Hepcidin in Anemic Chronic Heart Failure (CHF) Patients

Medical University of Vienna

Status

Completed

Conditions

Anemia

Chronic Heart Failure

Study type

Observational

Funder types

Other

Identifiers

NCT00437866

Version 1.0, 25.11.2006

Details and patient eligibility

About

Background: Anemia in chronic heart failure (CHF) is directly linked to increased mortality and reduced exercise capacity. The pathomechanism for the development of anemia in CHF is not well understood. Impairment of iron homeostasis is discussed to be one of the major triggers in anemia of chronic disease. Hepcidin was recently described as the central regulator of iron homeostasis.

Main hypothesis: Plasma hepcidin levels are altered in anemic CHF patients compared to non anemic controls and might be a main contributing factor of anemia in CHF.

Iron regulator-hypothesis High levels of cytokines in CHF patients cause up-regulation of hepcidin, which in turn leads to low iron uptake causing anemia. In this case venous hepcidin and hemoglobin concentrations should both correlate with cytokine levels.

Erythropoietin regulator-hypothesis Dysregulation of the erythropoietin system results in anemia, which represses hepcidin. This leads to a negative correlation between hemoglobin and hepcidin in plasma.

Methods: 100 consecutive patients diagnosed with systolic CHF will be prospectively included in the study. Iron status will be assessed and hepcidin, erythropoietin as well as interleukin-1, interleukin-6 and soluble TNF alpha receptor levels will be measured by ELISA.

Patients will be followed up for one year and mortality, rehospitalization and worsening of CHF will be documented.

Enrollment

100 patients

Sex

All

Ages

18+ years old

Volunteers

Accepts Healthy Volunteers

Inclusion criteria