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Erythropoese bei Eisenmangel

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Zusammenfassung

Die Kinetik der Erythroblastenproliferation wurde bei 5 Patienten mit Infekt- und Tumoranämie, 7 Patienten mit Eisenmangelanämie und 2 Patienten mit Blutungsanämie durch quantitative14C-Autoradiographie untersucht. Im Vergleich zu einem Kollektiv von 5 Normalpersonen wurde bei Infekt- und Tumoranämie ebenso wie bei der Eisenmangelanämie ein stark verzögerter Erythroblastenumsatz gefunden, während dieser bei der Blutungsanämie normal bis beschleunigt war. Die Verzögerung beruht auf einer mit der Erythroblastenreifung abnehmenden Proliferations- und Reifungsgeschwindigkeit. Hinweise auf Änderungen der Zahl von Teilungsschritten bei Infekt-, Tumor- und Eisenmangelanämie ergaben sich ebensowenig wie ein intramedullärer Erythroblastenuntergang.

Das zur Anämie führende Mißverhältnis zwischen Verlust und Neubildung von Erythrozyten läßt bei den 3 Patientengruppen unterschiedliche Konstellationen erkennen: Bei der Blutungsanämie liegt das Schwergewicht im Umfang des Blutverlustes. Die Insuffizienz der Nachbildung ist am Erythroblastenumsatz noch nicht erkennbar. Bei der Eisenmangel-, Infekt- und Tumoranämie kann der nur mäßig beschleunigte Erythrozytenverlust auf Grund mehrerer Hemmnisse nicht kompensiert werden: Der Erythroblastenumsatz ist vermindert, und zusätzlich geht ein allerdings eher geringer Teil der ausreifenden Zellen zugrunde, wahrscheinlich im Stadium der Retikulozyten. Der wichtigste Faktor ist das Unvermögen des Knochenmarks, mit einer adäquaten Hyperplasie zu antworten. Beim Infekt und Tumor fehlt sogar jegliche Kompensation durch eine erythropoetische Hyperplasie.

Summary

The kinetics of erythroblast proliferation were studied by means of quantitative14C-autoradiography in 5 patients showing anemia due to infection or malignancy, in 7 patients suffering from iron deficiency anemia, and in two individuals with bleeding anemia. Compared with a group of 5 healthy persons a markedly reduced turnover of erythroblasts was found in the anemia due to infection, malignancy, and iron defiency, whereas this turnover was normal or increased in the case of bleeding anemia. The reduction is caused by a progressively decreasing rate of erythroblast proliferation and maturation with advancing development into mature cells. No indications of a change in the number of cell divisions were found in the anemia of infection, malignancy, and of iron deficiency, nor was there evidence of an intramedullary death of nucleated red cell precursors.

The imbalance between production and loss of red cells causing anemia shows a different pattern in the 3 groups of disease: In bleeding anemia the insufficiency of supply is not yet apparent from the rate of erythroblast turnover giving weight to the factor of blood loss. In anemia due to infection, malignancy, and iron deficiency the but moderately increased rate of red cell destruction cannot be compensated because of several impairments: The rate of erythroblast turnover is reduced, and, in addition, a moderate portion of maturing cells is destroyed, probably at the reticulocyte stage. As the most significant factor, the bone marrow is unable to compensate the anemia by an effective erythroblast hyperplasia. In iron deficiency this hyperplasia is inadequately low, in infection and malignancies, however, it is more or less missing.

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Authors and Affiliations

  1. Institut für Hämatologie der Gesellschaft für Strahlen- und Umweltforschung, München

    Peter Dörmer & Barbara Lau

  2. Lehrstuhl für Hämatologie der Universität München, Deutschland

    Peter Dörmer & Barbara Lau

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  1. Peter Dörmer
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  2. Barbara Lau
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Herrn Prof. Dr. R. Marx zum 65. Geburtstag gewidmet

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Dörmer, P., Lau, B. Erythropoese bei Eisenmangel. Blut 34, 453–464 (1977). https://doi.org/10.1007/BF00996872

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