Leukotriene-mediated neuroinflammation, toxic brain damage, and neurodegeneration in acute methanol poisoning

Result code in IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F61388955%3A_____%2F17%3A00471295" target="_blank" >RIV/61388955:_____/17:00471295 - isvavai.cz</a>

Alternative codes found

RIV/00216208:11110/17:10361920 RIV/75010330:_____/17:00011796 RIV/00064165:_____/17:10361920

Result on the web

<a href="http://dx.doi.org/10.1080/15563650.2017.1284332" target="_blank" >http://dx.doi.org/10.1080/15563650.2017.1284332</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1080/15563650.2017.1284332" target="_blank" >10.1080/15563650.2017.1284332</a>

Result language

angličtina

Original language name

Leukotriene-mediated neuroinflammation, toxic brain damage, and neurodegeneration in acute methanol poisoning

Original language description

Context: The role of neuroinflammation in methanol- induced toxic brain damage has not been studied.nObjective: We studied acute concentrations and the dynamics of leukotrienes (LT) in serum in hospitalized patients with acute methanol poisoning and in survivors.nMethods: Series of acute cysteinyl-LT and LTB4 concentration measurements were performed in 28/101 hospitalized patients (mean observation time: 88 +/- 20 h). In 36 survivors, control LT measurements were performed 2 years after discharge.nResults: The acute maximum (C-max) LT concentrations were higher than concentrations in survivors: C-max for LTC4 was 80.7 +/- 5.6 versus 47.9 +/- 4.5 pg/mL, for LTD4, 51.0 +/- 6.6 versus 23.1 +/- 2.1 pg/mL, for LTE4, 64.2 +/- 6.0 versus 26.2 +/- 3.9 pg/mL, for LTB4, 59.8 +/- 6.2 versus 27.2 +/- 1.4 pg/mL (all p< 0.001). The patients who survived had higher LT concentrations than those who died (all p< 0.01). Among survivors, patients with CNS sequelae had lower LTE4 and LTB4 than did those without sequelae ( both p< 0.05). The LT concentrations increased at a rate of 0.4-0.5 pg/mL/h and peaked 4-5 days after admission. The patients with better outcomes had higher cys-LTs (all p< 0.01) and LTB4 (p< 0.05). More severely poisoned patients had lower acute LT concentrations than those with minor acidemia. The follow-up LT concentrations in survivors with and without CNS sequelae did not differ (all p> 0.05). The mean decrease in LT concentration was 30.9 +/- 9.0 pg/mL for LTC4, 26.3 +/- 8.6 pg/ mL for LTD4, 37.3 +/- 6.4 pg/mL for LTE4, and 32.0 +/- 8.8 pg/mL for LTB4.nConclusions: Our findings suggest that leukotriene- mediated neuroinflammation may play an important role in the mechanisms of toxic brain damage in acute methanol poisoning in humans. Acute elevation of LT concentrations was moderate, transitory, and was not followed by chronic neuroinflammation in survivors.

Czech name

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Czech description

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Type

J_imp - Article in a specialist periodical, which is included in the Web of Science database

CEP classification

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OECD FORD branch

10405 - Electrochemistry (dry cells, batteries, fuel cells, corrosion metals, electrolysis)

Project

<a href="/en/project/NV16-27075A" target="_blank" >NV16-27075A: NEURODEGENERATIVE PROCESSES IN PATIENTS EXPOSED TO METHANOL: PROSPECTIVE STUDY AFTER CZECH MASS METHANOL POISONING OUTBREAK IN 2012</a><br>

Continuities

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Publication year

2017

Confidentiality

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Name of the periodical

CLINICAL TOXICOLOGY

ISSN

1556-3650

e-ISSN

—

Volume of the periodical

55

Issue of the periodical within the volume

4

Country of publishing house

US - UNITED STATES

Number of pages

11

Pages from-to

249-259

UT code for WoS article

000394936500003

EID of the result in the Scopus database

2-s2.0-85011685025