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A vasanyagcsere-zavarok kezelésé nek lehetőségei, új perspektívák Irodalmi összefoglaló

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MAL 138 (10),631-640.(2016) (2.183Mb)
Date
2016-10
Author
Pásztiné Gere, Erzsébet
Barna, Réka Fanni
Szombath, Gergely
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Abstract
SUMMARY The authors summarize in their study the causes and the symptoms of iron toxicosis and iron deficiency anaemia and the diagnostic and treatment options of disturbances in iron homeostasis. Plasma iron level can be a reliable indica tor of iron deficiency anaemia, however, the low iron level can also be caused by chronic inflammation, infections and cancers. The iron supplementation of neonatal suckling piglets is of high veterinary importance, which is the most appropriate treatment for prevention of iron deficiency anaemia. The authors point out that iron toxicosis developed after administration of excessive iron can be compensated through parenteral deferoxamine, however other chelators applied mainly in human medicine such as deferiprone or deferasirox might be also effective in veterinary field. In this study the role of hepcidin in iron homeo stasis of the body is also discussed. The maintenance of physiological iron lev els in spite of rapid turnover of the iron suggests the regulation of hepcidin by plasma iron. In case of iron deficiency, the hepcidin amount is lowered, which then facilitates the rate of iron transport into the blood. In contrast, if the iron storage is saturated, the level of hepcidin produced by liver becomes elevated. Hepcidin oversecretion can also be induced by infection and inflammation with excessive interleukin-6 production. The authors also describe the compounds acting via hepcidin regulation which can be therapeutically beneficial in the treatment of iron homeostatic disturbances. The pharmacological intervention of the interplay between hepcidin and matriptase-2 has been one of the most recently discovered research fields which might involve the introduction of mat riptase modulators into the drug therapy of iron disorders.
URI
http://hdl.handle.net/10832/2811
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