Anemia Clinical Trial
Official title:
Hepcidin in the Pathogenesis of Anemia in Patients With Chronic Heart Failure
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.
n/a
Observational Model: Cohort, Time Perspective: Prospective
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