The Hypothesis of Circulus Hypoxicus and Its Clinical Relevance in Patients With Methanol Poisoning - An Observational Study of 35 Patients
Identifikátory výsledku
Kód výsledku v 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>
Nalezeny alternativní kódy
RIV/00064165:_____/18:10383020
Výsledek na webu
<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>
Alternativní jazyky
Jazyk výsledku
angličtina
Název v původním jazyce
The Hypothesis of Circulus Hypoxicus and Its Clinical Relevance in Patients With Methanol Poisoning - An Observational Study of 35 Patients
Popis výsledku v původním jazyce
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'.
Název v anglickém jazyce
The Hypothesis of Circulus Hypoxicus and Its Clinical Relevance in Patients With Methanol Poisoning - An Observational Study of 35 Patients
Popis výsledku anglicky
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'.
Klasifikace
Druh
J<sub>imp</sub> - Článek v periodiku v databázi Web of Science
CEP obor
—
OECD FORD obor
30108 - Toxicology
Návaznosti výsledku
Projekt
<a href="/cs/project/NV16-27075A" target="_blank" >NV16-27075A: NEURODEGENERATIVNÍ PROCESY U PACIENTŮ EXPONOVANÝCH METANOLU: PROSPEKTIVNÍ STUDIE PO HROMADNÉ OTRAVĚ METANOLEM V ČESKÉ REPUBLICE V ROCE 2012</a><br>
Návaznosti
I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Ostatní
Rok uplatnění
2018
Kód důvěrnosti údajů
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Údaje specifické pro druh výsledku
Název periodika
Basic & Clinical Pharmacology & Toxicology
ISSN
1742-7835
e-ISSN
—
Svazek periodika
123
Číslo periodika v rámci svazku
6
Stát vydavatele periodika
GB - Spojené království Velké Británie a Severního Irska
Počet stran výsledku
7
Strana od-do
749-755
Kód UT WoS článku
000449674400014
EID výsledku v databázi Scopus
2-s2.0-85050801785