The effect of anemia on serum hepcidin levels in patients with heart failure
Published on: 17th October, 2019
OCLC Number/Unique Identifier: 8303641326
Background: Anemia is an accelerating problem among patients with heart failure (HF) and its presence is associated with more symptoms. In this study, we investigated whether anemia in heart failure was related to hepcidin concentration.
Methods: 50 patients with heart failure and 20 healthy subjects with no history of a chronic illness including heart failure as control group, were included in the study. Heart failure was verified by echocardiography in each subject and patients were defined as ones with reduced ejection fraction (HFrEF) if EF ≤ 40% and with preserved ejection fraction (HFpEF) if EF 40% - 50%. Blood samples were taken from all patients after 10-12 hours fasting. Anemia assessment was performed according to World Health Organization (WHO) criterias.
Results: There was a positive correlation between hepcidin concentration and urea, ferritin, hemoglobin, hematocrite, C-reactive protein (p < 0,05). Hepcidin concentrations of anemic heart failure patients were significantly lower than the non-anemic heart failure patients (p < 0,05).
Conclusion: We found that serum hepcidin concentration in anemic patients with heart failure was lower than in heart failure patients without anemia. We believe that iron defiency occurs as a result of inflammatory process in heart failure and therefore hepcidin concentrations decrease as a response. However, long-term follow up studies are needed.
Serum Levels of the C-terminal Fragment of Fibroblast Growth Factor 23 (C-FGF23) and Hepcidin in Patients with Hemodialysis Undergoing Treatment with a Proline Hydroxylase Domain (PHD) Inhibitor
Published on: 14th October, 2024
Background: We previously reported, for the first time, serum levels of the C-terminal fragment of fibroblast growth factor 23 (C-FGF23) in patients undergoing hemodialysis (HD). Most HD patients have undergone treatment with either recombinant erythropoietin (r-EPO) or hypoxia-inducible factor (HIF) proline hydroxylase domain (PHD) inhibitor, both of which stimulate FGF23 production and cleavage. Methods: This cross-sectional observational study involved analyzing measuring FGF-related parameters and comparing results for subgroups of patients who received either r-EPO and or a PHD inhibitor. Results: No significant difference was observed for iron-related parameters or serum hepcidin levels in both subgroups of patients. Significant differences were found for certain FGF-23-related parameters. Conclusion: Both FGF23 production and cleavage were stimulated more in patients treated with the PHD inhibitor than in patients treated with r-EPO.
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