Reactive carbonyl compounds, carbonyl stress, and neuroinflammation in methyl alcohol intoxication

Hlusicka, Jiri; Löster, Tomáš; Lischková, Lucie; Vaněčková, Manuela; Diblik, Pavel; Urban, Pavel; Navrátil, Tomáš; Kačer, Petr; Kačerová, Tereza; Zakharov, Sergey

doi:10.1007/s00706-019-02429-z

Cited by 3 publications

(1 citation statement)

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“…Relatively high cancer mortality rate may be associated with acute exposure to metabolic formaldehyde produced by methanol oxidation. Possible mechanisms of reactive oxygen species production increased by formaldehyde and oxidative stress may play a role as well [43][44][45]. Alcoholic beverages per se, with low content of methanol, are classified by IARC as a Group 1 human carcinogen as well.…”

Section: Discussionmentioning

confidence: 99%

The impact of co-morbidities on a 6-year survival after methanol mass poisoning outbreak: possible role of metabolic formaldehyde

Zakharov

Rulíšek

Hlusicka

et al. 2019

Clinical Toxicology

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Context: The influence of co-morbid conditions on the outcome of acute methanol poisoning in mass poisoning outbreaks is not known. Objective: The objective of this is to study the impact of burden of co-morbidities, complications, and methanol-induced brain lesions on hospital, follow-up, and total mortality. Methods: All patients hospitalized with methanol poisoning during a mass poisoning outbreak were followed in a prospective cohort study until death or final follow-up after 6 years. The age-adjusted Charlson co-morbidity index (ACCI) score was calculated for each patient. A multivariate Cox regression model was used to calculate the adjusted hazards ratio (HR) for death. The survival was modeled using the Kaplan-Meier method. Results: Of 108 patients (mean age with SD 50.9 ± 2.6 years), 24 (54.4 ± 5.9 years) died during hospitalization (mean survival with SD 8 ± 4 days) and 84 (49.9 ± 3.0 years; p ¼ .159) were discharged, including 27 with methanol-induced brain lesions. Of the discharged patients, 15 (56.3 ± 6.8 years) died during the follow-up (mean survival 37 ± 11 months) and 69 (48.5 ± 3.3 years; p ¼ .044) survived. The hospital mortality was 22%, the follow-up mortality was 18%; the total mortality was 36%. Cardiac/respiratory arrest, acute respiratory failure, multiorgan failure syndrome, and arterial hypotension increased the HR for hospital and total (but not follow-up) mortality after adjustment for age, sex, and arterial pH (all p < .05). All patients who died in the hospital had at least one complication. A higher ACCI score was associated with greater total mortality (HR 1.22; 1.00-1.48 95% CI; p ¼ .046). Of those who died, 35 (90%) had a moderate-to-high ACCI. The Kaplan-Meier curve demonstrated that patients with a high ACCI had greater follow-up mortality compared to ones with low (p ¼ .027) or moderate (p ¼ .020) scores. For the patients who died during follow-up, cancers of different localizations were responsible for 7/15 (47%) of the deaths. Conclusions: The character and number of complications affected hospital but not follow-up mortality, while the burden of co-morbidities affected follow-up mortality. Methanol-induced brain lesions did not affect follow-up mortality. Relatively high cancer mortality rate may be associated with acute exposure to metabolic formaldehyde produced by methanol oxidation.

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Section: Discussionmentioning

confidence: 99%