Indication

Chronic iron overload in patient with non-transfusion-dependent thalassemia (NTDT)

Chronic iron overload in patients with non-transfusion-dependent thalassemia (NTDT) is a progressive state of systemic iron accumulation occurring in individuals with inherited hemoglobin disorders—such as ß-thalassemia intermedia, hemoglobin E/ß-thalassemia, and hemoglobin H disease—who do not require lifelong, regular blood transfusions for survival. Read more about Chronic iron overload in patient with non-transfusion-dependent thalassemia (NTDT)

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Common Chronic iron overload in patient with non-transfusion-dependent thalassemia (NTDT) therapies.

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DEFERASIROX

IRON CHELATING AGENTS·CHRONIC IRON OVERLOAD DUE TO REPEATED BLOOD TRANSFUSIONS·+1
NOVADOZ PHARMAC

DEFERASIROX

IRON CHELATING AGENTS·CHRONIC IRON OVERLOAD DUE TO REPEATED BLOOD TRANSFUSIONS·+1
OAKRUM PHARMA,

DEFERASIROX

IRON CHELATING AGENTS·CHRONIC IRON OVERLOAD DUE TO REPEATED BLOOD TRANSFUSIONS·+1
XIROMED, LLC

DEFERASIROX

IRON CHELATING AGENTS·CHRONIC IRON OVERLOAD DUE TO REPEATED BLOOD TRANSFUSIONS·+1
AVKARE

EXJADE (deferasirox)

IRON CHELATING AGENTS·CHRONIC IRON OVERLOAD DUE TO REPEATED BLOOD TRANSFUSIONS·+1
Novartis Pharmaceuticals

JADENU (deferasirox)

IRON CHELATING AGENTS·CHRONIC IRON OVERLOAD DUE TO REPEATED BLOOD TRANSFUSIONS·+1
Novartis Pharmaceuticals
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About Chronic iron overload in patient with non-transfusion-dependent thalassemia (NTDT).

Chronic iron overload in patients with non-transfusion-dependent thalassemia (NTDT) is a progressive state of systemic iron accumulation occurring in individuals with inherited hemoglobin disorders—such as ß-thalassemia intermedia, hemoglobin E/ß-thalassemia, and hemoglobin H disease—who do not require lifelong, regular blood transfusions for survival.

Rather than being transfusional, this iron loading is primarily driven by chronic ineffective erythropoiesis, which downregulates hepatic hepcidin production (largely via erythroferrone signaling) and induces unrestricted intestinal iron absorption and macrophage iron release.

The resulting excess iron preferentially accumulates in hepatocytes, leading to elevated liver iron concentration, secondary serum ferritin elevation, and potential long-term complications including hepatic fibrosis, cirrhosis, endocrinopathies, and vascular disease.

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