Skip to main content


Dr. Thomas Cochran Receives Discovery and Innovation Award from Western New York BloodCare


Dr. Thomas Cochran Receives Discovery and Innovation Award from Western New York BloodCare

Headshot of Thomas Cochran, MD
Thomas Cochran, MD
Clinical Assistant Professor of Pediatrics, University of Missouri-Kansas City School of Medicine
Full Biography

Thomas Cochran, MD, GME Fellowship Education, Hematology/Oncology/BMT, received a three-year, $185,704 Discovery and Innovation Award from Western New York BloodCare for his project, “Exploring Inflammatory States Related to Factor Deficiency and the Influence on Hepcidin and Iron Homeostasis in Children with Hemophilia.”

Iron deficiency is one of the most common nutritional deficiencies in children within the United States, and it has been associated with negative consequences on neurocognitive development and cardiovascular and immunological health. The prevalence of iron deficiency is higher in children with inherited bleeding disorders, such as hemophilia. Hemophilia is caused by deficiencies in clotting factors which are the proteins in blood responsible for normal blood clotting. Hemophilia A is caused by deficiencies in clotting factor 8, and hemophilia B is caused by deficiencies in clotting factor 9. 

There is growing evidence that children with hemophilia are in a low-grade inflammatory state due to the underlying factor deficit. Persistent inflammation can exacerbate the likelihood of iron deficiency by elevating hepcidin levels, a hormone that diminishes the intestinal absorption of iron. Hepcidin plays a pivotal role in maintaining iron homeostasis in the body. If hepcidin levels are unknowingly elevated in the iron deficient hemophilia population, patients with the disorder may be inappropriately started on enteric formulations of iron treatment that would not be adequately absorbed. This can prolong both treatment and the negative effects of iron deficiency on health and quality of life. 

“Further understanding of the role of hepcidin in the hemophilia population would directly improve outcomes and prevent the complications of iron deficiency in children with hemophilia,” said Dr. Cochran. “It could improve their quality of life.”

The goal of the study is to determine if there is an association of inflammatory markers, hepcidin, and factor activity with iron stores in children with hemophilia A and B. The study has two specific aims:

  1. Determine the association of factor 8 or 9 activity with C-reactive protein and leptin levels as a measure of chronic inflammation in children with hemophilia A or B. C-reactive protein is a biomarker used to assess inflammation. Leptin is a hormone that plays a role in regulating appetite, energy expenditure, and metabolism; it is also used as a biomarker for assessing chronic inflammation.
  2. Determine the association of hepcidin levels with transferrin saturation and ferritin levels in children with hemophilia A or B. Transferrin saturation and ferritin levels are used to evaluate iron status and diagnose iron deficiency.

The results from this study will be used as a foundation to develop a multi-site study collaboration with other hemophilia treatment centers. 

Shannon Carpenter, MD, MSCI, FAAP, Hematology/Oncology/BMT, is Dr. Cochran’s mentor and co-investigator for the study.