BACKGROUND:Chest CT supports quantitative COPD phenotyping, but diaphragm assessment remains limited by poor muscle conspicuity and labour-intensive analysis. We developed a fully automated, annotation-light framework extracting three-dimensional diaphragm-related inferior lung-interface surfaces from paired inspiratory-expiratory CT as surrogates of diaphragmatic dome geometry. METHODS:In this retrospective multicentre analysis of prospectively enrolled real-world cohort participants, paired CT examinations underwent automated lung isolation, mesh-based inferior-interface extraction, surface completion, and morphometry. After phase-ordering quality control, the internal cohort included 516 paired examinations. External analyses included 35 of 49 COPD participants with successful extraction for cross-scanner feasibility and 60 individuals for COPD-non-COPD replication. RESULTS:Automated dome-level localisation agreed strongly with independent readers (intraclass correlation coefficients, 0.92-0.96). COPD examinations showed larger expiratory surface area, longer unadjusted expiratory apico-diaphragmatic lung dimension, altered inspiratory convexity, and lower excursion. Bilateral surface-area differences persisted after adjustment for achieved expiratory CT lung volume, whereas cranio-caudal extent findings were attenuated. In exploratory COPD-non-COPD discrimination, adding diaphragm-related descriptors to expiratory LAA% increased the AUC from 0.780 (95% CI 0.738-0.820) to 0.824 (95% CI 0.794-0.867). Principal morphometric group differences were replicated externally; the ROC model was not externally validated. CONCLUSIONS:Automated paired-CT morphometry of the diaphragm-related inferior lung interface was feasible and reproducible, captured COPD-related thoraco-diaphragmatic geometry, and provided information complementary to parenchymal density measures.
BACKGROUND:Obesity and cardiometabolic dysfunction are increasingly recognized among people with cystic fibrosis (pwCF) in the CFTR modulator era. Emerging evidence suggests glucagon-like peptide-1 receptor agonists (GLP-1 RAs) may influence pulmonary physiology and respiratory outcomes in pwCF. However, factors associated with pulmonary response remain poorly understood. We hypothesized that pulmonary improvement following GLP-1 RA initiation would be associated with both metabolic response and treatment intensity. METHODS:We performed a retrospective cohort study of adults with CF-related diabetes (CFRD) treated with GLP-1 RAs. Clinical, metabolic, and pulmonary variables were assessed following GLP-1 RA initiation. Associations between baseline characteristics, treatment-related factors, and change in forced expiratory volume in 1 s (FEV1) were evaluated using regression analyses. RESULTS:Twenty-three adults with CFRD treated with GLP-1 RAs were included. Median FEV1 increased by 6.0 percentage points (IQR 3.5-10.0) over 6 months following therapy initiation. Greater reduction in body mass index (BMI) and achievement of therapeutic GLP-1 RA dosing were both associated with greater improvement in FEV1. Importantly, the association between therapeutic-dose GLP-1 RA therapy and improved FEV1 persisted after adjustment for BMI reduction, suggesting that pulmonary improvement may not be fully explained by weight loss alone. CONCLUSIONS:In adults with CFRD, greater BMI reduction and achievement of therapeutic GLP-1 RA dosing were associated with greater improvement in FEV1. These findings support further investigation of GLP-1 RAs as a potential therapeutic strategy that may influence pulmonary outcomes while improving metabolic health in pwCF.
BACKGROUND AND OBJECTIVES:- Exercise-induced bronchoconstriction (EIB) is the acute constriction of the airways during or after physical exertion. This transient obstruction results in symptoms such as coughing, wheezing, and dyspnea, which can affect exercise performance and overall quality of life. EIB affects a substantial proportion of individuals having asthma; however, it also affects non-asthmatics; nearly 5% to 20% of the general population is affected. Spirometry has been used to assess EIB; however, it has several limitations, including dependence on forced expiratory measurements that reflect large airway function and often overlook small airways. Impulse oscillometry addresses these limitations and enables assessment of small airways without requiring forced expiratory manoeuvres. In this study, we compared the post-exercise physiological responses detected by impulse oscillometry (IOS) and conventional spirometry following cardiopulmonary exercise testing. METHODS:Spirometry and impulse oscillometry were performed in healthy young adult males before and at 5, 10,15 and 20 min after completing symptom-limited incremental exercise testing. RESULTS:FEV1 decreased significantly 5 min post-exercise compared to baseline. Peak expiratory flow decreased significantly at 5, 10, 15, and 20 min postexercise. A significant increase in peripheral airway resistance (R5-R20) was observed at 5 min post-exercise. X5% pred. increased throughout post-exercise. Resonant frequency was significantly elevated at 5 min post-exercise. Additionally, the reactance area exhibited a significant reduction at 20 min post-exercise. INTERPRETATION AND CONCLUSION:This study demonstrates that serial IOS parameters detected statistically significant post-exercise peripheral airway changes that were not captured by conventional spirometry.
Both asthma and chronic obstructive pulmonary disease (COPD) are heterogeneous diseases characterised by airway obstruction. In recent years, they have received increasing attention due to the annual increase in morbidity and mortality. Asthma and COPD have different inflammatory patterns and underlying mechanisms. Asthma-COPD overlap (ACO) is a characteristic of both asthma and COPD. ACO is not simply a superposition of asthma and COPD but a heterogeneous multidimensional clinical construct. This not only increases the complexity of diagnosis, but also poses higher requirements for the selection of treatment strategies. This review presents an in-depth exploration of ACO from a multidimensional perspective, based on its heterogeneity, phenotypes, endotypes, and treatable characteristics. This study aimed to better address the diversity of the disease, explore more effective treatment approaches, reduce the disease burden, and improve patient prognosis.
Interleukin-5 (IL-5) is a central regulator of eosinophil differentiation, maturation, trafficking, activation and survival, and therapeutic targeting of the IL-5/IL-5 receptor alpha pathway has substantially changed the management of severe eosinophilic asthma and other eosinophil-associated disorders. However, clinical responses to anti-IL-5 and anti-IL-5Rα biologics remain heterogeneous, and persistent symptoms may reflect ongoing eosinophilic inflammation, partial clinical response, comorbidity-driven residual disease or inflammatory mechanisms not primarily dependent on IL-5. This narrative review summarizes current knowledge on IL-5 biology, eosinophil regulation and the pharmacological basis of IL-5 pathway inhibition, with particular focus on severe eosinophilic asthma, chronic rhinosinusitis with nasal polyps, eosinophilic granulomatosis with polyangiitis and hypereosinophilic syndromes. It also discusses eosinophil heterogeneity, biomarkers of response, IL-5-dependent and IL-5-independent pathways, epithelial alarmins, IL-4/IL-13 signalling, airway remodelling and treatable traits associated with residual symptoms. An illustrative retrospective real-world cohort of patients treated with mepolizumab or benralizumab is used to contextualize biomarker variability, clinical heterogeneity and comorbidity burden in routine severe-asthma care. Overall, interpretation of response to IL-5/IL-5Rα-targeted therapy should integrate blood eosinophils with clinical outcomes, lung function, corticosteroid exposure, sinonasal disease and other comorbidities. Future research should standardize definitions of remission, partial response and non-response, strengthen prospective real-world registries, and identify tissue-based or multi-omic biomarkers to guide biologic selection, sequencing and treatment optimization.
Chronic Obstructive Pulmonary Disease (COPD) is a long-lasting problem with the lungs that leads to many symptoms, poor quality of life, and greater use of the health care system. The aim of this study was to evaluate longitudinal changes in symptom distress among patients with chronic obstructive pulmonary disease (COPD) over a 6- months follow-up period and to examine the association between baseline symptom distress and disease severity. In total, 341 patients with COPD were recruited from the Department of Pulmonology at Maharishi Markandeshwar (Deemed to be University) Hospital in Mullana, Haryana, India. The Symptom Distress Scale (SDS) was used to calculate symptom distress at baseline, 3 months, and 6 months post-enrolment into the study. Demographics (age and sex) and clinical data (exacerbation history, number of medications take, etc.) were collected using a standardized data collection sheet and statistical analyses were done using SPSS version 25.0. Most of the patients were in GOLD Stage II (58.7%) or GOLD Stage III (28.4%). The mean SDS scores decreased substantially from a baseline score of 26.38 ± 8.18 to a score of 24.59 ± 8.18 at 3 months and a score of 21.65 ± 9.39 at 6 months (p < 0.001). There were strong correlations between baseline SDS scores and the SDS scores at 3 months (r = 0.951, p < 0.001) and at 6 months (r = 0.812, p < 0.001). Baseline SDS scores did not differ significantly between the COPD severity stages (p = 0.271). Multiple regression analysis revealed that age, gender, smoking status, COPD duration, and disease severity were not significant predictors of baseline symptom distress. A significant reduction in mean symptom distress scores was observed among patients with COPD over the 6-months follow-up period; however, the observation design does not allow conclusions regarding the factors responsible for these changes.
Background Risk stratification in fibrotic interstitial lung disease (F-ILD) traditionally relied on baseline physiological parameters. However, these static assessments may not adequately capture the dynamic nature of disease progression. Whether serial functional assessments provide prognostic information beyond baseline functional reserve remains uncertain. Methods We analyzed a prospectively established cohort of patients with fibrotic ILD who underwent routine functional assessments, including the one-minute sit-to-stand test (1MSTS) and the six-minute walk test (6MWT). Baseline predictors of mortality were evaluated using conventional Cox proportional hazards models, whereas longitudinal changes in functional performance were assessed using time-dependent Cox regression models. Overall survival was further examined according to baseline functional reserve and subsequent trajectories of functional change. Results Among 323 patients with fibrotic ILD, both baseline 1MSTS performance and six-minute walk distance (6MWD) were significantly associated with mortality. In time-dependent analyses, longitudinal decline in 6MWD remained an independent predictor of mortality, whereas longitudinal changes in 1MSTS did not provide additional prognostic value beyond baseline performance. Patients with impaired baseline walking capacity (<490 m) who subsequently experienced further decline had the highest mortality, whereas those with preserved baseline capacity and stable functional trajectories exhibited very low long-term mortality. Conclusion Baseline functional capacity and serial six-minute walk assessments provide complementary information for longitudinal risk stratification in fibrotic ILD. Serial monitoring of walking capacity may facilitate identification of clinically meaningful disease trajectories in routine clinical practice.
Cystic fibrosis transmembrane conductance regulator modulators (CFTRm) represent a major therapeutic advance for patients with cystic fibrosis (pwCF). Given their oral administration and high efficacy, they may be better suited than other cystic fibrosis treatments to optimize long-term adherence, which is crucial to ensuring effectiveness. To examine adherence patterns to CFTRm and their determinants, we conducted a population-based retrospective cohort study using data from the French CF Registry linked to the French National Health Data System. We included pwCF (>6 years) who initiated at least one CFTRm (ivacaftor or lumacaftor/ivacaftor) between 2012 and 2020 and were treated for at least six months. Implementation was measured using the continuous multiple-interval measure of medication availability version 7 (CMA-7), and longitudinal K-means clustering identified adherence trajectories based on monthly CMA-7 values over one-year follow-up. Multinomial logistic regression assessed associations between adherence patterns and sociodemographic and clinical characteristics. Among 1362 patients, three adherence trajectories were identified: optimal adherence (68%), gradual decline (16%), and initial drop-off followed by return to optimal adherence after 3-5 months (16%). Compared to optimal adherence, gradual decline trajectory was associated with age 15-25 years (reference: >25), while drop-off and rebound trajectory was linked to being younger than 15 and P. aeruginosa bronchial colonization. Socioeconomic disadvantage was also associated with nonoptimal adherence. This study highlights the need for age-tailored interventions to support long-term adherence, revealing a decline among adolescents and young adults, along with a specific pattern among children, which may relate to prescribing practices at treatment initiation.
BACKGROUND:Asthma is a common chronic disease worldwide, with most patients presenting with mild to moderate forms. Poor adherence to inhaled therapy is a recognized determinant of worse outcomes in chronic respiratory diseases. The aim of this study was to evaluate adherence to inhaled medications in a large cohort of adults with mild to moderate asthma and identify factors associated with suboptimal adherence. METHODS:This cross-sectional real-world study analyzed data from the Mild-Moderate Asthma Network of Italy (MANI) database. Adult patients (≥18 years) with a confirmed diagnosis of asthma according to Global Initiative for Asthma (GINA) criteria were eligible. Data from the first visit in which the Test of Adherence to Inhalers (TAI) questionnaire was available were extracted. Patient-reported outcomes included the Asthma Control Test (ACT), the Asthma Quality of Life Questionnaire (AQLQ), and TAI adherence categories. Patients were classified into three classes according to TAI score as follows: adherents (score ≥50), intermediate adherents (score 46-49), and non-adherents (score <46). RESULTS:A total of 832 patients were included. Adherent patients were older than intermediate and non-adherent subjects (p < 0.001). Current smoking was less frequent among adherent patients (11% vs 16%). Type 2 diabetes and anxiety were more prevalent among non-adherent individuals (5.3% vs 0.8% and 1.8%, p = 0.014; 10.7% vs 7.1% and 3.8%, p = 0.003, respectively). Higher adherence levels were associated with better asthma control (χ2 (2) = 47.706, p < 0.001) and quality of life (χ2 (2) = 42.068, p < 0.001). CONCLUSION:In adults with mild to moderate asthma, better adherence to inhaled therapy is associated with improved disease control and quality of life. Demographic factors, smoking status, and comorbidities may influence adherence behaviors. Routine assessment of adherence and targeted interventions addressing modifiable barriers may improve outcomes in this large asthma population.
BACKGROUND:Obesity is associated with poorly controlled asthma. One reason for this may be the increased mitochondrial oxidative stress in obese asthma. Indeed, targeting oxidative stress reduces airway reactivity in animal models. The purpose of this trial was to investigate the potential efficacy of the mitochondrial-targeted antioxidant MitoQuinone (MitoQ) for the treatment of poorly controlled asthma in people with obesity. METHODS:A twelve week, randomized, double-masked, placebo-controlled trial of 40 mg MitoQ versus placebo in adults with obesity and poorly controlled asthma was performed. The primary outcome was change in airway reactivity, with secondary outcomes of change in asthma control, quality of life, and lung function. RESULTS:Twenty participants were randomized to MitoQ, 18 to placebo. After 12 weeks, there was no difference in change in airway reactivity to methacholine (provocative dose producing a 20% decrease in FEV1) between the group assigned to MitoQ (median change = 0.0 μg [IQR -25.5 to 1.4]) or placebo (change = -0.8 μg [IQR -57 to 0.0]), p = 0.81. There was no difference in the change in Asthma Control Test score (MitoQ 1 [IQR -1 to 2], placebo 1 [-2 to 2]), p = 0.62, or Marks Asthma Quality of Life Score (MitoQ -0.08 [IQR -0.35 to 0.10], placebo -0.05 [-0.30 to 0.15]), p = 0.80. CONCLUSION:MitoQ was well tolerated but did not improve airway reactivity, asthma control, or lung function. Targeting oxidative stress in people with obesity and poorly controlled asthma with MitoQ is unlikely to be efficacious for the treatment of asthma.
BACKGROUND:Osteoporosis is a common comorbidity in patients with chronic obstructive pulmonary disease (COPD). However, most previous studies have been conducted in European populations. This study aims to explore whether patients with COPD are at increased risk of osteoporosis and osteoporosis-related fractures compared to a propensity score-matched (PSM) cohort of non-COPD patients in the TriNetX US Collaborative Network de-identified electronic health record (EHR) database. STUDY DESIGN AND METHODS:Adult patients aged 40-65 with a COPD diagnosis (ICD-10: J44.0-J44.9), confirmed by spirometry (FEV1/FVC <70%), and a minimum follow-up of 10 years (3650 days) were included. Both the ICD-10 code and spirometry criterion were required for COPD diagnosis. A 1:1 propensity score matching (PSM) was conducted to match non-COPD controls based on age, sex, BMI, smoking status, comorbidities, and medication use (including systemic corticosteroids, inhaled corticosteroids, and bone-active medications). The primary outcome was osteoporosis (ICD-10: M81.0). Secondary outcomes included osteoporosis with pathological fracture (M80) and pathological fractures (M84.4, M84.7). Cox proportional hazards models were used to estimate the hazard of osteoporosis after adjusting for confounding variables. RESULTS:Following PSM, 2682 COPD patients were compared with 2682 non-COPD controls. COPD patients exhibited a significantly increased risk of osteoporosis [HR: 1.95 (1.37-2.77), p = 0.0002]. Underweight status (BMI <18.5 kg/m2) further elevated osteoporosis risk [HR: 3.95 (2.19-7.13), p < 0.0001], while male sex was highly protective [HR: 0.15 (0.14-0.16), p < 0.0001]. Age-stratified analysis showed progressively increasing risk across older age groups, peaking at ages 61-65 [HR: 20.01 (18.77-21.33), p < 0.0001]. INTERPRETATION:COPD is independently associated with an increased risk of osteoporosis. These findings highlight the importance of systematic osteoporosis screening and monitoring as part of comprehensive COPD management, particularly in high-risk subgroups (older adults, females, and those with low BMI).
OBJECTIVES:This study aimed to compare lung patterns and disease progression in asbestosis and idiopathic pulmonary fibrosis (IPF) using qualitative and quantitative high-resolution computed tomography (HRCT) analysis. METHODS:HRCT scans were obtained at baseline (T0) and follow-up (T1) in 17 patients with asbestosis and 17 with IPF, after a median follow-up of 35 months (IQR = 3) and 35 months (IQR = 13), respectively. Lung parenchyma was segmented using CALIPER software, which quantifies reticulations (RET), ground-glass opacities (GGO), and honeycombing (HC), providing an interstitial lung disease (ILD) score based on the percentage of affected lung volume. Disease progression was defined as the change in ILD score from T0 to T1, normalized per year (DeltaILD/year). A comparative analysis was performed between the groups. Additionally, qualitative HRCT features at T0 were reviewed to identify distinguishing radiological signs. RESULTS:Patients with asbestosis showed significantly slower disease progression (median DeltaILD/year = 0.70%/month; IQR = 1.27) compared to IPF (median = 2.06%/month; IQR = 4.80) (p = 0.024). Subpleural lines (both <5 mm and >5 mm from pleura), pleural plaques, and pleural thickening were more common in asbestosis, whereas hypertrophic mediastinal fat and honeycombing predominated in IPF. CONCLUSION:Quantitative HRCT analysis with CALIPER effectively demonstrated slower progression in asbestosis compared to IPF. Specific imaging features, including subpleural lines and pleural involvement, distinguished asbestosis, while honeycombing and mediastinal fat hypertrophy were typical of IPF.
Asthma and chronic obstructive pulmonary disease (COPD) represent the two most prevalent chronic respiratory conditions worldwide, affecting hundreds of millions of individuals and imposing substantial morbidity and mortality. Despite their distinct biological mechanisms, these diseases frequently exhibit overlapping clinical features-including dyspnea, cough, and wheezing-that complicate differential diagnosis, particularly in smoking adults, older patients, and those with mild or fluctuating airflow obstruction. Spirometry remains the cornerstone of diagnostic evaluation, yet its limitations, including dependence on patient effort, reduced sensitivity for early disease, and inability to fully capture small airways involvement, contribute to persistent underdiagnosis and overdiagnosis in clinical practice. This review examines current diagnostic approaches for asthma and COPD, their inherent limitations, and the emerging biomarkers and functional technologies that may improve diagnostic precision. Established biomarkers, including blood eosinophils, fractional exhaled nitric oxide (FeNO), and induced sputum analysis, provide complementary information that refines clinical characterization but lack sufficient disease specificity for standalone use. Novel approaches, including lipidomics, metabolomics, and extracellular vesicle profiling, demonstrate potential for identifying disease-specific molecular signatures and biologically distinct phenotypes, particularly in asthma-COPD overlap. Concurrently, new functional tools-including novel spirometric indices such as Parameter D or FEV3/FEV6, respiratory oscillometry, and artificial intelligence-driven tidal breathing analysis-are enabling more sensitive, effort-independent, and multidimensional assessment of airway disease. The integration of these clinical, functional, inflammatory, and molecular approaches supports a transition toward multimodal diagnostic frameworks that may substantially improve the recognition and differential diagnosis of asthma and COPD, particularly in challenging clinical scenarios and early disease states.
BACKGROUND:The lactate-to-albumin ratio (LAR) has emerged as a potential prognostic biomarker in sepsis. This systematic review evaluated the prognostic value of LAR for mortality in adults with sepsis or septic shock. METHODS:PubMed/MEDLINE, Embase, Web of Science, Scopus, and the Cochrane Library were searched from inception through March 2026. Studies evaluating mortality-related prognostic performance of LAR in adults with sepsis or septic shock were included. Risk of bias was assessed using the Quality In Prognosis Studies (QUIPS) tool. Adjusted odds ratios (ORs) and hazard ratios (HRs) were evaluated separately because of methodological heterogeneity. Discrimination was assessed using study-specific area under the curve (AUC), sensitivity, specificity, and LAR thresholds. RESULTS:Fourteen primary studies were included. Higher LAR was consistently associated with increased mortality across emergency department and intensive care populations. AUC values generally ranged from approximately 0.65 to 0.87, although one smaller cohort reported an AUC of 0.976. Several multivariable analyses demonstrated associations between higher LAR and mortality after adjustment for clinical covariates. Adjusted ORs and HRs were not pooled because of differences in LAR scaling, thresholds, mortality endpoints, and adjustment strategies. Considerable variability was observed in reported cut-offs and diagnostic performance. CONCLUSIONS:Higher LAR is associated with mortality in adult sepsis and may provide complementary prognostic information. However, clinical and methodological heterogeneity precludes a universal cut-off or single pooled adjusted effect. Standardized prospective multicenter studies are required before routine clinical implementation.
BACKGROUND:Smoking exposure has been quantified using pack-years, which integrates smoking intensity and duration. However, pack-years may not fully capture the prognostic impact of prolonged exposure. We aimed to compare the prognostic value of smoking duration and cumulative smoking intensity for mortality risk stratification in patients with chronic obstructive pulmonary disease (COPD). METHODS:We analyzed data from the Korea COPD Subtype Study, an ongoing prospective multicenter cohort (NCT02800499). Smoking exposure was categorized using thresholds of 40 pack-years and 40 years of smoking duration. The primary outcome was all-cause mortality and the secondary outcome was cause-specific mortality. RESULTS:Among 2166 patients with COPD, 210 deaths occurred over a median follow-up of 7 years. Smoking duration ≥40 years was associated with increased all-cause mortality risk regardless of cumulative smoking intensity. Compared with patients with <40 pack-years and smoking duration <40 years, those with <40 pack-years but smoking duration ≥40 years had higher all-cause mortality risk (adjusted hazard ratio [aHR] = 1.66; 95% confidence interval [CI] = 1.01-2.73). Similarly, patients with ≥40 pack-years and smoking duration ≥40 years had increased all-cause mortality risk (aHR = 1.58; 95% CI = 1.15-2.16). In contrast, ≥40 pack-years without prolonged smoking duration was not associated with all-cause mortality. In cause-specific mortality analyses, prolonged smoking duration was also associated with increased cardiovascular and cancer-related mortality. CONCLUSIONS:Smoking duration was more strongly associated with mortality risk than cumulative smoking intensity alone and may provide additional prognostic information beyond pack-years for mortality risk stratification in patients with COPD.
This study aimed to investigate the prognostic value of the blood urea nitrogen-to-albumin ratio (BAR) for predicting all-cause mortality (ACM) in patients septic cardiomyopathy (SCM). An external validation was conducted in SCM patients from the Affiliated Hospital of Chengde Medical University. The results demonstrated that a higher BAR was significantly related to an increased sequential organ failure assessment (SOFA) score, a greater number of comorbidities, and worse clinical outcomes. Multiple regression analysis revealed that each unit increase in BAR was associated with a 4.1% rise in short-term mortality (OR = 1.041, P = 0.04). Receiver operating characteristic (ROC) curve analysis showed that the area under the curve (AUC) for BAR in predicting in-hospital mortality was < 0. 657, which was superior to that of blood urea nitrogen (BUN) alone or the SOFA score. In subgroup analyses, BAR remained stronger predictive ability in patients without any other comorbidities, such as renal insufficiency. In conclusion, BAR is an independent factor associated with short-term mortality in patients with SCM. As an easily accessible and broadly applicable marker reflecting both renal function and nutritional status, BAR may serve as a useful supplementary parameter for early risk stratification and medical treatment of patients with SCM. Receiver operating characteristic (ROC) analysis showed that BAR had modest discrimination for in-hospital mortality, with an AUC of 0.657 in the derivation cohort. Although this value was numerically higher than that of BUN alone and the SOFA score in the primary cohort, its overall discriminative ability remained limited. In the external validation cohort, BAR showed lower but still directionally consistent prognostic performance, with an AUC of 0.583. These findings suggest that BAR may serve as a simple and readily available supplementary marker for early risk stratification in patients with SCM, but it should not be interpreted as a stand-alone prognostic tool or a replacement for comprehensive clinical assessment. Multivariable regression analysis showed that each one-unit increase in BAR was associated with a higher risk of in-hospital mortality after full adjustment (OR = 1.041, 95% CI: 1.000-1.081, P = 0.04). However, the associations between BAR and 7-day, 30-day, and 365-day mortality after ICU discharge were attenuated and were no longer statistically significant in the fully adjusted model. These findings suggest that BAR is independently associated with in-hospital mortality in patients with SCM, whereas its relationship with post-ICU mortality should be interpreted as exploratory.
BACKGROUND:Chronic obstructive pulmonary disease (COPD) and osteoporosis are highly prevalent chronic conditions that frequently co-occur, yet their comorbid relationship remains systematically underrecognized in clinical practice. Approximately 38% of COPD patients have confirmed osteoporosis, yet fewer than 20% receive bone-protective pharmacotherapy. OBJECTIVE:To synthesize current evidence on the epidemiology, shared pathophysiological mechanisms, clinical consequences, and integrated management strategies for COPD-associated osteoporosis. METHODS:A narrative review was conducted through systematic searching of PubMed and MEDLINE (through December 2024) using the terms 'COPD,' 'osteoporosis,' 'bone mineral density,' 'fracture risk,' and 'corticosteroids.' Peer-reviewed original research, systematic reviews, meta-analyses, and clinical guidelines were included. Non-peer-reviewed sources were excluded. RESULTS:Shared mechanisms underlying COPD-associated osteoporosis include chronic systemic inflammation (elevated IL-6, TNF-α), corticosteroid-induced bone loss, sarcopenia, vitamin D deficiency, and overlapping risk factors including smoking, advanced age, and low BMI. Osteoporotic fractures, particularly vertebral and hip, independently increase all-cause mortality, worsen pulmonary mechanics, accelerate functional decline, and generate direct healthcare costs exceeding $17 billion annually in the United States (a general US osteoporotic-fracture cost estimate, not specific to COPD). Despite this burden, screening rates are low and treatment is substantially underutilized. CONCLUSIONS:Osteoporosis in COPD represents a modifiable comorbidity with major and measurable clinical impact. Proactive DXA-based screening, individualized pharmacotherapy with bisphosphonates or denosumab, pulmonary rehabilitation, and multidisciplinary coordinated care are evidence-supported strategies that remain underimplemented. Updating COPD clinical guidelines to mandate systematic bone health assessment is an urgent priority.
The escalating global burden of chronic obstructive pulmonary disease (COPD) has outpaced the capacity of conventional management paradigms to deliver truly individualized care. This review offers a critical, narrative synthesis of the role of artificial intelligence and computational modelling in advancing COPD precision management, integrating technical, clinical, and policy evidence streams that have largely been treated separately in prior surveys. Reporting follows the spirit of the PRISMA-ScR checklist, and the search strategy is fully described to permit replication. The scope is cross-modal and explicitly regional, spanning pathophysiological understanding, diagnostic and prognostic applications, personalized treatment regimen optimization, exacerbation prediction, and drug discovery and repurposing. Key computational approaches-including mechanistic, multiscale, and machine learning models-are appraised for their contributions to disease phenotyping and prediction. The review critically examines persistent challenges, including data availability and quality, model interpretability and explainability, ethical considerations and algorithmic bias, and barriers to clinical integration. Future directions encompass multimodal data integration, explainable AI development, and rigorous clinical validation and implementation. By consolidating evidence across disciplines, this review maps current capabilities, exposes critical gaps, and outlines strategic priorities for translating computational innovation into tangible improvements in COPD diagnosis, treatment, and patient outcomes.
