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Growth Differentiation Factor-15 Is a Novel Biomarker Predicting Acute Exacerbation of Chronic Obstructive Pulmonary Disease

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Abstract

Exacerbations in chronic obstructive pulmonary disease (COPD) reduce quality of life and are associated with a more rapid deterioration of the disease. Growth differentiation factor-15 (GDF-15) is a novel candidate exacerbation biomarker. In this study, we aimed to assess GDF-15 as a biomarker of acute exacerbation of COPD (AE-COPD). Lung function parameters, arterial blood gas analysis, and circulating levels of GDF-15, C-reactive protein (CRP), and fibrinogen were assessed in 29 patients on admission to the hospital for AE-COPD, in 29 age-, gender-, and body mass index (BMI)-matched patients with stable COPD, and 29 matched controls with normal lung function. Patients with AE-COPD had higher circulating concentrations of GDF-15 (p < 0.001), CRP (p < 0.001), and fibrinogen (p < 0.002) compared with patients with stable COPD and healthy controls. GDF-15 levels correlated with systemic inflammatory marker CRP in patients with AE-COPD (r = 0.677, p < 0.001) and with stable COPD (r = 0.417, p = 0.024). Multivariate logistic regression analysis revealed GDF-15 (odds ratio 18.16, 95 % confidence interval (CI) 2.51–134.32; p = 0.005) as an independent predictor of AE-COPD. In receiver operating characteristic analysis, GDF-15 achieved an area under the curve of 0.78 for the identification of AE-COPD. In conclusion, GDF-15 is a novel blood biomarker of AE-COPD that is more sensitive than that of CRP. GDF-15 may offer new insights into the pathogenesis of AE-COPD.

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Authors’ Contributions

All authors were involved in writing the paper and had final approval of the submitted and published versions.

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This is not an industry-supported study. The authors have indicated no conflict of interest.

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Correspondence to Nejat Altintas.

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Mutlu, L.C., Altintas, N., Aydin, M. et al. Growth Differentiation Factor-15 Is a Novel Biomarker Predicting Acute Exacerbation of Chronic Obstructive Pulmonary Disease. Inflammation 38, 1805–1813 (2015). https://doi.org/10.1007/s10753-015-0158-5

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