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Letter

Response to Letter: “Lithium poisoning: the value of early digestive tract decontamination”

, , &
Page 807 | Received 27 May 2013, Accepted 29 May 2013, Published online: 18 Jun 2013

To the Editor:

Thank you for your interest in our article. As you know, only randomized controlled trials can be the gold standard to demonstrate the efficacy of a given therapy. As already expressed in the section on limitations in our paper, this was a retrospective study so there was obviously some bias inherent in this design. We do not claim to have demonstrated the efficacy of these treatments but we were able to show, using multivariate analysis, that there was a statistical association between early digestive tract decontamination and decreased severity.

To respond to your concerns, the delayed attendance of patients at the Emergency Department is the main reason for late or no digestive decontamination. These two concepts are interrelated and given the retrospective design of the study, the two groups could not be similar regarding this point. We cannot agree that the time elapsing between ingestion and presentation in the Emergency Department has an influence on peak serum lithium levels or PSS, insofar as the estimated doses ingested were not statistically different and the PSS during the first 12 h was similar in both groups.

Given the lack of consensus or guidelines regarding the management of lithium poisoning using with whole bowel irrigation or sodium polystyrene sulphonate, differences in treatment modalities were inevitable in a study of this type. But no rises in serum lithium concentrations were observed in patients following the initiation of whole bowel irrigation (n = 12).

Finally, the results of studies in humans have shown that sodium polystyrene sulphonate acts in two ways: it reduces the absorption of lithium by the gastrointestinal tractCitation1–3 but also ensures “gut dialysis” by accelerating the elimination of lithium from plasma.Citation4 We mentioned in our article that whole bowel irrigation appears to be more appropriate for gastrointestinal tract decontamination because the binding of sodium polystyrene sulphonate to unabsorbed lithium is relatively weak. However, it is not null (reduction in the AUC of between 11% and 48%, depending on the studiesCitation1–3). Moreover, sodium polystyrene sulphonate enables a significant acceleration in the elimination half-life of lithium (Li T1/2 ˜50% shorter).Citation4 This activity, alongside digestive adsorption, may also have influenced the clinical course of the patients in our study.

As expressed in our article, we are in strong agreement that further studies are now necessary on this subject.

Declaration of interest

The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.

References

  • Tomaszewski C, Musso C, Pearson JR, Kulig K, Marx JA. Lithium absorption prevented by sodium polystyrene sulfonate in volunteers. Ann Emerg Med 1992; 21:1308–1311.
  • Belanger DR, Tierney MG, Dickinson G. Effect of sodium polystyrene sulfonate on lithium bioavailability. Ann Emerg Med 1992; 21: 1312–1315.
  • Gehrke JC, Watling SM, Gehrke CW, Zumwalt R. In vivo binding of lithium using the cation exchange resin sodium polystyrene sulfonate. Am J Emerg Med 1996; 14:37–38.
  • Ghannoum M, Lavergne V, Seng Yue C, Ayoub P. Successful treatment of lithium toxicity with sodium polystyrene sulfonate: a retrospective cohort study. Clin Toxicol 2010; 48:34–41.

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