Serum YKL-40 concentrations in patients with rheumatoid arthritis: relation to disease activity

Citation
Js. Johansen et al., Serum YKL-40 concentrations in patients with rheumatoid arthritis: relation to disease activity, RHEUMATOLOG, 38(7), 1999, pp. 618-626
Citations number
40
Categorie Soggetti
Rheumatology
Journal title
RHEUMATOLOGY
ISSN journal
14620324 → ACNP
Volume
38
Issue
7
Year of publication
1999
Pages
618 - 626
Database
ISI
SICI code
1462-0324(199907)38:7<618:SYCIPW>2.0.ZU;2-S
Abstract
Objective. YKL-40, also called human cartilage glycoprotein-39, is secreted by chondrocytes, synovial cells, macrophages and neutrophils. Studies have shown that YKL-40 is an autoantigen in rheumatoid arthritis (RA). We evalu ated whether serum YKL-40 was related to disease activity in patients with RA. Methods. Serum YKL-40 was determined by radioimmunoassay in 156 patients wi th RA during a 1 yr longitudinal study. Results. Serum YKL-40 was increased in 54% of the patients with clinically active disease. Patients with clinically active disease initially who becam e inactive after 12 months had a significant decrease in serum YKL-40 (-30% , P < 0.002) and patients who changed from inactive to active disease had a n increase in serum YKL-40. Patients who remained active had unchanged seru m YKL-40 during the study. Serum YKL-40 decreased rapidly (-24% after 7 day s, P < 0.01) during prednisolone therapy, and more slowly in patients treat ed with methotrexate only (-15% after 60 days, P < 0.01). Patients with ear ly RA (disease duration <3 yr, n = 50) and a persistently elevated serum YK L-40 were at risk of radiological disease progression as determined by Lars en score. Conclusion. Serum YKL-40 varies according to disease activity in RA, but pr ovides in some respect information different from conventional markers. Our previous studies are consistent with a local release of YKL-40 in the arth ritic joint followed by a secondary increase in serum YKL-40. YKL-40 may pr ove to be a new tool for the study of disease activity and pathophysiology of RA.