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Discussion Starter · #1 ·
So I'm well aware of sulfonamide drugs being able to cause hemolysis in G6PD Deficiency, but I can't seem to understand how.

I know they antagonize the synthesis of folate but I don't understand what that has to do with HMS?
 

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Have you read biochem? When you do it you'll undersand. Actually G6PD is the major enzyme required for generation of NADPH ( in the step where g6pd converts glucose6P into 6phosphogluconate. NAPDH is produced as a byproduct. This NADPH has the capability to lend its hydrogen to glutathione thus reducing glutathione. The reduced glutathione causes scavenging of free radicals like H2O2 converting them into H2O. As a result glutathione is oxidized, now again we need to reduce this glutathione inorder for it to be effective again.. Which u already know takes place cz of G6PD.
 

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Discussion Starter · #4 ·
Sulfa drugs produce free radicals and G6PD deficient individuals are unable to detoxify them causing RBC damage
The first part of your response, I am well aware. But HOW do sulfa drugs place stress on the hexomonophosphate shunt? How do they produce free radicals? The biochem does not go into that. In fact most websites just say it puts "stress" on the system and causes hemolysis.

I did just find a source that lists sulfonamides as "alanine radicals"...but the mechanism of action is still unknown. It seems like we know sulfa drugs can precipitate RBC destruction from empirical evidence but nothing from a theoretical perspective.
 

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Oh sorry for misunderstanding your question :) well i'm not sure about the mechanism of free radical production by sulfa drugs probably something to do with their chemical structure etc. i dont think thats too high yield on the USMLE.
 
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