Glucose-6-phosphate dehydrogenase (G6PD) deficiency is an inherited condition. Which of the following best describes the mechanism of its clinical consequence?

Correct answer: D. Reduced G6PD leads to decreased NADPH, impairing glutathione regeneration and making red blood cells vulnerable to oxidative destruction

• A. G6PD deficiency does NOT affect platelet function or bleeding time. It exclusively affects red blood cells via the pentose phosphate pathway. Bleeding disorders are associated with conditions like hemophilia, von Willebrand disease, or thrombocytopenia — not G6PD deficiency.
• B. Glycogen storage diseases (e.g., Pompe disease) involve glycogen accumulation, but not G6PD deficiency. G6PD is an enzyme in the pentose phosphate pathway; its deficiency leads to oxidative stress-induced hemolysis, not glycogen accumulation. These are entirely different metabolic pathways.
• C. This is incorrect. G6PD does not regulate glucose uptake into RBCs. RBCs take up glucose via GLUT1 transporters independently of G6PD. G6PD’s role is specifically in the pentose phosphate pathway (hexose monophosphate shunt), which generates NADPH for oxidative protection — not in glucose transport or glycolysis per se.
• D. CORRECT — G6PD deficiency reduces NADPH production in the pentose phosphate pathway. NADPH is essential for regenerating glutathione (the cell’s antioxidant defense). Without adequate glutathione, oxidizing drugs (dapsone, primaquine, nitrofurantoin, sulfonamides) and fava beans cause oxidative damage to RBC membranes, leading to hemolytic anemia. In dentistry: avoid aspirin in high doses; metronidazole, amoxicillin, and common LA agents are generally safe.