• Pathophysiology/Etiology
    • Anemia resulting from chronic inflammatory states (e.g., autoimmune diseases like RA, chronic infections like TB, malignancies, or chronic kidney disease).
    • Key mediator: Hepcidin. An acute-phase reactant produced by the liver in response to inflammatory cytokines (esp. IL-6).
    • Mechanism: ↑ Hepcidin → binds to and degrades ferroportin (iron exporter) on enterocytes and macrophages → ↓ intestinal iron absorption & ↓ iron release from macrophage stores (iron sequestration).
    • This leads to functional iron deficiency: adequate total body iron stores, but iron is unavailable for erythropoiesis.
    • Inflammatory cytokines also suppress erythropoietin (EPO) production and bone marrow response to EPO.
  • Clinical Presentation
    • Symptoms of anemia (fatigue, pallor, SOB) are often mild and may be overshadowed by the underlying chronic disease.
    • Associated with chronic inflammatory conditions, infections, or cancer.
    • Anemia is typically mild to moderate, with Hb rarely < 8 g/dL.
  • Diagnosis
    • CBC: Initially normocytic, normochromic anemia. Can become microcytic over time as iron-restricted erythropoiesis persists.
    • Iron Studies (Classic Pattern):
      • ↓ Serum Iron
      • ↓ Total Iron-Binding Capacity (TIBC) / Transferrin
      • ↑/Normal Serum Ferritin (an acute phase reactant, reflects high iron stores).
      • ↓ Transferrin Saturation (% sat)
    • Low reticulocyte count for the degree of anemia.
    • Elevated inflammatory markers (e.g., CRP, ESR).
  • DDx (Differential Diagnosis)
    • Iron Deficiency Anemia (IDA): The key differential. Can also coexist with ACD.
      • IDA vs. ACD: In IDA, TIBC is high and ferritin is low. In ACD, TIBC is low and ferritin is high/normal.
      • A serum ferritin <100 ng/mL in an inflammatory state suggests concomitant IDA.
    • Thalassemia: Microcytic anemia with normal/high iron studies; diagnosed via Hb electrophoresis.
    • Sideroblastic Anemia: Can be microcytic; diagnosed by ring sideroblasts on bone marrow biopsy.
  • Management/Treatment
    • Primary goal: Treat the underlying chronic disease. This is the most effective long-term strategy.
    • Iron supplementation is generally not effective and avoided unless true co-existing iron deficiency is confirmed, as the issue is iron utilization, not absolute deficiency.
    • Erythropoiesis-stimulating agents (ESAs) (e.g., recombinant erythropoietin) may be used for anemia of CKD or chemotherapy-induced anemia.
    • RBC transfusions for severe, symptomatic anemia (e.g., Hb < 7-8 g/dL or hemodynamic instability).
  • Key Associations/Complications
    • Associated Conditions: Rheumatoid arthritis (RA), SLE, inflammatory bowel disease (IBD), chronic kidney disease (CKD), chronic infections (TB, HIV), and malignancy.
    • Buzzwords: “Anemia of inflammation,” high hepcidin, sequestered iron, low TIBC, high ferritin.