Effects of the administration of ferric citrate hydrate on inflammatory and oxidative stress markers as well as improvements in anemia treatment

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  • Hara Masaki
    Department of Internal Medicine, Saiyu Soka Hospital
  • Nakamura Yuya
    Department of Internal Medicine, Saiyu Soka Hospital Division of Medical Pharmacology, Department of Pharmacology, Showa University
  • Suzuki Hiroki
    Department of Internal Medicine, Saiyu Soka Hospital
  • Nishida Kazumasa
    Department of Internal Medicine, Saiyu Soka Hospital
  • Ohsawa Isao
    Department of Internal Medicine, Saiyu Soka Hospital
  • Inagaki Masahiro
    Chemistry Division, Department of Education, Showa University Fuji Yoshida
  • Hasegawa Hitomi
    Division of Medical Pharmacology, Department of Pharmacology, Showa University
  • Oguti Katsuji
    Division of Medical Pharmacology, Department of Pharmacology, Showa University
  • Goto Yoshikazu
    Department of Internal Medicine, Saiyu Soka Hospital
  • Gotoh Hiromichi
    Department of Internal Medicine, Saiyu Soka Hospital

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Other Title
  • クエン酸第二鉄水和物投与による炎症マーカー, 酸化ストレス関連マーカーへの影響と貧血改善効果について
  • クエンサン ダイニテツ スイワブツ トウヨ ニ ヨル エンショウ マーカー,サンカ ストレス カンレン マーカー エ ノ エイキョウ ト ヒンケツ カイゼン コウカ ニ ツイテ

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<p>This prospective 12-week study aimed to evaluate the changes in the levels of inflammatory and oxidative stress markers after the administration of ferric citrate hydrate (FCH) and to determine whether the serum hepcidin-25 level could serve as a prognostic indicator during the treatment of anemia with FCH. The serum levels of inorganic phosphorus, hemoglobin (Hb), iron, erythropoiesis-stimulating agents (ESA), inflammatory and oxidative stress markers, and serum hepcidin-25 together with the erythropoietin resistance index (ERI) were studied in both the FCH treatment group (1,500 mg/day FCH) and control group (who were administered a phosphate binder other than FCH). The patients that exhibited changes of <10% in their serum hepcidin-25 levels were designated the “invariant group”, whereas those that exhibited changes of >10% in their serum hepcidin-25 levels were designated the “gain group”. In the FCH group, significant increases in the serum ferritin level and significant reductions in the ERI and the serum ESA level were observed after the administration of FCH. There were no significant changes in inflammatory or oxidative stress markers in either group. The invariant group exhibited significantly higher Hb levels than the gain group (2.2±0.4 vs. −0.6±1.4 g/dL, respectively ; p=0.0105). Therefore, the serum hepcidin-25 level could be a novel prognostic marker of the increase in the Hb level induced by the administration of FCH.</p>

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