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Enhanced Concentrations of Interleukin 16 Are Associated with Joint Destruction in Patients with Rheumatoid Arthritis
LEROY R. LARD, BART O. ROEP, RENE E.M. TOES, and THOMAS W.J. HUIZINGA
ABSTRACT.
Methods. We measured systemic IL-16 levels longitudinally in 39 patients with recent-onset RA, in 13 patients with initially undifferentiated arthritis who will develop RA over time, in 15 patients with undifferentiated arthritis, and in 12 healthy controls, and correlated the levels with joint damage and disease activity. Systemic IL-16 levels were measured by ELISA. Joint destruction was measured according to the Sharp method and the disease activity variables included C-reactive protein (CRP) and Disease Activity Score (DAS) measured at disease onset, and after one and 2 years of followup. Results. A significantly increased IL-16 level in RA patients at disease onset [median (25th-75th percentile) 45.2 (37.7–82.4) pg/ml] was observed compared to both controls [30.4 (24.4–37.0) pg/ml, p = 0.0008], and to patients with undifferentiated arthritis [29.0 (21.5–52.4) pg/ml; p = 0.005]. The IL-16 levels of the patients who presented with undifferentiated arthritis but who developed RA over time were also increased [47.9 (34.5–108.2) pg/ml] compared to the controls (p = 0.004) and to the patients who over time remained diagnosed with undifferentiated arthritis (p = 0.01). We found that high IL-16 levels correlated positively with joint destruction during the 2-year followup (p = 0.02) and not with the disease activity variables. Conclusion. Our results suggest that the cytokine IL-16 plays a role in the disease process underlying RA and joint destruction. (J Rheumatol 2004;31:35-9) Key Indexing Terms:
INTERLEUKIN 16
From the Departments of Rheumatology and Immunohaematology and Blood Transfusion, Leiden University Medical Center, Leiden, The Netherlands. L.R. Lard, MD; R.E.M. Toes, PhD; T.W.J. Huizinga, MD, PhD, Department of Rheumatology; B.O. Roep, PhD, Department of Immunohaematology and Blood Transfusion. Address reprint requests to Dr. T.W.J. Huizinga, Department of Rheumatology, Leiden University Medical Center, PO Box 9600, 2300 RC, Leiden, The Netherlands. E-mail: t.w.j.huizinga@lumc.nl Submitted November 25, 2002; revision accepted June 9, 2003. |