Outcome of iron reduction therapy in ex-thalassemics

Aboobacker, Fouzia N.; Dixit, Gaurav; Lakshmi, Kavitha M; Korula, Anu; Abraham, Aby; George, Biju; Srivastava, Alok

doi:10.1371/journal.pone.0238793

Cited by 4 publications

(2 citation statements)

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“…This may be due to the short duration of administration of deferasirox which does not exceed 6 months or may be due to those patients in group B were older than that of group A (mean of age 21.12 and 40.68 months respectively. The results of the present work are in accordance with that of other investigators (26,27) where they reported, evidence of iron overload manifested as elevated serum ferritin levels in all patients with βTM whether were using or not using chelating agents. They proved that the serum ferritin level is in correlation with age.…”

Section: Table5 Effect Of Ferritin Levels On Serum Alt Ast and Alp Insupporting

confidence: 93%

Evaluation of Hepatic Enzymes in major β-thalassemic Patients using Deferasirox

Bashi

Fathi²

2022

IJPS

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β-thalassemia major is a genetic disease that causes sever defect in normal hemoglobin synthesis. The patients with β-thalassemia major need periodic blood transfusions that can result in accumulation of body iron, so treatment with iron chelating agent is required. Complications of this iron overload affecting many vital organs, including the liver. The aim of this work was to evaluate liver enzymes in β -thalassemia major patients with deferasirox versus without it. Two groups of β-thalassemia major patients were involved in this study named group A; 40 β-thalassemia patients of blood transfusion dependent without deferasirox, group B; 40 β-thalassemia patients of blood transfusion dependent on deferasirox. In addition to group C, 40 normal subjects as a control group. Samples of serum were obtained from all participants to be tested for alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase and ferritin. The biochemical data of the patients on blood transfusion without deferasirox showed significant increases in the mean serum levels of aminotransferases and ferritin in comparison with control. Whereas the patients on blood transfusion with deferasirox exhibit significant increases in the means serum levels of alkaline phosphatase activity and ferritin in comparison with control. Iron overload may cause liver injury, shown by significant increases of; ALT and AST activities and elevated ferritin level in serum of transfusion dependent patients of β-thalassemia major. Administration of deferasirox for β-thalassemia major patients causes elevation of serum ALP activity and ferritin level.

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Section: Table5 Effect Of Ferritin Levels On Serum Alt Ast and Alp Insupporting

confidence: 93%

Evaluation of Hepatic Enzymes in major β-thalassemic Patients using Deferasirox

Bashi

Fathi²

2022

IJPS

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“…The same standard diagnostic techniques, including MRI T2* and serum ferritin, are used for monitoring iron overload and the progress of therapeutic intervention, including phlebotomy and chelation therapy in idiopathic hemochromatosis, thalassemia intermedia, post-allogeneic HCT patients, and other categories of patients with non-transfusion-dependent iron overloading conditions ( Table 1 ) [ 122 , 123 , 124 , 125 , 126 , 127 ].…”

Section: Excess Iron Deposition and Toxicity In Non-transfusional Iro...mentioning

confidence: 99%

Iron Load Toxicity in Medicine: From Molecular and Cellular Aspects to Clinical Implications

Kontoghiorghes

2023

IJMS

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Iron is essential for all organisms and cells. Diseases of iron imbalance affect billions of patients, including those with iron overload and other forms of iron toxicity. Excess iron load is an adverse prognostic factor for all diseases and can cause serious organ damage and fatalities following chronic red blood cell transfusions in patients of many conditions, including hemoglobinopathies, myelodyspasia, and hematopoietic stem cell transplantation. Similar toxicity of excess body iron load but at a slower rate of disease progression is found in idiopathic haemochromatosis patients. Excess iron deposition in different regions of the brain with suspected toxicity has been identified by MRI T2* and similar methods in many neurodegenerative diseases, including Alzheimer’s disease and Parkinson’s disease. Based on its role as the major biological catalyst of free radical reactions and the Fenton reaction, iron has also been implicated in all diseases associated with free radical pathology and tissue damage. Furthermore, the recent discovery of ferroptosis, which is a cell death program based on free radical generation by iron and cell membrane lipid oxidation, sparked thousands of investigations and the association of iron with cardiac, kidney, liver, and many other diseases, including cancer and infections. The toxicity implications of iron in a labile, non-protein bound form and its complexes with dietary molecules such as vitamin C and drugs such as doxorubicin and other xenobiotic molecules in relation to carcinogenesis and other forms of toxicity are also discussed. In each case and form of iron toxicity, the mechanistic insights, diagnostic criteria, and molecular interactions are essential for the design of new and effective therapeutic interventions and of future targeted therapeutic strategies. In particular, this approach has been successful for the treatment of most iron loading conditions and especially for the transition of thalassemia from a fatal to a chronic disease due to new therapeutic protocols resulting in the complete elimination of iron overload and of iron toxicity.

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