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Title: Model of reticuloendothelial iron metabolism in humans: Abnormal behavior in idiopathic hemochromatosis and in inflammation

Abstract

Iron transport in the reticuloendothelial (RE) system plays a central role in iron metabolism, but its regulation has not been characterized physiologically in vivo in humans. In particular, why serum iron is elevated and RE cells are much less iron-loaded than parenchymal cells in idiopathic hemochromatosis is not known. The processing of erythrocyte iron by the RE system was studied after intravenous (IV) injection of 59Fe heat-damaged RBCs (HDRBCs) and 55Fe transferrin in normal subjects and in patients with iron deficiency, idiopathic hemochromatosis, inflammation, marrow aplasia, or hyperplastic erythropoiesis. Early release of 59Fe by the RE system was calculated from the plasma iron turnover and the 59Fe plasma reappearance curve. Late release was calculated from the ratio of 59Fe/55Fe RBC utilization in 2 weeks. The partitioning of iron between the early (release from heme catabolism) and late (release from RE stores) phases depended on the size of RE iron stores, as illustrated by the inverse relationship observed between early release and plasma ferritin (P less than .001). There was a strong correlation between early release and the rate of change of serum iron levels during the first three hours in normal subjects (r = .85, P less than .001). Inflammationmore » produced a blockade of the early release phase, whereas in idiopathic hemochromatosis early release was considerably increased as compared with subjects with similar iron stores. Based on these results, we describe a model of RE iron metabolism in humans. We conclude that the RE system appears to determine the diurnal fluctuations in serum iron levels through variations in the immediate output of heme iron. In idiopathic hemochromatosis, a defect of the RE cell in withholding iron freed from hemoglobin could be responsible for the high serum iron levels and low RE iron stores.« less

Authors:
; ;  [1]
  1. (Univ. of Liege (Belgium))
Publication Date:
OSTI Identifier:
5606070
Resource Type:
Journal Article
Resource Relation:
Journal Name: Blood; (USA); Journal Volume: 74:2
Country of Publication:
United States
Language:
English
Subject:
59 BASIC BIOLOGICAL SCIENCES; HEMIC DISEASES; PATHOGENESIS; IRON; METABOLISM; BLOOD PLASMA; ERYTHROCYTES; ERYTHROPOIESIS; HEAT; INFLAMMATION; IRON 55; IRON 59; MEMBRANE TRANSPORT; PATIENTS; RETICULOENDOTHELIAL SYSTEM; TRACER TECHNIQUES; TRANSFERRIN; ANIMAL TISSUES; BETA DECAY RADIOISOTOPES; BETA-MINUS DECAY RADIOISOTOPES; BIOLOGICAL MATERIALS; BLOOD; BLOOD CELLS; BLOOD FORMATION; BODY; BODY FLUIDS; DAYS LIVING RADIOISOTOPES; DISEASES; ELECTRON CAPTURE RADIOISOTOPES; ELEMENTS; ENERGY; EVEN-ODD NUCLEI; GLOBULINS; GLOBULINS-BETA; INTERMEDIATE MASS NUCLEI; IRON ISOTOPES; ISOTOPE APPLICATIONS; ISOTOPES; MATERIALS; METALLOPROTEINS; METALS; NUCLEI; ORGANIC COMPOUNDS; PATHOLOGICAL CHANGES; PROTEINS; RADIOISOTOPES; SYMPTOMS; TISSUES; TRANSITION ELEMENTS; YEARS LIVING RADIOISOTOPES; 550501* - Metabolism- Tracer Techniques; 550901 - Pathology- Tracer Techniques

Citation Formats

Fillet, G., Beguin, Y., and Baldelli, L. Model of reticuloendothelial iron metabolism in humans: Abnormal behavior in idiopathic hemochromatosis and in inflammation. United States: N. p., 1989. Web.
Fillet, G., Beguin, Y., & Baldelli, L. Model of reticuloendothelial iron metabolism in humans: Abnormal behavior in idiopathic hemochromatosis and in inflammation. United States.
Fillet, G., Beguin, Y., and Baldelli, L. Tue . "Model of reticuloendothelial iron metabolism in humans: Abnormal behavior in idiopathic hemochromatosis and in inflammation". United States.
@article{osti_5606070,
title = {Model of reticuloendothelial iron metabolism in humans: Abnormal behavior in idiopathic hemochromatosis and in inflammation},
author = {Fillet, G. and Beguin, Y. and Baldelli, L.},
abstractNote = {Iron transport in the reticuloendothelial (RE) system plays a central role in iron metabolism, but its regulation has not been characterized physiologically in vivo in humans. In particular, why serum iron is elevated and RE cells are much less iron-loaded than parenchymal cells in idiopathic hemochromatosis is not known. The processing of erythrocyte iron by the RE system was studied after intravenous (IV) injection of 59Fe heat-damaged RBCs (HDRBCs) and 55Fe transferrin in normal subjects and in patients with iron deficiency, idiopathic hemochromatosis, inflammation, marrow aplasia, or hyperplastic erythropoiesis. Early release of 59Fe by the RE system was calculated from the plasma iron turnover and the 59Fe plasma reappearance curve. Late release was calculated from the ratio of 59Fe/55Fe RBC utilization in 2 weeks. The partitioning of iron between the early (release from heme catabolism) and late (release from RE stores) phases depended on the size of RE iron stores, as illustrated by the inverse relationship observed between early release and plasma ferritin (P less than .001). There was a strong correlation between early release and the rate of change of serum iron levels during the first three hours in normal subjects (r = .85, P less than .001). Inflammation produced a blockade of the early release phase, whereas in idiopathic hemochromatosis early release was considerably increased as compared with subjects with similar iron stores. Based on these results, we describe a model of RE iron metabolism in humans. We conclude that the RE system appears to determine the diurnal fluctuations in serum iron levels through variations in the immediate output of heme iron. In idiopathic hemochromatosis, a defect of the RE cell in withholding iron freed from hemoglobin could be responsible for the high serum iron levels and low RE iron stores.},
doi = {},
journal = {Blood; (USA)},
number = ,
volume = 74:2,
place = {United States},
year = {Tue Aug 01 00:00:00 EDT 1989},
month = {Tue Aug 01 00:00:00 EDT 1989}
}