Publication | Closed Access
Lactic Acidosis, a Complication of Papaverine Overdose
12
Citations
15
References
1981
Year
Lactic AcidosisPapaverine-induced Acid-base DisturbanceBiochemistryMitochondrial FunctionSevere Lactic AcidosisMedicinePhysiologyLipid PeroxidationPoisoningToxicologyMitochondrial ToxinMetabolomicsMetabolismPharmacologyRedox BiologyClinical ToxicologyOxidative Stress
A 61-year-old female developed severe lactic acidosis after ingesting approximately 15 g of papaverine. This was associated with intense respiratory alkalosis, elevated plasma pyruvate, mild hyperglycemia, and hypokalemia. Severe lactic acidosis with elevated plasma pyruvate level and profound respiratory drive observed in this patient can be explained by the inhibition of mitochondrial oxidative reactions by papaverine. The clinical and biochemical features of papaverine-induced acid-base disturbance closely resemble those caused by salicylates, another known mitochondrial toxin.
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