Serum hepcidin: a direct link between anemia of inflammation and coronary artery atherosclerosis in patients with rheumatoid arthritis

Abstract

Objective: To investigate the role of hepcidin as an inducer of anemia of inflammation in patients with rheumatoid arthritis (RA), and its correlation to coronary artery atherosclerosis.

Methods: Our study included 60 patients with RA and 20 healthy controls. Anemic RA patients with serum transferrin receptors/log ferritin (sTfR-F) index value < 1.5 were classified as having pure anemia of chronic disease (ACD), and patients with sTfR-F index value > 1.5 were classified as having anemia of chronic disease with coexistent iron deficiency anemia (ACD+IDA). Measurements were taken for Disease Activity Score for 28 joints (DAS28), Modified Health Assessment Questionnaire (MHAQ), erythrocyte sedimentation rate (ESR), high sensitivity C-reactive protein (hsCRP), rheumatoid factor (RF), lipid profile, serum interleukin 6 (IL-6), tumor necrosis factor-α, iron studies, and serum hepcidin. Coronary calcium score (CCS) was measured using multislice spiral computed tomography as a marker of atherosclerosis.

Results: Serum hepcidin was found to be higher in anemic patients with RA than in controls (p < 0.001), and higher in the pure ACD subgroup than in the ACD+IDA subgroup (p < 0.001). Hepcidin concentration was positively correlated with disease duration, ESR, hsCRP, RF, DAS28, MHAQ, serum ferritin, IL-6, and mean CCS and inversely correlated with hemoglobin, sTfR, and the sTfR-F index.

Conclusion: Hepcidin can be considered a key inducer of anemia of inflammation in patients with RA. This inflammation was proved to be directly linked to coronary artery atherosclerosis. The correlations between serum hepcidin with disease activity and IL-6 raise the possibility of using it as a surrogate marker for disease activity.