Hepcidin and Anemia in Trauma
Lena Napolitano, MD

Anemia (low hemoglobin and red blood cell count) is common in trauma patients and is associated with a high rate of blood transfusion. Anemia is a problem in trauma patients, particularly in the recovery phase, since it can inhibit trauma patients from participating in physical therapy.

This study is designed to determine how long anemia persists in trauma patients and why anemia does not resolve. Hepcidin, a peptide made in the liver, has recently been identified as the key regulator of iron homeostasis, and plays a major role in how and why anemia develops. Hepcidin reduces iron availability by: (1) decreased iron absorption across the intestine and (2) decreased release of iron– iron is locked in the cells and not available to make red blood cells. High levels of hepcidin induce a state of functional iron deficiency. Hepcidin is increased in states of inflammation, and likely plays an important role in the acute inflammation that occurs with trauma. However, no studies have measured hepcidin in trauma patients.

If hepcidin levels are elevated in trauma, this will confirm that inability to use iron stores is key to the anemia of trauma. The researchers suspect that hepcidin will be increased early after trauma and that anemia will not resolve in trauma until late. By measuring changes in red blood cells, hepcidin and other markers of inflammation in trauma patients, the researchers can critically examine potential therapeutic strategies for the treatment and of anemia in trauma and critical care.