Hepcidin and Anemia in Trauma

The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Read our disclaimer for details. Identifier: NCT01580267
Recruitment Status : Completed
First Posted : April 18, 2012
Last Update Posted : April 28, 2014
Information provided by (Responsible Party):
Lena Napolitano, MD, University of Michigan

Brief Summary:

Anemia (decreased number of red blood cells) is common in critically ill trauma patients admitted to an Intensive Care Unit and is associated with a high rate of blood transfusions. This "anemia of inflammation" is a result of three mechanisms: impaired iron regulation, shortened red blood cell life span, and reduced rate of erythropoiesis (a protein that helps make new red blood cells).

Hepcidin, a protein made in the liver, regulates iron and is decreased when iron in the blood is low. This can lead to anemia.

This research study is being conducted to learn how inflammation, hepcidin, and erythropoietin interact in critically ill patients. The findings will help in determining effective treatment for patients with anemia of inflammation.

Condition or disease

Detailed Description:

Anemia is common in trauma patients and is associated with a high rate of blood transfusion. The pathophysiology of this anemia is "anemia of inflammation" and develops via 3 mechanisms: impaired iron regulation, shortened red blood cell life span, and reduced rate of erythropoiesis. Once iron enters cells (enterocytes and macrophages), the iron export protein ferroportin controls egress. Hepcidin, a peptide made in the liver, is the key regulator of iron homeostasis. Hepcidin binds to ferroportin, leading to its ultimate degradation. Hepcidin reduces iron availability via 2 mechanisms: decreased absorption of iron across the GI tract and decreased release of iron from the reticuloendothelial system. It therefore induces a functional iron deficiency by shuttling iron into the macrophages and making it unavailable for erythropoiesis. Hepcidin is decreased by iron deficiency, most anemias, and tissue hypoxia. Hepcidin is upregulated by iron excess and inflammation. Hepcidin 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 will 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 with resultant suppression of native erythropoiesis.

The investigators hypothesize that hepcidin will be increased and erythropoietin decreased early after trauma and that resolution of anemia will not occur until late (28-31 days). By measuring time-dependent changes in hemoglobin, hepcidin, cytokine, and erythropoietin concentrations in trauma patients, the investigators can critically examine the inter-relationships to target potential therapeutic strategies for the treatment and amelioration of anemia in trauma and critical care.

Study Type : Observational
Actual Enrollment : 74 participants
Observational Model: Case-Only
Time Perspective: Prospective
Official Title: Hepcidin and Anemia in Trauma
Study Start Date : June 2012
Actual Primary Completion Date : April 2014
Actual Study Completion Date : April 2014

Resource links provided by the National Library of Medicine

Biospecimen Retention:   Samples Without DNA

Information from the National Library of Medicine

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Ages Eligible for Study:   18 Years and older   (Adult, Older Adult)
Sexes Eligible for Study:   All
Accepts Healthy Volunteers:   No
Sampling Method:   Probability Sample
Study Population
Trauma patients, 18 years of age or older, admitted to a University of Michigan ICU

Inclusion Criteria:

  1. Trauma patient
  2. Age 18 years or older
  3. Admitted to ICU
  4. Anemic (Hct < 34.5%)

Exclusion Criteria:

  1. Pre-existing hematological disorder
  2. Pre-existing diagnosis of anemia or other known iron disorder
  3. Chronic renal failure
  4. Use of recombinant erythropoietin
  5. Treatment with systemic immunosuppressant or cytotoxic drugs
  6. Pregnancy
  7. Patients not expected to survive

Information from the National Library of Medicine

To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.

Please refer to this study by its identifier (NCT number): NCT01580267

United States, Michigan
University of Michigan Health System
Ann Arbor, Michigan, United States, 48109
Sponsors and Collaborators
University of Michigan
Principal Investigator: Lena M Napolitano, MD University of Michigan

Responsible Party: Lena Napolitano, MD, Principal Investigator, University of Michigan Identifier: NCT01580267     History of Changes
Other Study ID Numbers: HUM00053750
First Posted: April 18, 2012    Key Record Dates
Last Update Posted: April 28, 2014
Last Verified: April 2014

Keywords provided by Lena Napolitano, MD, University of Michigan:
Anemia in trauma

Additional relevant MeSH terms:
Hematologic Diseases
Anti-Infective Agents