G۶PD deficiency might offer protection against fatal poisoning caused by Aluminum phosphide: A Case Series in North Iran

Introduction: Aluminum phosphide (AlP) is a highly toxic pesticide with a high mortality rate due to the lack of a specific antidote. Its toxicity is primarily mediated through the generation of phosphine gas, leading to severe oxidative stress, mitochondrial dysfunction, and multi-organ failure. Recent studies suggest that glucose-۶-phosphate dehydrogenase (G۶PD) deficiency may offer a protective effect by modulating oxidative stress pathways.Case Reports: We report three cases of patients with confirmed AlP poisoning who were also diagnosed with G۶PD deficiency. All patients presented to Razi hospital in Qaem Shahr, Mazandaran, Iran in February, July and December ۲۰۲۳ respectively with severe metabolic acidosis, hemolysis, hematuria, and systemic toxicity. They received intensive supportive care, including antioxidant therapy (N-acetylcysteine, vitamin C), magnesium sulfate, methylprednisolone, and aggressive hemodynamic support. Despite the usual high fatality rate associated with AlP poisoning, all three patients survived without major complications, suggesting a potential protective role of G۶PD deficiency.Discussion: G۶PD deficiency impairs the pentose phosphate pathway, reducing NADPH availability, which may limit oxidative damage induced by phosphine gas. This paradoxical effect could contribute to improved outcomes in AlP poisoning. Early recognition and aggressive supportive management were crucial in achieving positive clinical outcomes.Conclusion: These cases suggest that G۶PD deficiency may confer a protective advantage in AlP poisoning by altering oxidative stress responses. Further research is warranted to explore the underlying mechanisms and potential therapeutic implications for AlP toxicity management.

کلیدواژه ها:

Aluminum phosphide poisoning ، G۶PD deficiency ، Oxidative stress