Chapter 098. Iron Deficiency and Other
Hypoproliferative Anemias
(Part 2)
Figure 98-1

Internal iron exchange.
Normally about 80% of iron passing through the
plasma transferrin pool is
recycled from broken-
down red cells. Absorption of about 1 mg/d is required from
the diet in men, 1.4 mg/d in women to maintain homeostasis.
As long as transferrin saturation is maintained between 20–
60% and
erythropoiesis is no
t increased, iron stores are not required. However, in the event
of blood loss, dietary iron deficiency, or inadequate iron absorption, up to 40 mg/d
of iron can be mobilized from stores. RE, reticuloendothelial.
The iron-transferrin complex circulates in the plasma until it interacts with
specific transferrin receptors on the surface of marrow erythroid cells. Diferric
transferrin has the highest affinity for transferrin receptors; apotransferrin
(transferrin not carrying iron) has very little affinity. While transferrin receptors
are found on cells in many tissues within the body—and all cells at some time
during development will display transferrin receptors—the cell having the greatest
number of receptors (300,000 to 400,000/cell) is the developing erythroblast.
Once the iron-bearing transferrin interacts with its receptor, the complex is

However, to achieve a maximum proliferative erythroid marrow response to
anemia, additional iron must be available. With markedly stimulated
erythropoiesis, demands for iron are increased by as much as six- to eightfold.
With extravascular hemolytic anemia, the rate of red cell destruction is increased,
but the iron recovered from the red cells is efficiently reutilized for hemoglobin
synthesis. In contrast, with intravascular hemolysis or blood loss anemia, the rate
of red cell production is limited by the amount of iron that can be mobilized from
stores. Typically, the rate of mobilization under these circumstances will not
support red cell production more than 2.5 times normal. If the delivery of iron to
the stimulated marrow is suboptimal, the marrow's proliferative response is
blunted, and hemoglobin synthesis is impaired. The result is a hypoproliferative
marrow accompanied by microcytic, hypochromic anemia.
While blood loss or hemolysis places a demand on the iron supply,
conditions associated with inflammation interfere with iron release from stores and
can result in a rapid decrease in the serum iron (see below).