Elevated serum adiponectin is related to elevated serum ferritin and interleukin-6 in β-thalassaemia major children

El-Rasheidy, Farida H; Essa, Enas Said; Mahmoud, Asmaa A.; Nada, Ali

doi:10.1515/jpem-2016-0014

Cited by 10 publications

(17 citation statements)

References 25 publications

(28 reference statements)

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“…Individuals with β-thalassemia major, characterized by marked ineffective erythropoiesis and severe hemolysis, as well as with β-thalassemia intermedia, characterized by widely variable symptoms and severity ranging between the two extremes of the major and minor forms, require frequent to occasional RBCs transfusions to sustain life ( 24 – 26 ). Among β-thalassemic ( 27 , 28 ), the subjects affected by minor β-thalassemia, clinically asymptomatic and characterized by morphological abnormalities of erythrocytes as well as by a slight lowering of the hemoglobin levels, show the disorders of iron homeostasis sometimes leading to a mild anemia ( 24 ). During pregnancy, despite the progress of therapies, maternal and fetal complications, such as risk of abortion, thromboembolism, pre-term delivery and intrauterine growth restriction, appear to be increased in patients with β-thalassemia major, occurring in almost 40% of pregnancies, as well as in patients with β-thalassemia intermedia, occurring in 20–30% of pregnancies, compared to healthy ones ( 25 , 26 ).…”

Section: Introductionmentioning

confidence: 99%

Efficacy of Lactoferrin Oral Administration in the Treatment of Anemia and Anemia of Inflammation in Pregnant and Non-pregnant Women: An Interventional Study

et al. 2018

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The discovery of the ferroportin-hepcidin complex has led to a critical review on the treatment of anemia and anemia of inflammation (AI). Ferroportin, the only known mammalian iron exporter from cells to blood, is negatively regulated by hepcidin, a hormone peptide able to bind to ferroportin, leading to its degradation. Therefore, new efficient therapeutic interventions acting on hepcidin and ferroportin are imperative to manage anemia and AI. Bovine milk derivative lactoferrin (bLf), a glycoprotein able to chelate two ferric ions per molecule, is emerging as a natural anti-inflammatory substance able to modulate hepcidin and ferroportin synthesis through the down-regulation of interleukin-6 (IL-6). Here, an interventional study (ClinicalTrials.gov Identifier: NCT01221844) was conducted by orally administering 100 mg of 20–30% iron-saturated bLf (corresponding to 70–84 μg of elemental iron) twice a day. This treatment was compared with the Italian standard therapy, consisting in the oral administration of 329.7 mg of ferrous sulfate once a day (corresponding to 105 mg of elemental iron). Treatments were carried out on 29 anemic women with minor β-thalassemia (20 pregnant and 9 non-pregnant), 149 women with hereditary thrombophilia (HT) (70 pregnant and 79 non-pregnant) affected by AI and 20 anemic pregnant women suffering from various pathologies. In anemic pregnant and non-pregnant women with minor β-thalassemia, presenting undetectable hepcidin levels, differently from ferrous sulfate management, bLf decreased IL-6 (from 25 ± 8 to 6 ± 3 pg/ml) and increased total serum iron (TSI) (from 54 ± 17 to 80 ± 9 μg/dl). BLf was also more efficient than ferrous sulfate in AI treatment in HT pregnant and non-pregnant women by decreasing both serum IL-6 (from 89 ± 8 to 58 ± 6 pg/ml) and hepcidin (from 115 ± 23 to 65 ± 10 ng/ml), thus increasing hematological parameters, such as the number of red blood cells (RBCs), the concentration of hemoglobin, TSI and serum ferritin. BLf was also efficient in treating anemia in other pathological pregnancies. Taken together all the results, bLf, showing a greater benefit and efficacy than the standard ferrous sulfate management, can be considered as a promising compound in treating anemia and AI through its ability to down-regulate IL-6, thus restoring ferroportin-mediated iron export from cells to blood in a hepcidin-dependent or independent way.

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Section: Introductionmentioning

confidence: 99%

Efficacy of Lactoferrin Oral Administration in the Treatment of Anemia and Anemia of Inflammation in Pregnant and Non-pregnant Women: An Interventional Study

et al. 2018

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“…Likewise, Neopterin, a proinflammatory mediator produced by activated macrophage, was described in higher levels in TM patients compared to control individuals (12). Furthermore, TM patients showed higher levels of IL-6 (13-15), , and C-reactive protein (15). Despite the impoverished cellular components, the humoral determinants of innate immunity seem to be augmented in TM.…”

Section: Innate Immunitymentioning

confidence: 95%

The Role of Immune System in Thalassemia Major: A Narrative Review

Bazi¹,

Shahramian²,

Yaghoobi³

et al. 2017

J Pediatr Rev

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Context: Thalassemia is a genetic disorder of hemoglobin production. Patients with thalassemia major (TM) require regular blood transfusions to keep a compatible hemoglobin level for oxygenating organs. These patients suffer from different complications such as infections, autoimmunity and alloimmunization due to transfusion. Such complications link the immune system to TM pathogenesis. In the present study, we have reviewed the latest data available on interactions of TM pathophysiologic determinants and immune system components. Evidence Acquisition: A comprehensive search was performed on PubMed, Scopous, and Web of Knowledge databases using keywords thalassemia, immune system, autoimmune, alloimmune, adaptive immunity, innate immunity, complications, and immunesenescnce. Results: It seems that persistent antigenic stimulation and oxidative stress from excessive iron are the two main pathophysiologic factors of TM impacting the immune system. Regarding innate immunity, functional activity of neutrophils, and natural killer cells (NKCs) is decreased in TM. On the other hand, higher levels of TNF-α and IL-1β, IL-6, IL-8, and C-reactive protein proinflammatory cytokines have been observed in the serum of patients. TM patients have demonstrated higher ratios of regulatory B lymphocytes (CD19+, CD38+, CD24+), helper T cells, suppressor T cells, and T regulatory (CD4+/CD25+/Foxp3+) lymphocytes. TM patients have shown significant higher levels of IgA immunoglobin respective to normal counterparts that may predispose them to diabetes and coeliac disease. Immune cells, however, rendered lower than optimal activity in TM patients, which may be due to nutritional insufficiencies. Potential relationships have been suggested between immune system and various thalassemia compilations including heart infraction, hypertension, atherosclerosis, diabetes, thyroid dysfunction, and osteoporosis. Conclusions: Immune genetic determinants may be involved in modulating the clinical picture of TM. TM patients generally represents with higher immune cell counts, likely as a result of persistent antigenic challenge from blood transfusions. However, these patients face compromised immune cell functions. The role of immunologic interactions in pathogenesis of TM needs to be further divulged in future studies.

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“…Four cross-sectional clinical studies investigated adiponectin levels in thalassemia patients (Chaliasos et al, 2010;El-Rasheidy, Essa, Mahmoud, & Nada Ael, 2016;Enli, Balci, Gonen, Uzun, & Polat, 2014;Elsayh, Mohammed, Zahran, & Saad, 2016). Three studies were conducted in β-thalassemia major (Chaliasos et al, 2010;El-Rasheidy et al, 2016;Elsayh et al, 2016), while the other one was conducted in a heterogeneous group of β-thalassemia major, intermedia, and minor (Enli et al, 2014). All of these studies demonstrated elevated serum TABLE 5 Associations between serum adiponectin and iron burden, severity of anemia, and inflammation in β-thalassemia patients adiponectin levels in thalassemia patients compared with healthy individuals (Chaliasos et al, 2010;El-Rasheidy et al, 2016;Enli et al, 2014;Elsayh et al, 2016).…”

Section: Lcn2 and Adiponectin Are Associated With Iron Burden Sevementioning

confidence: 99%

“…Three studies were conducted in β-thalassemia major (Chaliasos et al, 2010;El-Rasheidy et al, 2016;Elsayh et al, 2016), while the other one was conducted in a heterogeneous group of β-thalassemia major, intermedia, and minor (Enli et al, 2014). All of these studies demonstrated elevated serum TABLE 5 Associations between serum adiponectin and iron burden, severity of anemia, and inflammation in β-thalassemia patients adiponectin levels in thalassemia patients compared with healthy individuals (Chaliasos et al, 2010;El-Rasheidy et al, 2016;Enli et al, 2014;Elsayh et al, 2016). Positive correlations were found between serum adiponectin and ferritin (El-Rasheidy et al, 2016;Enli et al, 2014), CRP (El-Rasheidy et al, 2016;Elsayh et al, 2016), and interleukin (IL)-6 (El- Rasheidy et al, 2016).…”

Section: Lcn2 and Adiponectin Are Associated With Iron Burden Sevementioning

confidence: 99%

“…All of these studies demonstrated elevated serum TABLE 5 Associations between serum adiponectin and iron burden, severity of anemia, and inflammation in β-thalassemia patients adiponectin levels in thalassemia patients compared with healthy individuals (Chaliasos et al, 2010;El-Rasheidy et al, 2016;Enli et al, 2014;Elsayh et al, 2016). Positive correlations were found between serum adiponectin and ferritin (El-Rasheidy et al, 2016;Enli et al, 2014), CRP (El-Rasheidy et al, 2016;Elsayh et al, 2016), and interleukin (IL)-6 (El- Rasheidy et al, 2016). Serum adiponectin was reported to be negatively correlated with hemoglobin (El-Rasheidy et al, 2016).…”

Section: Lcn2 and Adiponectin Are Associated With Iron Burden Sevementioning

confidence: 99%

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Roles of lipocalin 2 and adiponectin in iron overload cardiomyopathy

Siri‐Angkul

Chattipakorn

2018

Journal Cellular Physiology

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Thalassemia is among the most common genetic diseases worldwide. Ineffective erythropoiesis, chronic hemolysis, and regular blood transfusion in thalassemia patients lead to increased iron burden. Iron overload cardiomyopathy is the most severe co-morbidity and most common cause of mortality in thalassemia patients. Although its associated mechanisms are still not completely understood, cellular iron mishandling, chronic inflammation, and oxidative stress appear to be the key processes involved. In order to acquire a more comprehensive insight of the impact of cardiac iron overload, these alterations need to be intensively investigated. This comprehensive mini-review focuses on two emergent molecules which have been shown to potentially play significant roles in iron overload cardiomyopathy. These two molecules are an iron-transporting protein, lipocalin 2, and an anti-inflammatory adipokine, adiponectin. Reports from in vitro and in vivo studies are comprehensively summarized. Clinical studies examining the roles of these molecules in thalassemia patients are also presented and discussed.

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Elevated serum adiponectin is related to elevated serum ferritin and interleukin-6 in β-thalassaemia major children

Abstract: Serum adiponectin was increased in β-thalassaemia major as were pro-inflammatory markers (CRP and IL-6). Its level is directly associated with ferritin and IL-6 levels.

Cited by 10 publications

References 25 publications

Efficacy of Lactoferrin Oral Administration in the Treatment of Anemia and Anemia of Inflammation in Pregnant and Non-pregnant Women: An Interventional Study

Efficacy of Lactoferrin Oral Administration in the Treatment of Anemia and Anemia of Inflammation in Pregnant and Non-pregnant Women: An Interventional Study

The Role of Immune System in Thalassemia Major: A Narrative Review

Roles of lipocalin 2 and adiponectin in iron overload cardiomyopathy

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