Advances in Respiratory Medicine

15 pages, 870 KB

Open AccessArticle

COPD Assessment Test Variability as a Predictor of Exacerbations in Patients with COPD: A Prospective Study Using Virtual Assistant Monitoring

by Cristina Aljama, Robson Aparecido Prudente, Ane Lopez-Gonzalez, María Sáez, Suzana E. Tanni, Júlia Sampol, Núria Rodés, Yesly Esthepannie Carlos, Mercedes Pallero, Sergi Martí, Gerard Orriols, Marian Ramon, Galo Granados, Cristina Esquinas, Marc Miravitlles and Miriam Barrecheguren

Adv. Respir. Med. 2026, 94(5), 64; https://doi.org/10.3390/arm94050064 - 7 Sep 2026

Abstract

Although short-term CAT score variability has been associated with COPD exacerbations, evidence supporting its integration into virtual assistant-based monitoring remains limited. The aim of this study was to assess the short-term variability in CAT scores using a virtual management tool in patients with [...] Read more.

Although short-term CAT score variability has been associated with COPD exacerbations, evidence supporting its integration into virtual assistant-based monitoring remains limited. The aim of this study was to assess the short-term variability in CAT scores using a virtual management tool in patients with COPD and to examine its relationship with the prediction of exacerbations. A prospective observational single-center study was conducted in patients aged >35 with COPD and an exacerbator phenotype (≥2 outpatient exacerbations or ≥1 hospitalization in the previous year). Follow-up was performed weekly, including the CAT questionnaire, through calls were conducted by the virtual assistant Tucuvi Health Manager^® during a period of one year. A total of 106 patients were included; 64.2% were male, with a mean (SD) age of 66.8 (7.9) years and a median FEV₁(%) of 38.8 (30.1–45.0). The mean follow-up was 25 weeks [IQR 20–35], during which 73 (69%) patients experienced ≥1 exacerbation, accounting for 192 episodes (26% of which required hospitalization). A total of 2550 CAT scores were collected. The mean baseline CAT score was 17.9 (7.6), and scores increased significantly during exacerbations compared with non-exacerbation periods and according to exacerbation severity. Each one-point increase in absolute CAT score was associated with an 11.1% increase in the odds of exacerbation (OR: 1.11; 95% CI: 1.08–1.13), while a weekly variation of ≥2 points (MCID) was associated with more than sixfold higher odds (OR: 6.30; 95% CI: 4.28–9.27). The optimal cut-off for CAT change in the prediction of exacerbation risk was 3 points with a ROC curve of 0.773. Weekly deterioration in CAT scores was associated with increased exacerbation risk in patients with COPD. Short-term increases in CAT may serve as clinically useful warning signals for exacerbation. Full article

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22 pages, 863 KB

Open AccessReview

Precision Medicine in Overlap Syndrome (COPD–Obstructive Sleep Apnea): From Phenotypes and Endotypes to Treatable Traits

by Carina Adina Afloarei, Andreea Zabara Antal, David Toma, Adriana Loredana Pintilie, Georgiana Pitusac, Raluca Tiron, Tudor Birladeanu, Teodor Zaharia and Radu Crisan Dabija

Adv. Respir. Med. 2026, 94(5), 63; https://doi.org/10.3390/arm94050063 - 1 Sep 2026

Abstract

Introduction: COPD-OSA overlap syndrome (OVS) is defined by the coexistence of chronic obstructive pulmonary disease and obstructive sleep apnea syndrome in the same patient; it affects 28.3% of patients evaluated for either condition and is associated with significantly higher mortality compared to either [...] Read more.

Introduction: COPD-OSA overlap syndrome (OVS) is defined by the coexistence of chronic obstructive pulmonary disease and obstructive sleep apnea syndrome in the same patient; it affects 28.3% of patients evaluated for either condition and is associated with significantly higher mortality compared to either pathology in isolation. Current therapeutic approaches, involving PAP therapy and bronchodilation, treat this syndrome as a homogeneous entity and ignore the biological heterogeneity of this patient population. Objectives: This review proposes a systematic framework for the endotypic classification of biological interactions between COPD and OSA, integrating current literature on the pathophysiological mechanisms underlying the OVS, clinically accessible biomarkers, and emerging therapies. Methods: A narrative review based on available literature, focusing on studies published between 2010 and 2026 identified via searches in PubMed, PMC, and Dove Medical Press using the terms: COPD-OSA overlap syndrome, endotype, precision medicine, phenotype, biomarker, dupilumab, and incretin-based therapies. Results: Four clinical phenotypes (obese-metabolic, emphysematous, bronchitic-hypoxemic, and hypercapnic) and three molecular endotypes (Th2/eosinophilic, neutrophilic/oxidative, and metabolic-adipokine) are proposed, each with distinct pathophysiological mechanisms and specific therapeutic implications. The interaction between the two conditions generates a unique, pronounced hypoxemic profile. We propose the “double-hit hypoxemia” model as a conceptual framework characterized by amplified systemic inflammation and increased cardiovascular risk compared to either pathology in isolation. This proposed model has not yet been prospectively validated. Dupilumab (approved for an inflammatory phenotype in COPD patients characterized by eosinophil counts ≥ 300 cells/μL) represents a promising option, though currently unsupported in the OVS population, that could nonetheless be relevant to the Th2/eosinophilic endotype of this syndrome and tirzepatide (which reduced the AHI by up to 23.8 events/hour versus placebo in the SURMOUNT-OSA trial, conducted in patients with obesity and moderate-to-severe OSA, rather than in patients with confirmed OVS) could represent a promising therapy for the metabolic-adipokine endotype of obese patients with OVS. A minimal biomarker panel, comprising blood eosinophils, FeNO, daytime PaCO₂, BMI, and T90, allows for a practical approach to identifying the dominant endotype. Conclusions: Endotyping of OVS may provide a framework for moving beyond a uniform therapeutic approach toward more individualized management based on the dominant underlying biological mechanism. Randomized clinical trials focusing on endotypic stratification and OVS cohorts remain research priorities. Full article

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17 pages, 1198 KB

Open AccessArticle

Patterns of Comorbidity in Asthma–COPD Overlap Cohort According to Various ACO Definitions

by Andrzej Obojski, Krzysztof Kuziemski, Marek Barczyk, Rafał Krenke, Ewa Wycinka and Adam Barczyk

Adv. Respir. Med. 2026, 94(5), 62; https://doi.org/10.3390/arm94050062 - 31 Aug 2026

Abstract

Background: The asthma–COPD overlap is widely recognized, but its characteristics are not fully understood. This is largely true for the clinical presentation characterized by various ACO definitions. The purpose of this study was to investigate the pattern of comorbidities among patients with ACO, [...] Read more.

Background: The asthma–COPD overlap is widely recognized, but its characteristics are not fully understood. This is largely true for the clinical presentation characterized by various ACO definitions. The purpose of this study was to investigate the pattern of comorbidities among patients with ACO, defined by various criteria. Methods: The data came from the multicenter cross-sectional study conducted in a mixed population of patients with asthma and COPD. Patients were classified into five groups according to five different definitions of ACO (GINA/GOLD/30%, Spanish criteria, COPD + asthma < 40, Gibson’s criteria, clinician’s diagnosis), reference ACO groups, and a group of patients with obstructive pulmonary diseases who were not diagnosed with ACO. To demonstrate the differences between groups, we compared the prevalence of comorbidities between all ACO and non-ACO groups. Data on age, severity of airflow obstruction, and smoking history were recorded for all patients. Results: For the final analysis, 1609 patients were included. Patients belonging to the ACO groups had a higher burden of comorbidities, poorer lung function, and a higher number of pack-years of smoking history compared to patients without an ACO diagnosis. Comorbidities were significantly more prevalent in ACO groups. Compared to the non-ACO group, nine diseases were more common in the GINA/GOLD/30% group, seven in both the COPD + asthma < 40 group and the clinician’s diagnosis group, five in the Gibson’s criteria group, and two in the Spanish criteria group. The most common comorbidities in the ACO groups were hypertension, coronary artery disease, GERD, musculoskeletal disorders, diabetes, and chronic sinusitis. Chronic sinusitis was more frequent in ACO groups defined by more precise asthma criteria. Conclusions: The definitions of ACO used in clinical practice vary widely and describe different populations. ACO populations vary in terms of comorbidities, lung function, smoking history, and age. Chronic sinusitis is a comorbidity that occurs more frequently in ACO groups defined by more precise asthma criteria. Patients with ACO differ in their clinical outcomes from those with other obstructive airway diseases. Full article

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16 pages, 426 KB

Open AccessReview

Morphological Analysis of the Flow–Volume Curve for Identifying Fixed Airflow Obstruction: A Scoping Review

by Alirio Bastidas-Goyes, Luis F. Giraldo-Cadavid, Eduardo Tuta-Quintero, Diana Diaz-Quijano, Daniel Botero-Rosas, Adriana Maldonado-Franco, Alejandra Vargas, Paula Rincón, Lina López, Juan S. Hernández, Juan Castro, Isabella Criado, Charbel Faizal-Gómez, David Jiménez, Ingrid Mora and Juan León

Adv. Respir. Med. 2026, 94(5), 61; https://doi.org/10.3390/arm94050061 - 29 Aug 2026

Abstract

Background/Objective: The morphology of the flow–volume curve has emerged as a potential source of additional functional information by enabling the analysis of concavity, slope-based metrics, area-derived measures, and mathematical models extracted from the expiratory tracing. Therefore, the aim of this study was to [...] Read more.

Background/Objective: The morphology of the flow–volume curve has emerged as a potential source of additional functional information by enabling the analysis of concavity, slope-based metrics, area-derived measures, and mathematical models extracted from the expiratory tracing. Therefore, the aim of this study was to map and describe the available evidence on morphological analysis methods of the expiratory flow–volume curve for the identification and characterization of fixed airflow obstruction. Methods: A scoping review was conducted following the methodological frameworks proposed by Arksey and O’Malley, Levac et al., the Joanna Briggs Institute, and the PRISMA Extension for Scoping Reviews (PRISMA-ScR). Studies published between 1 January 1990, and 31 December 2025, that evaluated morphological flow–volume curve metrics for the diagnosis or characterization of Chronic Obstructive Pulmonary Disease (COPD) were included, without language restrictions. Searches were performed in PubMed/MEDLINE, Embase, Scopus, Web of Science, IEEE Xplore, OpenGrey, and Google Scholar. Study selection was conducted by independent reviewers, with disagreements resolved by consensus, and data extraction was performed using a standardized form. Results were synthesized narratively and organized according to metric families. Results: The search identified 13,577 records; after duplicate removal and screening, 24 studies met the inclusion criteria. The evidence included observational studies, diagnostic validation studies, longitudinal cohorts, and methodological modeling studies. Identified metrics were grouped into four main categories: concavity and geometric indices of the flow–volume curve, expiratory slope and flow-decay metrics, area-based or volumetric-derived measures, and mathematical or computational models applied to the tracing. Concavity indices, the β-angle, slope-ratio, Peak Index, and the D parameter showed consistent associations with airflow obstruction, emphysema, small airway disease, or functional impairment. Expiratory slope metrics and Flow Decay demonstrated high diagnostic performance in several studies, whereas area-based measures such as AEX, AEX-FV, AreaFE%, and AUC3/AT3 integrated the overall loss of expiratory flow during forced expiration. Mathematical and computational models suggested that the complete shape of the curve contains additional diagnostic and prognostic information, although methodological variability and the need for external validation remain important limitations. Conclusions: Morphological analysis of the flow–volume curve represents a promising approach to complement conventional spirometry in the identification and characterization of fixed airflow obstruction. These metrics may provide additional information regarding airflow limitation, non-uniform lung emptying, emphysema, small airway disease, hyperinflation, and clinically relevant outcomes. Full article

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19 pages, 3719 KB

Open AccessArticle

Chlorogenic Acid Attenuates Bleomycin-Induced Pulmonary Fibrosis in a Murine Model by Modulating TGF-β1 Expression

by Juan Manuel Velázquez-Enríquez, Alma Aurora Ramírez-Hernández, Jovito César Santos-Álvarez, Edilburga Reyes-Jiménez, Antonio Arcos-Román, Jaime Arellanes-Robledo, Carlos Alberto Matias-Cervantes, María del Socorro Pina-Canseco, Verónica Rocío Vásquez-Garzón and Rafael Baltiérrez-Hoyos

Adv. Respir. Med. 2026, 94(5), 60; https://doi.org/10.3390/arm94050060 - 25 Aug 2026

Abstract

Background: Idiopathic pulmonary fibrosis (IPF) is a progressive interstitial lung disease driven by aberrant extracellular matrix deposition, with the activity of transforming growth factor-beta 1 (TGF-β1) orchestrating fibrogenesis. Current therapies are limited by severe adverse effects, highlighting the unmet need for safer treatments. [...] Read more.

Background: Idiopathic pulmonary fibrosis (IPF) is a progressive interstitial lung disease driven by aberrant extracellular matrix deposition, with the activity of transforming growth factor-beta 1 (TGF-β1) orchestrating fibrogenesis. Current therapies are limited by severe adverse effects, highlighting the unmet need for safer treatments. In this study, the therapeutic potential of chlorogenic acid (CGA) in a murine model of pulmonary fibrosis was evaluated. Methods: Pathology was induced on day 0 via subcutaneous osmotic minipumps delivering bleomycin (BLM) for one week, followed by pump removal on day 10. Therapeutic interventions with intragastric CGA (60 mg/kg) were administered daily from days 14 to 20. Lung tissue samples obtained on day 21 were analyzed via histological, immunohistochemical, and RT–PCR methods. Results: Histological analysis via H&E and Masson’s trichrome staining revealed that CGA treatment significantly attenuated alveolar thickening, restored the alveolar space, and reduced the total cell density and Ashcroft fibrosis score. Furthermore, CGA markedly decreased collagen deposition. Quantitative RT–PCR and immunohistochemical assays revealed that CGA effectively decreased the expression of Col1a1, TGF-β1, and the myofibroblast marker alpha-smooth muscle actin (α-SMA). Conclusions: CGA exerts important therapeutic effects by decreasing the expression of TGF-β1 and the activation of myofibroblasts, indicating that this natural polyphenol is a promising candidate for mitigating the progression of pulmonary fibrosis. Full article

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11 pages, 3526 KB

Open AccessArticle

Serum Angiopoietin-1 and Angiopoietin-2 as Biomarkers of Pulmonary Hemodynamic Burden in COPD-Associated Pulmonary Hypertension: A Cross-Sectional Study

by Jyoti Bajpai, Akshyaya Pradhan, Mohammed Kaleem Ahmad, Surya Kant, Ajay Kumar Verma, Darshan Kumar Bajaj, Rishi Sethi and Mario Cazzola

Adv. Respir. Med. 2026, 94(4), 59; https://doi.org/10.3390/arm94040059 - 11 Aug 2026

Abstract

Purpose: Pulmonary hypertension (PH) is a serious complication of COPD associated with worse outcomes. Reliable circulating biomarkers of pulmonary vascular involvement are lacking. Angiopoietin-1 (ANGP-1) and angiopoietin-2 (ANGP-2) regulate endothelial homeostasis, but their relationship with echocardiographically estimated pulmonary pressure in COPD remains uncertain. [...] Read more.

Purpose: Pulmonary hypertension (PH) is a serious complication of COPD associated with worse outcomes. Reliable circulating biomarkers of pulmonary vascular involvement are lacking. Angiopoietin-1 (ANGP-1) and angiopoietin-2 (ANGP-2) regulate endothelial homeostasis, but their relationship with echocardiographically estimated pulmonary pressure in COPD remains uncertain. Methods: This prospective cross-sectional study included 70 consecutively recruited adults with COPD, stratified using a study-specific echocardiographic threshold into the COPD PH group (mPAP > 20 mmHg; n = 46) and the COPD without PH (mPAP < 20 mmHg; n = 24), together with 20 additional controls. This non-invasive stratification was not considered equivalent to PH confirmed by right heart catheterization. Serum ANGP-1 and ANGP-2 were measured using ELISA. Group differences and associations with e-mPAP and right atrial pressure (RAP) were assessed. Results: Median ANGP-1 was higher in the elevated e-mPAP group [8780.06 (IQR 7955.29–9902.88) pg/mL] than in the lower e-mPAP group [3065.14 (1170.69–6200.41)] and controls [2997.19 (1292.13–3278.18); p < 0.001]. ANGP-2 showed a similar pattern [6152.92 (5380.27–8652.50), 2669.77 (1802.18–4744.00), and 2405.54 (1779.73–3751.76) pg/mL; p < 0.001]. Among COPD participants, ANGP-1 and ANGP-2 correlated with e-mPAP (r = 0.64 and r = 0.54) and RAP (r = 0.54 and r = 0.52; all Holm-adjusted p < 0.001). In multivariable models, e-mPAP and RAP were independently associated with ANGP-1, whereas RAP was independently associated with ANGP-2. Conclusions: Higher circulating ANGP-1 and ANGP-2 were associated with an elevated echo-estimated pulmonary-pressure phenotype in COPD. These findings are exploratory and require validation in larger cohorts using direct hemodynamic assessment. Full article

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21 pages, 7267 KB

Open AccessArticle

Effects of Inhaled Amitriptyline on Airway Function and Immune Responses in Experimental Asthma

by Anna Michely, Svenja Böll, Lida Yao, Regina Ben Hamza, Irina Rachimow, Klaus Tenbrock, Christian Martin and Eva Verjans

Adv. Respir. Med. 2026, 94(4), 58; https://doi.org/10.3390/arm94040058 - 6 Aug 2026

Abstract

Background: Bronchial asthma is a chronic inflammatory airway disease characterized by acute bronchoconstriction and type 2-driven inflammation. This study investigated whether inhaled amitriptyline, a functional inhibitor of acid sphingomyelinase, exerts both bronchodilatory and immunomodulatory effects in experimental murine models of allergic airway inflammation [...] Read more.

Background: Bronchial asthma is a chronic inflammatory airway disease characterized by acute bronchoconstriction and type 2-driven inflammation. This study investigated whether inhaled amitriptyline, a functional inhibitor of acid sphingomyelinase, exerts both bronchodilatory and immunomodulatory effects in experimental murine models of allergic airway inflammation (AAI) and human cellular systems. Methods: Acute AAI was induced in mice using ovalbumin (OVA) and house dust mite (HDM) protocols, respectively. Inhaled amitriptyline (3.3 mg/mL) was administered for either 20 days (short-term) or 36 days (long-term). Lung function was assessed using FlexiVent^®, and inflammatory markers including IgE, eosinophils, and type 2 cytokines were measured in bronchoalveolar lavage fluid and lung tissue. Complementary experiments were included using passively sensitized PCLSs and human type 2-differentiated CD4⁺ T cells. Results: Inhaled amitriptyline improved lung mechanics in both the OVA and HDM models, reducing total respiratory resistance and elastance. In the OVA model, eosinophil and T cell counts in BALF were decreased, whereas immunomodulatory effects were less pronounced in the short-term HDM model. In human T_H2 cells, no significant changes in cytokine production or gene expression were observed. Ex vivo, amitriptyline dose-dependently inhibited allergen-induced bronchoconstriction in PCLSs. Conclusions: Inhaled amitriptyline improves lung function across murine models of AAI, supporting its potential in exhibiting model-dependent immunomodulatory effects, and directly attenuates allergen-induced bronchoconstriction, supporting its potential as a bronchodilator with context-dependent immunomodulatory properties. Full article

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12 pages, 1324 KB

Open AccessArticle

Left Ventricular Diastolic Dysfunction in Patients with Interstitial Lung Disease—A Potential Treatable Trait

by Ophir Freund, Uriel Katsoff, Tzlil Hershko, Ayala Ron, Shir Frydman, Doron Cohn-Schwartz, Aviv Kupershmidt, Neta Mano, Ariel Melloul, Eyal Kleinhendler, Amir Bar-Shai and Avraham Unterman

Adv. Respir. Med. 2026, 94(4), 57; https://doi.org/10.3390/arm94040057 - 4 Aug 2026

Abstract

Cardiovascular comorbidities complicate interstitial lung disease (ILD) and represent potential therapeutic targets, yet the prevalence and clinical impact of left ventricular diastolic dysfunction (LVDD) remain poorly characterized. We aimed to evaluate LVDD as a potential treatable trait within a prospective cohort. Using data [...] Read more.

Cardiovascular comorbidities complicate interstitial lung disease (ILD) and represent potential therapeutic targets, yet the prevalence and clinical impact of left ventricular diastolic dysfunction (LVDD) remain poorly characterized. We aimed to evaluate LVDD as a potential treatable trait within a prospective cohort. Using data from an ILD registry (January 2021–October 2024), we defined clinically relevant LVDD as echocardiographic grade 2 or 3 diastolic dysfunction. Out of 276 patients (median age 69, 44% female), 14% had LVDD, which was almost entirely in patients with fibrosis (97%, p = 0.045) and associated with lower diffusing capacity for carbon monoxide. Survival and clinical analyses restricted to the fibrotic ILD subgroup (n = 241) showed that LVDD was independently associated with a higher hazard for a combined adverse outcome of acute exacerbation, lung transplantation, or death (adjusted HR 1.82, 95% CI 1.03–3.38, p = 0.043), which persisted after 1:2 propensity score matching (HR 2.04). LVDD also independently predicted increased all-cause mortality (adjusted HR 2.10) and reduced 6-min walk distance (median 413 vs. 465 m, β = −0.14, p = 0.036). In conclusion, LVDD is prevalent in fibrotic ILD and carries significant prognostic implications. Given its objective measurability and actionable treatment pathways, LVDD represents a potentially important treatable trait requiring multi-disciplinary care. Full article

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14 pages, 1353 KB

Open AccessArticle

Timothy Grass Pollen-Specific Immunoglobulin E in Nasal Secretions During Natural Allergen Exposure and After a Nasal Provocation Test in Patients with Suspected Local Allergic Rhinitis

by Mohamad Mahdi Mortada, Waleed Aman Ur Rahman, Alaa Sherri, Gabriela Pawlak, Krystian Kowalski, Anna Piłat, Edyta Pietrowska, Marta Popławska, Iwona Dziembała-Gładysz, Barbara Majkowska-Wojciechowska and Marcin Kurowski

Adv. Respir. Med. 2026, 94(4), 56; https://doi.org/10.3390/arm94040056 - 3 Aug 2026

Abstract

Introduction: Allergic rhinitis (AR) imposes a substantial burden on individuals worldwide. Local allergic rhinitis (LAR) patients exhibit symptoms similar to those of AR without a positive skin prick test (SPT) or the presence of sIgE specific to one or more allergens. Our study [...] Read more.

Introduction: Allergic rhinitis (AR) imposes a substantial burden on individuals worldwide. Local allergic rhinitis (LAR) patients exhibit symptoms similar to those of AR without a positive skin prick test (SPT) or the presence of sIgE specific to one or more allergens. Our study evaluated specific and total grass pollen IgE in the nasal secretions of patients with suspected LAR, examining the effects of natural pollen exposure and nasal provocation testing (NPT). Methods: Twenty-nine subjects (18 with suspected LAR and 11 with AR) were included in this study. The total nasal symptom score (TNSS) and visual analog scale (VAS) were used for subjective assessment. NPT was performed using grass pollen allergen. Nasal lavage was used to obtain nasal secretions, and the levels of sIgE and total IgE were measured. Results: During the exposure vs. the off-exposure period, the TNSS and VAS were significantly higher in LAR (p < 0.0001 and p = 0.0061, respectively). sIgE and total IgE were significantly higher in the AR group than in the LAR group during the exposure period (p = 0.0008 and p = 0.0491, respectively). LAR diagnosis was confirmed in seven subjects. TNSS and VAS scores were higher after a positive NPT. The median level of sIgE was lower in the negative and positive NPT. A higher median total IgE level was observed post-provocation in both groups. A significantly higher median relative sIgE level was noted after positive and negative provocation (p = 0.0156 and p = 0.0143, respectively). Conclusions: The assessment of local sIgE levels in nasal secretions can be used as a method for the diagnostic workup of patients with suspected LAR. Achieving a well-defined and standardized protocol for the assessment of sIgE concentrations in nasal secretions of LAR is a goal of future larger studies. Full article

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17 pages, 1179 KB

Open AccessArticle

Who Really Benefits from CPAP? Disease Severity, Response Quality, and Long-Term Survival in Obstructive Sleep Apnea

by Wojciech Kuczyński, Karol Pierzchała, Weronika Bielska, Zuzanna Boczar, Aleksandra Kudrycka and Piotr Białasiewicz

Adv. Respir. Med. 2026, 94(4), 55; https://doi.org/10.3390/arm94040055 - 28 Jul 2026

Abstract

Obstructive sleep apnea (OSA) is associated with increased cardiovascular, respiratory, and all-cause mortality, yet the long-term survival impact of continuous positive airway pressure (CPAP) remains contested, and treatment is usually analysed as a binary exposure rather than by the quality of the response [...] Read more.

Obstructive sleep apnea (OSA) is associated with increased cardiovascular, respiratory, and all-cause mortality, yet the long-term survival impact of continuous positive airway pressure (CPAP) remains contested, and treatment is usually analysed as a binary exposure rather than by the quality of the response achieved. In a single-centre cohort of 4368 adults referred for polysomnography and followed for 8–20 years (prespecified subgroup with apnea–hypopnea index [AHI] ≥ 15, n = 2304), we applied cause-specific Cox and Fine–Gray competing-risks models, together with machine-learning classifiers, to characterise all-cause, cardiovascular, and pulmonary mortality. CPAP was associated with reduced all-cause (hazard ratio [HR] 0.75), cardiovascular (HR 0.75), and pulmonary mortality (HR 0.54), with the benefit confined to severe OSA (HR 0.66) and absent in moderate disease (HR 0.95). Good responders showed a significant 34% reduction in all-cause mortality (HR 0.66), whereas poor responders showed no significant reduction. Nocturnal desaturation (time with oxygen saturation < 90%) was the dominant independent predictor of pulmonary mortality, and baseline features predicted response category only moderately (macro-averaged AUC 0.76). Long-term CPAP confers a severity- and response-dependent survival benefit; nocturnal hypoxaemia is a key, modifiable driver of respiratory death. Full article

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21 pages, 6332 KB

Open AccessArticle

Microglia-Mediated Ependymal Injury in Bacille Calmette-Guérin-Induced Meningitis Is Attenuated by Sodium Butyrate with Restoration of Hmgcs2 Expression

by Yang Ren, Danni Chen, Shiqi Xie, Yawen He, Xuanru Zhuang, Dan Ye, Zhentao Fei, Lu Xia, Yongjie Wang and Feng Li

Adv. Respir. Med. 2026, 94(4), 54; https://doi.org/10.3390/arm94040054 - 27 Jul 2026

Abstract

Background: Tuberculous meningitis (TBM) is the most severe form of central nervous system tuberculosis, associated with high mortality and neurological sequelae. Microglia-driven neuroinflammation is a key contributor to TBM pathogenesis; however, its specific effects on ependymal cells—critical for cerebrospinal fluid dynamics and barrier [...] Read more.

Background: Tuberculous meningitis (TBM) is the most severe form of central nervous system tuberculosis, associated with high mortality and neurological sequelae. Microglia-driven neuroinflammation is a key contributor to TBM pathogenesis; however, its specific effects on ependymal cells—critical for cerebrospinal fluid dynamics and barrier function—and potential therapeutic strategies remain unclear. Methods: A murine TBM model was established by tail vein injection of BCG. Although the virulence of BCG, an attenuated strain of Mycobacterium bovis, is different from that of clinically isolated human Mycobacterium tuberculosis, its induced phenotypes such as periventricular inflammatory infiltration, microglia activation, and ependymal dysfunction highly reproduce the key histopathological features of human TBM. Primary ependymal cells were cultured and treated either directly with BCG or indirectly with conditioned medium from BCG-stimulated BV2 microglial cells (BCG+BV2-CM). Transcriptomic profiling was conducted via RNA sequencing, with validation by qPCR and Western blot. Functional outcomes, including ciliary morphology and apoptosis, were assessed using immunofluorescence and flow cytometry. The therapeutic effect of sodium butyrate (NaB) was evaluated through pretreatment experiments. Results: BCG infection induced characteristic TBM pathology, with persistent bacteria in the brain and lungs, ventricular inflammation, and pulmonary damage. Transcriptomic analysis showed that direct BCG treatment altered the expression of 1036 genes in ependymal cells, whereas BCG+BV2-CM treatment induced 3558 differentially expressed genes, highlighting microglia’s role in amplifying ependymal injury. Integrated analysis identified 64 consistently dysregulated genes across in vitro and in vivo models, enriched in immune and metabolic pathways. BCG challenge significantly downregulated Hmgcs2, leading to ciliary shortening and increased apoptosis. Sodium butyrate treatment restored Hmgcs2 expression, preserved ciliary structure, and reduced apoptosis. Conclusion: Microglia profoundly exacerbate transcriptional dysregulation in ependymal cells during TBM. Sodium butyrate confers protection against BCG-induced ependymal damage by upregulating Hmgcs2, revealing a novel therapeutic target for tuberculous meningitis. Full article

(This article belongs to the Special Issue Infectious Diseases in Respiratory Medicine)

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20 pages, 3512 KB

Open AccessReview

Awake Prone Positioning in Non-Intubated Non-COVID-19 ARDS: A Comprehensive Review

by Mairi Ziaka and Aristomenis Exadaktylos

Adv. Respir. Med. 2026, 94(4), 53; https://doi.org/10.3390/arm94040053 - 27 Jul 2026

Cited by 1

Abstract

Despite advances in the understanding of the pathophysiology of acute respiratory distress syndrome (ARDS), treatment options remain limited and are mainly supportive, while mortality remains high. Prone positioning (PP) has been shown to improve oxygenation and lung mechanics in ARDS by reducing the [...] Read more.

Despite advances in the understanding of the pathophysiology of acute respiratory distress syndrome (ARDS), treatment options remain limited and are mainly supportive, while mortality remains high. Prone positioning (PP) has been shown to improve oxygenation and lung mechanics in ARDS by reducing the imbalance in ventilation distribution between ventral and dorsal lung regions, altering pulmonary blood flow distribution, modifying the density distribution of edematous lung tissue, and limiting areas with low ventilation–perfusion ratios. During the coronavirus disease 2019 (COVID-19) pandemic, the use of PP, referred to as awake prone positioning (APP), was extended to non-intubated patients with severe hypoxemic respiratory failure. However, several concerns remain, including worsening oxygenation following the transition from prone to supine position, the potential development of patient self-inflicted lung injury (P-SILI), and delays in endotracheal intubation and initiation of invasive mechanical ventilation. Evidence regarding the use of APP in non-COVID-19 ARDS is scarce and consists mainly of small case series and a limited number of prospective studies with small and heterogeneous populations. Therefore, in the present work, we aim to summarize the existing evidence on APP in non-COVID-19 ARDS and acute hypoxemic respiratory failure (AHRF), describe the underlying pathophysiological mechanisms, and highlight areas for future research. Full article

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14 pages, 2345 KB

Open AccessArticle

Association Between Physical Function, Pulmonary Function, and Social Determinants of Health in Individuals with Post-Tuberculosis Lung Disease

by Nielza Moreira de Souza, Pedro Henrique Perpetuo de Lima Silva, Estephane Ramos de Souza Penna, Amanda Oliveira dos Anjos, Alícia Sales Carneiro, Walter Costa, Bruna Cuoco Provenzano, Ana Paula Santos and Agnaldo José Lopes

Adv. Respir. Med. 2026, 94(4), 52; https://doi.org/10.3390/arm94040052 - 27 Jul 2026

Abstract

Although poverty and tuberculosis are insidiously linked, knowledge of the relationship between social determinants of health (SDoHs) and post-tuberculosis lung disease (PTLD) is limited. This study aimed to analyze the association between physical function, pulmonary function, and SDoHs in individuals with PTLD (iwPTLD), [...] Read more.

Although poverty and tuberculosis are insidiously linked, knowledge of the relationship between social determinants of health (SDoHs) and post-tuberculosis lung disease (PTLD) is limited. This study aimed to analyze the association between physical function, pulmonary function, and SDoHs in individuals with PTLD (iwPTLD), considering the impact of social inequalities on physical performance. This cross-sectional study collected social data from 69 iwPTLDs using a standardized assessment form. The patients underwent pulmonary function testing via spirometry and body plethysmography, as well as respiratory muscle strength and quadriceps muscle strength (QMS) testing. They also completed the six-minute step test (6MST). The median value of steps climbed by participants on the 6MST was 88 (57–117), corresponding to 50.1% (34.9–73.2) of the predicted value. The mean QMS was 28.7 ± 11.9 kgf, with 11 participants (17.4%) showing QMS below the cutoff point. Spirometry revealed normal, obstructive, restrictive, and mixed patterns in 19 (27.5%), 20 (29%), 18 (26.1%), and 12 (17.4%) of the participants, respectively. Performance on the 6MST showed no statistically significant association with SDoHs. QMS showed a statistically significant association with treated sewage (W = 84, p = 0.026). Forced expiratory volume in one second showed significant correlations with education level (ρ = 0.248, p = 0.040), social protection (W = 207, p = 0.050, r = 0.238), and treated water (W = 24.5, p = 0.029, r = 0.264). Maximum inspiratory pressure showed significant correlations with education level (ρ = 0.246, p = 0.042) and treated water (W = 20, p = 0.021, r = 0.280). The regression model for 6MST and QMS performance showed that 12% and 45% of the variability was explained by the studied variables, respectively. In iwPTLD, impairments in physical function and damage to lung function are weakly associated with the deterioration of SDoHs. While this relationship is weak, it should not be ignored because it may operate through indirect pathways. Full article

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9 pages, 822 KB

Open AccessArticle

Interstitial Lung Disease in the United States: CDC Mortality Trends (1999–2024)

by Palak Grover, Rahul Jain, Gurleen Kaur and Bipneet Singh

Adv. Respir. Med. 2026, 94(4), 51; https://doi.org/10.3390/arm94040051 - 24 Jul 2026

Abstract

Interstitial lung diseases (ILDs) comprise a heterogeneous group of pulmonary disorders associated with substantial morbidity and mortality. We examined mortality attributed to selected J84-coded ILDs in the United States from 1999 to 2024 using CDC WONDER underlying-cause-of-death data. Age-adjusted mortality rates (AAMRs) per [...] Read more.

Interstitial lung diseases (ILDs) comprise a heterogeneous group of pulmonary disorders associated with substantial morbidity and mortality. We examined mortality attributed to selected J84-coded ILDs in the United States from 1999 to 2024 using CDC WONDER underlying-cause-of-death data. Age-adjusted mortality rates (AAMRs) per 100,000 population were standardized to the 2000 U.S. population and stratified by sex and race. Joinpoint regression was used to identify changes in temporal slope and estimate annual percent change (APC), average annual percent change (AAPC), 95% confidence intervals (CIs), and p-values. After the removal of overlapping years between the CDC WONDER database series, 444,573 unique deaths occurred. Annual deaths increased from 11,358 in 1999 to 22,849 in 2024, while AAMR increased from 4.2 to 5.1 per 100,000. Overall, AAMR increased during 1999–2004 (APC 2.32%, 95% CI 1.39–3.26; p < 0.001) and more slowly during 2004–2024 (APC 0.36%, 95% CI 0.16–0.56; p = 0.001), with an overall AAPC of 0.75% (95% CI 0.60–0.90; p < 0.001). Male AAMRs remained higher than female AAMRs, while race-specific trends were heterogeneous. No temporal reduction in population mortality coincided with the introduction of antifibrotic therapies; however, this ecological analysis cannot evaluate treatment effectiveness or individual treatment exposure. Full article

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15 pages, 587 KB

Open AccessReview

Nanocarrier-Based Drug Delivery Systems for Lung Cancer: A Systematic Review and Meta-Analysis of Preclinical Studies

by Pranvera Breznica Selmani, Arlinda Daka Grapci, Blerina Koshi, Zana Sllamniku Dalipi and Rozafa Koliqi

Adv. Respir. Med. 2026, 94(4), 50; https://doi.org/10.3390/arm94040050 - 24 Jul 2026

Abstract

Drug delivery systems (DDS) may improve the therapeutic performance of chemotherapy in lung cancer, but their preclinical efficacy has not been quantitatively synthesized. We conducted a systematic review and meta-analysis of controlled in vivo mouse studies evaluating DDS-based chemotherapeutic formulations for lung cancer. [...] Read more.

Drug delivery systems (DDS) may improve the therapeutic performance of chemotherapy in lung cancer, but their preclinical efficacy has not been quantitatively synthesized. We conducted a systematic review and meta-analysis of controlled in vivo mouse studies evaluating DDS-based chemotherapeutic formulations for lung cancer. Databases were searched from inception to 15 February 2025, and methodological quality was assessed using the SYRCLE risk-of-bias tool. Thirty studies comprising 47 experiments were included. Compared with corresponding free-drug treatments, DDS-based chemotherapy significantly reduced tumor volume (WMD −310.67 mm³; 95% CI: −375.51 to −245.83; p < 0.001), although substantial heterogeneity was observed. Both targeted and non-targeted DDS were associated with tumor growth inhibition, and targeted formulations showed a larger average reduction; however, this finding should be interpreted in light of differences in formulation properties, tumor models, and treatment protocols. Nanoparticle, liposomal, and micellar platforms all demonstrated significant antitumor effects, while combination DDS and docetaxel- or cisplatin-based systems showed large effects in subgroup analyses with variable sample sizes. These findings support the continued development of DDS-based chemotherapy for lung cancer, but standardized reporting of nanocarrier characterization, pharmacokinetics, biodistribution, toxicity, and rigorous animal-study design is required to improve reproducibility and translational relevance. Full article

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11 pages, 553 KB

Open AccessArticle

Association of ICD-10-Coded Pneumonia Events with Interstitial Lung Disease Outcomes in Patients with Rheumatoid Arthritis: A Large Database Retrospective Cohort

by Esteban Kosak Lopez, Luis Rodriguez Donís, Justin Lam, Andrew Geller, Raul Leguizamon, Michael Vera Ricaurte, Priscilla Nethala, Maria Planchart Ferretto, Maria Laura Fernandez-Wever, Jose M. Martinez-Manzano, Enrique Pacheco and Shahrzad Abdollahi

Adv. Respir. Med. 2026, 94(4), 49; https://doi.org/10.3390/arm94040049 - 22 Jul 2026

Abstract

Introduction: Patients with rheumatoid arthritis (RA) have higher risk for pneumonia, interstitial lung disease (ILD) and pulmonary fibrosis (PF). However, the association between an ICD-10-coded pneumonia event (CPE) and the incidence of ILD or PF in the RA population remains unclear. Methods: We [...] Read more.

Introduction: Patients with rheumatoid arthritis (RA) have higher risk for pneumonia, interstitial lung disease (ILD) and pulmonary fibrosis (PF). However, the association between an ICD-10-coded pneumonia event (CPE) and the incidence of ILD or PF in the RA population remains unclear. Methods: We conducted a retrospective cohort study using the TriNetX database. Patients with ICD-10 for RA aged 50 or older who had a CPE within one year of RA diagnosis (CPE cohort, n = 4553) were matched 1:1 by propensity score for key factors, including demographics, comorbidities (i.e., COPD), and medication use (DMARDs, corticosteroids) to RA patients without a CPE (Control cohort, n = 4553). Cox proportional hazard models assessed the incidence of a composite ILD outcome, PF, and secondary complications over a 4-year follow-up after the index event defined as 1-year after RA diagnosis for both cohorts. Results: The CPE cohort showed an increased risk for all outcomes. Patients with CPE had a 2.48-fold increased risk for PF (HR = 2.48; 95% CI, 1.78–3.45; p < 0.01) and a 2.87-fold increased risk for the composite ILD outcome (HR = 2.87; 95% CI, 2.18–3.80; p < 0.01). The risk of rheumatoid lung disease was 4.15 times higher (HR = 4.15; 95% CI, 2.30–7.50; p < 0.01). Furthermore, the CPE group had a higher risk for all-cause mortality (HR = 1.82; 95% CI, 1.58–2.09; p < 0.01). Conclusions: The CPE within one year of RA diagnosis is associated with an increase in subsequent ILD-coded outcomes. While this retrospective design cannot establish causality, an unspecified pneumonia code in early RA may represent an early clinical manifestation of unrecognized ILD, serving as a high-risk marker that warrants pulmonary surveillance. Full article

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13 pages, 831 KB

Open AccessArticle

Artificial Intelligence-Induced Deskilling in Interventional Pulmonology: An International Cross-Sectional Survey on Risk Perception and Mitigation Strategies

by Guido Marchi and Lorenzo Corbetta

Adv. Respir. Med. 2026, 94(4), 48; https://doi.org/10.3390/arm94040048 - 20 Jul 2026

Abstract

Artificial intelligence (AI) is progressively reshaping interventional pulmonology (IP), yet its potential to erode procedural and cognitive competencies through AI-induced deskilling remains poorly characterized in this specialty. An international, observational, cross-sectional survey was conducted in May 2026 among 118 expert interventional pulmonologists from [...] Read more.

Artificial intelligence (AI) is progressively reshaping interventional pulmonology (IP), yet its potential to erode procedural and cognitive competencies through AI-induced deskilling remains poorly characterized in this specialty. An international, observational, cross-sectional survey was conducted in May 2026 among 118 expert interventional pulmonologists from 10 different countries across 5 continents. Participants completed a structured questionnaire comprising five demographic items and 12 Likert-scale statements addressing deskilling risk perception and mitigation attitudes; percentage agreement was calculated for each item (scores 4–5). High perceived clinical value of AI was reported (87%), alongside substantial concern for procedural deskilling (73%) and upskilling inhibition (83%). Familiarity with automation bias was limited (38%), yet its clinical relevance was widely recognized after definition provision (81%)—a gap of 43 percentage points. Strong support emerged for AI-free training (84%), simulation-based training (86%), and longitudinal performance monitoring (78%). Concern for institutional fragility in the absence of AI was expressed by 74%, and governance frameworks, including minimum non-AI-assisted procedural volume requirements, were endorsed by 70%. Deskilling was identified as a high research priority by 89%. These findings indicate that AI-induced deskilling is perceived as a relevant and emerging risk by expert interventional pulmonologists internationally, even before the widespread clinical deployment of AI technologies. Although the extent to which these concerns will translate into measurable effects on procedural competence is currently uncertain, the results underscore the need for prospective research, educational initiatives, and appropriate governance frameworks to ensure the preservation of core procedural skills. Full article

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13 pages, 705 KB

Open AccessArticle

Cystic Fibrosis Mortality Trends 1999–2024—A CDC Wonder Study

by Palak Grover, Rahul Jain, Gurleen Kaur, Niroshan Ranjan and Bipneet Singh

Adv. Respir. Med. 2026, 94(4), 47; https://doi.org/10.3390/arm94040047 - 14 Jul 2026

Abstract

Cystic fibrosis (CF) is an autosomal recessive disorder caused by mutations in the CFTR gene. The sequential approval of CFTR modulators ivacaftor (2012), lumacaftor/ivacaftor (2015), tezacaftor/ivacaftor (2018), and elexacaftor/tezacaftor/ivacaftor (2019) has transformed CF care, but population-level mortality trends across therapeutic periods have not [...] Read more.

Cystic fibrosis (CF) is an autosomal recessive disorder caused by mutations in the CFTR gene. The sequential approval of CFTR modulators ivacaftor (2012), lumacaftor/ivacaftor (2015), tezacaftor/ivacaftor (2018), and elexacaftor/tezacaftor/ivacaftor (2019) has transformed CF care, but population-level mortality trends across therapeutic periods have not been comprehensively assessed. We conducted a retrospective analysis of CF mortality in the United States from 1999 to 2024 using CDC WONDER Underlying Cause of Death data (ICD-10 codes E84.0–E84.9). Age-adjusted mortality rates (AAMR) per 100,000 were calculated using the 2000 U.S. standard population. The study period was divided into three periods: pre-modulator (1999–2011), early modulator (2012–2018), and elexacaftor/tezacaftor/ivacaftor (2019–2024). Annual mortality trends were evaluated using segmented log-linear Poisson regression, with annual death counts as the outcome and the corresponding U.S. population as an offset. Candidate models with multiple change points were compared to identify distinct temporal segments. Annual percent changes (APCs) and 95% confidence intervals (CIs) were estimated for each segment. Prespecified therapeutic periods, including pre-modulator (1999–2011), early modulator (2012–2018), and ETI period (2019–2024), were retained for descriptive analyses. Trends were stratified by sex and U.S. Census Region. A total of 10,959 CF deaths were recorded over 26 years. In the pre-modulator period, mortality was stable at a mean of 478 deaths/year (AAMR 0.14–0.17). The early modulator period showed a modest 5.4% reduction in mean annual deaths (452/year). The period following ETI availability was associated with a decline to 263/year, a 47% reduction from the pre-modulator period (AAPC −8.6%/year). The AAMR declined from 0.17 (1999) to 0.07 (2024). The female-to-male death count ratio shifted from 1.05 to 0.97 across periods, though age-adjusted rates were identical between sexes within each period, and this finding should be interpreted cautiously. Regionally, the South’s share of CF deaths grew from 37.2% to 41.6% despite absolute declines in all regions, suggesting potential geographic disparities that warrant further investigation with individual-level data. Segmented regression identified change points in 2005 and 2015. Mortality declined significantly from 1999 through 2005 (APC, −2.70%; 95% CI, −4.01% to −1.37%), remained stable from 2006 through 2015 (APC, +0.21%; 95% CI, −0.47% to +0.90%), and declined sharply from 2016 through 2024 (APC, −9.76%; 95% CI, −10.66% to −8.84%). CF mortality in the United States has declined by more than half since the introduction of CFTR modulators. The shift in the sex-based death count ratio and the concentration of remaining deaths in the South are hypothesis-generating observations that require confirmation with individual-level data. These ecological findings cannot establish causation, as concurrent changes in supportive care, lung transplantation practices, and COVID-19 pandemic effects may have contributed to the observed trends. Full article

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14 pages, 1448 KB

Open AccessSystematic Review

Prevalence and Impact of Pulmonary Hypertension Associated with Arteriovenous Fistulas and Grafts in End-Stage Renal Disease: A Systematic Review and Meta-Analysis

by Ahmed A. Zayed, Mohammad Aldalahmeh, Salim Barakat, Georges Khattar, Walid Sange, Elie Bou Sanayeh, Zaid Khamis, Bahy Abofrekha, Suzanne El-Sayegh and Michel N. Chalhoub

Adv. Respir. Med. 2026, 94(4), 46; https://doi.org/10.3390/arm94040046 - 6 Jul 2026

Abstract

Background/Objectives: Pulmonary hypertension (PH) is an increasingly recognized complication in patients with end-stage renal disease (ESRD) undergoing hemodialysis, particularly those utilizing arteriovenous fistulas (AVF) or grafts (AVG) for vascular access. The prevalence and clinical impact of PH in this population remain unclear due [...] Read more.

Background/Objectives: Pulmonary hypertension (PH) is an increasingly recognized complication in patients with end-stage renal disease (ESRD) undergoing hemodialysis, particularly those utilizing arteriovenous fistulas (AVF) or grafts (AVG) for vascular access. The prevalence and clinical impact of PH in this population remain unclear due to methodological heterogeneity and variable diagnostic criteria. This systematic review and meta-analysis aimed to quantify the association between AVF/AVG use and PH prevalence in ESRD patients and to explore sources of heterogeneity. Methods: A systematic search of PubMed, Embase, Scopus, and Web of Science was conducted for studies published through 31 December 2024, without language or date restrictions. Eligible studies included adults (≥18 years) with ESRD on dialysis, comparing those with AVF/AVG access to non-AVF/AVG controls (e.g., tunneled dialysis catheters or peritoneal dialysis), and reporting PH prevalence or mean pulmonary artery pressures. Study quality was assessed using the Newcastle–Ottawa Scale, and risk of bias was evaluated. A random-effects meta-analysis calculated pooled odds ratios (OR) for PH prevalence, with heterogeneity assessed by I² and Cochran’s Q. Sensitivity analyses and tests for publication bias (Egger’s and Begg’s) were performed. Secondary analysis compared pooled mean pulmonary artery pressures between groups. Results: Eleven observational studies (1299 dialysis patients) met the inclusion criteria; ten studies (1224 patients) contributed to the quantitative meta-analysis after exclusion of one study with a zero-event control arm. Most studies were small, predominantly cross-sectional, and of moderate methodological quality. The pooled analysis showed a statistically significant association between AVF/AVG use and PH (OR 2.06, 95% CI: 1.69–2.52), with low statistical heterogeneity (I² = 0%). This estimate was sensitive to individual studies: in leave-one-out analysis the association lost statistical significance when the single most influential study was removed indicating that the pooled result is driven in part by a small number of studies rather than being uniformly robust. No statistical evidence of publication bias was detected. Five studies reported continuous pulmonary artery pressures, which were directionally higher in AVF/AVG patients but were not pooled because of extreme heterogeneity (I² = 99.4%). Conclusions: In this synthesis of observational data, AVF/AVG use was associated with higher odds of pulmonary hypertension than non-AVF/AVG access. Because all included studies were observational and the pooled estimate is sensitive to individual influential studies, these findings indicate a possible association rather than a causal effect and should be interpreted with caution. They support the rationale for prospective hemodynamic studies and for evaluating—rather than presuming the benefit of—PH monitoring and individualized access strategies in higher-risk dialysis patients. Full article

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