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Open Access Research article

Effect of tocilizumab on haematological markers implicates interleukin-6 signalling in the anaemia of rheumatoid arthritis

John D Isaacs15*, Olivier Harari2, Uwe Kobold3, Janet S Lee4 and Corrado Bernasconi2

Author Affiliations

1 Institute of Cellular Medicine, The Medical School, Framlington Place, Newcastle upon Tyne, NE2 4HH, UK

2 Roche, Basel, Switzerland

3 Roche Diagnostics GmbH, Penzberg, Germany

4 Roche, Nutley, New Jersey

5 Newcastle University, Institute of Cellular Medicine (Musculoskeletal Research Group), Newcastle upon Tyne, NE2 4HH, UK

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Arthritis Research & Therapy 2013, 15:R204  doi:10.1186/ar4397

Published: 2 December 2013

Abstract

Introduction

Our objective was to determine the interrelationships of interleukin (IL)-6 receptor inhibition with haemoglobin, acute-phase reactants and iron metabolism markers (including hepcidin) in patients with rheumatoid arthritis (RA).

Methods

Data of patients receiving tocilizumab or placebo in the MEASURE study were analysed. We investigated associations at baseline and during tocilizumab treatment among haemoglobin, parameters of haemoglobin and iron homeostasis [ferritin, total iron-binding capacity (TIBC), hepcidin, haptoglobin], IL-6 and acute-phase reactants [C-reactive protein (CRP), erythrocyte sedimentation rate (ESR)] to identify statistical correlates of rise in haemoglobin level.

Results

At baseline, CRP and haptoglobin were inversely correlated (modestly) with haemoglobin levels. After treatment with tocilizumab, CRP, hepcidin, ferritin and haptoglobin levels fell alongside increases in TIBC and haemoglobin. The falls in CRP, hepcidin and haptoglobin levels in the first 2 weeks correlated with a week 12 rise in TIBC and haemoglobin.

Conclusions

Inflammatory anaemia improves in patients with RA treated with tocilizumab. This improvement correlates with the degree of suppression of systemic inflammation, reduction in hepcidin and haptoglobin and increase in iron-binding capacity. These clinical data provide evidence of a role for IL-6 signalling in the inflammatory anaemia of RA.