Hepcidin and Anemia in Trauma
Principal Investigator: Lena M. Napolitano, MD
Institution: University of Michigan Health System, Ann Arbor MI
Anemia is common in trauma patients and is associated with a high rate of blood transfusion. This “anemia of inflammation” develops via three mechanisms: 1) impaired iron regulation, 2) shortened red blood cell life span, and 3) reduced rate of erythropoiesis. Hepcidin is decreased by iron deficiency, most anemias, and tissue hypoxia. It likely plays an important role in the acute inflammatory response that occurs with trauma. However, no studies have measured hepcidin in critically ill trauma patients. If serum hepcidin levels are elevated in trauma, this would confirm that inability to use existing iron stores is part of, if not key to, the anemia of trauma and critical illness. This has important implications, since the use of blood transfusion for anemia treatment may further induce an inflammatory response.
The hypothesis for this study was that hepcidin would be increased and erythropoietin decreased early after trauma and that resolution of anemia would not occur until late (28-31 days). This study addressed two specific aims: 1) to define the temporal relationship between serum and urine hepcidin concentrations, anemia, and iron and erythropoiesis studies in critically ill trauma patients, and 2) to assess the correlation between hepcidin levels, anemia, and degree of inflammation. The study provided the first available data regarding the time-dependent changes of the peptide hormone hepcidin in anemia associated with trauma and critical illness. The temporal relationship between serum hepcidin concentrations, anemia, and iron and erythropoiesis studies was defined and the correlation between hepcidin levels, anemia, and degree of inflammation as determined.