Pub Date : 2025-11-06DOI: 10.1016/s2213-2600(25)00338-8
For over seven decades, oral corticosteroids have been the cornerstone of sarcoidosis management. Oral corticosteroids suppress sarcoidosis inflammati…
70多年来,口服皮质类固醇一直是结节病治疗的基石。口服糖皮质激素抑制结节病炎症…
{"title":"A paradigm shift in corticosteroid therapy for sarcoidosis: a World Association of Sarcoidosis and Other Granulomatous Disorders Position Paper, endorsed by the Americas Association of Sarcoidosis and Other Granulomatous Disorders","authors":"","doi":"10.1016/s2213-2600(25)00338-8","DOIUrl":"https://doi.org/10.1016/s2213-2600(25)00338-8","url":null,"abstract":"For over seven decades, oral corticosteroids have been the cornerstone of sarcoidosis management. Oral corticosteroids suppress sarcoidosis inflammati…","PeriodicalId":51307,"journal":{"name":"Lancet Respiratory Medicine","volume":"28 1","pages":""},"PeriodicalIF":76.2,"publicationDate":"2025-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145455103","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 : 2025-11-06DOI: 10.1016/s2213-2600(25)00402-3
Tony Kirby
No Abstract
没有抽象的
{"title":"US lung cancer report suggests years of encouraging progress under threat from health agency cuts","authors":"Tony Kirby","doi":"10.1016/s2213-2600(25)00402-3","DOIUrl":"https://doi.org/10.1016/s2213-2600(25)00402-3","url":null,"abstract":"No Abstract","PeriodicalId":51307,"journal":{"name":"Lancet Respiratory Medicine","volume":"39 1","pages":""},"PeriodicalIF":76.2,"publicationDate":"2025-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145455104","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 : 2025-11-06DOI: 10.1016/s2213-2600(25)00391-1
Katie Bechman, James Galloway, Surinder S Birring
No Abstract
没有抽象的
{"title":"Towards a new treatment era in sarcoidosis","authors":"Katie Bechman, James Galloway, Surinder S Birring","doi":"10.1016/s2213-2600(25)00391-1","DOIUrl":"https://doi.org/10.1016/s2213-2600(25)00391-1","url":null,"abstract":"No Abstract","PeriodicalId":51307,"journal":{"name":"Lancet Respiratory Medicine","volume":"135 1","pages":""},"PeriodicalIF":76.2,"publicationDate":"2025-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145454791","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 : 2025-10-30DOI: 10.1016/s2213-2600(25)00329-7
Matthew J Saunders, Delia Boccia, Palwasha Y Khan, Lara Goscé, Antonio Gasparrini, Rebecca A Clark, Julia M Pescarini, Salome Charalambous, Lelisa Fekadu, Fernanda Dockhorn da Costa Johansen, Irina Vasilyeva, Gopalan Narendran, Tao Li, Norbert Ndjeka, Richard G White, Rein M G J Houben, Matteo Zignol, Nebiat Gebreselassie, Christopher Finn McQuaid
Climate change is likely to exacerbate a range of determinants that drive tuberculosis, the world's leading cause of death from a single infectious agent. However, tuberculosis is often neglected in wider climate health discussions. Commissioned by WHO, we developed an analytical framework outlining potential causal relationships between climate change and tuberculosis. We drew on existing knowledge of tuberculosis determinants, identified determinants likely to be sensitive to the effects of climate change, and conceptualised the mechanistic pathways through which these effects might occur. We collated evidence for these pathways, but found no studies directly linking climate change and tuberculosis, warranting research to build evidence for action. Nevertheless, the available indirect evidence supports the existence of plausible causal links between climate change and tuberculosis. This evidence highlights the need to consider tuberculosis as a climate-sensitive disease, and include tuberculosis in climate risk adaptation and mitigation programmes, and climate-resilient funding and response mechanisms. Only through urgent research and comprehensive action can we address this overlooked intersection and ensure that climate change does not become a barrier to ending the global tuberculosis epidemic.
{"title":"Climate change and tuberculosis: an analytical framework","authors":"Matthew J Saunders, Delia Boccia, Palwasha Y Khan, Lara Goscé, Antonio Gasparrini, Rebecca A Clark, Julia M Pescarini, Salome Charalambous, Lelisa Fekadu, Fernanda Dockhorn da Costa Johansen, Irina Vasilyeva, Gopalan Narendran, Tao Li, Norbert Ndjeka, Richard G White, Rein M G J Houben, Matteo Zignol, Nebiat Gebreselassie, Christopher Finn McQuaid","doi":"10.1016/s2213-2600(25)00329-7","DOIUrl":"https://doi.org/10.1016/s2213-2600(25)00329-7","url":null,"abstract":"Climate change is likely to exacerbate a range of determinants that drive tuberculosis, the world's leading cause of death from a single infectious agent. However, tuberculosis is often neglected in wider climate health discussions. Commissioned by WHO, we developed an analytical framework outlining potential causal relationships between climate change and tuberculosis. We drew on existing knowledge of tuberculosis determinants, identified determinants likely to be sensitive to the effects of climate change, and conceptualised the mechanistic pathways through which these effects might occur. We collated evidence for these pathways, but found no studies directly linking climate change and tuberculosis, warranting research to build evidence for action. Nevertheless, the available indirect evidence supports the existence of plausible causal links between climate change and tuberculosis. This evidence highlights the need to consider tuberculosis as a climate-sensitive disease, and include tuberculosis in climate risk adaptation and mitigation programmes, and climate-resilient funding and response mechanisms. Only through urgent research and comprehensive action can we address this overlooked intersection and ensure that climate change does not become a barrier to ending the global tuberculosis epidemic.","PeriodicalId":51307,"journal":{"name":"Lancet Respiratory Medicine","volume":"48 1","pages":""},"PeriodicalIF":76.2,"publicationDate":"2025-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145404680","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 : 2025-10-28DOI: 10.1016/s2213-2600(25)00361-3
Ewan C Mackay, Peter S P Cho, Surinder S Birring, James H Hull
{"title":"Remission in chronic cough: an achievable target?","authors":"Ewan C Mackay, Peter S P Cho, Surinder S Birring, James H Hull","doi":"10.1016/s2213-2600(25)00361-3","DOIUrl":"https://doi.org/10.1016/s2213-2600(25)00361-3","url":null,"abstract":"","PeriodicalId":51307,"journal":{"name":"Lancet Respiratory Medicine","volume":"39 1","pages":""},"PeriodicalIF":76.2,"publicationDate":"2025-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145382800","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 : 2025-10-28DOI: 10.1016/s2213-2600(25)00368-6
Huib A M Kerstjens, Maarten van den Berge
{"title":"FeNO or no FeNO in COPD?","authors":"Huib A M Kerstjens, Maarten van den Berge","doi":"10.1016/s2213-2600(25)00368-6","DOIUrl":"https://doi.org/10.1016/s2213-2600(25)00368-6","url":null,"abstract":"","PeriodicalId":51307,"journal":{"name":"Lancet Respiratory Medicine","volume":"7 14 1","pages":""},"PeriodicalIF":76.2,"publicationDate":"2025-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145382793","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 : 2025-10-11DOI: 10.1016/s2213-2600(25)00322-4
Mark van den Boogaard, Thomas Ottens
No Abstract
没有抽象的
{"title":"Deep sedation in the ICU: at what cost?","authors":"Mark van den Boogaard, Thomas Ottens","doi":"10.1016/s2213-2600(25)00322-4","DOIUrl":"https://doi.org/10.1016/s2213-2600(25)00322-4","url":null,"abstract":"No Abstract","PeriodicalId":51307,"journal":{"name":"Lancet Respiratory Medicine","volume":"135 1","pages":""},"PeriodicalIF":76.2,"publicationDate":"2025-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145282707","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 : 2025-10-11DOI: 10.1016/s2213-2600(25)00264-4
Karuna Wongtangman, Felix Borngaesser, Maíra I Rudolph, Flora T Scheffenbichler, Michael E Kiyatkin, Ibraheem M Karaye, William J Sauer
<h3>Background</h3>Deep sedation can be used during invasive mechanical ventilation without proven indication to treat the signs and symptoms of emotional distress or insomnia. However, medication-induced deep sedation is associated with delayed recovery and increased mortality. We tested the hypothesis that medication-induced deep sedation, but not emotional distress, is associated with loss of independent living.<h3>Methods</h3>In this retrospective cohort study, we included adult patients (age ≥18 years) who lived independently before hospital admission and were mechanically ventilated for at least 24 h in any of 20 ICUs at an academic health system in the Bronx, New York (NY, USA), and adjacent counties. The primary exposure was the proportion of time spent in medication-induced deep sedation (defined as a Richmond Agitation Sedation Score of –3 to –5) within the first week of ICU admission. The secondary exposure was the proportion of time with indicators of emotional distress within the first week of ICU admission. The exposures were categorised as none, a low proportion, or a high proportion using the median (42·9% for medication-induced deep sedation and 10·7% for emotional distress) as the cutoff between low and high. The primary outcome was loss of independent living (defined as in-hospital death or postoperative discharge to a long-term skilled nursing facility). Modified Poisson regression with an a priori-defined confounder control model were used to assess the association between exposures and outcomes. Mediation analysis was done to evaluate whether patient mobilisation level during mechanical ventilation contributed to the association between deep sedation and loss of independent living.<h3>Findings</h3>Among 10 204 patients receiving invasive mechanical ventilation between Jan 30, 2016 and July 11, 2023, 6369 (62·4%) had a loss of independent living. The proportion of patients who received deep sedation was a mean 2·84-fold (SD 1·51) higher than the proportion of patients who had an order for deep sedation. 7289 (71·4%) patients had at least one episode of medication-induced deep sedation within the first week of mechanical ventilation in the ICU. A high proportion of medication-induced deep sedation was associated with an increased risk of loss of independent living (adjusted risk ratio [RR<sub>adj</sub>] 1·18 [95% CI 1·13–1·23], p<0·0001) compared with no medication-induced deep sedation. There were 30 022 documented episodes of emotional distress. Having a high proportion of emotional distress was associated with a decreased risk of loss of independent living (RR<sub>adj</sub> 0·88 [0·84–0·92], p<0·0001) compared with no emotional distress. Clinicians provided deeper sedation in response to emotional distress and during the night (p<0·0001 for both comparisons). Symptom control with antipsychotics or non-opioid analgesics was associated with a decreased risk of loss of independent living compared with no treatment (RR
{"title":"Association of medication-induced deep sedation and emotional distress during mechanical ventilation with loss of independent living: an observational cohort study","authors":"Karuna Wongtangman, Felix Borngaesser, Maíra I Rudolph, Flora T Scheffenbichler, Michael E Kiyatkin, Ibraheem M Karaye, William J Sauer","doi":"10.1016/s2213-2600(25)00264-4","DOIUrl":"https://doi.org/10.1016/s2213-2600(25)00264-4","url":null,"abstract":"<h3>Background</h3>Deep sedation can be used during invasive mechanical ventilation without proven indication to treat the signs and symptoms of emotional distress or insomnia. However, medication-induced deep sedation is associated with delayed recovery and increased mortality. We tested the hypothesis that medication-induced deep sedation, but not emotional distress, is associated with loss of independent living.<h3>Methods</h3>In this retrospective cohort study, we included adult patients (age ≥18 years) who lived independently before hospital admission and were mechanically ventilated for at least 24 h in any of 20 ICUs at an academic health system in the Bronx, New York (NY, USA), and adjacent counties. The primary exposure was the proportion of time spent in medication-induced deep sedation (defined as a Richmond Agitation Sedation Score of –3 to –5) within the first week of ICU admission. The secondary exposure was the proportion of time with indicators of emotional distress within the first week of ICU admission. The exposures were categorised as none, a low proportion, or a high proportion using the median (42·9% for medication-induced deep sedation and 10·7% for emotional distress) as the cutoff between low and high. The primary outcome was loss of independent living (defined as in-hospital death or postoperative discharge to a long-term skilled nursing facility). Modified Poisson regression with an a priori-defined confounder control model were used to assess the association between exposures and outcomes. Mediation analysis was done to evaluate whether patient mobilisation level during mechanical ventilation contributed to the association between deep sedation and loss of independent living.<h3>Findings</h3>Among 10 204 patients receiving invasive mechanical ventilation between Jan 30, 2016 and July 11, 2023, 6369 (62·4%) had a loss of independent living. The proportion of patients who received deep sedation was a mean 2·84-fold (SD 1·51) higher than the proportion of patients who had an order for deep sedation. 7289 (71·4%) patients had at least one episode of medication-induced deep sedation within the first week of mechanical ventilation in the ICU. A high proportion of medication-induced deep sedation was associated with an increased risk of loss of independent living (adjusted risk ratio [RR<sub>adj</sub>] 1·18 [95% CI 1·13–1·23], p<0·0001) compared with no medication-induced deep sedation. There were 30 022 documented episodes of emotional distress. Having a high proportion of emotional distress was associated with a decreased risk of loss of independent living (RR<sub>adj</sub> 0·88 [0·84–0·92], p<0·0001) compared with no emotional distress. Clinicians provided deeper sedation in response to emotional distress and during the night (p<0·0001 for both comparisons). Symptom control with antipsychotics or non-opioid analgesics was associated with a decreased risk of loss of independent living compared with no treatment (RR","PeriodicalId":51307,"journal":{"name":"Lancet Respiratory Medicine","volume":"19 1","pages":""},"PeriodicalIF":76.2,"publicationDate":"2025-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145282778","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 : 2025-10-08DOI: 10.1016/s2213-2600(25)00366-2
Priya Venkatesan
<h2>Section snippets</h2><section><section><h2>Early-life exposure to paracetamol versus ibuprofen</h2>Previous non-experimental studies suggest an association between paracetamol exposure in the first year of life and subsequent asthma and eczema developing in childhood; however, randomised trials are needed to establish whether a causal link truly exists. Stuart R Dalziel (University of Auckland, Auckland, New Zealand) presented 1-year results from the PIPPA Tamariki randomised <span><span>study</span><svg aria-label="Opens in new window" focusable="false" height="20" viewbox="0 0 8 8"><path d="M1.12949 2.1072V1H7V6.85795H5.89111V2.90281L0.784057 8L0 7.21635L5.11902 2.1072H1.12949Z"></path></svg></span> comparing the use of paracetamol versus ibuprofen in early life. The study included 3908 infants in New Zealand</section></section><section><section><h2>Astegolimab for COPD</h2>Triggers of exacerbations in chronic obstructive pulmonary disease (COPD) can release IL-33 that binds to the ST2 receptor and increase inflammation; therefore, targeting the IL-33/SL2 pathway is an area of therapeutic interest. Neil J Greening (University of Leicester, Leicester, UK) presented results from the phase 2b <span><span>ALIENTO trial</span><svg aria-label="Opens in new window" focusable="false" height="20" viewbox="0 0 8 8"><path d="M1.12949 2.1072V1H7V6.85795H5.89111V2.90281L0.784057 8L0 7.21635L5.11902 2.1072H1.12949Z"></path></svg></span> comparing astegolimab, a human IgG2 monoclonal antibody targeting ST2 and blocking IL-33 activity, versus placebo in current or former smokers aged 40–90 years</section></section><section><section><h2>Sotatercept for PAH</h2>Two studies were presented on sotatercept, a fusion protein that inhibits activin signalling, for the treatment of pulmonary arterial hypertension (PAH). In the first, Ioana R Preston (Tufts Medical Center, Boston, MA, USA) presented new safety data from the <span><span>SOTERIA</span><svg aria-label="Opens in new window" focusable="false" height="20" viewbox="0 0 8 8"><path d="M1.12949 2.1072V1H7V6.85795H5.89111V2.90281L0.784057 8L0 7.21635L5.11902 2.1072H1.12949Z"></path></svg></span> long-term follow-up study, the interim results for which were published <span><span>previously</span><svg aria-label="Opens in new window" focusable="false" height="20" viewbox="0 0 8 8"><path d="M1.12949 2.1072V1H7V6.85795H5.89111V2.90281L0.784057 8L0 7.21635L5.11902 2.1072H1.12949Z"></path></svg></span>. Chalmers commented “Sotatercept is a game changer in PAH supported by a series of impactful trials, [but] long-term safety of new therapies is</section></section><section><section><h2>Nerandomilast for IPF</h2>Justin M Oldham (University of Michigan, Ann Arbor, MI, USA) presented final data from the <span><span>FIBRONEER-IPF</span><svg aria-label="Opens in new window" focusable="false" height="20" viewbox="0 0 8 8"><path d="M1.12949 2.1072V1H7V6.85795H5.89111V2.90281L0.784057 8L0 7.21635L5.11902 2.1072H1.12949Z"></pat
早期接触扑热息痛与布洛芬之前的非实验研究表明,在生命的第一年接触扑热息痛与随后在儿童时期发生哮喘和湿疹之间存在关联;然而,需要随机试验来确定因果关系是否真的存在。Stuart R Dalziel(新西兰奥克兰大学)介绍了PIPPA Tamariki随机研究1年的结果,比较了早期使用扑热息痛和布洛芬的情况。该研究包括新西兰的3908名婴儿,阿司哥利单抗治疗COPD慢性阻塞性肺疾病(COPD)恶化的触发因素可以释放与ST2受体结合的IL-33并增加炎症;因此,靶向IL-33/SL2通路是一个治疗领域。Neil J Greening (University of Leicester, Leicester, UK)发表了2b期ALIENTO试验的结果,比较了阿斯特戈利单抗(一种靶向ST2并阻断IL-33活性的人IgG2单克隆抗体)与安慰剂在40-90岁当前或曾经吸烟者中的疗效。首先,Ioana R Preston (Tufts Medical Center, Boston, MA, USA)介绍了SOTERIA长期随访研究的新安全性数据,该研究的中期结果已在之前发表。Chalmers评论道:“Sotatercept是一系列有影响力的试验支持的PAH的游戏规则改变者,[但是]新疗法的长期安全性是nerandomilast治疗IPF。justin M Oldham(密歇根大学,Ann Arbor, MI, USA)提交了磷酸二酯酶4B抑制剂nerandomilast治疗特发性肺纤维化(IPF)患者的FIBRONEER-IPF 3期试验的最终数据。1117名平均年龄约为70岁的患者被分配到12周的nerandomilast 9 mg每日2次,nerandomilast 18 mg每日2次或安慰剂组。77.7%的患者在入组时正在服用尼达尼布或吡非尼酮。先前发表的试验结果:高渗盐水和卡西汀治疗支气管扩张加重粘液活性药物,如高渗盐水和卡西汀,通常用于支气管扩张患者,以防止加重;然而,几乎没有证据表明它们的有效性。朱迪·M·布拉德利(英国贝尔法斯特女王大学威尔康-沃尔夫森实验医学研究所)评论说:“支气管扩张患者经常对服用似乎没有效果的药物感到沮丧。”布拉德利介绍了英国CLEAR试验的结果
{"title":"European Respiratory Society International Congress 2025","authors":"Priya Venkatesan","doi":"10.1016/s2213-2600(25)00366-2","DOIUrl":"https://doi.org/10.1016/s2213-2600(25)00366-2","url":null,"abstract":"<h2>Section snippets</h2><section><section><h2>Early-life exposure to paracetamol versus ibuprofen</h2>Previous non-experimental studies suggest an association between paracetamol exposure in the first year of life and subsequent asthma and eczema developing in childhood; however, randomised trials are needed to establish whether a causal link truly exists. Stuart R Dalziel (University of Auckland, Auckland, New Zealand) presented 1-year results from the PIPPA Tamariki randomised <span><span>study</span><svg aria-label=\"Opens in new window\" focusable=\"false\" height=\"20\" viewbox=\"0 0 8 8\"><path d=\"M1.12949 2.1072V1H7V6.85795H5.89111V2.90281L0.784057 8L0 7.21635L5.11902 2.1072H1.12949Z\"></path></svg></span> comparing the use of paracetamol versus ibuprofen in early life. The study included 3908 infants in New Zealand</section></section><section><section><h2>Astegolimab for COPD</h2>Triggers of exacerbations in chronic obstructive pulmonary disease (COPD) can release IL-33 that binds to the ST2 receptor and increase inflammation; therefore, targeting the IL-33/SL2 pathway is an area of therapeutic interest. Neil J Greening (University of Leicester, Leicester, UK) presented results from the phase 2b <span><span>ALIENTO trial</span><svg aria-label=\"Opens in new window\" focusable=\"false\" height=\"20\" viewbox=\"0 0 8 8\"><path d=\"M1.12949 2.1072V1H7V6.85795H5.89111V2.90281L0.784057 8L0 7.21635L5.11902 2.1072H1.12949Z\"></path></svg></span> comparing astegolimab, a human IgG2 monoclonal antibody targeting ST2 and blocking IL-33 activity, versus placebo in current or former smokers aged 40–90 years</section></section><section><section><h2>Sotatercept for PAH</h2>Two studies were presented on sotatercept, a fusion protein that inhibits activin signalling, for the treatment of pulmonary arterial hypertension (PAH). In the first, Ioana R Preston (Tufts Medical Center, Boston, MA, USA) presented new safety data from the <span><span>SOTERIA</span><svg aria-label=\"Opens in new window\" focusable=\"false\" height=\"20\" viewbox=\"0 0 8 8\"><path d=\"M1.12949 2.1072V1H7V6.85795H5.89111V2.90281L0.784057 8L0 7.21635L5.11902 2.1072H1.12949Z\"></path></svg></span> long-term follow-up study, the interim results for which were published <span><span>previously</span><svg aria-label=\"Opens in new window\" focusable=\"false\" height=\"20\" viewbox=\"0 0 8 8\"><path d=\"M1.12949 2.1072V1H7V6.85795H5.89111V2.90281L0.784057 8L0 7.21635L5.11902 2.1072H1.12949Z\"></path></svg></span>. Chalmers commented “Sotatercept is a game changer in PAH supported by a series of impactful trials, [but] long-term safety of new therapies is</section></section><section><section><h2>Nerandomilast for IPF</h2>Justin M Oldham (University of Michigan, Ann Arbor, MI, USA) presented final data from the <span><span>FIBRONEER-IPF</span><svg aria-label=\"Opens in new window\" focusable=\"false\" height=\"20\" viewbox=\"0 0 8 8\"><path d=\"M1.12949 2.1072V1H7V6.85795H5.89111V2.90281L0.784057 8L0 7.21635L5.11902 2.1072H1.12949Z\"></pat","PeriodicalId":51307,"journal":{"name":"Lancet Respiratory Medicine","volume":"33 1","pages":""},"PeriodicalIF":76.2,"publicationDate":"2025-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145247360","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}