Determination of ferritin and hemosiderin iron in patients with normal iron stores and iron overload by serum ferritin kinetics

Hiroshi Saito, Akihiro Tomita, Haruhiko Ohashi, Hideaki Maeda, Hisao Hayashi, Tomoki Naoe

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

We attempted to clarify the storage iron metabolism from the change in the serum ferritin level. We assumed that the nonlinear decrease in serum ferritin was caused by serum ferritin increase in iron mobilization. Under this assumption, we determined both ferritin and hemosiderin iron levels by computer-assisted simulation of the row of decreasing assay-dots of serum ferritin in 11 patients with normal iron stores free of both iron deficiency and iron overload; chronic hepatitis C (CHC) and iron deficiency anemia after treatment, and 11 patients with iron overload; hereditary hemochromatosis (HH) and transfusion-dependent anemias (TD). We determined the iron removal rates of 20 and 17 mg/day by administering mean doses of deferasirox at 631 and 616 mg/day in 2 TD during the period of balance of iron addition and removal as indicated by the serum ferritin returned to the previous level. The ferritin-per-hemosiderin ratio was almost the same in both HH and CHC. This matched the localized hepatic hemosiderin deposition in CHC with normal iron stores. We detected the ferritin increased by utilizing the hemosiderin iron in iron removal and the ferritin reduced by transforming ferritin into hemosiderin in iron additions. The iron storing capacity of hemosiderin was limitless, while that of ferritin was suppressed when ferritin iron exceeded around 5 grams. We confirmed the pathway of iron from hemosiderin to ferritin in iron mobilization, and that from ferritin to hemosiderin in iron deposition. Thus, serum ferritin kinetics enabled us to be the first to clinically clarify storage iron metabolism.

Original languageEnglish
Pages (from-to)39-49
Number of pages11
JournalNagoya Journal of Medical Science
Volume74
Issue number1-2
Publication statusPublished - 01-12-2012
Externally publishedYes

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Hemosiderin
Iron Overload
Ferritins
Iron
Serum
Chronic Hepatitis C
Hemochromatosis
Anemia
Iron-Deficiency Anemias

All Science Journal Classification (ASJC) codes

  • Medicine(all)

Cite this

Saito, Hiroshi ; Tomita, Akihiro ; Ohashi, Haruhiko ; Maeda, Hideaki ; Hayashi, Hisao ; Naoe, Tomoki. / Determination of ferritin and hemosiderin iron in patients with normal iron stores and iron overload by serum ferritin kinetics. In: Nagoya Journal of Medical Science. 2012 ; Vol. 74, No. 1-2. pp. 39-49.
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Determination of ferritin and hemosiderin iron in patients with normal iron stores and iron overload by serum ferritin kinetics. / Saito, Hiroshi; Tomita, Akihiro; Ohashi, Haruhiko; Maeda, Hideaki; Hayashi, Hisao; Naoe, Tomoki.

In: Nagoya Journal of Medical Science, Vol. 74, No. 1-2, 01.12.2012, p. 39-49.

Research output: Contribution to journalArticle

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T1 - Determination of ferritin and hemosiderin iron in patients with normal iron stores and iron overload by serum ferritin kinetics

AU - Saito, Hiroshi

AU - Tomita, Akihiro

AU - Ohashi, Haruhiko

AU - Maeda, Hideaki

AU - Hayashi, Hisao

AU - Naoe, Tomoki

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N2 - We attempted to clarify the storage iron metabolism from the change in the serum ferritin level. We assumed that the nonlinear decrease in serum ferritin was caused by serum ferritin increase in iron mobilization. Under this assumption, we determined both ferritin and hemosiderin iron levels by computer-assisted simulation of the row of decreasing assay-dots of serum ferritin in 11 patients with normal iron stores free of both iron deficiency and iron overload; chronic hepatitis C (CHC) and iron deficiency anemia after treatment, and 11 patients with iron overload; hereditary hemochromatosis (HH) and transfusion-dependent anemias (TD). We determined the iron removal rates of 20 and 17 mg/day by administering mean doses of deferasirox at 631 and 616 mg/day in 2 TD during the period of balance of iron addition and removal as indicated by the serum ferritin returned to the previous level. The ferritin-per-hemosiderin ratio was almost the same in both HH and CHC. This matched the localized hepatic hemosiderin deposition in CHC with normal iron stores. We detected the ferritin increased by utilizing the hemosiderin iron in iron removal and the ferritin reduced by transforming ferritin into hemosiderin in iron additions. The iron storing capacity of hemosiderin was limitless, while that of ferritin was suppressed when ferritin iron exceeded around 5 grams. We confirmed the pathway of iron from hemosiderin to ferritin in iron mobilization, and that from ferritin to hemosiderin in iron deposition. Thus, serum ferritin kinetics enabled us to be the first to clinically clarify storage iron metabolism.

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