Hepcidin Modulators: A Potential Alternative Treatment of Iron Deficiency and Iron Deficiency Anemia in Heart Failure

AbstractHeart failure affects roughly 6.7 million Americans and is associated with many comorbidities and complications, including iron deficiency and anemia. Iron homeostasis is integral to optimal body function. Hepcidin, a hepatically produced peptide, is a major modulator in iron homeostasis. Its synthesis is induced in part by inflammatory states. Iron deficiency in heart failure is currently diagnosed with the assessment of serum ferritin and percent of transferrin saturation. Iron deficiency in the setting of hepcidin excess in inflammatory conditions, such as heart failure, is discussed in this literature review. Iron deficiency is associated with worse prognosis and poorer outcomes in heart failure patients. Targeted treatment of iron deficiency and iron deficiency anemia may provide improved quality of life and decrease mortality and morbidity among heart failure patients. Current treatment options for iron deficiency and anemia include intravenous and oral iron supplementation, as well as other erythropoiesis-stimulating agents. However, concerns regarding safety have been raised in regards to these options. An emerging possibility for the treatment of iron deficiency in the setting of hepcidin overload is hepcidin modulators, including hepcidin antagonists or inhibitors. This review has addressed iron deficiency and anemia in heart failure and suggests that hepcidin antagonists/inhibitors may provide a viable alternative to the classic treatment methods.