Oxidative Stress (Malondialdehyde) in Adults Beta-Thalassemia Major and Intermedia: Comparison Between Before and After Blood Transfusion and Its Correlation with Iron Overload

Abstract

Background: Iron overload is a major problem in both transfusion-dependent (TDT) and non-transfusion-dependent thalassemia (NTDT). It has been known to increase oxidative stress. Meanwhile, blood transfusion as main therapy for thalassemia increases iron overload. One of the markers of oxidative stress is malondialdehyde (MDA). This study aims to provide data on MDA levels in adult thalassemia patients, and to compare the levels before and after transfusion in patients with TDT and NTDT. Methods: This is a cross-sectional, pre-post study in adult patients with thalassemia major and intermedia that received blood transfusion with or without iron-chelating agents in Cipto Mangunkusumo Hospital. Blood samples were taken immediately before the transfusion and one day after. Serum ferritin (SF) assays were conducted by electrochemiluminescence immunoassay method, while transferrin saturation (TS) was calculated by dividing serum iron by the binding capacity. Subsequently, plasma MDA levels assays were performed using the Wills method, and data analysis was conducted using the t-test/Mann-Whitney and Pearson/Spearman correlation test, depending on the data distribution. Results:The 63 respondents recruited consist of 51 TDT and 12 NTDT patients, and their median plasma MDA level before and after transfusion was 0.49 µmol/L and 0.45 µmol/L, respectively. Before transfusion, there was no correlation between SF and MDA, and TS and MDA levels. After the transfusion, there was no correlation between, SF and MDA, or TS and MDA levels. Conclusion:There is no significant difference in MDA levels before and after transfusion. Although blood transfusion increases the iron load in thalassemia patients, there was no increase in median MDA level after transfusion. Meanwhile, there was no correlation between markers of iron overload and MDA level in thalassemia patients both before and after transfusion.

Real‐world complication burden and disease management paradigms in transfusion‐related β‐thalassaemia in Greece: Results from ULYSSES, an epidemiological, multicentre, retrospective cross‐sectional study

“…Maintenance of serum ferritin below 1000 μg/L has been associated with improved clinical outcomes among all patients [18]; LIC up to 7 mg/g dw generally has no apparent adverse effects, while sustained LIC above 15–20 mg/g dw is linked with worsening prognosis [19, 20] and abnormalities [21]. Thus, patients in ULYSSES seem to have rather adequately controlled iron levels, compared with other previously published observational studies [14–16, 22–31]. Several factors could contribute to the observed differences, including variability in patient populations, genetic background, regions and observation periods, which determine available resources and application of different treatment modalities.…”

New Insights of Oxidative Stress and Thalassemia May Lead to Antioxidant Therapy

“…Thalassemia is a genetic disease of abnormal hemoglobin moieties of red blood cells (RBCs) 1 , resulting of abnormal and unpaired α-globin chain, or by abnormal globin molecules synthesis leading to fragility of RBCs membrane, with subsequent easily broken down of erythrocytes, resulting in chronic hemolytic anaemia. [2][3][4] Moreover, the formed severe anaemia resulted in lifelong dependence on blood transfusions to sustain life 5 , a therapy that causes additional iron overload, with its complications and toxic effects. 6 Accumulation of iron lead to elevation of free toxic ferrous in plasma.…”

“…7 Moreover, the accumulated ferrous form induces production of reactive oxygen species (ROS) including hydroxyl radicals (OH • ). [8][9][10] this dualistic impact of acculated unpaired globin chain and LPI facilitate the oxidant load on erythrocyte consequently reducing erythrocytes lifespan 11 increasing the chance of membrane lipid peroxidation 4 , increased lipid peroxidation processes with subsequent consumption of antioxidants. This consumption of antioxidants is responsible for constant intracellular oxidative stress, although oxidative stress is not the primary cause of thalassemia, it mediates several of its pathologies.…”

Food‐borne polyphenols: A biocompatible anchor recuperating iron homeostasis

“…Polyphenols can chelate iron ions or interfere with iron-related proteins (ferroportin (Fpn), hepcidin, ferritin, etc.) to participate in iron homeostasis, and multiple pathways have been reported that are involved in polyphenols-mediated bioactivities (Atmakusuma et al, 2021;Hatairaktham et al, 2021).…”

“…Polyphenols can chelate iron ions or interfere with iron‐related proteins (ferroportin (Fpn), hepcidin, ferritin, etc.) to participate in iron homeostasis, and multiple pathways have been reported that are involved in polyphenols‐mediated bioactivities (Atmakusuma et al., 2021; Hatairaktham et al., 2021). Administrated via daily dietary supplementation, polyphenols offer more convenient and biosafe strategies for the prevention and medication of these diseases.…”