Serum level of osteopontin as an inflammatory marker does not indicate disease activity or responsiveness to therapeutic treatments in patients with rheumatoid arthritis

Hye In Ji, Sang Hoon Lee, Ran Song, Hyung In Yang, Yeon Ah Lee, Seung Jae Hong, Somi Kim, YongBeom Park, Soo Kon Lee, Myung Chul Yoo, Kyoung Soo Kim

Research output: Contribution to journalArticle

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Abstract

Osteopontin (OPN) is known to be significantly involved in the pathogenesis of rheumatoid arthritis (RA). This study aimed to evaluate if the serum concentration of OPN in patients with RA before and after therapeutic treatments was correlated to disease activity and response to therapy. Blood samples from 40 patients with RA were collected at baseline and six months after starting treatment with disease-modifying antirheumatic drugs (DMARDs) and/or tumor necrosis factor (TNF)-α blockers. Serum levels of OPN were measured by ELISA. At baseline, the serum OPN level in RA patients was significantly higher than that of the healthy group. The OPN level at baseline in RA patients with severe disease activity as evaluated by DAS28 was slightly higher than that of those with moderate disease activity. The serum OPN level in RA patients was not significantly correlated with the DAS28 level. The serum OPN level in both responders and non-responders after therapy was significantly decreased regardless of responsiveness to therapy. Also, the OPN level at baseline did not affect the responsiveness to therapeutic treatments. In conclusion, serum OPN level was not correlated with disease activity or responsiveness of RA patients to therapeutic treatments.

Original languageEnglish
Pages (from-to)397-402
Number of pages6
JournalClinical Rheumatology
Volume33
Issue number3
DOIs
Publication statusPublished - 2014 Jan 1

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Osteopontin
Rheumatoid Arthritis
Serum
Therapeutics
Antirheumatic Agents
Tumor Necrosis Factor-alpha
Enzyme-Linked Immunosorbent Assay

All Science Journal Classification (ASJC) codes

  • Rheumatology

Cite this

Ji, Hye In ; Lee, Sang Hoon ; Song, Ran ; Yang, Hyung In ; Lee, Yeon Ah ; Hong, Seung Jae ; Kim, Somi ; Park, YongBeom ; Lee, Soo Kon ; Yoo, Myung Chul ; Kim, Kyoung Soo. / Serum level of osteopontin as an inflammatory marker does not indicate disease activity or responsiveness to therapeutic treatments in patients with rheumatoid arthritis. In: Clinical Rheumatology. 2014 ; Vol. 33, No. 3. pp. 397-402.
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abstract = "Osteopontin (OPN) is known to be significantly involved in the pathogenesis of rheumatoid arthritis (RA). This study aimed to evaluate if the serum concentration of OPN in patients with RA before and after therapeutic treatments was correlated to disease activity and response to therapy. Blood samples from 40 patients with RA were collected at baseline and six months after starting treatment with disease-modifying antirheumatic drugs (DMARDs) and/or tumor necrosis factor (TNF)-α blockers. Serum levels of OPN were measured by ELISA. At baseline, the serum OPN level in RA patients was significantly higher than that of the healthy group. The OPN level at baseline in RA patients with severe disease activity as evaluated by DAS28 was slightly higher than that of those with moderate disease activity. The serum OPN level in RA patients was not significantly correlated with the DAS28 level. The serum OPN level in both responders and non-responders after therapy was significantly decreased regardless of responsiveness to therapy. Also, the OPN level at baseline did not affect the responsiveness to therapeutic treatments. In conclusion, serum OPN level was not correlated with disease activity or responsiveness of RA patients to therapeutic treatments.",
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Serum level of osteopontin as an inflammatory marker does not indicate disease activity or responsiveness to therapeutic treatments in patients with rheumatoid arthritis. / Ji, Hye In; Lee, Sang Hoon; Song, Ran; Yang, Hyung In; Lee, Yeon Ah; Hong, Seung Jae; Kim, Somi; Park, YongBeom; Lee, Soo Kon; Yoo, Myung Chul; Kim, Kyoung Soo.

In: Clinical Rheumatology, Vol. 33, No. 3, 01.01.2014, p. 397-402.

Research output: Contribution to journalArticle

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