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Chapter 13: Anemia of Chronic Inflammation

DEFINITION

Anemia associated with chronic infection, inflammatory or neoplastic disease.
Also referred to as anemia of chronic disease.
One to 2 months of sustained disease is required for anemia to develop.
Anemia is moderate, with a hemoglobin level between 7 and 11 g/dL, and is rarely symptomatic.
The characteristic features of anemia of inflammation (AI) are listed in Table 13–1.

TABLE 13–1LABORATORY STUDIES OF IRON METABOLISM IN IRON-DEFICIENCY ANEMIA (IDA), ANEMIA OF INFLAMMATION (AI), AND A COMBINATION OF THE TWO.

TABLE 13–1 LABORATORY STUDIES OF IRON METABOLISM IN IRON-DEFICIENCY ANEMIA (IDA), ANEMIA OF INFLAMMATION (AI), AND A COMBINATION OF THE TWO.

IDA (n = 48)

AI (n = 58)

Combination (n = 17)

Hemoglobin, g/L

93 ± 16 (96)

102 ± 12 (103)

88 ± 20 (90)

MCV, fL

75 ± 9 (75)

90 ± 7 (91)

78 ± 9 (79)

Iron, μmol/L (10–40)

8 ± 11 (4)

10 ± 6 (9)

6 ± 3 (6)

Transferrin, g/L (2.1–3.4m, 2.0–3.1f)

3.3 ± 0.4 (3.3)

1.9 ± 0.5 (1.8)

2.6 ± 0.6 (2.4)

Transferrin saturation, %

12 ± 17 (5.7)

23 ± 13 (21)

12 ± 7 (8)

Ferritin, μg/L (15–306m, 5–103f)

21 ± 55 (11)

342 ± 385 (195)

87 ± 167 (23)

TfR, mg/L (0.85–3.05)

6.2 ± 3.5 (5.0)

1.8 ± 0.6 (1.8)

5.1 ± 2.0 (4.7)

TfR/log ferritin

6.8 ± 6.5 (5.4)

0.8 ± 0.3 (0.8)

3.8 ± 1.9 (3.2)

Reproduced with permission from Punnonen K, Irjala K, Rajamaki A: Blood 89:1052, 1997.

Source: Williams Hematology, 8th ed, Chap. 37, Table 37–2, p. 506.

Inflammation leads to interleukin (IL)-6 production, which induces hepatocyte hepcidin production, which blocks intestinal iron absorption and iron release from macrophages and hepatocytes. Hepcidin binds to and leads to feroportin degradation, the primary cell surface iron exporter.
Impaired intestinal iron uptake and impaired release of iron from macrophages leads to a low level of serum iron and consequent low saturation of transferrin.
Enhanced activity of macrophages increases erythrocyte destruction.
Production of erythropoietin (EPO) is decreased in response to anemia, and the ability of erythroid precursors to respond to EPO is impaired, both also related to inflammatory cytokine production (IL-1, tumor necrosis factor, interferons).