The Role of Iron and Iron Overload in Chronic Liver Disease

Milić, Sandra; Mikolašević, Ivana; Orlić, Lidija; Devcic, Edita; Čizmarević, Nada Starčević; Stimac, Davor; Kapović, Miljenko; Ristić, Smiljana

doi:10.12659/msm.896494

Cited by 147 publications

(118 citation statements)

References 66 publications

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“…The significance of maintaining the homeostasis of essential microelements cannot be overrated, considering the participation of iron and copper in the development of diseases of this organ [15,16], the role of manganese superoxide dismutase in liver tumour suppression [17], or the protective effect of zinc in the case of hepatoxicity of lithium [12]. Additionally, the necessity of maintaining the proper liver functions must be highlighted, considering that lithium therapy in psychiatric subjects is usually used for some years [4].…”

Section: Discussionmentioning

confidence: 99%

Homeostasis of chosen microelements in liver of rats receiving lithium and/or selenium orally

Kiełczykowska¹,

Kopciał²,

Marzec³

et al. 2017

J Pre Clin Clin Res.

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Introduction and objective. Lithium and selenium have been the subjects of extensive research for many years. Concern about the physiological action of these elements results from the application of lithium in medicine, as well as the beneficial influence of selenium supplementation in different pathological states. However, little data are available concerning their effect on the homeostasis of essential microelements in organs. Therefore, the aim of the current study was to evaluate the influence of lithium and/or selenium administration on homeostasis of iron, zinc, copper and manganese in the liver of rats. Materials and method. The experiment was carried on 24 male Wistar rats (4 groups of 6 animals) subjected to the treatment with: group I (control) -saline; group II -lithium carbonate at a dose of 2.7 mg Li/kg b.w.; group III -sodium selenite at a dose of 0.5 mg Se/kg b.w.; group IV -both lithium carbonate and sodium selenite at the doses mentioned above. Administration was performed for 6 weeks, once a day by stomach tube, in the form of water solutions. Results. The tissue content of zinc, iron and manganese showed no statistical differences among the studied groups. Zn was slightly decreased in group III vs. control and group II. Fe was insignificantly enhanced in groups II and IV vs. control. Mn in group IV was slightly increased vs. groups II and III. Cu in group III was significantly decreased vs. group IV and slightly depleted vs. groups I and II. Conclusion. With the exception of Cu in the Se-treated group, lithium and/or selenium did not affect the studied microelements' liver homeostasis in a significant way. These results may contribute to the knowledge of essential microelements homeostasis in human organisms undergoing lithium therapy, and/or selenium supplementation.

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Section: Discussionmentioning

confidence: 99%

Homeostasis of chosen microelements in liver of rats receiving lithium and/or selenium orally

Kiełczykowska¹,

Kopciał²,

Marzec³

et al. 2017

J Pre Clin Clin Res.

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“…For instance, the cellular pattern of iron deposition within the liver during states of positive iron balance appears to greatly impact the risk of tissue damage and subsequent adverse outcomes [57-59]. When “excess” iron is predominately deposited in hepatocytes (i.e., parenchymal deposition), as might be observed in hereditary HFE -associated hemochromatosis, tissue damage is common [57].…”

Section: When Does Positive Iron Balance Become Iron Toxicity?mentioning

confidence: 99%

“…When “excess” iron is predominately deposited in hepatocytes (i.e., parenchymal deposition), as might be observed in hereditary HFE -associated hemochromatosis, tissue damage is common [57]. In such conditions, iron deposition into Kupffer cells is a later finding [59]. In contrast, when reticuloendothelial deposition of iron predominates, as is expected with IV iron administration, tissue damage is less frequent.…”

Section: When Does Positive Iron Balance Become Iron Toxicity?mentioning

confidence: 99%

Positive Iron Balance in Chronic Kidney Disease: How Much is Too Much and How to Tell?

et al. 2018

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Background: Regulation of body iron occurs at cellular, tissue, and systemic levels. In healthy individuals, iron absorption and losses are minimal, creating a virtually closed system. In the setting of chronic kidney disease and hemodialysis (HD), increased iron losses, reduced iron absorption, and limited iron availability lead to iron deficiency. Intravenous (IV) iron therapy is frequently prescribed to replace lost iron, but determining an individual’s iron balance and stores can be challenging and imprecise, contributing to uncertainty about the long-term safety of IV iron therapy. Summary: Patients on HD receiving judicious doses of IV iron are likely to be in a state of positive iron balance, yet this does not appear to confer an overt risk for clinically relevant iron toxicity. The concomitant use of iron with erythropoiesis-stimulating agents, the use of maintenance iron dosing regimens, and the reticuloendothelial distribution of hepatic iron deposition likely minimize the potential for iron toxicity in patients on HD. Key Messages: Because no single diagnostic test can, at present, accurately assess iron status and risk for toxicity, clinicians need to take an integrative approach to avoid iron doses that impose excessive exposure while ensuring sufficient replenishment of iron stores capable of overcoming hepcidin blockade and allowing for effective erythropoiesis.

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“…The accumulation of iron in hepatocytes prevents the binding of transcription factors to DNA, decreasing the hepatic synthesis of hepcidin [117]. …”

Section: Hepcidinmentioning

confidence: 99%

Hepcidin: Homeostasis and Diseases Related to Iron Metabolism

et al. 2017

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Iron is an essential metal for cell survival that is regulated by the peptide hormone hepcidin. However, its influence on certain diseases is directly related to iron metabolism or secondary to underlying diseases. Genetic alterations influence the serum hepcidin concentration, which can lead to an iron overload in tissues, as observed in haemochromatosis, in which serum hepcidin or defective hepcidin synthesis is observed. Another genetic imbalance of iron is iron-refractory anaemia, in which serum concentrations of hepcidin are increased, precluding the flow and efflux of extra- and intracellular iron. During the pathogenesis of certain diseases, the resulting oxidative stress, as well as the increase in inflammatory cytokines, influences the transcription of the HAMP gene to generate a secondary anaemia due to the increase in the serum concentration of hepcidin. To date, there is no available drug to inhibit or enhance hepcidin transcription, mostly due to the cytotoxicity described in the in vitro models. The proposed therapeutic targets are still in the early stages of clinical trials. Some candidates are promising, such as heparin derivatives and minihepcidins. This review describes the main pathways of systemic and genetic regulation of hepcidin, as well as its influence on the disorders related to iron metabolism.

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The Role of Iron and Iron Overload in Chronic Liver Disease

Cited by 147 publications

References 66 publications

Homeostasis of chosen microelements in liver of rats receiving lithium and/or selenium orally

Homeostasis of chosen microelements in liver of rats receiving lithium and/or selenium orally

Positive Iron Balance in Chronic Kidney Disease: How Much is Too Much and How to Tell?

Hepcidin: Homeostasis and Diseases Related to Iron Metabolism

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