A 19-year-old man develops sudden dark urine, jaundice, and abdominal pain two days after taking primaquine for malaria prophylaxis. Hb drops from 13 to 7.5 g/dL with a normal MCV, high LDH and low haptoglobin. Peripheral smear shows red cells with a portion of cytoplasm appearing bitten out. The underlying defect involves:
- A Autoantibodies against band 3 protein causing extravascular haemolysis
- B Deficiency of glucose-6-phosphate dehydrogenase with denatured haemoglobin removed by splenic macrophages ✓
- C Defective assembly of GPI anchors leading to complement lysis
- D Mutation in the ankyrin gene reducing membrane stability
Correct answer: B. Deficiency of glucose-6-phosphate dehydrogenase with denatured haemoglobin removed by splenic macrophages
Explanation
Primaquine generates oxidative stress; in G6PD deficiency, reduced glutathione cannot be regenerated, so oxidised haemoglobin precipitates as Heinz bodies attached to the membrane. Splenic macrophages pluck these inclusions out, producing the characteristic bite cells seen here. Band 3 autoantibodies describe warm AIHA, GPI anchor defects describe paroxysmal nocturnal haemoglobinuria, and ankyrin mutations cause hereditary spherocytosis; none of these are drug triggered with bite cells.
Reference: Robbins and Cotran Pathologic Basis of Disease, 10th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.