Viewing Study NCT01201135


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Study NCT ID: NCT01201135
Status: UNKNOWN
Last Update Posted: 2010-09-14
First Post: 2010-09-12
Is NOT Gene Therapy: True
Has Adverse Events: False

Brief Title: GDF 15 in Sickle Cell Disease and Hereditary Spherocytosis
Sponsor: Wolfson Medical Center
Organization:

Study Overview

Official Title: The Impact of Growth Differentiating Factor (GDF) 15 in Sickle Cell Disease and Hereditary Spherocytosis
Status: UNKNOWN
Status Verified Date: 2010-09
Last Known Status: NOT_YET_RECRUITING
Delayed Posting: No
If Stopped, Why?: Not Stopped
Has Expanded Access: False
If Expanded Access, NCT#: N/A
Has Expanded Access, NCT# Status: N/A
Acronym: GDF 15
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 Oversight

Has Oversight DMC: False
Is a FDA Regulated Drug?: None
Is a FDA Regulated Device?: None
Is an Unapproved Device?: None
Is a PPSD?: None
Is a US Export?: None
Is an FDA AA801 Violation?: