A 60-year-old diabetic woman has unexplained anemia with iron studies showing low serum iron, normal ferritin, and iron overload confirmed on MRI. Serum ceruloplasmin is undetectable and genetic testing shows a homozygous CP gene mutation. The anemia results from failure of which process?

• A Endocytosis of transferrin receptor complexes in erythroid precursors
• B Reduction of dietary ferric iron by duodenal cytochrome b reductase
• C Oxidation of ferrous iron exported from macrophages and hepatocytes by ceruloplasmin ferroxidase activity ✓
• D Proteolytic cleavage of membrane ferroportin by hepcidin

Explanation

Aceruloplasminemia is caused by CP gene mutations abolishing ceruloplasmin ferroxidase activity. Iron released from stores as Fe2+ must be oxidized to Fe3+ before loading onto transferrin; without this oxidation, iron becomes trapped inside macrophages and hepatocytes, producing parenchymal iron overload together with iron-restricted anemia and diabetes. Hepcidin cleavage of ferroportin is intact here, and DMT1 reduction concerns luminal absorption rather than iron egress from storage cells.

Reference: Williams Hematology, 10th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.