8  Anemia of Inflammation

Key Points
  • AI = most common anemia in malignancy, autoimmune dz, chronic infection
  • Labs: normo/microcytic, ↓ retic, ↓ Fe, ↓/normal TSAT, normal/↑ ferritin
  • Path: IL-6 → ↑ hepcidin → Fe sequestration (iron-restricted erythropoiesis)
  • Tx: treat underlying dz; IV Fe only if concurrent IDA proven

8.1 Overview

  • AI = most common anemia cause in inflammatory dz worldwide (2nd after IDA)
  • Etiologies: malignancy, autoimmune dz, chronic infection, trauma, acute illness
  • Children: minor bacterial/viral infection → mild normocytic anemia w/ blunted retic (self-limited)
  • Also: COPD, CHF, obesity, aging → chronic systemic inflammation

8.2 Pathophysiology

Cytokine-mediated: - IL-6, TNF, IFN-γ → ↓ EPO production relative to Hb level - ↓ EPO responsiveness - ↓ BM precursor survival

Hepcidin-iron axis (central): - Hepcidin = iron regulatory hormone (↑ by inflammation via STAT3) - Binds ferroportin → ↓ GI iron absorption & ↓ Fe release from macrophages - Results: iron sequestration in macrophages/hepatocytes = iron-restricted erythropoiesis

8.3 Diagnosis

Clinical: normo/microcytic anemia (Hb 7-11) in inflammatory dz background - Evolves: microcytic & hypochromic over time - Blunted retic count is key

Labs:

Anemia of Inflammation
Parameter AI IDA AI/IDA
Ferritin Normal/↑
Serum Fe
TSAT (%)
TIBC Normal/↓ Normal
MCV Normal/↓
RDW Normal/↑
sTfR <2
% Hypochromic RBCs Normal/↓

Key distinction: - ↑ ferritin = expected in AI (acute phase reactant), argues AGAINST IDA alone - sTfR/log ferritin ratio > useful when inflammatory stress present - AI/IDA: sTfR ≥2; AI alone: sTfR <1

8.4 Treatment

Primary: - Treat underlying dz (cornerstone) - Hb improvement = better indicator of dz control than Fe supplementation alone

Iron supplementation: - Only if AI/IDA proven (not just suspected) - Confirm: sTfR ↑, TSAT <20%, hypochromic RBCs, RBC Hb content ↓ - IV Fe > PO (↑ hepcidin limits absorption); expect slow response - Response: gradual Hb ↑ over weeks (competing AI effects)

Erythropoietin-stimulating agents (ESAs): - Limited use outside CKD/myelofibrosis (not approved for AI alone) - ↑ adverse events w/ malignancy; caution w/ Hb correction

Future: - JAK inhibitors (baricitinib, momelotinib): ↓ hepcidin → Fe availability ↑ - Hepcidin-ferroportin axis targeting (trials ongoing)

Clinical Pearl
  • ↑ ferritin = argues AGAINST IDA alone (reflects inflammation, not Fe stores)
  • Distinguish: true IDA (ferritin ↓, TIBC ↑) vs. IDA/AI combo (ferritin normal/↑, TIBC normal)
  • Document hypochromia (RBC Hb content, % hypochromic RBCs) before Fe supplementation