Session Type: Abstract Submissions (ACR)
Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by joint inflammation and eventually destruction, where TNFa is a central mediator of both processes. Soluble CD163 is a plasma marker of macrophage activation. CD163 is a scavenger receptor specifically expressed by macrophages and responsible for binding hemoglobin-haptoglobin complexes. The soluble form is cleaved from the cell surface by TACE/ADAM17, the metalloproteinase also responsible for the cleavage of TNFa, suggesting a close association between sCD163 and TNFa. In RA, sCD163 has been suggested as a marker of disease activity and progression 1. We aimed to investigate plasma sCD163 in very early RA (eRA) patients.
Soluble CD163 was measured by ELISA in plasma samples from 154 eRA patients belonging to the OPERA cohort2. Age 53.5 years (51-56), 70% females, average disease duration: 3 months. Patients were randomized to conventional methotrexate and placebo (MTX+PLA) or MTX and adalimummab (MTX+ADA) treatment. Clinical disease was assessed by: Disease activity index (DAS28), health assessment questionnaire (HAQ), CRP, swollen joints (SJC40), tender joints (TJC40), simple disease activity index (SDAI), clinical disease activity index (CDAI), visual analogue scale (VAS) for pain, total sharp score (TSS), IgM-RF and ACPA. Statistical analysis was performed by student’s t-test, Spearman’s Rank correlation and linear regression.
Plasma concentration of sCD163 at baseline was 2.40 mg/l (CI: 2.21 mg/l-2.56 mg/l)) corresponding to the upper part of the HV reference interval (0.69mg/l – 3.86mg/l). After three months of treatment sCD163 had decreased significantly in both treatment groups (to 1.81 mg/l (1.68mg/l – 1.95 mg/l), p<0.001). Though the decrease in the MTX+ADA group was more prominent than in the MTX+PLA group. Withdrawal of ADA after 12 months of treatment was followed by incremental sCD163 levels during the subsequent 12 months (1.73mg/l (1.55mg/l -1.94mg/l to 2.07mg/l (1.88mg/l – 2.28mg/l (p<0.001)). At baseline sCD163 correlated with CRP and all investigated markers of disease activity (ρ = 0.16-0.28, p<0.05). We observed no correlation with TSS, IgM-RF and ACPA. The correlation between sCD163 and CRP at baseline could be fitted to a linear regression model (β=8.28, p<0.001). In the MTX+PLA group, this linear regression was also observed after 6 months and 1 year of treatment (β=7.5 and 9.9, respectively, both p<0.001). In the MTX+ADA group the close association was only observed after 3 months of treatment (β=10.9, p<0.007).
Soluble CD163 correlated with markers of disease activity in eRA. The correlation with CRP was very close and followed a linear regression model. Our results also indicate that sCD163 is associated with TNFa, as withdrawal of anti-TNF treatment was clearly reflected in increased sCD163 levels and correlation with CRP is diminished in the MTX+ADA treatment group. Plasma sCD163 thus reflects anti-TNF treatment and is a potential new disease activity marker in eRA.
H. J. Møller,
M. L. Hetland,
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ACR Meeting Abstracts - https://acrabstracts.org/abstract/soluble-cd163-is-a-marker-of-disease-activity-in-early-rheumatoid-arthritis-and-reflects-tnf%ce%b1-levels/