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Tocilizumab (TCZ) has been approved for giant cell arteritis (GCA). Interleukin-6 (IL-6) receptor blockade suppresses clinical disease and is steroid sparing.1 2 Since IL-6 induces the acute-phase response, the clinically used inflammation markers (C reactive protein (CRP), erythrocyte sedimentation rate (ESR)) are suppressed during TCZ treatment. Whether serum IL-6 is useful in monitoring disease activity and detecting infections in TCZ-treated GCA is unknown.
We longitudinally measured IL-6 in 23 patients with intravenous TCZ–treated GCA, two patients with polymyalgia rheumatica and one patient with Takayasu arteritis of our GCA cohort (EKBB-239/09), and in 13/26 patients additionally before TCZ treatment. Patient characteristics are shown in table 1. At each visit, clinical and laboratory parameters (white blood cell (WBC), CRP, ESR) were assessed. Relapse was defined as the need for treatment intensification following new or increasing symptoms, or rising CRP/ESR not otherwise explained.2
During TCZ therapy, CRP, ESR and WBC rapidly declined and were sustainably suppressed. IL-6 levels rose and remained elevated throughout TCZ treatment (figure 1). Daily prednisone doses were successfully tapered after TCZ was initiated (figure 1C). During 23.8 patient-years of TCZ therapy, eight infections were documented with available IL-6 levels (online supplementary table S1). IL-6, but not CRP, ESR …
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