TY - JOUR
T1 - Lung function trajectory and biomarkers in the tasmanian longitudinal health study
AU - Bui, Dinh S.
AU - Agusti, Alvar
AU - Walters, Haydn
AU - Lodge, Caroline
AU - Perret, Jennifer L.
AU - Lowe, Adrian
AU - Bowatte, Gayan
AU - Cassim, Raisa
AU - Hamilton, Garun S.
AU - Frith, Peter
AU - James, Alan
AU - Thomas, Paul S.
AU - Jarvis, Debbie
AU - Abramson, Michael J.
AU - Faner, Rosa
AU - Dharmage, Shyamali C.
N1 - Funding Information:
Support statement: TAHS was supported by the National Health and Medical Research Council (NHMRC) of Australia under NHMRC project grant scheme (299901 and 1021275) and NHMRC European collaborative grant scheme (1101313) as part of ALEC (Ageing Lungs in European Cohorts funded by the European Union’s Horizon 2020 research and innovation programme under grant agreement number 633212); The University of Melbourne; Clifford Craig Medical Research Trust of Tasmania; the Victorian, Queensland & Tasmanian Asthma Foundations; The Royal Hobart Hospital; Helen MacPherson Smith Trust; and GlaxoSmithKline. S.C. Dharmage, A. Lowe, J.L. Perret, C. Lodge and H. Walters are supported by the NHMRC of Australia. R. Faner is recipient of a Miguel Servet Research Program Contract of the Instituto de Salud Carlos III (FEDER, CP16/00039, PI17/00379 and PI18/00018).
Publisher Copyright:
© The authors 2021.
Copyright:
Copyright 2021 Elsevier B.V., All rights reserved.
PY - 2021/7/1
Y1 - 2021/7/1
N2 - Background and objective Different 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. Methods 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 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. Conclusions 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.
AB - Background and objective Different 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. Methods 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 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. Conclusions 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.
UR - https://www.scopus.com/pages/publications/85116977231
U2 - 10.1183/23120541.00020-2021
DO - 10.1183/23120541.00020-2021
M3 - Article
C2 - 34527727
AN - SCOPUS:85116977231
SN - 2312-0541
VL - 7
JO - ERJ Open Research
JF - ERJ Open Research
IS - 3
M1 - 00020-2021
ER -