Background CT attenuation is affected by lung volume, dosage, and scanner bias, leading to inaccurate emphysema progression measurements in multicenter studies. Purpose To develop and validate a method that simultaneously corrects volume, noise, and interscanner bias for lung density change estimation in emphysema progression at CT in a longitudinal multicenter study. Materials and Methods In this secondary analysis of the prospective Genetic Epidemiology of Chronic Obstructive Pulmonary Disease (COPDGene) study, lung function data were obtained from participants who completed baseline and 5-year follow-up visits from January 2008 to August 2017. CT emphysema progression was measured with volume-adjusted lung density (VALD) and compared with the joint volume-noise-bias-adjusted lung density (VNB-ALD). Reproducibility was studied under change of dosage protocol and scanner model with repeated acquisitions. Emphysema progression was visually scored in 102 randomly selected participants. A stratified analysis of clinical characteristics was performed that considered groups based on their combined lung density change measured by VALD and VNB-ALD. Results A total of 4954 COPDGene participants (mean age, 60 years ± 9 [SD]; 2511 male, 2443 female) were analyzed (1329 with repeated reduced-dose acquisition in the follow-up visit). Mean repeatability coefficients were 30 g/L ± 0.46 for VALD and 14 g/L ± 0.34 for VNB-ALD. VALD measurements showed no evidence of differences between nonprogressors and progressors (mean, -5.5 g/L ± 9.5 vs -8.6 g/L ± 9.6; = .11), while VNB-ALD agreed with visual readings and showed a difference (mean, -0.67 g/L ± 4.8 vs -4.2 g/L ± 5.5; < .001). Analysis of progression showed that VNB-ALD progressors had a greater decline in forced expiratory volume in 1 second (-42 mL per year vs -32 mL per year; Tukey-adjusted = .002). Conclusion Simultaneously correcting volume, noise, and interscanner bias for lung density change estimation in emphysema progression at CT improved repeatability analyses and agreed with visual readings. It distinguished between progressors and nonprogressors and was associated with a greater decline in lung function metrics. Clinical trial registration no. NCT00608764 © RSNA, 2024 See also the editorial by Goo in this issue.
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http://dx.doi.org/10.1148/radiol.231632 | DOI Listing |
Respir Res
December 2024
Department of Pulmonary and Critical Care Medicine, Shengjing Hospital of China Medical University, No.36 Sanhao Street, Shenyang, 110004, Liaoning, China.
Background: Alveolar macrophages (AMs) modulate pulmonary inflammation in chronic obstructive pulmonary disease (COPD), contributing to its progression. The PPARγ/RXRα heterodimer influences AM polarization induced by cigarette smoke (CS). Although PPARγ agonists suppress CS-induced M1 macrophage polarization, the impact of RXRα agonists on this process has not been determined.
View Article and Find Full Text PDFRespir Investig
December 2024
Division of Respirology, Neurology, and Rheumatology, Department of Internal Medicine, Kurume University School of Medicine, 67 Asahi-machi, Kurume, Fukuoka, 830-0011, Japan.
Background: The prognostic factors in mild fibrosing interstitial lung disease (FILD) have not been established.
Methods: We retrospectively attempted to identify predictive factors of annual progression in mild FILD with gender-age-physiology (GAP) score of 3 or less using logistic regression analysis. Annual FILD progression was defined as meeting any two or more of the following conditions: 1, more than 10% decrease in forced vital capacity (FVC) or 15% decrease in diffusing capacity of the lungs for carbon monoxide (D); 2, worsening of dyspnea; 3, worsening of fibrotic change on CT at 1 year after admission.
J Bras Pneumol
December 2024
. Vall d'Hebron Institut de Recerca - VHIR - Hospital Universitário Valld'Hebron, Barcelona, España.
Alpha-1 antitrypsin deficiency (AATD) is a relatively rare genetic disorder, inherited in an autosomal codominant manner, that results in reduced serum AAT concentrations, with a consequent reduction in antielastase activity in the lungs, as well as an increased risk of diseases such as pulmonary emphysema, liver cirrhosis, and necrotizing panniculitis. It results from different mutations in the SERPINA1 gene, leading to changes in the AAT glycoprotein, which can alter its concentration, conformation, and function. Unfortunately, underdiagnosis is quite common; it is possible that only 10% of cases are diagnosed.
View Article and Find Full Text PDFInt J Chron Obstruct Pulmon Dis
December 2024
Institute and Outpatient Clinic for Occupational, Social and Environmental Medicine, University Hospital, LMU Munich, Comprehensive Pneumology Center Munich (CPC-M), German Center for Lung Research (DZL), Munich, Germany.
Background: The COPD Assessment Test (CAT) comprises eight questions. We evaluated the information that each of the questions and the total score contributed to outcomes and characteristics of chronic obstructive lung disease (COPD), including their dependence on smoking status.
Methods: Patients with COPD of the COSYCONET cohort with Global Initiative for Chronic Obstructive Lung Disease (GOLD) grades 1-4 and the former grade 0 were included.
Comput Biol Med
December 2024
Applied Chest Imaging Laboratory, Department of Radiology and Medicine, Brigham and Women's Hospital, 399 Revolution Drive, Somerville, 02145, MA, USA; Harvard Medical School, 25 Shattuck Street, Boston, 02115 MA, USA. Electronic address:
Emphysema, marked by irreversible lung tissue destruction, poses challenges in progression prediction due to its heterogeneity. Early detection is particularly critical for patients with Alpha-1 Antitrypsin Deficiency (AATD), a genetic disorder reducing ATT protein levels. Heterozygous carriers (PiMS and PiMZ) have variable AAT levels thus complicating their prognosis.
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