal,Parthasarathi Bhattacharyya,Parvaiz A Koul,Raja Dhar,Kripesh Ranjan Sarmah,Dipesh Maskey,Ravi Dosi,Gayathri Devi H Jayadevappa,Dipti Gothi,Asmita Mehta,Richa Gupta,Arpana Neopane,Padmanabhan Arjun,Alok Kumar Singh,Soibam Pahal Meitei,Bodhika Samarasekera,Sonia Dalal,Sujeet Madhukar,Sandeep Katiyar,Loganathan Nattusamy,Devi Jyoti Dash,Harjit Dumra,Deepak Talwar,Sonam Spalgais,Viswesvaran Balasubramanian,Murali Mohan,Saima Saeed,Matiur Rehman,Sunil K Chhabra,Zarir F Udwadia,Aditya Agrawal,Naveen Dutt,Eshanth Perera,Alok Nath,Rohit Kumar,Virendra Singh,Kerri A Johannson","doi":"10.1136/thorax-2025-223960","DOIUrl":"https://doi.org/10.1136/thorax-2025-223960","url":null,"abstract":"INTRODUCTIONThere is an unmet need for a validated qualitative and quantitative tool to assess environmental exposures in patients with interstitial lung disease (ILD). This study aimed to develop and validate a comprehensive tool to systematically identify exposures in patients with ILD.METHODSA systematic literature search was completed to identify exposures associated with more than five documented hypersensitivity pneumonitis (HP) cases. These exposures were evaluated through a two-round Delphi survey involving 39 pulmonologists from India, Sri Lanka, Pakistan and Nepal. The questionnaire was prospectively derived at one centre and validated across five centres in India and Sri Lanka. The HP South Asian Questionnaire for Exposure (HP-SAQE) was validated against the gold standard multidisciplinary discussion diagnosis, distinguishing HP from non-HP ILD.RESULTSThe literature search screened 5170 records and included 407 studies, identifying 24 exposures. A 50-item Delphi survey achieved expert consensus (>70%) on 17 qualitative and 4 quantitative items (six questions) by 39 pulmonologists. HP-SAQE score ranged from 0 to 14. After pilot testing, the questionnaire was translated into Hindi, Tamil and Sinhala. In the derivation cohort (n=40), the HP-SAQE score was significantly higher in patients with HP versus non-HP (mean: 10.2±1.6 vs 6.7±4.2; p=0.001). This finding was validated in a separate cohort (n=163; mean: 9.4±2.2 vs 4.13±4.28; p<0.001). Receiver operating characteristic curve analysis showed good diagnostic performance (area under the receiver operating characteristic curve, AUC: 0.791 derivation; 0.858 validation, centre-wise AUCs 0.705-0.967).CONCLUSIONThe HP-SAQE is the first qualitative and quantitative exposure assessment tool for patients with ILD that has a good diagnostic performance.","PeriodicalId":23284,"journal":{"name":"Thorax","volume":"45 1","pages":""},"PeriodicalIF":10.0,"publicationDate":"2026-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147359210","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-03-04DOI: 10.1136/thorax-2025-223922
Ludovico Messineo,Molly Kim,Ali Azarbarzin,Daniel Vena,Madison Preuss,Neda Esmaeili,Atqiya Aishah,Natalie V Lawrence,Dillon C Gilbertson,David P White,Andrew Wellman,Scott A Sands
BACKGROUNDObstructive sleep apnoea (OSA) pathogenesis during rapid-eye movement (REM) sleep has been linked to dips in ventilatory drive and downstream genioglossus hypotonia. The carbonic anhydrase inhibitor acetazolamide is known to increase ventilatory drive and improve OSA severity. Therefore, we tested the effect of acetazolamide on REM-predominant OSA severity (apnoea hypopnoea index (AHI) and hypoxic burden, co-primary outcomes) and underlying physiological mechanisms (ventilatory drive, ventilation and pharyngeal muscle activity).METHODS11 participants with REM-predominant OSA per baseline polysomnography (REM AHI/non-REM AHI≥2) were allocated to receiving acetazolamide 500 mg for three nights (first night at half dose) or placebo according to a randomised, crossover, double-blind design. Detailed physiological polysomnography with recording of diaphragm and genioglossus electromyography was conducted after each intervention, with a 1-week washout in between.RESULTSAs hypothesised, acetazolamide reduced AHI by 35.5% (95% CI 23.1% to 46.3%) and hypoxic burden by 35.9% (95% CI 21.1% to 48.4%) vs placebo (p<0.001), meeting the primary endpoint. Mechanistic analysis in REM revealed that, unexpectedly, acetazolamide did not mitigate dips in ventilatory drive versus placebo (first decile (+0.1 (-1.0 to 1.3) L/min, p=0.8). Rather, acetazolamide reduced collapsibility (increased ventilation at eupneic drive: +1.4 (1.2 to 1.8) L/min) and raised muscle responsiveness (ventilation vs drive slope: +32 (25 to 41) %ventilation/drive, p<0.001; genioglossus versus drive slope: +0.33 (0.13 to 0.54) %max/(L/min), p=0.001).CONCLUSIONSAcetazolamide modestly improved REM OSA, with meaningful improvements in upper airway physiology, but failed to mitigate the dips in ventilatory drive responsible for REM OSA.TRIAL REGISTRATION NUMBERNCT05589792.
背景：阻塞性睡眠呼吸暂停（OSA）在快速眼动（REM）睡眠期间的发病机制与通气驱动下降和下游的颏舌肌张力低下有关。已知碳酸酐酶抑制剂乙酰唑胺可增加通气驱动并改善OSA严重程度。因此，我们测试了乙酰唑胺对rem期为主的OSA严重程度（呼吸暂停低通气指数（AHI）和缺氧负担，共同主要结局）和潜在生理机制（通气驱动、通气和咽肌活动）的影响。方法根据随机、交叉、双盲设计，11例基线多导睡眠图（REM AHI/非REM AHI≥2）以REM为主的OSA患者被分配给乙酰唑胺500 mg，连续3晚（第一晚剂量为一半）或安慰剂。每次干预后进行详细的生理多导睡眠图，记录膈肌和颏舌肌肌电图，中间有1周的洗脱期。与安慰剂相比，乙酰唑胺降低了35.5% （95% CI 23.1%至46.3%）的AHI和35.9% （95% CI 21.1%至48.4%）的缺氧负担（p<0.001），达到了主要终点。REM的机制分析显示，出乎意料的是，乙酰唑胺与安慰剂相比并没有减轻通气驱动的下降(前十分位数（+0.1(-1.0至1.3)L/min, p=0.8）。相反，乙酰唑胺降低了湿缩性（增加了通气：+1.4(1.2至1.8)L/min）并提高了肌肉反应性(通气vs通气坡度：+32(25至41)%通气/通气，p<0.001；颏舌肌与驱动斜率：+0.33（0.13至0.54)%max/(L/min), p=0.001）。结论头孢唑胺可适度改善REM睡眠呼吸暂停，对上气道生理有明显改善，但不能减轻REM睡眠呼吸暂停引起的通气驱动下降。试验注册号05589792。
{"title":"Acetazolamide to prevent ventilatory drive withdrawal in REM sleep apnoea: a randomised controlled trial.","authors":"Ludovico Messineo,Molly Kim,Ali Azarbarzin,Daniel Vena,Madison Preuss,Neda Esmaeili,Atqiya Aishah,Natalie V Lawrence,Dillon C Gilbertson,David P White,Andrew Wellman,Scott A Sands","doi":"10.1136/thorax-2025-223922","DOIUrl":"https://doi.org/10.1136/thorax-2025-223922","url":null,"abstract":"BACKGROUNDObstructive sleep apnoea (OSA) pathogenesis during rapid-eye movement (REM) sleep has been linked to dips in ventilatory drive and downstream genioglossus hypotonia. The carbonic anhydrase inhibitor acetazolamide is known to increase ventilatory drive and improve OSA severity. Therefore, we tested the effect of acetazolamide on REM-predominant OSA severity (apnoea hypopnoea index (AHI) and hypoxic burden, co-primary outcomes) and underlying physiological mechanisms (ventilatory drive, ventilation and pharyngeal muscle activity).METHODS11 participants with REM-predominant OSA per baseline polysomnography (REM AHI/non-REM AHI≥2) were allocated to receiving acetazolamide 500 mg for three nights (first night at half dose) or placebo according to a randomised, crossover, double-blind design. Detailed physiological polysomnography with recording of diaphragm and genioglossus electromyography was conducted after each intervention, with a 1-week washout in between.RESULTSAs hypothesised, acetazolamide reduced AHI by 35.5% (95% CI 23.1% to 46.3%) and hypoxic burden by 35.9% (95% CI 21.1% to 48.4%) vs placebo (p<0.001), meeting the primary endpoint. Mechanistic analysis in REM revealed that, unexpectedly, acetazolamide did not mitigate dips in ventilatory drive versus placebo (first decile (+0.1 (-1.0 to 1.3) L/min, p=0.8). Rather, acetazolamide reduced collapsibility (increased ventilation at eupneic drive: +1.4 (1.2 to 1.8) L/min) and raised muscle responsiveness (ventilation vs drive slope: +32 (25 to 41) %ventilation/drive, p<0.001; genioglossus versus drive slope: +0.33 (0.13 to 0.54) %max/(L/min), p=0.001).CONCLUSIONSAcetazolamide modestly improved REM OSA, with meaningful improvements in upper airway physiology, but failed to mitigate the dips in ventilatory drive responsible for REM OSA.TRIAL REGISTRATION NUMBERNCT05589792.","PeriodicalId":23284,"journal":{"name":"Thorax","volume":"61 1","pages":""},"PeriodicalIF":10.0,"publicationDate":"2026-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147350515","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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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