scholarly journals Expression of Hepcidin and Growth Differentiation Factor 15 (GDF-15) Levels in Thalassemia Patients with Iron Overload and Positive Anti Hepatitis C Virus

2017 ◽  
Vol 17 (2) ◽  
pp. 106 ◽  
Author(s):  
Nuri Dyah Indrasari ◽  
Ina Susianti Timan ◽  
Pustika Amalia
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Iron Overload ◽  
Growth Differentiation Factor 15 ◽  
Differentiation Factor

Growth differentiation factor-15 in young sickle cell disease patients: Relation to hemolysis, iron overload and vascular complications

2014 ◽  
Vol 53 (4) ◽  
pp. 189-193 ◽  
Author(s):  
Azza Abdel Gawad Tantawy ◽  
Amira Abdel Moneam Adly ◽  
Eman Abdel Rahman Ismail ◽  
Yasser Wagih Darwish ◽  
Marwa Ali Zedan
Keyword(s):  
Sickle Cell Disease ◽  
Iron Overload ◽  
Sickle Cell ◽  
Vascular Complications ◽  
Cell Disease ◽  
Growth Differentiation Factor 15 ◽  
Differentiation Factor

Mechanisms of Liver Injury. III. Oxidative stress in the pathogenesis of hepatitis C virus

2006 ◽  
Vol 290 (5) ◽  
pp. G847-G851 ◽  
Author(s):  
Jinah Choi ◽  
J.-H. James Ou
Keyword(s):  
Oxidative Stress ◽  
Hepatocellular Carcinoma ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Liver Injury ◽  
Iron Overload ◽  
Antioxidant Defense ◽  
Hcv Infection ◽  
Nitrogen Species ◽  
Systemic Oxidative Stress

Hepatitis C virus (HCV) is a major cause of viral hepatitis that can progress to hepatic fibrosis, steatosis, hepatocellular carcinoma, and liver failure. HCV infection is characterized by a systemic oxidative stress that is most likely caused by a combination of chronic inflammation, iron overload, liver damage, and proteins encoded by HCV. The increased generation of reactive oxygen and nitrogen species, together with the decreased antioxidant defense, promotes the development and progression of hepatic and extrahepatic complications of HCV infection. This review discusses the possible mechanisms of HCV-induced oxidative stress and its role in HCV pathogenesis.

scholarly journals Iron Overload and Hepatitis C Virus Infection

2018 ◽  
Vol 131 (2) ◽  
pp. 251
Author(s):  
Antonio Ponzetto ◽  
Natale Figura
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Virus Infection ◽  
Iron Overload ◽  
Hepatitis C Virus Infection

scholarly journals Megaloblastic anemia-related iron overload and erythroid regulators: a case report

2021 ◽  
Vol 15 (1) ◽  
Author(s):  
Nicolas Vallet ◽  
Jean-Baptiste Delaye ◽  
Martine Ropert ◽  
Amélie Foucault ◽  
Noémie Ravalet ◽  
...  
Keyword(s):  
Iron Overload ◽  
Vitamin B12 ◽  
Megaloblastic Anemia ◽  
Transferrin Saturation ◽  
Cardiac Insufficiency ◽  
Ineffective Erythropoiesis ◽  
Growth Differentiation Factor 15 ◽  
Differentiation Factor ◽  
Biological Tests ◽  
Previously Treated

Abstract Background In ineffective erythropoiesis, hepcidin synthesis is suppressed by erythroid regulators, namely erythroferrone and growth differentiation factor-15. For the first time, the hypothesis that iron overload in megaloblastic anemia may be related to ineffective erythropoiesis is explored by describing the kinetics of hepcidin, erythroferrone, and growth differentiation factor-15 levels in a patient diagnosed with megaloblastic anemia associated with iron overload. Case presentation An 81-year-old Caucasian male was admitted for fatigue. He had type-2 diabetes previously treated with metformin, ischemic cardiac insufficiency, and stage-3 chronic kidney disease. Vitiligo was observed on both hands. Biological tests revealed normocytic non-regenerative anemia associated with hemolysis, thrombocytopenia, and elevated sideremia, ferritin, and transferrin saturation levels. Megaloblastic anemia was confirmed with undetectable blood vitamin B12 and typical cytological findings like hyper-segmented neutrophils in blood and megaloblasts in bone marrow. The patient received vitamin B12 supplementation. At 3 months, biological parameters reached normal values. Hepcidin kinetics from diagnosis to 3 months inversely correlated with those of erythroferrone and growth differentiation factor-15. Conclusions This case suggests that iron-overload mechanisms of dyserythropoietic anemias may apply to megaloblastic anemias.

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