A 55-year-old woman with long-standing rheumatoid arthritis presents with fatigue. Hemoglobin is 9.8 g/dL, MCV 74 fL, serum iron low, transferrin saturation 12%, and ferritin 190 ng/mL. CRP is elevated. The primary mechanism responsible for her anemia is:

• A Hepcidin-mediated degradation of ferroportin, trapping iron within macrophages ✓
• B Defective mitochondrial heme synthesis causing ring sideroblast formation
• C Autoimmune destruction of gastric parietal cells with loss of intrinsic factor
• D Imbalanced globin chain synthesis precipitating in red cell precursors

Explanation

Anemia of chronic disease results from inflammatory cytokines (IL-6) driving hepatic hepcidin release. Hepcidin binds ferroportin on enterocytes and macrophages, causing its internalization and degradation, so absorbed iron is sequestered rather than released into plasma. The key discriminator here is ferritin: values above 100 ng/mL indicate adequate stores and argue strongly against true iron deficiency, where ferritin would be low. Sideroblastic change, pernicious anemia, and thalassemia do not fit the ferritin and inflammatory picture.

Reference: Robbins and Cotran Pathologic Basis of Disease, 10th ed.

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Written and medically reviewed by the StethoPrep medical team.