GDF 15 in Sickle Cell Disease and Hereditary Spherocytosis (GDF 15)
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|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 ]
To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.
Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT01201135
|Contact: Ghoti Hossam, email@example.com|
|Principal Investigator:||GHOTI HOSSAM, doctor||HEMATOLOGY DEPARTMENT ON WOLFSSON MEDICAL CENTER|