Plasma butyrylcholinesterase as a marker of clinical outcome in diethyl organophosphorus insecticide poisoned patients treated with pralidoxime.

We are grateful for Lucyk and colleagues’ interest in our work on the value of plasma butyrylcholinesterase (BuChE) as a marker of pralidoxime effect. We note their interest in the association between early BuChE reactivation and clinical outcome. Most importantly, the original randomized controlled trial (RCT; Eddleston et al., 2009) assessed the effectiveness of pralidoxime in patients proven by laboratory analysis to have been poisoned by the organophosphorus (OP) insecticide, chlorpyrifos. Both red cell acetylcholinesterase (AChE; Eddleston et al., 2005) and BuChE (Konickx et al., 2013) inhibited by chlorpyrifos are rapidly reactivated by pralidoxime. Unfortunately, in a preplanned subgroup analysis of these patients we found no evidence of benefit from pralidoxime (case fatality: placebo arm 2/42 [4.8%] vs. pralidoxime arm 6/54 [11.1%]; odds ratio 3.34 [95% CI 0.57–19.37]) despite clear reactivation of AChE in diethyl OP poisoned patients (Eddleston et al., 2009, Fig. 3). Concerning intubation, this occurred earlier in patients receiving pralidoxime (and reactivating their cholinesterases) than those receiving placebo in the RCT (Eddleston et al., 2009, Fig. 7). Looking at patients with confirmed diethyl OP poisoning (the great majority of whom ingested chlorpyrifos), there was no reduction in need for intubation after pralidoxime administration (proportion intubated: placebo arm 6/50 [12.0%] vs. 10/62 [16.1%]; odds ratio 1.41 [95% CI 0.47–4.19], unpublished). Themedian (interquartile range, IQR) time to admission and treatment was 4.4 (2.9–7.6) h in the two arms of the study. Of note, patients in the placebo arm, with no reactivation of their red cell AChE (Eddleston et al., 2009) or BuChE (Konickx