Pathology Thread

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 resolves.

ACD is the most common anemia in hospitalized patients.

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 MCHC).

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 increased.

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 deficiency.

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.

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.