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Medication-induced hemolytic anemia -> glucose-6-phosphate dehydrogenase (G6PD) deficiency. Exposure to oxidant drugs (eg, antimalarial drugs) or infections (eg, hepatitis A) -> production of peroxides and free radicals. Normally quickly inactivated by reduced glutathione (GSH). GSH is then replenished via glutathione reductase, which requires reduced nicotinamide adenine dinucleotide phosphate (NADPH). G6PD regenerates NADPH from NADP+. As such, the regeneration of GSH is impaired in G6PD-deficient individuals, and the peroxides and free radicals accumulate -> denaturation of hemoglobin -> formation of methemoglobin and denatured globin that attach to the RBC membranes (aka Heinz bodies) -> destruction by reticuloendothelial macrophages.

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