Increased plasma osteopontin in frequent exacerbator and acute exacerbation of COPD Seung Jun Lee 1 , Sung Hwan Kim 2 , Wanchul Kim 1 , Sujin Lim 1 , Seung Hun Lee 1 , Yu Eun Kim 1 , Yu Ji Cho 1 , Yi Yeong Jeong 1 , Ho Cheol Kim 1 , Jong Deog Lee 1 and Young Sil Hwang 1 1 Division Pulmonology and Allergy, Department of Internal Medicine, College of Medicine, Gyeongsang National University, Jinju, Korea 2 Department of Thoracic and Cardiovascular Surgery, College of Medicine, Gyeongsang National University, Jinju, Korea Abstract Introduction: Osteopontin (OPN) is a phosphorylated glycoprotein expressed by diverse tissues including bone, brain, kidney, liver and lung. Limited data exist regarding OPN in chronic obstructive pulmonary disease (COPD) and the exac- erbation of this condition. Objectives: The aim of this study was to evaluate plasma OPN levels and investigate the clinical usefulness of plasma OPN measurement in patients with COPD. Methods: Plasma OPN levels were measured and compared in patients with COPD exacerbation (n = 64), patients with stable COPD (n = 68) and healthy controls (n = 30). In patients with COPD exacerbation, plasma OPN levels were measured repeatedly in convalescence. Patients with stable COPD were categorized into fre- quent and infrequent exacerbators according to their frequency of exacerbation, and plasma OPN levels were compared between these two groups. Plasma OPN levels were determined by enzyme-linked immunosorbent assay. Results: Patients with COPD exacerbation had increased plasma OPN levels com- pared with those with stable COPD and healthy controls (32.6 ± 29.6, 17.6 ± 11.1, 8.4 ± 6.1 ng/mL, respectively; P < 0.001). In patients with COPD exacerbation, plasma OPN levels were significantly decreased in convalescence (44.8 ± 43.5 vs 24.6 ± 13.6 ng/mL; P = 0.034). Frequent exacerbators had higher plasma OPN levels compared with infrequent exacerbators (22.5 ± 12.0 vs 15.0 ± 9.8 ng/mL; P = 0.008). Conclusions: Plasma OPN levels were increased in patients with COPD exacerba- tion and frequent exacerbators, which suggests a possible role for OPN as a biomarker of COPD exacerbation. Please cite this paper as: Lee SJ, Kim SH, Kim W, Lim S, Lee SH, Kim YE, Cho YJ, Jeong YY, Kim HC, Lee JD and Hwang YS. Increased plasma osteopontin in frequent exacerbator and acute exacerbation of COPD. Clin Respir J 2014; 8: 305–311. Key words biomarker – chronic obstructive pulmonary disease – convalescence – disease exacerbation – osteopontin Correspondence Jong Deog Lee, PhD MD, Division of Pulmonology and Allergy, Department of Internal Medicine, School of Medicine, Gyeongsang National University, 92 Chilam-dong, 660-751 Jinju, Gyeongnam, Korea. Tel: +82 55 750 8611 Fax: +82 55 758 9122 email: ljd8611@nate.com Received: 04 March 2013 Revision requested: 03 July 2013 Accepted: 30 October 2013 DOI:10.1111/crj.12072 Authorship and contributorship J.D. Lee and S.J. Lee are guarantors of the manuscript. J.D. Lee contributed as the corresponding author, reviewing all data and revising the manuscript. S.J. Lee contributed as the primary author, reviewing all data and writing the manuscript. S.H. Kim contributed to the preparation of the manuscript, and read and approved the final manuscript. W. Kim contributed to the preparation of the manuscript, and read and approved the final manuscript. S. Lim contributed to the preparation of the manuscript, and read and approved the final manuscript. S.H. Lee contributed to the preparation of the manuscript, and read and approved the final manuscript. Y.E. Kim contributed to the preparation of the manuscript, and read and approved the final manuscript. Y.J. Cho contributed to the preparation of the manuscript, and read and approved the final manuscript. Y.Y. Jeong contributed to the preparation of the manuscript, and read and approved the final manuscript. H.C. Kim contributed to the preparation of the manuscript, and read and approved the final manuscript. Y.S. Hwang contributed to the preparation of the manuscript, and read and approved the final manuscript. Conflict of interest The authors have stated explicitly that there are no conflicts of interest in connection with this article. The Clinical Respiratory Journal ORIGINAL ARTICLE 305 The Clinical Respiratory Journal (2014) • ISSN 1752-6981 © 2013 John Wiley & Sons Ltd