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ABSTRACTBackground and ObjectiveProactive palliative interventions can improve symptom control and quality of life in individuals with chronic obstructive pulmonary disease (COPD); however, they are often underutilised. This study aimed to develop and validate a prediction model to identify women with COPD in their last year of life to facilitate timely palliative care referrals and interventions.MethodsData from 1236 women diagnosed with COPD from the 1921–1926 Australian Longitudinal Study on Women's Health cohort, linked to administrative health records, were analysed. We employed Lasso regression and multivariable logistic regression to select predictors. To assess the predictive performance of the model, we used the area under the receiver operating characteristic (AUROC) curve, calibration plot, and calibration metrics. The Youden index was used to establish the optimal cutoff point for risk classification. The clinical utility of the model was evaluated using decision curve analysis (DCA).ResultsThe final model to predict 1‐year all‐cause mortality included six predictors: smoking status, body mass index, needing regular assistance with daily activities, number of supplied medications, duration of illness, and number of hospital admissions. The model performed well, with AUROC of 0.82 (95% CI: 0.80–0.85) and showed excellent calibration. Using a cutoff of 56.6% predicted risk, the model achieved a sensitivity of 72.3%, specificity of 77.7%, and accuracy of 75.0%. The DCA indicated that the model provided a greater net benefit for clinical decision‐making.ConclusionOur prediction model for identifying women with COPD who may benefit from palliative care has shown robust predictive performance and can be easily applied, but requires external validation.

ABSTRACTBackground and ObjectiveWe determined the impact of genetic susceptibility and its interaction with smoking and air pollution on the risk of developing lung adenocarcinoma.MethodsThis retrospective case–control study utilised data from Taiwan Precision Medicine Initiative (TPMI) project conducted between June 2019 and November 2022. The study population consisted of lung adenocarcinoma patients and 1:4 age‐, gender‐, and index year‐matched non‐lung cancer controls. We analysed polygenic risk scores (PRS), smoking status, as well as PM2.5 and PM10 exposures.ResultsA total of 681 lung adenocarcinoma patients and 2724 non‐lung cancer participants were included. PRS was significantly higher among lung adenocarcinoma patients than controls (p < 0.001). Overall, a higher PRS was associated with a higher risk of lung adenocarcinoma. A high PM2.5 exposure was associated with a higher risk of lung adenocarcinoma (OR 1.88 [95% CI 1.12–3.14], p = 0.0163) among never‐smokers with low genetic risk. Never‐smokers with a higher genetic risk were associated with a higher OR for lung adenocarcinoma with the highest OR among Q4 participants with high PM2.5 exposure (4.97 [95% CI 3.10–7.97], p < 0.001). There was no significant impact of PM2.5 exposure among individuals with higher genetic risks. Similar phenomena were observed in the PM10 analyses. There were no significant correlations of PRS with risk of lung adenocarcinoma among smokers.ConclusionPRS significantly predicted lung adenocarcinoma incident cases in a dose‐dependent manner among never‐smokers. The PRS effect was not noted in smokers. The results were consistent among participants exposed to different air pollution levels. image

ABSTRACTBackground and ObjectiveSymptom‐based questionnaires and handheld lung function devices are widely used for COPD case finding, but the optimal combination remains unclear. This study aimed to compare the diagnostic accuracy (DA) of various combinations of handheld lung function devices and questionnaires and develop a COPD case‐finding strategy.MethodsThis cross‐sectional, prospective, observational study enrolled participants aged ≥ 40 years with respiratory symptoms and ≥ 10 smoking pack‐years. Participants completed three questionnaires (COPD diagnostic questionnaire [CDQ], lung function questionnaire; COPD Population Screener) and 2 handheld lung function devices (peak flow meter, microspirometer), followed by spirometry to confirm COPD (post‐bronchodilation FEV1/FVC < 0.7). DA is assessed using the area under the ROC curve (AUROC).ResultsAmong 224 participants, COPD incidence was 29%. Individually, handheld devices showed significantly higher DA than questionnaires (AUROC 0.678–0.69 for questionnaires vs. 0.807 for peak expiratory flow rate [PEFR] and 0.888 for FEV1/FEV6; all pairwise p < 0.05). FEV1/FEV6‐based combinations outperformed PEFR‐based combinations (all n = 224; AUROC 0.897–0.903 vs. 0.810–0.818; p < 0.05). The CDQ and FEV1/FEV6 combination reached the highest DA (AUROC 0.903). FEV1/FEV6 < 0.76 was the optimal cutoff value. A two‐staged strategy (sensitivity/specificity 0.82/0.84) was proposed: low‐risk participants (CDQ ≤ 13) need no further testing; middle‐risk (CDQ 14–26) should undergo FEV1/FEV6; and high‐risk (CDQ ≥ 27) and middle‐risk with FEV1/FEV6 < 0.76 require confirmatory spirometry. This approach would reduce misdiagnoses and save costs and time compared to FEV1/FEV6 alone.ConclusionFEV1/FEV6 and CDQ combination achieves the highest DA. A two‐staged, risk‐stratified strategy combining CDQ and FEV1/FEV6 can be accurate and cost‐effective to detect at‐risk, undiagnosed COPD subjects. External validation is required. image

ABSTRACTBackground and ObjectiveWhile short‐term weight changes are known to influence obstructive sleep apnoea (OSA), the impact of body mass index (BMI) changes over the life course has been poorly documented. We examined the association between BMI trajectories from childhood to middle age and adult OSA, 10 years later.MethodsFive BMI trajectories were previously identified in the population‐based cohort Tasmanian Longitudinal Health Study (TAHS), using eight time‐point BMI from age 5 to 43 years. The primary outcome was probable OSA at 53 years, defined using STOP‐Bang questionnaire, with Berlin and OSA‐50 questionnaires used to ensure consistency of findings. Clinically significant diagnosed OSA was defined as self‐reported medical diagnosis or mild OSA with symptoms or moderate‐to‐severe OSA, using type‐4 sleep studies. Associations were examined using multivariable logistic regression.ResultsCompared with the average BMI trajectory, the child average‐increasing (aOR = 5.28, 95% CI 3.38–8.27) and persistently high trajectories (aOR = 3.73, 2.06–6.74) were associated with increased risk of probable OSA. These associations were consistent when using clinically significant diagnosed OSA (child average‐increasing trajectory: aOR = 2.95, 1.30–6.72; high trajectory: aOR = 2.23, 0.82–6.09). Individuals belonging to the low trajectory were less likely than the average trajectory to have OSA. Notably, the child high‐decreasing trajectory was not associated with OSA.ConclusionPhysicians and the public should be aware of the potential risk of OSA in middle‐aged adults when BMI is high or continuously increasing from childhood to mid‐40s. Obese children who subsequently lose weight were not at higher risk of OSA in middle age—a novel and key finding. image

ABSTRACTBackground and ObjectiveAn imbalanced fat and muscle mass ratio might impact exacerbation of chronic obstructive pulmonary disease (COPD). We investigated the association of visceral fat‐to‐muscle ratio (VMR) with severe COPD exacerbation requiring hospitalisation.MethodsThis prospective cohort study in COPD patients was performed along with the Xinjiang Multi‐Ethnic Cohort study between May 2018 and December 2023. Baseline VMR was calculated from visceral fat area and muscle mass measured by bioelectrical impedance analysis. Numbers of COPD exacerbation hospitalizations were monitored. Associations between various variables and exacerbation were assessed by logistics regression and Zero‐inflated Poisson regression analyses.ResultsA total of 631 COPD patients were included, with 186 (29.48%) and 304 (48.18%) severe COPD exacerbation within 1 and 5 years, respectively. Compared with body mass index and other obesity indicators, VMR had stronger associations with severe exacerbation. A higher VMR was associated with increased risks of 1‐year and 5‐year exacerbation (odds ratio [OR] = 1.34 and 1.44, respectively). The subgroup female and overweight individuals showed a strong association (female OR = 1.89 and 1.99, overweight OR = 1.80 and 1.88, for 1 and 5‐year exacerbation, respectively). The number of COPD exacerbation increased by 46% for each one‐point VMR increase. These results remained unchanged in the sensitivity analyses after removing underweight patients or smoke influence, as well as in the competing risk analysis when considering other causes for death.ConclusionVMR was a risk factors of severe COPD exacerbation. Proactive assessment of VMR might be helpful to guide management of COPD patients.

ABSTRACTBackground and ObjectiveIdiopathic pulmonary fibrosis (IPF) is a chronic progressive lung disease with a poor prognosis. Antifibrotics slow the decline of pulmonary function after 12‐months, but limited studies have examined the role of circulatory biomarkers in antifibrotic treated IPF patients.MethodsSerum from 98 IPF participants, from the Australian Idiopathic Pulmonary Fibrosis Registry were collected at four time‐points over 1 year post‐antifibrotic treatment and analysed as two separate cohorts. Patients were stratified as progressive, if they experienced ≥ 10% decline in FVC or ≥ 15% decline in DLCO or were deceased within 1 year of treatment initiation: or otherwise as stable. Ten molecules of interest were measured by ELISAs in patient serum.ResultsBaseline MMP7 levels were higher in progressive than stable patients in Cohort 1 (p = 0.02) and Cohort 2 (p = 0.0002). Baseline MMP7 levels also best differentiated progressive from stable patients (Cohort 1, AUC = 0.74, p = 0.02; Cohort 2, AUC = 0.81, p = 0.0003). Regression analysis of the combined cohort showed that elevated MMP7 levels predicted 12‐month progression (OR = 1.530, p = 0.010) and increased risk of overall mortality (HR = 1.268, p = 0.002). LASSO regression identified a multi‐biomarker panel (MMP7, ICAM‐1, CHI3L1, CA125) that differentiated progression more accurately than MMP7 alone. Furthermore, GAP combined with MMP7, ICAM‐1, CCL18 and SP‐D was more predictive of 3‐year mortality than GAP alone.ConclusionMMP7 along with a multi‐biomarker and GAP panel can predict IPF progression and mortality, with the potential for optimising management.

ABSTRACTBackground and ObjectivePrevious observational studies reported a complex relationship between snoring and coronary artery disease (CAD). We aimed to estimate the causal associations between snoring and CAD among East Asian people, and the effects independent of BMI.MethodsBased on 497,250 adults from China Kadoorie Biobank (CKB), we performed a conventional prospective analysis between snoring and CAD outcomes, using the multivariable Cox regression. We also leveraged genome‐wide association (GWAS) summary statistics of snoring and BMI from CKB (n = 100,626, 47,208 snorers) and CAD outcomes from Biobank of Japan (BBJ, 5891–25,892 cases, 142,336–168,186 controls). Single‐variable and multivariable two‐sample bi‐directional Mendelian randomization (MR) analyses were performed.ResultsDuring a median follow‐up of 12.32 years, 48,997 participants developed CAD. Snoring and habitual snoring were associated with incident CAD and myocardial infarction (MI), habitual snoring was also associated with stable angina pectoris (SAP). The HRs (95% CIs) of habitual snoring were 1.06 (1.04, 1.08), 1.06 (1.04, 1.08) and 1.14 (1.03, 1.25). The associations remained among non‐adiposity participants. Genetically predicted habitual snoring was associated with CAD and MI, the corresponding IVW‐ORs (95% CIs) were 1.09 (1.005, 1.19) and 1.15 (1.05, 1.25). Further adjusted BMI, habitual snoring retained independent effects on MI and CAD, and showed impact on SAP (1.09 [1.01, 1.17]). No reverse associations were observed between CADs on snoring traits.ConclusionHabitual snoring elevated the risks of total CAD, MI and SAP. The causal associations were independent of BMI. These findings indicated that snoring intervention might contribute to the decrease of CAD risk among Asians.

ABSTRACTBackground and ObjectiveFibrotic interstitial lung disease (ILD) is associated with high morbidity and mortality. Patients often exhibit impaired nutritional status and alterations in body composition, such as dynapenia and sarcopenia, which correlate with poor pulmonary function, reduced exercise tolerance and diminished quality of life. However, the impact of dynapenia and sarcopenia on prognosis has not been examined extensively in ILD patients.We assessed the impact of dynapenia and sarcopenia as risk factors for mortality and their prevalence in ILD.MethodsProspective cohort study. ILD was classified into idiopathic pulmonary fibrosis (IPF), connective tissue disease‐related ILD (CTD‐ILD) and chronic hypersensitivity pneumonitis (CHP). Patients over 18 years old with a confirmed diagnosis of ILD were included, while those with diagnoses of cancer, human immunodeficiency virus and neurological disease were excluded. Dynapenia and sarcopenia were determined according to EWGSOP2 criteria.ResultsNinety‐eight ILD patients were included; 33.66% had IPF, 47.96% had CTD‐ILD, and 18.37% had CHP. The mean age was 63.89 ± 12.02 years; 37.76% were male.The risk factors associated with mortality included dynapenia (HR: 2.04, 95% CI: 1.10–3.77, p = 0.022), sarcopenia (HR: 1.88, 95% CI; 1.00–3.33, p = 0.049) and exercise tolerance (HR: 0.99, 95% CI; 0.99–0.99, p = 0.023), adjusted for confounding variables.The prevalence of dynapenia was 45% in ILD; 51% in IPF, 35% in CTD‐ILD and 61% in CHP. The prevalence of sarcopenia was 29%; both IPF (39%) and CHP (50%) had a higher prevalence of sarcopenia than CTD‐ILD (14%).ConclusionSarcopenia and dynapenia are independent risk factors for mortality in ILD. image