Table 2.

Laboratory evaluation of absolute iron deficiency anemia and anemia of inflammation severe enough to be considered for transfusion

Iron sufficientAbsolute iron deficiency anemia Anemia of inflammation with functional iron deficiency Combined absolute and functional iron deficiency§ 
Bone marrow iron stores Normal Absent Present or increased Absent 
Hb (g/dL) Normal Low Low Low 
Mean corpuscular volume (MCV) (fL) Normal Decreased Slightly decreased or normal Decreased 
Red cell distribution width (RDW) (%) Normal Increased Slightly increased or normal Increased 
Transferrin saturation (%)  Normal <20% Decreased <20% 
Ferritin (μg/L) Normal Decreased Increased Increased 
Soluble transferrin receptor (mg/L) Normal Increased Normal Increased 
Hepcidin (ng/mL)  Normal Decreased Increased Normal or decreased 
Iron sufficientAbsolute iron deficiency anemia Anemia of inflammation with functional iron deficiency Combined absolute and functional iron deficiency§ 
Bone marrow iron stores Normal Absent Present or increased Absent 
Hb (g/dL) Normal Low Low Low 
Mean corpuscular volume (MCV) (fL) Normal Decreased Slightly decreased or normal Decreased 
Red cell distribution width (RDW) (%) Normal Increased Slightly increased or normal Increased 
Transferrin saturation (%)  Normal <20% Decreased <20% 
Ferritin (μg/L) Normal Decreased Increased Increased 
Soluble transferrin receptor (mg/L) Normal Increased Normal Increased 
Hepcidin (ng/mL)  Normal Decreased Increased Normal or decreased 

Absolute iron deficiency is a deficit in total body iron with absent or reduced iron stores that cannot meet erythroid and tissue iron needs. Absolute iron deficiency develops from an (1) inadequate dietary iron absorption, (2) increased iron requirements, and (3) iron loss, or some combination of these causes. Increased iron loss is almost always due to blood loss (from GI, gynecological, and less commonly, urinary, or respiratory sources).9 

Anemia of inflammation, also known as the anemia of chronic disease, results from sustained functional iron deficiency. Although functional iron deficient erythropoiesis is the principial cause of the anemia of inflammation, coexisting hepcidin-independent mechanisms may also be involved, including inflammatory suppression of erythropoiesis, decreased erythropoietin secretion, and a reduced erythrocyte survival.9 

Functional iron deficiency, common in patients that are hospitalized or chronically ill, develops with sufficient or increased body iron stores that are unable to meet iron requirements because of iron sequestration produced by increased hepcidin or increased erythropoietic demand resulting from endogenous (hemolysis) or exogenous (erythropoiesis-stimulating agents) causes.

§

Absolute and functional iron deficiency may coexist.

With decreased transferrin saturation, the TIBC is generally increased with absolute iron deficiency and decreased with functional iron deficiency.

Laboratory measurement of hepcidin is a research procedure at present.

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