GDF 15 in Sickle Cell Disease and Hereditary Spherocytosis (GDF 15)
Recruitment status was: Not yet recruiting
Patients With Thalassemia Intermedia,
Congenital Dyserythropoietic Anemia Type I
|Study Design:||Time Perspective: Prospective|
|Official Title:||The Impact of Growth Differentiating Factor (GDF) 15 in Sickle Cell Disease and Hereditary Spherocytosis|
- GDF 15 [ Time Frame: year ]
- Hepcidine [ Time Frame: year ]
|Study Start Date:||September 2010|
|Estimated Study Completion Date:||September 2011|
|Estimated Primary Completion Date:||September 2011 (Final data collection date for primary outcome measure)|
|Sickle cell disease|
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.
Please refer to this study by its ClinicalTrials.gov identifier: NCT01201135
|Principal Investigator:||GHOTI HOSSAM, doctor||HEMATOLOGY DEPARTMENT ON WOLFSSON MEDICAL CENTER|