View clinical trials related to Iron Overload.
Filter by:The scientific rationale for this study is the evolving understanding that iron-induced tissue damage is not only a process of progressive bulking of organs through high-volumes iron deposition, but also a reactive iron species related "toxic" damage. Iron mediated damage can occur prior reaching high iron storage thresholds derived from thalassemia major setting, free toxic iron species being already present when transferrin saturation >60-70% (25); therefore a timely early adoption of iron chelation may be of benefit before overt iron overload is seen. Our hypothesis is that early and low dose DFX-FCT is better tolerated and is able to prevent iron accumulation and consequently tissue iron related damage, by consistently suppressing iron reactive oxygen species (NTBI and LPI). If this hypothesis is confirmed this approach could contribute to an improvement of clinical practice of patients managements. Additionally this approach might also be a contribute in preventing future iron overloaded related complication, in this already frail and co-treated patient population.
A serum ferritin level can reflect the total body iron content, thus a very low serum ferritin is commonly used as an indicator of iron deficiency and a very high serum ferritin is commonly used as a marker of iron overload. Ferritin is a shell of protein in which iron is stored. Ferritin is an acute phase reactant, and serum ferritin levels can increase during inflammatory conditions. Consequently, an elevated ferritin level might mean there is an excess of storage iron, or might simply mean that inflammation has resulted in high levels of the ferritin shell, containing little iron. The research team is able to quantify the amount of iron in ferritin using inductively conducted plasma mass spectrometry, in the Heme and Iron Core Laboratory at the University of Utah. Thus, it can be determined whether in a child with a very high serum ferritin level, that ferritin is loaded with iron or is actually very low in iron. Neonates and young children with certain liver disorders characteristically have a very high serum ferritin level. These conditions are gestational alloimmune liver disease (GALD) and hemophagocytic lymphohistiocytosis (HLH). It is not clear what the iron content of the ferritin is in these neonates. Knowing this will be a step toward understanding whether the pathogenesis of these conditions involves iron overload. Additionally, if urine ferritin and iron levels correlate with serum ferritin and iron levels, urine may be used as a non-invasive way to monitor iron status. In this study, serum and urine samples will be collected from children with high serum ferritin levels and confirmed iron toxicity. Both ferritin and iron content within ferritin will be measured in the serum and urine samples and compared for correlation.
This study is a Phase 2 multicenter, randomized, open-label, parallel-group study. The primary objective of the study is to evaluate the effect of LJPC-401 (synthetic human hepcidin) on iron levels in patients with transfusion-dependent beta thalassemia with myocardial iron overload.
This is a long-term follow-up to an earlier study, LA38-0411. Its purpose is to gather more information about the safety and efficacy of deferiprone in patients with sickle cell disease or other anemias who suffer from iron overload caused by regular blood transfusions.
The purpose of this study is to assess safety and amount of the study drug in the blood after increasing doses of SP-420. The study will be conducted in patients with β-thalassemia.
This research is being done so that we can look at the safety and efficacy of deferiprone in people with sickle cell disease or other anemias. Deferiprone is a drug that removes iron from the body. We will be comparing deferiprone with deferoxamine, another drug that removes iron from the body.
Evaluated Exjade efficacy and safety in patients with aplastic anemia and transfusion-dependent iron overload, undergoing treatment programs of immunosuppressive treatment (Cyclosporine A) , in comparison with a group of patients undergoing treatment programs of immunosuppressive treatment (Cyclosporine A) without chelation therapy.
The purpose of this extension study is to evaluate SSP-004184AQ in patients with transfusional iron overload and to provide data on long term safety and efficacy. SSP-004184AQ is an iron chelator under development for chronic daily oral administration to patients with transfusional iron overload
The purpose of this study is to evaluate SSP-004184AQ in patients with transfusional iron overload whose primary diagnosis is hereditary or congenital anemia. SSP-004184AQ is an iron chelator under development for chronic daily oral administration to patients with transfusional iron overload.
Chronic iron overload is responsible for morbidity and mortality. There are many genetic and acquired causes. One of them is an hepcidin deficiency. Hepcidin is the regulating hormone for iron. The study explores this specific cause, and aim to characterize this iron overload in term of clinical, biological, genetic and functional specificities.