Intravenous pyridoxine-induced metabolic acidosis

Study objective: Pyridoxine hydrochloride, the antidote for isonicotinic ac id hydrazide (INH)-induced seizures, is available in solution at a concentr ation of 100 mg/mL at a pH of less than 3. Pyridoxine is often infused rapi dly in targe doses for INH-induced seizures. Effects of pyridoxine infusion on base deficit in amounts given for INH poisoning have not been studied i n human subjects. We hypothesized that this infusion would result in transi ent worsening of acidosis. Methods: We conducted a randomized, controlled crossover trial in human vol unteers. Five healthy volunteers (mean age, 35 years; range, 29 to 43 years ) were randomized to receive intravenous placebo (50 mL of normal saline so lution) or 5 g of pyridoxine (50 mL) over 5 minutes. A peripheral intraveno us catheter was established in each arm, and a heparinized Venous blood sam ple was obtained for base deficit at baseline and 3, 6, 10, 20, and 30 minu tes after infusion. After at least a 1-week washout period, the volunteers were assigned to the alternate arms of the experiments, thus acting as thei r own control subjects. Data were analyzed by using the 2-tailed paired t t est, controlling for multiple comparisons. Results: No difference was noted between groups at baseline. A statisticall y significant increased base deficit was noted after the pyridoxine infusio n versus control at 3 to 20 minutes but not at 30 minutes (P = .1). Maximal mean increase in base deficit (2.74 mEq/L) was noted at 3 minutes. Conclusion: A transient increase in base deficit occurs after the infusion of 5 g of pyridoxine in normal: volunteers.