Hepcidin is an iron-regulating peptide hormone made in the liver. It controls the delivery of iron to blood plasma from intestinal cells absorbing iron, from erythrocyte-recycling macrophages, and from iron-storing hepatocytes.
In patients with Transfusion-Dependent Thalassemia (TDT), hepcidin and soluble Transferrin Receptor 1 (sTfR1) play important roles in iron metabolism and are associated with the management of iron overload, a common complication in thalassemia patients.Hepcidin:Function: Hepcidin is a key regulator of iron homeostasis. It controls the absorption of dietary iron in the intestines and the release of iron from macrophages and hepatocytes.Role in TDT: In TDT patients, chronic blood transfusions can lead to iron accumulation, primarily in the liver and other organs. Hepcidin levels are often suppressed in thalassemia, contributing to increased iron absorption and deposition. Monitoring hepcidin levels is crucial for assessing iron status and guiding iron chelation therapy.sTfR1 (soluble Transferrin Receptor 1):Function: Transferrin receptors are proteins involved in cellular iron uptake. sTfR1 is a soluble form of the transferrin receptor found in the blood.Role in TDT: Increased levels of sTfR1 in the serum are associated with enhanced erythropoiesis (formation of red blood cells) in response to chronic anemia, as seen in thalassemia. sTfR1 can be a marker of erythropoietic activity and iron deficiency. Monitoring sTfR1 levels helps in assessing the degree of anemia and the need for transfusions.