Hepcidin and Anemia in Trauma

This study has been completed.
Sponsor:
Information provided by (Responsible Party):
Lena Napolitano, MD, University of Michigan
ClinicalTrials.gov Identifier:
NCT01580267
First received: April 17, 2012
Last updated: April 24, 2014
Last verified: April 2014

April 17, 2012
April 24, 2014
June 2012
April 2014   (final data collection date for primary outcome measure)
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Complete list of historical versions of study NCT01580267 on ClinicalTrials.gov Archive Site
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Hepcidin and Anemia in Trauma
Hepcidin and Anemia in Trauma

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.

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.

Observational
Observational Model: Case-Only
Time Perspective: Prospective
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Retention:   Samples Without DNA
Description:

Serum

Probability Sample

Trauma patients, 18 years of age or older, admitted to a University of Michigan ICU

Anemia
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*   Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
 
Completed
74
April 2014
April 2014   (final data collection date for primary outcome measure)

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
Both
18 Years and older
No
Contact information is only displayed when the study is recruiting subjects
United States
 
NCT01580267
HUM00053750
No
Lena Napolitano, MD, University of Michigan
University of Michigan
Not Provided
Principal Investigator: Lena M Napolitano, MD University of Michigan
University of Michigan
April 2014

ICMJE     Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP