The Relationship between Cadherin Polymorphisms and the Risk of Delayed Encephalopathy after Acute Carbon Monoxide Poisoning in the Chinese Han Population

Abstract

Objective. The purpose of this study was to analyze the relationship between cadherin gene single-nucleotide polymorphisms (SNPs) and the risk of delayed encephalopathy after acute carbon monoxide poisoning (DEACMP). Materials and Methods. A total of 416 patients with DEACMP and 754 patients with acute carbon monoxide poisoning (ACMP) were recruited. We used the Sequenom MassARRAY® system to detect cadherin gene SNPs related to DEACMP. Using different genetic analysis models, we evaluated the relationship between the cadherin gene polymorphisms and risk of DEACMP. Results. We found that rs1944294 in the N-cadherin (CDH2) gene showed significant differences in genotype frequencies between the two groups under codominant and dominant inheritance models. Similarly, rs2513796 in the cadherin-17 (CDH17) gene showed significant differences under the codominant, dominant, and overdominant genetic models. And the T allele frequency of rs1944294 in the DEACMP group was significantly higher than that in the ACMP group ( P = 0.023 ). Conclusions. Cadherin gene SNPs (rs1944294, rs2513796) are associated with an increased risk of DEACMP in the Chinese population.

Analysis of factors associated with the development of delayed encephalopathy following acute carbon monoxide poisoning

“…In other words, longer CO exposure was associated with a greater amount of inhaled CO, longer coma, and more severe poisoning, thereby raising the risk of DEACMP, which may be related to the following mechanism: neuronal necrosis and apoptosis after ACOP. Similarly, prior studies revealed that longer durations of CO exposure and coma were associated with more severe neurological damage, and longer durations of hypoxia were associated with more severe brain damage and demyelination changes in the brain in patients with moderate to severe poisoning, thereby increasing the risk of DEACMP [20][21][22] . It is clinically more important to actively provide HBOT to patients with more severe conditions or longer durations of CO exposure or coma to improve the hypoxic state of the organism of the patients in time, alleviate the disease, and reduce the risk of DEACMP.…”