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Fetal Hb Production during Acute Erythroid Expansion: I. OBSERVATIONS IN PATIENTS WITH TRANSIENT ERYTHROBLASTOPENIA AND POST‐PHLEBOTOMY
Author(s) -
Papayannopoulou Th.,
Vichinsky E.,
Stamatoyannopoulos G.
Publication year - 1980
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.1980.tb08707.x
Subject(s) - reticulocytosis , erythropoiesis , phlebotomy , immunology , andrology , fetal hemoglobin , medicine , anemia , biology , fetus , endocrinology , pregnancy , genetics
Summary. In order to study fetal haemoglobin production during acute erythroid expansion we did sequential measurements of Hb F‐containing erythrocytes (F‐cells) and of relevant haematological parameters in 10 subjects recovering from erythroid aplasia, iron deficiency anaemia or following phlebotomy. An increased production of F‐cells was consistently observed during the acute marrow expansion, but there were significant differences in the maximum F‐cell response among individuals. These differences could not be explained by differences in the degree of anaemia alone, nor could they be correlated with the level of peak reticulocytosis. Two patients who reached the highest F‐cell numbers were probably carriers of heterocellular hereditary persistence of Hb F, suggesting that this gene may play a role in determining the magnitude of F‐cell production in anaemic patients. It is speculated that the main reason for the consistently observed increase in F cell production during acute marrow expansion is the premature terminal differentiation of earlier erythroid precursors (burst forming units; BFUe). This proposition is in accord with observations in vitro which suggest that Hb F is expressed in erythroid clones derived from BFUe's. It is further proposed that differences in the degree of BFUe recruitment may underly the disparities in Hb F response among individuals subjected to similar anaemic stimuli.