A patient with rheumatoid arthritis has hemoglobin 10.2 g/dL, MCV 78 fL, low serum iron, low total iron binding capacity, and ferritin of 210 ng/mL. Which mechanism best explains the restricted availability of iron for erythropoiesis in this condition?
- A Hepcidin induced internalization of ferroportin, trapping iron in macrophages and enterocytes ✓
- B Autoantibody mediated destruction of duodenal enterocytes
- C Competition between bacterial siderophores and transferrin for circulating iron
- D Suppression of erythropoietin production by inflammatory cytokines alone
Correct answer: A. Hepcidin induced internalization of ferroportin, trapping iron in macrophages and enterocytes
Explanation
Interleukin-6 released in chronic inflammation stimulates hepatic hepcidin secretion. Hepcidin binds ferroportin on macrophages and enterocytes, triggering its internalization and degradation, so absorbed and recycled iron cannot leave these cells and plasma iron falls. Reduced marrow response to erythropoietin contributes but is not the primary block on iron release, making option D incomplete. Low hepcidin states such as hereditary hemochromatosis produce the opposite picture.
Reference: Harrison's Principles of Internal Medicine, 21st ed.
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