Laboratory Interpretation: Anemia of Chronic Disease (Inflammation)
These labs demonstrate normocytic anemia with elevated ferritin and low iron/TIBC/transferrin, a classic pattern of anemia of chronic disease (ACD) caused by underlying inflammation—not true iron deficiency. 1
Key Laboratory Findings
Anemia Pattern:
- Hemoglobin 10.8 g/dL indicates mild-to-moderate anemia 2, 3
- MCV 92.5 fL confirms normocytic anemia (normal red cell size) 1
- RDW 16.6% is elevated, suggesting mixed red cell populations or early iron-restricted erythropoiesis 1
Iron Studies Pattern - Diagnostic of ACD:
- Ferritin 480 μg/L is markedly elevated, excluding absolute iron deficiency and indicating either inflammation or adequate-to-increased iron stores 1
- Iron 39 μg/dL is low, reflecting inflammation-driven iron sequestration in macrophages, not true depletion 2, 3
- TIBC 188 μg/dL is low (normal ~250-450), characteristic of ACD where transferrin production decreases during inflammation 1
- Transferrin 131 mg/dL is low, consistent with inflammatory suppression of hepatic transferrin synthesis 1
- Transferrin saturation is approximately 21% (Iron 39/TIBC 188 × 100), which is borderline low but above the critical <16% threshold for absolute iron deficiency 1, 4
White Blood Cell Findings:
- Monocytes 13.1% are elevated (normal ~2-10%), supporting an inflammatory or infectious process 1
- Lymphocytes 22.7% are relatively low, which can occur with chronic inflammation 1
Pathophysiology Explanation
This pattern occurs because inflammation triggers:
- Increased hepcidin production by the liver, which blocks iron release from macrophages and reduces intestinal iron absorption 2, 5
- Iron becomes "trapped" in the reticuloendothelial system despite adequate total body stores 3, 6
- Cytokine-mediated suppression of erythropoietin function and erythroid progenitor cells 2, 7
- Shortened red blood cell lifespan 7
Differential Diagnosis Algorithm
Step 1: Rule out absolute iron deficiency
- Ferritin >100 μg/L essentially excludes true iron deficiency, even in the presence of inflammation 1
- Ferritin >150 μg/L rarely occurs with absolute iron deficiency 4
- Verdict: Absolute iron deficiency is excluded 1
Step 2: Distinguish ACD from functional iron deficiency
- Functional iron deficiency shows ferritin 100-700 μg/L with TSAT <20% and declining ferritin over time during erythropoietin therapy 1
- ACD shows stable or rising ferritin with low TIBC/transferrin 1
- Verdict: The low TIBC and low transferrin confirm ACD, not functional iron deficiency 1
Step 3: Identify the underlying inflammatory condition
- Look for: chronic infections (TB, HIV, endocarditis), autoimmune diseases (rheumatoid arthritis, lupus, inflammatory bowel disease), malignancy, chronic kidney disease, heart failure 2, 3, 6
- Check CRP and ESR to quantify inflammation 1
- Elevated monocytes suggest active inflammation or infection 1
Critical Pitfall to Avoid
Do NOT treat with oral iron supplementation based solely on the low serum iron. 1 In ACD, the problem is not iron deficiency but rather inflammation-driven iron sequestration. Oral iron will be poorly absorbed due to elevated hepcidin and may cause gastrointestinal side effects without improving anemia 2, 5. The elevated ferritin confirms adequate iron stores are present but inaccessible 1.
Management Priorities
Primary intervention: Identify and treat the underlying inflammatory disease. 2, 3, 6 This is the only approach that addresses the root cause and typically normalizes hemoglobin over time 2.
If anemia persists despite treating inflammation:
- Consider intravenous iron (not oral) if TSAT remains <20% and functional iron deficiency develops 1, 5
- Trial of IV iron: 50-125 mg weekly for 8-10 doses; if no erythropoietic response occurs, inflammatory block is confirmed and further iron should be stopped 1
- Erythropoiesis-stimulating agents may be considered for persistent symptomatic anemia 2, 5
Additional workup needed: