Serum transferrin receptor as a new index of erythropoiesis. 1987

Y Kohgo, and Y Niitsu, and H Kondo, and J Kato, and N Tsushima, and K Sasaki, and M Hirayama, and T Numata, and T Nishisato, and I Urushizaki
Department of Internal Medicine, Sapporo Medical College, Japan.

Serum transferrin receptors were measured by a sandwich radioimmunoassay procedure in patients with iron deficiency anemia, autoimmune hemolytic anemia and aplastic anemia. The mean circulating transferrin receptor concentration of normal subjects and patients with iron deficiency anemia, autoimmune hemolytic anemia and aplastic anemia are 253 +/- 82 ng/mL, 730 +/- 391 ng/mL, 1,426 +/- 1,079 ng/mL, and 182 +/- 39 ng/mL, respectively. The values for those with iron deficiency anemia and autoimmune hemolytic anemia were significantly higher than that of normal controls and the values for those with aplastic anemia were lower than that of normal controls. After iron supplementation in iron deficiency anemia, the serum transferrin receptor values increased twofold over those of pretreatment values. This increase parallels an increase in peripheral reticulocytes. Therefore, the number of circulating transferrin receptors in anemic patients may reflect the level of bone marrow erythropoiesis and is a potentially useful new index for red cell production.

UI MeSH Term Description Entries
D011990 Receptors, Transferrin Membrane glycoproteins found in high concentrations on iron-utilizing cells. They specifically bind iron-bearing transferrin, are endocytosed with its ligand and then returned to the cell surface where transferrin without its iron is released. Transferrin Receptors,Transferrin Receptor,Receptor, Transferrin
D012156 Reticulocytes Immature ERYTHROCYTES. In humans, these are ERYTHROID CELLS that have just undergone extrusion of their CELL NUCLEUS. They still contain some organelles that gradually decrease in number as the cells mature. RIBOSOMES are last to disappear. Certain staining techniques cause components of the ribosomes to precipitate into characteristic "reticulum" (not the same as the ENDOPLASMIC RETICULUM), hence the name reticulocytes. Reticulocyte
D004920 Erythropoiesis The production of red blood cells (ERYTHROCYTES). In humans, erythrocytes are produced by the YOLK SAC in the first trimester; by the liver in the second trimester; by the BONE MARROW in the third trimester and after birth. In normal individuals, the erythrocyte count in the peripheral blood remains relatively constant implying a balance between the rate of erythrocyte production and rate of destruction. Erythropoieses
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D000740 Anemia A reduction in the number of circulating ERYTHROCYTES or in the quantity of HEMOGLOBIN. Anemias
D000741 Anemia, Aplastic A form of anemia in which the bone marrow fails to produce adequate numbers of peripheral blood elements. Anemia, Hypoplastic,Aplastic Anaemia,Aplastic Anemia,Anaemia, Aplastic,Aplastic Anaemias,Aplastic Anemias,Hypoplastic Anemia,Hypoplastic Anemias
D000744 Anemia, Hemolytic, Autoimmune Acquired hemolytic anemia due to the presence of AUTOANTIBODIES which agglutinate or lyse the patient's own RED BLOOD CELLS. Anemia, Hemolytic, Idiopathic Acquired,Autoimmune Haemolytic Anaemia,Autoimmune Hemolytic Anemia,Cold Agglutinin Disease,Hemolytic Anemia, Autoimmune,Acquired Autoimmune Hemolytic Anemia,Anemia, Hemolytic, Cold Antibody,Cold Antibody Disease,Cold Antibody Hemolytic Anemia,Idiopathic Autoimmune Hemolytic Anemia,Agglutinin Disease, Cold,Anaemia, Autoimmune Haemolytic,Anemia, Autoimmune Hemolytic,Autoimmune Haemolytic Anaemias,Autoimmune Hemolytic Anemias,Cold Agglutinin Diseases,Cold Antibody Diseases,Haemolytic Anaemia, Autoimmune
D000747 Anemia, Hypochromic Anemia characterized by a decrease in the ratio of the weight of hemoglobin to the volume of the erythrocyte, i.e., the mean corpuscular hemoglobin concentration is less than normal. The individual cells contain less hemoglobin than they could have under optimal conditions. Hypochromic anemia may be caused by iron deficiency from a low iron intake, diminished iron absorption, or excessive iron loss. It can also be caused by infections or other diseases, therapeutic drugs, lead poisoning, and other conditions. (Stedman, 25th ed; from Miale, Laboratory Medicine: Hematology, 6th ed, p393) Chlorosis,Anemias, Hypochromic,Chloroses,Hypochromic Anemia,Hypochromic Anemias
D014168 Transferrin An iron-binding beta1-globulin that is synthesized in the LIVER and secreted into the blood. It plays a central role in the transport of IRON throughout the circulation. A variety of transferrin isoforms exist in humans, including some that are considered markers for specific disease states. Siderophilin,Isotransferrin,Monoferric Transferrins,Serotransferrin,Transferrin B,Transferrin C,beta 2-Transferrin,beta-1 Metal-Binding Globulin,tau-Transferrin,Globulin, beta-1 Metal-Binding,Metal-Binding Globulin, beta-1,Transferrins, Monoferric,beta 1 Metal Binding Globulin,beta 2 Transferrin,tau Transferrin

Related Publications

Y Kohgo, and Y Niitsu, and H Kondo, and J Kato, and N Tsushima, and K Sasaki, and M Hirayama, and T Numata, and T Nishisato, and I Urushizaki
August 1990, British journal of haematology,
Y Kohgo, and Y Niitsu, and H Kondo, and J Kato, and N Tsushima, and K Sasaki, and M Hirayama, and T Numata, and T Nishisato, and I Urushizaki
February 1999, American journal of hematology,
Y Kohgo, and Y Niitsu, and H Kondo, and J Kato, and N Tsushima, and K Sasaki, and M Hirayama, and T Numata, and T Nishisato, and I Urushizaki
July 2000, [Rinsho ketsueki] The Japanese journal of clinical hematology,
Y Kohgo, and Y Niitsu, and H Kondo, and J Kato, and N Tsushima, and K Sasaki, and M Hirayama, and T Numata, and T Nishisato, and I Urushizaki
January 2001, Acta clinica Belgica,
Y Kohgo, and Y Niitsu, and H Kondo, and J Kato, and N Tsushima, and K Sasaki, and M Hirayama, and T Numata, and T Nishisato, and I Urushizaki
January 2002, Archives of internal medicine,
Y Kohgo, and Y Niitsu, and H Kondo, and J Kato, and N Tsushima, and K Sasaki, and M Hirayama, and T Numata, and T Nishisato, and I Urushizaki
January 2011, Journal of Ayub Medical College, Abbottabad : JAMC,
Y Kohgo, and Y Niitsu, and H Kondo, and J Kato, and N Tsushima, and K Sasaki, and M Hirayama, and T Numata, and T Nishisato, and I Urushizaki
October 1999, Haematologica,
Y Kohgo, and Y Niitsu, and H Kondo, and J Kato, and N Tsushima, and K Sasaki, and M Hirayama, and T Numata, and T Nishisato, and I Urushizaki
January 1993, Bulletin et memoires de l'Academie royale de medecine de Belgique,
Y Kohgo, and Y Niitsu, and H Kondo, and J Kato, and N Tsushima, and K Sasaki, and M Hirayama, and T Numata, and T Nishisato, and I Urushizaki
October 1998, Blood,
Y Kohgo, and Y Niitsu, and H Kondo, and J Kato, and N Tsushima, and K Sasaki, and M Hirayama, and T Numata, and T Nishisato, and I Urushizaki
September 1998, European journal of haematology,
Copied contents to your clipboard!