Abstract
Background: We examined whether high-sensitivity CRP (hsCRP) reflected the inflammatory disease status evaluated by clinical and ultrasound (US) parameters in RA patients receiving IL-6 receptor antibodies (anti-IL-6R) or JAK inhibitors (JAKi). Methods: We conducted a cross-sectional study of patients with established RA receiving anti-IL-6R (tocilizumab, sarilumab) or JAKi (tofacitinib, baricitinib). Serum hsCRP and US synovitis in both hands were measured. Associations between hsCRP and clinical inflammatory activity were evaluated using composite activity indices. The association between hsCRP and US synovitis was analyzed. Results: 63 (92% female) patients (42 anti- IL-6R and 21 JAKi) were included, and the median disease duration was 14.4 (0.2–37.5) years. Most patients were in remission or had low levels of disease. Overall hsCRP values were very low, and significantly lower in anti-IL-6R patients (median 0.04 mg/dL vs. 0.16 mg/dL). Anti-IL-6R (82.4%) patients and 48% of JAKi patients had very low hsCRP levels (≤0.1 mg/dL) (p = 0.002). In the anti-IL-6R group, hsCRP did not correlate with the composite activity index or US synovitis. In the JAKi group, hsCRP moderately correlated with US parameters (r = 0.5) but not clinical disease activity, and hsCRP levels were higher in patients with US synovitis (0.02 vs. 0.42 mg/dL) (p = 0.001). Conclusion: In anti-IL-6R RA-treated patients, hsCRP does not reflect the inflammatory disease state, but in those treated with JAKi, hsCRP was associated with US synovitis.
Highlights
Rheumatoid arthritis (RA) is a chronic progressive disease characterized by inflammation of the synovial joints, leading to joint destruction and disability that can be prevented by promptly initiated and effective therapy [1]
In patients treated with anti-IL-6R, C-reactive protein (CRP) does not satisfactorily reflect the degree of inflammation, since their production is aborted with these biological therapies, without this being reflected in a substantial improvement in synovitis [7]
We hypothesized that there is no association in patients treated with anti-IL-6R due to the dramatic impact on high-sensitivity CRP (hsCRP) serum levels with these therapies whereas, in patients treated with JAK inhibitors (JAKi), hsCRP may be a sensitive biomarker of disease activity
Summary
Rheumatoid arthritis (RA) is a chronic progressive disease characterized by inflammation of the synovial joints, leading to joint destruction and disability that can be prevented by promptly initiated and effective therapy [1]. Less well known and studied, this occurs in patients treated with JAKi, which partially inhibits IL6 signaling [8]. It has been questioned whether CRP reflects the inflammatory state in patients receiving these therapies. We examined whether high-sensitivity CRP (hsCRP) reflected the inflammatory disease status evaluated by clinical and ultrasound (US) parameters in RA patients receiving IL-6 receptor antibodies (anti-IL-6R) or JAK inhibitors (JAKi). Associations between hsCRP and clinical inflammatory activity were evaluated using composite activity indices. Results: 63 (92% female) patients (42 anti- IL-6R and 21 JAKi) were included, and the median disease duration was 14.4 (0.2–37.5) years
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