Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/28079
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dc.contributor.authorBui, Dinh S-
dc.contributor.authorAgusti, Alvar-
dc.contributor.authorWalters, Haydn-
dc.contributor.authorLodge, Caroline-
dc.contributor.authorPerret, Jennifer L-
dc.contributor.authorLowe, Adrian-
dc.contributor.authorBowatte, Gayan-
dc.contributor.authorCassim, Raisa-
dc.contributor.authorHamilton, Garun S-
dc.contributor.authorFrith, Peter-
dc.contributor.authorJames, Alan-
dc.contributor.authorThomas, Paul S-
dc.contributor.authorJarvis, Debbie-
dc.contributor.authorAbramson, Michael J-
dc.contributor.authorFaner, Rosa-
dc.contributor.authorDharmage, Shyamali C-
dc.date2021-07-
dc.date.accessioned2021-11-24T05:39:44Z-
dc.date.available2021-11-24T05:39:44Z-
dc.date.issued2021-09-13-
dc.identifier.citationERJ Open Research 2021; 7(3): 00020-2021.en
dc.identifier.issn2312-0541-
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/28079-
dc.description.abstractDifferent lung function trajectories through life can lead to COPD in adulthood. This study investigated whether circulating levels of biomarkers can differentiate those with accelerated (AD) from normal decline (ND) trajectories. The Tasmanian Longitudinal Health Study (TAHS) is a general population study that measured spirometry and followed up participants from ages 7 to 53 years. Based on their forced expiratory volume in 1 s (FEV1) trajectories from age 7 to 53 years, this analysis included those with COPD at age 53 years (60 with AD and 94 with ND) and controls (n=720) defined as never-smokers with an average FEV1 trajectory. Circulating levels of selected biomarkers determined at 53 and 45 years of age were compared between trajectories. Results showed that CC16 levels (an anti-inflammatory protein) were lower and C-reactive protein (CRP) (a pro-inflammatory marker) higher in the AD than in the ND trajectory. Higher CC16 levels were associated with a decreased risk of belonging to the AD trajectory (OR=0.79 (0.63-0.98) per unit increase) relative to ND trajectory. Higher CRP levels were associated with an increased risk of belonging to the AD trajectory (OR=1.07, 95% CI: 1.00-1.13, per unit increase). Levels of CC16 (area under the curve (AUC)=0.69, 95% CI: 0.56-0.81, p=0.002), CRP (AUC=0.63, 95% CI: 0.53-0.72, p=0.01) and the combination of both (AUC=0.72, 95% CI: 0.60-0.83, p<0.001) were able to discriminate between the AD and ND trajectories. Other quantified biomarkers (interleukin (IL)-4, IL-5, IL-6, IL-10 and tumour necrosis factor-α (TNF-α)) were not significantly different between AD, ND and controls. Circulating levels of CRP and CC16 measured in late adulthood identify different lung function trajectories (AD versus ND) leading to COPD at age 53 years.en
dc.language.isoeng-
dc.titleLung function trajectory and biomarkers in the Tasmanian Longitudinal Health Study.en
dc.typeJournal Articleen
dc.identifier.journaltitleERJ Open Researchen
dc.identifier.affiliationInstitute for Breathing and Sleepen
dc.identifier.affiliationDept of Pulmonary Physiology and Sleep Medicine, Sir Charles Gairdner Hospital, Nedlands, Australiaen
dc.identifier.affiliationSchool of Public Health & Preventive Medicine, Monash University, Melbourne, Australiaen
dc.identifier.affiliationRespiratory Epidemiology and Public Health Group, National Heart and Lung Institute, Imperial College London, London, UKen
dc.identifier.affiliationAllergy and Lung Health Unit, School of Population and Global Health, The University of Melbourne, Melbourne, Australiaen
dc.identifier.affiliationLung and Sleep Dept at Monash Health, Melbourne, Australiaen
dc.identifier.affiliationSchool of Clinical Sciences, Monash University, Melbourne, Australiaen
dc.identifier.affiliationCollege of Medicine and Public Health, Flinders University, Adelaide, Australiaen
dc.identifier.affiliationDept of Epidemiology and Biostatistics, MRC-PHE Centre for Environment and Health, School of Public Health, Imperial College London, London, UKen
dc.identifier.affiliationFaculty of Medicine, Inflammation and Infection Research, University of New South Wales, Sydney, Australiaen
dc.identifier.affiliationCentro de Investigación Biomédica en Red Enfermedades Respiratorias (CIBERES), Barcelona, Spainen
dc.identifier.affiliationInstitut d'Investigacions Biomediques August Pi i Sunyer (IDIBAPS), Barcelona, Spainen
dc.identifier.affiliationRespiratory Institute, Hospital Clinic, Barcelona, Spainen
dc.identifier.affiliationUniversity of Barcelona, Barcelona, Spainen
dc.identifier.pubmedurihttps://pubmed.ncbi.nlm.nih.gov/34527727/en
dc.identifier.doi10.1183/23120541.00020-2021en
dc.type.contentTexten
dc.identifier.orcid0000-0002-4388-784Xen
dc.identifier.orcid0000-0001-7034-0615en
dc.identifier.orcid0000-0003-3265-0131en
dc.identifier.orcid0000-0002-1753-3896en
dc.identifier.orcid0000-0002-9954-0538en
dc.identifier.orcid0000-0002-4388-784Xen
dc.identifier.pubmedid34527727-
local.name.researcherPerret, Jennifer L
item.languageiso639-1en-
item.cerifentitytypePublications-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.grantfulltextnone-
item.openairetypeJournal Article-
item.fulltextNo Fulltext-
crisitem.author.deptInstitute for Breathing and Sleep-
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