The anemia of prematurity is an ill defined entity with a multicausative pathogenesis.
Therefore, before one can speak about news, one has to analyze, which are the facts,
which are proven? What is in doubt?
It is well known that the erythropoiesis in fetusses as well as in children and adults
is mainly regulated by one of the multiple hematopoietic growth factors, a 34 KD
glycoprotein named erythropoietin(Epo), which-beyond the fetal period is produced in
peritubular cells of the kidney. In the human fetus, however, liver macrophages and
v.Kupfer cells as well as hepatocytes appear to be the primary source of erythropoietin.
The Epo production shifts from the liver to the kidney sometime during the last three
months of fetal life.
Epo induces proliferation and differentiation of erythroid precursors. This holds true
also for preterm infants. At least two receptors are active, one stimulating the
hemoglobin synthesis, one stimulating the synthesis of membrane constituents.
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