Hepcidin plasma levels are not associated with changes in haemoglobin in early rheumatoid arthritis patients

Abstract

Objective: A reduction in haemoglobin level is a frequent complication among rheumatoid arthritis (RA) patients. Hepcidin has been linked to disturbed erythropoiesis. The objective of this study was to investigate the longitudinal changes in hepcidin in patients with early RA.

Method: Hepcidin plasma concentrations were measured by enzyme-linked immunosorbent assay in patients with early RA (n = 80) and healthy volunteers (HV, n = 40). Haemoglobin and other iron-related proteins were also measured. At baseline, all patients had active disease and were treatment naïve. Patients were treated with disease-modifying anti-rheumatic drugs (DMARDs) and with additional adalimumab (ADA, n = 42) or placebo (PLA, n = 38) during 52 weeks, using a treat-to-target strategy, aiming for a 28-joint Disease Activity Score (DAS28) < 3.2.

Results: At baseline, hepcidin levels [median (interquartile range)] were 9.7 ng/mL (5.2–19.4 ng/mL) in DMARD + ADA and 11.3 ng/mL (5.9–19.1 ng/mL) in DMARD + PLA. Both were significantly higher than seen in HV (6.0 ng/mL (3.3–9.3 ng/mL) (p < 0.001). After 12 months, both treatment regimens resulted in normalization of hepcidin. DAS28 correlated with hepcidin at baseline (r = 0.48, p < 0.001). No correlation was observed between levels of haemoglobin and hepcidin at baseline or during the 52 week follow-up. No change in haemoglobin levels was seen as a function of hepcidin changes. In a mixed statistical model, no single factor was connected with the regulation of haemoglobin in early RA.

Conclusion: The changes in hepcidin were not associated with changes in haemoglobin levels. Thus, hepcidin could not be used as a prognostic marker in patients with early RA.

Acknowledgements

We thank the OPERA Study Group for collecting the material and Julia Johansen, Copenhagen University Hospital at Glostrup, Denmark, for handling the samples. We are grateful to Karin Skovgaard Sørensen, Department of Biomedicine, Aarhus University, for technical assistance.

The study was supported by a grant from the Danish Rheumatism Association.

Additional information

Funding

This work was supported by the Gigtforeningen: [Grant Number R92-A1604].