Abstract
Background: Accelerated ageing in the lungs and systemic vasculature has been proposed as a mechanism in chronic obstructive pulmonary disease (COPD). However, with the exception of lung function decline, biomarkers indicating age-related deterioration in COPD are scarce. Elastin degradation occurs in COPD and in normal ageing, and is known to be increased in COPD. The aim of this study was to determine whether the pattern of elastin turnover as a function to age is different between COPD, control smokers and non-smokers.
Methods: We analyzed the levels of circulating desmosine, a specific marker of elastin turnover, in three independent cohorts comprising a total of 1,973 subjects (261 non-smoker controls, 380 smoker controls, and 1,332 COPD patients) using linear mixed effect model.
Results: Circulating desmosine levels were positively correlated with age in all groups (p<0.0001). Further analysis of circulating desmosine as a function of age in each group as a whole show that the slope of this relationship was greater in the COPD group (6.6 ng/L per year, p<0.0001) compared with non-smoker (2.9 ng/L per year) or smoker control group (3.1 ng/L per year), suggesting that in COPD age-dependent systemic elastin degradation is amplified. A similar age-dependent amplification was not observed in the smoker control group (p=0.68), although a slightly higher circulating desmosine level was found (median (IQR): 0.23 (0.18-0.28) in smoker and 0.20 (0.16-0.25) in non-smoker controls, p=0.008).
Conclusion: Our results provide evidence of age-associated increase on elastin turnover in COPD, supporting accelerated ageing in this condition.
- Copyright ©the authors 2016