BACKGROUND: The etiology of anemia is still unclear in patients with chronic heart failure (CHF). Hepcidin is an iron regulatory peptide that is synthesized in the liver to suppress iron absorption and utilization. Hepcidin synthesis is suppressed by anemia, hypoxia and erythropoiesis, and induced by inflammation. Inflammatory cytokines, such as interleukin-6 (IL-6), increase the synthesis of hepcidin, resulting in anemia of inflammation (AI). The serum hepcidin concentration in CHF patients with anemia was measured in order to better understand anemia in CHF. METHODS AND RESULTS: Serum hepcidin-25, erythropoietin (EPO), ferritin and IL-6 concentrations were measured in 61 CHF patients. Among these patients, 36 patients had anemia. A group of 16 patients without cardiac disease or anemia were recruited as controls. Serum IL-6 and EPO were higher and hepcidin-25 was lower in CHF patients with anemia than in controls. Hepcidin-25 correlated with EPO and ferritin but not with IL-6. Results of multivariable regression analysis showed that independent predictors of serum hepcidin-25 included EPO and ferritin but not IL-6. CONCLUSIONS: Serum hepcidin-25 concentrations were regulated by iron storage and erythropoiesis but not by IL-6 in CHF patients with anemia. These findings might indicate that AI is a minor cause of anemia in CHF.
BACKGROUND: The etiology of anemia is still unclear in patients with chronic heart failure (CHF). Hepcidin is an iron regulatory peptide that is synthesized in the liver to suppress iron absorption and utilization. Hepcidin synthesis is suppressed by anemia, hypoxia and erythropoiesis, and induced by inflammation. Inflammatory cytokines, such as interleukin-6 (IL-6), increase the synthesis of hepcidin, resulting in anemia of inflammation (AI). The serum hepcidin concentration in CHFpatients with anemia was measured in order to better understand anemia in CHF. METHODS AND RESULTS: Serum hepcidin-25, erythropoietin (EPO), ferritin and IL-6 concentrations were measured in 61 CHFpatients. Among these patients, 36 patients had anemia. A group of 16 patients without cardiac disease or anemia were recruited as controls. Serum IL-6 and EPO were higher and hepcidin-25 was lower in CHFpatients with anemia than in controls. Hepcidin-25 correlated with EPO and ferritin but not with IL-6. Results of multivariable regression analysis showed that independent predictors of serum hepcidin-25 included EPO and ferritin but not IL-6. CONCLUSIONS: Serum hepcidin-25 concentrations were regulated by iron storage and erythropoiesis but not by IL-6 in CHFpatients with anemia. These findings might indicate that AI is a minor cause of anemia in CHF.
Authors: G Fenna van Breda; Lennart G Bongartz; Wenqing Zhuang; Rachel P L van Swelm; Jeanne Pertijs; Branko Braam; Maarten-Jan Cramer; Dorine W Swinkels; Pieter A Doevendans; Marianne C Verhaar; Roos Masereeuw; Jaap A Joles; Carlo A J M Gaillard Journal: Am J Nephrol Date: 2016-10-22 Impact factor: 3.754
Authors: Vijay Divakaran; Sachin Mehta; David Yao; Saamir Hassan; Steven Simpson; Erwin Wiegerinck; Dorine W Swinkels; Douglas L Mann; Vahid Afshar-Kharghan Journal: Am J Hematol Date: 2011-01 Impact factor: 10.047
Authors: Ewa A Jankowska; Jolanta Malyszko; Hossein Ardehali; Ewa Koc-Zorawska; Waldemar Banasiak; Stephan von Haehling; Iain C Macdougall; Guenter Weiss; John J V McMurray; Stefan D Anker; Mihai Gheorghiade; Piotr Ponikowski Journal: Eur Heart J Date: 2012-11-23 Impact factor: 29.983