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
  Purpose

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
Anemia

Study Type: Observational
Study Design: Observational Model: Case-Only
Time Perspective: Prospective
Official Title: Hepcidin and Anemia in Trauma

Resource links provided by NLM:


Further study details as provided by University of Michigan:

Biospecimen Retention:   Samples Without DNA

Serum


Enrollment: 74
Study Start Date: June 2012
Study Completion Date: April 2014
Primary Completion Date: April 2014 (Final data collection date for primary outcome measure)
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.

  Eligibility

Ages Eligible for Study:   18 Years and older
Genders Eligible for Study:   Both
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

Criteria

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
  Contacts and Locations
Choosing to participate in a study is an important personal decision. Talk with your doctor and family members or friends about deciding to join a study. To learn more about this study, you or your doctor may contact the study research staff using the Contacts provided below. For general information, see Learn About Clinical Studies.

Please refer to this study by its ClinicalTrials.gov identifier: NCT01580267

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

No publications provided

Responsible Party: Lena Napolitano, MD, Principal Investigator, University of Michigan
ClinicalTrials.gov Identifier: NCT01580267     History of Changes
Other Study ID Numbers: HUM00053750
Study First Received: April 17, 2012
Last Updated: April 24, 2014
Health Authority: United States: Institutional Review Board

Keywords provided by University of Michigan:
Anemia in trauma

Additional relevant MeSH terms:
Anemia
Hematologic Diseases
Hepcidin
Anti-Bacterial Agents
Anti-Infective Agents
Therapeutic Uses
Pharmacologic Actions

ClinicalTrials.gov processed this record on July 23, 2014