A patient with Plasmodium vivax malaria is started on primaquine for radical cure. Prior to initiating treatment, testing for G6PD deficiency is mandatory because primaquine undergoes hepatic metabolism to reactive oxygen species that preferentially damage:
- A G6PD-deficient red blood cells unable to regenerate NADPH for glutathione reduction ✓
- B Reticulocytes with high RNA content
- C Schizont-infected erythrocytes expressing parasite aldolase
- D Mature hepatocytes containing CYP2D6 isoenzyme
Explanation
Primaquine is metabolized to reactive intermediates (hydroxylated metabolites) that generate oxidative stress. Normally, red blood cells detoxify these via the glutathione reductase system, which requires NADPH regenerated by glucose-6-phosphate dehydrogenase (G6PD). In G6PD-deficient individuals, NADPH cannot be regenerated, glutathione is depleted, and oxidative haemolysis of red blood cells results, causing acute intravascular haemolytic anaemia. This particularly affects older RBCs but can cause severe haemolysis across all red cell ages in severe deficiency. CYP2D6 is needed to activate primaquine; G6PD deficiency does not affect hepatic metabolism.
Reference: Ananthanarayan & Paniker's Textbook of Microbiology, 11th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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