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Letter

Reply to letter re paper “Methanol and ethylene glycol acute poisonings—predictors of mortality”

Page 226 | Received 12 Jan 2012, Accepted 12 Jan 2012, Published online: 10 Feb 2012

To the Editor:

We are grateful for the interest in our paper “Methanol and ethylene glycol acute poisonings—predictors of mortality.” I have looked over the four papers cited in detail to reassess why they were not originally included.

The paper by Naraqi S et al. published in Aust NZ J Med (1979;9:65–68) contained pH data, but no anion gap or osmolal gap data. It was deemed unsuitable as individual patient data were not reported, some pH data were post treatment with bicarbonate, and there was ingestion of ethanol prior to poisoning in some patients—where ethanol is protective and acts as “treatment.”

The paper by Sanaei-Zadeh et al. published in J Med Toxicol (2011;7:189–194) assessed blood glucose and only reported mean and range data for pH measurements, with no data on anion gap or osmolal gap. It was also unsuitable due to the lack of individual data presented; additionally, the age ranged from 10 years of age and our inclusion criterion was restricted to adults (children less than 16 years were excluded).

The paper by Paasma et al. published in Clin Toxicol (Phila) (2007;45:152–157) reported pH data, but again no anion gap or osmolal gap data. It too was unsuitable due to the lack of individual patient data, and also again the lowest age category (< 30years) could not be guaranteed to exclude children.

The paper by Hovda et al. published in J Intern Med (2005;258: 181–190) did report individual data for the 51 patients followed and did report pH, anion gap, and osmolal gap data. However, some of these patients received ethanol treatment prior to the pH, anion gap, and osmolal gap data being collected; hence, they were excluded from our study. On re-examining this paper, the 10 patients to whom this applied were identified, so the others may have been able to be included. However, the discussion in this paper does question whether these patients were also alcoholics and whether co-ingestion of ethanol with methanol also occurred—again this would have acted as “treatment.”

In light of this, we do feel our analysis was appropriate. In our inclusion criteria, we may have been better to state that “reports of poisonings with methanol and ethylene glycol were extracted from the literature reports which reported individual patient data on at least one of the three biomarkers: osmolal gap, anion gap and arterial blood pH.” We would also like to emphasize that these four papers mentioned looked at methanol poisoning for which the three biomarkers behave in a predictable manner. The purpose of our paper was to compare this to the case for ethylene glycol—where it is less clear how the biomarkers should be interpreted. Thus, we are satisfied that we have not missed out any cases that could have been included, so we do not feel that our conclusions are questionable. We would be happy to reassess these conclusions if data on these biomarkers, for both methanol and ethylene glycol, did become available in the future.

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