Anemia of chronic disease (ACD) is difficult to
define as its eitology and pathogenesis is not clear. ACD is
associated with an underlying disease (usually inflammation,
infection, or malignancy), but is without apparent cause
(not due to a lack of the nutrients iron, vitamin B 12, or
folic acid). ACD resolves when the underlying disease
ACD is the most common anemia in hospitalized patients.
Anemia of chronic disease with normochromic
The anemia is usually mild (Hct = 30-40%), but may be
lower. The RBCs of ACD are usually normochromic/normocytic,
but, especially in time, may be mildly
hypochromic/microcytic (mild decrease MCV and decrease
Typically ACD is associated with low serum iron, normal
or low transferrin, low transferrin saturation, and high
serum ferritin. Bone marrow iron stores are usually
Ferritin (an acute phase reactant) may be elevated in
inflammation. Low-normal levels of ferritin in a patient
with acute inflammation may be consistent with Fe
The primary mechanism for the pathogenesis of ACD is
decreased red blood cell production. Why red blood cell
production is decreased is unclear.
It is known that inflammatory and infectious disorders
release factors (IL-1, tumor necrosis factor, etc.) that
suppress erythropoiesis. IL-1 causes the release of
lactoferrin from neutrophils. Lactoferrin binds Fe more
avidly than transferrin and thus may shunt Fe to macrophages
rather than to erythroid precursors.
Abnormalities of Fe mobilization from marrow stores are
also recognized which may prevent reutilization of Fe
salvaged from dead RBCs.
Note: The decreased availability of iron
(hypoferremia) in ACD may reduce the amount of
available Fe below the level necessary for optimal
In most instances treatment of ACD requires treatment of
the underlying disease.
Inappropriately low serum erythropoietin levels for the
degree of anemia have been reported in ACD. Human
recombinant erythropoietin (EPO) therapy can correct the
anemia in such cases.
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