Page 42 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

Erythrocyte Turnover: Abnormalities, Compensation, and Diagnosis
Proliferation and differentiation of the ery- mality of cell formation (→ A3) because the
throid precursor cells up to the mature eryth- second, theoretically possible cause, a prolon-
rocytes takes barely a week. This time can be gation of RBC life-span, does not occur. On the
shortened to a few days if erythropoiesis is other hand, a longer lasting increase in reticu-
stimulated, for example, by an increase in cell locyte numbers (reticulocytosis) is evidence for
loss (hemolysis or bleeding). As the average a chronically shortened life-span in the circu-
life-span of RBCs in peripheral blood is more lation on the part of the RBCs (chronic bleed-
than 100 days, a brief disorder of cell forma- ing or hemolysis). Transitory reticulocytosis is
tion is not detectable, but increased cell loss a sign of stimulated erythropoiesis, for exam-
quickly results in anemia. (With neutrophil ple, after acute blood loss, after acute hemoly-
leukocytes, whose differentiation time is sis, or after correction of abnormal cell forma-
roughly as long, the reverse is the case, be- tion (with a high level of erythropoietin;
cause their life-span in peripheral blood is → B2,3).
only about 10 hours: neutropenia occurs if ! When erythrocytes are broken down in
there is an acute disorder of cell formation, macrophages (→ p. 30), bilirubin, formed from
but not after cell loss.) liberated heme, is excreted in the bile after
With a survival time of ca.10 sec and a total conjugation in the liver. The concentration of
7
RBC count of ca. 1.6 × 10 13 in blood, the rate unconjugated (“indirect”) bilirubin in serum
Blood of formation is 1.6 million erythrocytes per is increased in hemolysis (→ A4 and p.164ff.),
second. If necessary, this production rate in-
but in some circumstances also if hemoglobin
3 creases up to tenfold without causing bone turnover is increased as a result of ineffective
marrow exhaustion. Life-long hemolytic ane- erythropoiesis.
mia, for example, can thus largely be compen- ! The life-span of RBCs (shortened in hemo-
sated. lytic anemia; → A5) as well as their total vol-
Disorders of erythrocyte metabolism, be it ume can be measured by marking the eryth-
abnormal erythropoiesis in its various steps rocytes in vitro with radioactive 51 Cr (binding
(→ A), a shortened life-span, or chronic blood Cr to the Hb-β chain) and then re-infusing
loss, can be differentiated by means of a num- them. As 51 Cr is released in hemolysis and
ber of diagnostic parameters: then excreted by the kidneys, the erythrocyte
! Stem cells obtained by bone marrow punc- life-span can be calculated from the loss of
ture can be stimulated to proliferate and differ- radioactivity measured daily. Total erythrocyte
entiate by erythropoietin in a cell culture. Col- volume can be determined from the amount of
onies of more or less differentiated, hemoglo- 51 Cr injected and the initial 51 Cr concentration
bin-containing cells (E) are formed in this way in blood, using the principle of indicator dilu-
(burst-forming units [BFU-E] or colony-forming tion.
units [CFU-E]). Their number is decreased if ! Measuring erythropoietin (→ A6). Lowered
the anemia is caused by abnormal cell forma- concentration of plasma erythropoietin sug-
tion; it is increased if the cells are lost in a late gests the anemia is caused nephrogenically
stage of differentiation (erythroblast, erythro- (→ B4). However, most anemias are associated
cyte) (→ A1). with a (compensatory) increase in erythro-
! Erythroblasts can be morphologically iden- poietin concentration (→ B2,3).
tified and quantified in a stained bone marrow
sample. They decrease in number in aplasia
and in defects of stem cell differentiation;
they increase if erythropoiesis is stimulated,
for example, by increased hemolysis (→ A2).
! The efficiency of the entire erythropoiesis can
be measured by determining the number of re-
32 ticulocytes (→ p. 30). If the number of reticulo-
cytes is reduced, one must assume an abnor-
Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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