Liver congestion in heart failure contributes to inappropriately increased serum hepcidin despite anemia

The Tohoku Journal of Experimental Medicine
Yukako OhnoTohru Minamino

Abstract

Hepcidin is a key regulator of mammalian iron metabolism and mainly produced by the liver. Hepcidin excess causes iron deficiency and anemia by inhibiting iron absorption from the intestine and iron release from macrophage stores. Anemia is frequently complicated with heart failure. In heart failure patients, the most frequent histologic appearance of liver is congestion. However, it remains unclear whether liver congestion associated with heart failure influences hepcidin production, thereby contributing to anemia and functional iron deficiency. In this study, we investigated this relationship in clinical and basic studies. In clinical studies of consecutive heart failure patients (n = 320), anemia was a common comorbidity (41%). In heart failure patients without active infection and ongoing cancer (n = 30), log-serum hepcidin concentration of patients with liver congestion was higher than those without liver congestion (p = 0.0316). Moreover, in heart failure patients with liver congestion (n = 19), the anemia was associated with the higher serum hepcidin concentrations, which is a type of anemia characterized by induction of hepcidin. Subsequently, we produced a rat model of heart failure with liver congestion by injecting m...Continue Reading

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Dec 17, 2015·Heart, Lung & Circulation·Christopher C Y WongAndrew P Sindone
Feb 24, 2021·European Journal of Preventive Cardiology·Jeness CampodonicoPiergiuseppe Agostoni
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May 5, 2021·Molecular and Cellular Biochemistry·Rengin Elsurer AfsarBaris Afsar

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