GDF 15 in Sickle Cell Disease and Hereditary Spherocytosis

• Conditions: Patients With Thalassemia Intermedia,; Congenital Dyserythropoietic Anemia Type I

• Registration Number: NCT01201135
• Lead Sponsor: Wolfson Medical Center

Brief Summary

Patients with thalassemia intermedia, congenital dyserythropoietic anemia type I , and sideroblastic anemia were found to express very high levels of serum GDF15, and this contributed to the inappropriate suppression of hepcidin with subsequent secondary iron overload.The aim of our present study is to asses the levels of GDF15 and hepcidin in patients with Sickle cell disease and hereditary spherocytosis

Detailed Description

The identification of the ferroportin/hepcidin axis has allowed the effect of erythroid activity on iron balance to be studied and has created the basis for better defining the erythroid regulators.

In iron-loading anemias, ineffective erythropoiesis suppresses hepcidin production, which result in dysregulating iron homeostasis. Miller and co-workers showed that release of cytokines like growth differentiation factor 15 (GDF15) during the process of ineffective erythropoiesis inhibits hepcidin production, thus defining a molecular link between ineffective erythropoiesis, suppression of hepcidin production and parenchymal iron loading.

Study Timeline

• Status Verified: 2010-09
• Study Start: 2010-09
• Study First Submitted: 2010-09-12
• Study First Submitted QC: 2010-09-12
• Last Update Submitted: 2010-09-12
• Study First Posted: 2010-09-14
• Last Update Posted: 2010-09-14
• Primary Completion: 2011-09
• Study Completion: 2011-09

Recruitment & Eligibility

• Status: UNKNOWN
• Sex: All
• Target Recruitment: 80

Inclusion Criteria

• non

Exclusion Criteria

• non

Study & Design

• Study Type: OBSERVATIONAL
• Study Design: Not specified

Primary Outcome Measures

Name	Time	Method
GDF 15	year

Secondary Outcome Measures

Name	Time	Method
Hepcidine	year