The Hypothesis of Circulus Hypoxicus and Its Clinical Relevance in Patients With Methanol Poisoning - An Observational Study of 35 Patients
The result's identifiers
Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11110%2F18%3A10383020" target="_blank" >RIV/00216208:11110/18:10383020 - isvavai.cz</a>
Alternative codes found
RIV/00064165:_____/18:10383020
Result on the web
<a href="https://doi.org/10.1111/bcpt.13074" target="_blank" >https://doi.org/10.1111/bcpt.13074</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1111/bcpt.13074" target="_blank" >10.1111/bcpt.13074</a>
Alternative languages
Result language
angličtina
Original language name
The Hypothesis of Circulus Hypoxicus and Its Clinical Relevance in Patients With Methanol Poisoning - An Observational Study of 35 Patients
Original language description
Methanol mass poisoning is a global problem with high fatality rates and often severe sequelae in survivors. Patients typically present late to the hospital with severe metabolic acidosis followed by a rapid deterioration in their clinical status. The hypothesis 'Circulus hypoxicus' describes the metabolic acidosis following methanol poisoning as a self-enhancing hypoxic circle responsible for methanol toxicity. We wanted to test the validity of this hypothesis by an observational study based on 35 patients from the methanol outbreaks in Norway (2004) and the Czech Republic (2012). Comprehensive laboratory values, including S(serum)-methanol, S-formate, S-lactate, arterial blood gases, anion and osmolal gaps, were used in the calculations. Laboratory values and calculated gaps were compared to each other using linear regression. S-lactate and S-formate correlated better with the increased base deficit and anion gap than did S-formate alone. Base deficit rose to about 20 mmol/L and S-formate rose to 12 mmol/L prior to a significant rise in S-lactate - most likely caused by formate inhibition of mitochondrial respiration (type B lactacidosis). The further rise in S-lactate was not linear to S-formate most likely due to the self-enhancing pathophysiology, but may also be associated with hypotension in critically ill patients and variable ethanol drinking habits. Our study suggests that the primary metabolic acidosis leads to a secondary lactic acidosis mainly due to the toxic effects of formate. The following decline in pH will further increase this toxicity. As such, a vicious and self-enhancing acidotic circle may explain the pathophysiology in methanol poisoning, namely the 'Circulus hypoxicus'.
Czech name
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Czech description
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Classification
Type
J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database
CEP classification
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OECD FORD branch
30108 - Toxicology
Result continuities
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
Others
Publication year
2018
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Data specific for result type
Name of the periodical
Basic & Clinical Pharmacology & Toxicology
ISSN
1742-7835
e-ISSN
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Volume of the periodical
123
Issue of the periodical within the volume
6
Country of publishing house
GB - UNITED KINGDOM
Number of pages
7
Pages from-to
749-755
UT code for WoS article
000449674400014
EID of the result in the Scopus database
2-s2.0-85050801785