GDF 15 in Sickle Cell Disease and Hereditary Spherocytosis (GDF 15)
|ClinicalTrials.gov Identifier: NCT01201135|
Recruitment Status : Unknown
Verified September 2010 by Wolfson Medical Center.
Recruitment status was: Not yet recruiting
First Posted : September 14, 2010
Last Update Posted : September 14, 2010
|Condition or disease|
|Patients With Thalassemia Intermedia, Congenital Dyserythropoietic Anemia Type I|
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 Type :||Observational|
|Estimated Enrollment :||80 participants|
|Official Title:||The Impact of Growth Differentiating Factor (GDF) 15 in Sickle Cell Disease and Hereditary Spherocytosis|
|Study Start Date :||September 2010|
|Estimated Primary Completion Date :||September 2011|
|Estimated Study Completion Date :||September 2011|
|Sickle cell disease|
- GDF 15 [ Time Frame: year ]
- Hepcidine [ Time Frame: year ]
Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT01201135
|Contact: Ghoti Hossam, firstname.lastname@example.org|
|Principal Investigator:||GHOTI HOSSAM, doctor||HEMATOLOGY DEPARTMENT ON WOLFSSON MEDICAL CENTER|