C-REACTIVE PROTEIN IN RHEUMATOID ARTHRITIS TREATED WITH INTERLEUKIN-6 INHIBITOR

Abstract

Rheumatoid arthritis (RA) is a chronic immune-me-diated systemic inflammatory disease characterized by chronic synovial inflammation and hyperplasia, which cause joint erosion and damage along with systemic manifestations. Proinflammatory pathways result in localized joint and systemic inflammation with cytokines, such as interleukin-6 (IL-6), tumour necrosis factor-α (TNF-α), interleukin 1β (IL-1β), as well as downstream signalling pathways. One function of IL-6 is to drive production of the acute-phase reactant C-reactive pro-tein (CRP) following an inflammatory event. C-reactive protein is not only a marker of inflamma-tion or infection, but it is also an immune regulator. C-reactive protein level is a component of several com-posite disease activity measures. Higher CRP levels are associated with greater RA disease activity, radiogra-phic progression and joint destruction. Yet, the usefulness of CRP testing as a routine measure of RA disease activity is not universal due to the sub-stantial proportion of treated patients who experience flares in their RA but still have normal CRP levels. There may be challenges in assessing remission with 28-joint Disease Activity Score -CRP (DAS28-CRP) when patients are treated with IL-6 inhibitors and other drugs that directly affect CRP levels because a reduction in CRP may not reflect disease activity decrease. The case that we present is a patient with seropositive RA in whom we tried all available RA treatment modalities including IL-6 inhibitor and two other biologicals, and despite the fact that we achieved low disease activity and sometimes even remission of the underlying disease, radiographic progression and sub-jective complaints of the patient continued.