## G6PD Deficiency and Antileprotic Drugs **Key Point:** Dapsone is an oxidizing agent that causes hemolysis in G6PD-deficient patients by generating reactive oxygen species that overwhelm the reduced glutathione (GSH) defense system. **High-Yield:** This is a frequently tested contraindication in NEET PG. Dapsone-induced hemolysis in G6PD deficiency is a classic pharmacogenetic interaction that every candidate must know. **Warning:** Do not confuse dapsone's hemolytic potential with its other side effects (methemoglobinemia, agranulocytosis). The G6PD-related hemolysis is specifically due to oxidative stress. ## Mechanism of Dapsone-Induced Hemolysis in G6PD Deficiency 1. Dapsone is metabolized to hydroxylamine and nitroso metabolites 2. These metabolites generate reactive oxygen species (ROS) 3. ROS oxidize hemoglobin to methemoglobin and damage RBC membranes 4. In G6PD deficiency, the pentose phosphate pathway is impaired → reduced NADPH production 5. Reduced NADPH → decreased reduced glutathione (GSH) regeneration 6. Without adequate GSH, RBCs cannot neutralize ROS → hemolysis ## Antileprotic Drugs and G6PD Status | Drug | G6PD Safe? | Mechanism if Unsafe | Severity | |------|-----------|-------------------|----------| | Dapsone | **No** | Oxidizing metabolites | Severe hemolysis | | Rifampicin | Yes | Not an oxidizing agent | — | | Clofazimine | Yes | Minimal oxidative stress | — | | Ofloxacin | Yes | Not an oxidizing agent | — | **Clinical Pearl:** Before starting dapsone in any patient, especially those from malaria-endemic regions (where G6PD prevalence is high), G6PD screening is mandatory. Even heterozygous females can develop hemolysis with dapsone. ## Why Dapsone? Dapsone is the only antileprotic in this list with significant oxidative potential that directly threatens RBC survival in G6PD-deficient individuals.
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