Serum hepcidin levels and stroke in thalassemia patients

Petrova, Jordanka; Manolov, V.; Dimitrov, Georgi; Tarnovska-Kadreva, Р.; Yaneva-Sirakova, Teodora; Velizarova, M.; Vasilev, V.; Atanasova, Б.; Tzatchev, К.; Marinov, B; Emilova, Radoslava; Genchev, G.

doi:10.1177/1747493015623557

Cited by 4 publications

(2 citation statements)

References 7 publications

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“…These results indicate that β-thalassemia patients with higher HAMP levels and other complications should be paid attention to. 70 Blood transfusion and iron chelating are the main therapeutic strategies for β-thalassemia. However, iron chelators have severe side effects, and blood transfusion would cause secondary iron overload.…”

Section: Iron Disorders Due To Deregulation Of Hepcidinmentioning

confidence: 99%

Hepcidin

et al. 2016

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Iron is required for most forms of organisms, and it is the most essential element for the functions of many iron-containing proteins involved in oxygen transport, cellular respiration, DNA replication, and so on. Disorders of iron metabolism are associated with diverse diseases, including anemias (e.g., iron-deficiency anemia and anemia of chronic diseases) and iron overload diseases, such as hereditary hemochromatosis and β-thalassemia. Hepcidin (encoded by Hamp gene) is a peptide hormone synthesized by hepatocytes, and it plays an important role in regulating the systematic iron homeostasis. As the systemic iron regulator, hepcidin, not only controls dietary iron absorption and iron egress out of iron storage cells, but also induces iron redistribution in various organs. Deregulated hepcidin is often seen in a variety of iron-related diseases including anemias and iron overload disorders. In the case of iron overload disorders (e.g., hereditary hemochromatosis and β-thalassemia), hepatic hepcidin concentration is significantly reduced.Since hepcidin deregulation is responsible for iron disorder-associated diseases, the purpose of this review is to summarize the recent findings on therapeutics targeting hepcidin.Continuous efforts have been made to search for hepcidin mimics and chemical compounds that could be used to increase hepcidin level. Here, a literature search was conducted in PubMed, and research papers relevant to hepcidin regulation or hepcidin-centered therapeutic work were reviewed. On the basis of literature search, we recapitulated recent findings on therapeutic studies targeting hepcidin, including agonists and antagonists to modulate hepcidin expression or its downstream signaling. We also discussed the molecular mechanisms by which hepcidin level and iron metabolism are modulated.Elevating hepcidin concentration is an optimal strategy to ameliorate iron overload diseases, and also to relieve β-thalassemia phenotypes by improving ineffective erythropoiesis. Relative to the current conventional therapies, such as phlebotomy and blood transfusion, therapeutics targeting hepcidin would open a new avenue for treatment of iron-related diseases.

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Section: Iron Disorders Due To Deregulation Of Hepcidinmentioning

confidence: 99%

Hepcidin

et al. 2016

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“…On the other hand cases of acute stroke in thalassemia patients might seriously mask the anemia picture and clinicians might make an incorrect therapeutic choice [14].…”

Section: Discussionmentioning

confidence: 99%

Serum Hepcidin Quantification in Stroke in β-Thalassemia and Rheumatoid Arthritis Patients

Manolov¹

2017

Austin J Cerebrovasc Dis & Stroke

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Background and Purpose: Anemia occurs often in different conditions, associated with iron metabolism and flowing in a number of diseases. Variations in serum levels of iron is due to a number of reasons, such as bleeding from the gastrointestinal tract, inflammation, production of inflammatory cytokines, deposition of iron in various tissue structures, and etc. Oxidative stress plays an important role in neuronal injuries caused by cerebral ischemia. We aimed to quantify serum hepcidin in rheumatoid arthritis patients with ischemic stroke and β-thalassemia with stroke and evaluate peptide changes in combination of two diseases.Methods: For a period of two years 138 patients with ischemic stroke were enrolled. They were separated into three groups -49 with ischemic stroke, caused by vascular reasons (ISVR), 43 patients with rheumatoid arthritis (RA) and 46 β-thalassemia cases (BTM). Their results were compared to age and gender matched healthy controls. Established parameters from rheumatoid arthritis and β-thalassemia cases were compared with RA and BTM patients without stroke. Statistical analysis of established results was performed using Pearson's correlation and Student's paired t-test. Results:We found statistically different results from included groups for serum hepcidin levels. They differ in case if an acute stroke occurs during rheumatoid arthritis or β-thalassemia. Serum hepcidin levels statistically differ in three ischemic stoke groups: ISVR 87.6±9.4 µg/L, RA 19.4±0.9 µg/L and BTM 7.9±1.1 µg/L (P<0.001). In patients with RA and BTM without stroke hepcidin shows serum concentrations from 35.6±1.4 µg/L and 0.95±0.3 µg/L (P<0.001). In healthy controls we quantified serum hepcidin as 22.7±5.1 µg/L. Conclusion:Our study in patients with acute stroke, rheumatoid arthritis and stroke and β-thalassemia and stroke confirms the ability of verified immunochemical method for evaluation of iron homeostasis. It provides a basis for the correct choice of therapeutic approach in anemia treatment. Rheumatoid arthritis increases serum hepcidin levels in stroke; in patients with β-thalassemia peptide's concentration decreases. Dissimilar diseases are accompanied with iron disorders, thereby masking the state of this trace element in human body.

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