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SAT0096 Serum hepcidin level is a surrogate marker of disease activity but does not independently predict radiographic progression in early rheumatoid arthritis: Results from the ESPOIR cohort
  1. J. Sellam1,
  2. S. Kotti2,
  3. S. Fellahi3,
  4. J.-P. Bastard3,
  5. M. Meyer4,
  6. F. Lioté5,
  7. O. Meyer6,
  8. T. Simon7,
  9. J. Capeau3,
  10. F. Berenbaum1
  1. 1Department of Rheumatology, UPMC Paris-6, Saint-Antoine Hospital, Ap-Hp
  2. 2Unité de Recherche Clinique Paris-Est URCEST, Hôpital Saint-Antoine, Ap-Hp
  3. 3UMR_S938, Inserm U938, Department of Biochemistry and Hormonology, UPMC Paris-6, Tenon Hospital, Ap-Hp
  4. 4Rheumatology Department, Hôpital Saint-Antoine, Ap-Hp
  5. 5Department of Rheumatology, Paris Diderot Paris VII University, Lariboisière Hospital, Ap-Hp
  6. 6Department of Rheumatology, Paris Diderot Paris VII University, Bichat Hospital, Ap-Hp
  7. 7Unité de Recherche Clinique Paris-Est URCEST, UPMC Paris-6, Saint-Antoine Hospital, Ap-Hp, Paris, France

Abstract

Background Hepcidin is an interleukin 6-induced peptide hormone produced by the liver and involved in iron homeostasis and inflammation. Previous published studies have suggested that hepcidin could be a key biomarker of severity in rheumatoid arthritis (RA).

Objectives We investigated whether serum hepcidin level may represent a novel surrogate biomarker of RA features, disease activity, or of structural progression.

Methods Serum hepcidin level was assessed by enzyme immunoassay kit (Bachem, UK) in 791 patients from the French ESPOIR early arthritis cohort (at least 2 swollen joints for more than 6 weeks and less than 6 months) who met the 2010 EULAR-ACR criteria for RA (n=632) or had undifferentiated arthritis (UA) (n=159) at inclusion. We compared baseline hepcidin levels between RA and UA, searched for a cross-sectional association with the baseline clinical, immunological and radiological RA features, and determined, using univariate and multivariate analyses, whether log-transformed hepcidin level may predict the progression of X-ray alterations defined by an increase of the total Sharp/van der Heijde score ≥1.

Results Mean (±SD) level of hepcidin was higher in RA than in UA patients (53.02±48.45 vs 39.63±39.87 ng/mL, p<0.0001). In RA patients, serum hepcidin was higher when rheumatoid factor (RF) or anti-CCP were positive compared to their absence (57.5±51.6 vs 46.9±43.2 ng/mL, p=0.0007; 58.3±52.1 vs 47.8±44.0 ng/mL, p=0.0007, respectively). Correlation between hepcidin levels and DAS28 (r=0.1, p=0.01) was mainly explained by its correlation with erythrocyte sedimentation rate (ESR) (r=0.21, p<0.0001) and with C reactive protein (r=0.24, p<0.0001). A higher hepcidin concentration was significantly associated with an increased HAQ (r=0.14, p=0.0005), but not with fatigue level. Hepcidin level was unchanged whether anaemia was present or not (p=0.4), was not correlated with haemoglobin level but correlated with ferritinemia (r=0.27, p<0.0001). Baseline hepcidin level was higher in erosive compared with non erosive RA patients at inclusion (62.77±50.01 versus 51.01±47.93 ng/mL, p=0007). Log (hepcidin level) was associated with radiographic progression at 1 year (odds ratio=1.38 [95%CI:1.10-1.72]; p<0.0001) in the univariate but not in the multivariate analysis which included relevant confounders (gender, DAS28 at inclusion, HAQ level at inclusion, RF positivity, antiCCP antibodies positivity) (odds ratio=1.24 [95%CI:0.92-1.67]; p=0.16).

Conclusions Serum hepcidin level is elevated in RF/anti-CCP-positive RA patients and in erosive RA. Serum hepcidin increase reflects a higher disease activity and correlates with HAQ, suggesting a clinical relevance of its assessment beyond its link with the ESR. However, its measurement does not give additional information compared to the usual biomarkers of inflammation nor it predicts radiographic progression.

Disclosure of Interest None Declared

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