Influence of Liver Congestion and Hypoxemia in Heart Failure on Hematological and Iron Status via Hepcidin

Abstract

BackgroundAnemia and relative iron deficiency (RID) frequently occurs in patients with heart failure (HF). Hepcidin is known to be a main regulator of iron metabolism and recently, we reported that liver congestion (LC) contributed to anemia and RID via inappropriate expression of hepcidin.ObjectiveThis study aims to assess whether LC in HF influences hematological and iron status via expression of hepcidin.MethodRats received subcutaneous injection of monocrotaline (MCT) and we examined anemia, markers of iron state, percutaneous oxygen saturation (SpO2), hepcidin and pathological finding in the liver. Moreover, we examined inferior vena cava diameter as an indicator of LC and serum hepcidin levels in forty nine patients admitted with HF and anemia.ResultsLC was observed 4 weeks after injection of MCT and SpO2 markedly decrease 5 weeks. On week 4 and 5, decrease of Hb, serum iron and transferring saturations with inappropriate expression of hepcidin was observed but on week 6, increase of them with decreased expression of hepcidin were observed. LC was frequently found in HF patients with anemia and serum hepcidin levels in patients with severe anemia and LC were significantly higher than those in without LC and inflammation.ConclusionLC in HF influences hematological and iron status via inappropriate hepcidin expression but severe hypoxemia in HF may inversely influence them. BackgroundAnemia and relative iron deficiency (RID) frequently occurs in patients with heart failure (HF). Hepcidin is known to be a main regulator of iron metabolism and recently, we reported that liver congestion (LC) contributed to anemia and RID via inappropriate expression of hepcidin. Anemia and relative iron deficiency (RID) frequently occurs in patients with heart failure (HF). Hepcidin is known to be a main regulator of iron metabolism and recently, we reported that liver congestion (LC) contributed to anemia and RID via inappropriate expression of hepcidin. ObjectiveThis study aims to assess whether LC in HF influences hematological and iron status via expression of hepcidin. This study aims to assess whether LC in HF influences hematological and iron status via expression of hepcidin. MethodRats received subcutaneous injection of monocrotaline (MCT) and we examined anemia, markers of iron state, percutaneous oxygen saturation (SpO2), hepcidin and pathological finding in the liver. Moreover, we examined inferior vena cava diameter as an indicator of LC and serum hepcidin levels in forty nine patients admitted with HF and anemia. Rats received subcutaneous injection of monocrotaline (MCT) and we examined anemia, markers of iron state, percutaneous oxygen saturation (SpO2), hepcidin and pathological finding in the liver. Moreover, we examined inferior vena cava diameter as an indicator of LC and serum hepcidin levels in forty nine patients admitted with HF and anemia. ResultsLC was observed 4 weeks after injection of MCT and SpO2 markedly decrease 5 weeks. On week 4 and 5, decrease of Hb, serum iron and transferring saturations with inappropriate expression of hepcidin was observed but on week 6, increase of them with decreased expression of hepcidin were observed. LC was frequently found in HF patients with anemia and serum hepcidin levels in patients with severe anemia and LC were significantly higher than those in without LC and inflammation. LC was observed 4 weeks after injection of MCT and SpO2 markedly decrease 5 weeks. On week 4 and 5, decrease of Hb, serum iron and transferring saturations with inappropriate expression of hepcidin was observed but on week 6, increase of them with decreased expression of hepcidin were observed. LC was frequently found in HF patients with anemia and serum hepcidin levels in patients with severe anemia and LC were significantly higher than those in without LC and inflammation. ConclusionLC in HF influences hematological and iron status via inappropriate hepcidin expression but severe hypoxemia in HF may inversely influence them. LC in HF influences hematological and iron status via inappropriate hepcidin expression but severe hypoxemia in HF may inversely influence them.