Choline as a specific manifestation of delayed encephalopathy after acute carbon monoxide poisoning: a description of two cases.
Ontology highlight
ABSTRACT:
SUBMITTER: Zhai H
PROVIDER: S-EPMC10784035 | biostudies-literature | 2024 Jan
REPOSITORIES: biostudies-literature
Publications
Choline as a specific manifestation of delayed encephalopathy after acute carbon monoxide poisoning: a description of two cases.
Zhai Huige H Mao Yumeng Y Wang Qianqi Q Cui Yunmei Y Xu Dongyuan D Yan Gen G
Quantitative imaging in medicine and surgery 20231117 1
Similar Datasets
Project description:ObjectiveThe aim of this study is to explore the relationship between neuron-specific enolase (NSE) gene polymorphism and delayed encephalopathy after acute carbon monoxide poisoning (DEACMP) and provide a theoretical basis for DEACMP pathogenesis, diagnosis, and prognosis.MethodsTo investigate this relationship, we screened 6 NSE single nucleotide polymorphisms (SNPs), based on the results of the previous genome-wide association studies (GWAS). A total of 1,201 patients, including 416 in the DEACMP group and 785 in the acute carbon monoxide poisoning (ACMP) group, were detected by the Sequenom MassARRAY® method. The genotype frequencies and alleles of the 6 NSE SNPs (rs2071074, rs2071417, rs2071419, rs11064464, rs11064465, and rs3213434) were compared using different genetic models.ResultsIn the SNPs rs2071419 and rs3213434, we found that the genotypes and allele frequencies in the two groups significantly correlated with the grouping of patients (χ 2 = 6.596, p = 0.037; χ 2 = 8.769, p = 0.012). The haplotypes GGTTTC and CCTTTC of ACMP and DEACMP were different (χ 2 = 6.563, p = 0.010; χ 2 = 4.151, p = 0.042). We also observed that rs2071419 and rs3213434 significantly correlated with DEACMP-increased risk in the dominant, codominant, and overdominant genetic models. In addition, we speculated that the C allele of the rs2071419 polymorphism and the T allele of the rs3213434 polymorphism in NSE may increase the DEACMP risk (p = 0.011, p = 0.006).ConclusionsThe results show that rs2071419 and rs3213434 are susceptible sites of DEACMP. The NSE C allele of rs2071419 and T allele of rs3213434 and the haplotypes GGTTTC and CCTTTC may be risk factors for DEACMP.
| S-EPMC7584970 | biostudies-literature
Project description: Not available
| S-EPMC10689858 | biostudies-literature
Project description:Delayed encephalopathy after acute carbon monoxide poisoning (DEACMP) is a disease with an incomplete pathological mechanism, long treatment time, and uncertain factors affecting the therapeutic effect. This study explored prognostic factors for DEACMP patients treated with hyperbaric oxygen therapy (HBOT) in 15 hospitals in China. The findings might provide a theoretical basis for further improving the prognosis of DEACMP patients. In this study, data from 330 patients with DEACMP who were admitted to HBOT centers of 15 hospitals in Hunan Province (China) from June 2015 to June 2020 were retrospectively analyzed, and their medical records related to disease prognosis were collected and followed up by telephone. Univariate and multivariate analyses were used to identify independent risk factors for the prognosis of DEACMP patients after HBOT. Univariate analysis revealed 11 possible prognostic factors. Consistent with univariate analysis, multivariate analysis found that underlying diseases (Odds radio(OR) = 2.886, P = 0.048), hypermyotonia (OR = 5.2558, P = 0.008), and HBOT pressure no less Than 2.3 atm absolute (ATA) ((OR = 7.812, P = 0.004) were identified as independent prognostic factors among 20 variables for poor prognosis of DEACMP patients treated with HBOT in the study. This multicenter retrospective analysis revealed that the adverse prognostic markers for DEACMP patients treated with HBOT might be underlying diseases, hypermyotonia, and an HBOT pressure of 2.3 ATA or higher.
| S-EPMC9792756 | biostudies-literature
Project description:AimsThe objective of this study is to explore the regulatory role of DNA methylation in delayed encephalopathy after carbon monoxide poisoning (DEACMP) and to identify candidate epigenetic biomarkers.MethodsIn this study, multi-omics analyses such as methylomics, transcriptomics, pyrophosphate sequencing, qRT-PCR, immunohistochemistry, and western blotting were utilized to investigate the role of epigenetic regulation and altered gene expression in the pathogenesis of DEACMP.ResultsUsing integrated analysis, we identified 168 differentially methylated CpGs sites, 334 differentially expressed genes, and two differentially methylated and differentially expressed genes (DAB2IP and SMYD3) in the DEACMP group. The pyrosequencing results further revealed hypomethylation of DAB2IP and hypermethylation of SMYD3. Moreover, we verified the upregulation of DAB2IP expression accompanied by the downregulation of SMYD3 expression in the DEACMP rats model.ConclusionThis study, based on dysregulated DNA methylation and gene expression profiles, identified and validated two DEACMP-related genes (DAB2IP and SMYD3) that could serve as epigenetic biomarkers and potential therapeutic targets for DEACMP.
| S-EPMC11829117 | biostudies-literature
Project description: Not available
| S-EPMC4016057 | biostudies-literature
Project description:Carbon monoxide (CO) is the leading cause of poisoning deaths in many countries, including Japan. Annually, CO poisoning claims about 2000-5000 lives in Japan, which is over half of the total number of poisoning deaths. This paper discusses the physicochemical properties of CO and the toxicological evaluation of CO poisoning.
| S-EPMC6992844 | biostudies-literature
Project description:Delayed encephalopathy after acute carbon monoxide poisoning (DEACMP) is more characteristic of anoxic encephalopathy than of other types of anoxia. Those who have the same poisoning degree and are of similar age and gender have a greater risk of getting DEACMP. This has made it clear that there are obvious personal differences. Genetic factors may play a very important role. The authors performed a genome-wide association study involving pooling of DNA obtained from 175 patients and 244 matched acute carbon monoxide poisoning without delayed encephalopathy controls. The Illumina HumanHap 660 Chip array was used for DNA pools. Allele frequencies of all SNPs were compared between delayed encephalopathy after acute carbon monoxide poisoning and control groups and ranked. A total of 123 SNPs gave an OR >1.4. Of these, 46 mapped in or close to known genes. Forty-eight SNPs located in 19 genes were associated with DEACMP after correction for 5% FDR in the genome-wide association of pooled DNA. Two SNPs (rs11845632 and rs2196447) locate in the Neurexin 3 gene were selected for individual genotyping in all samples and another cohort consisted of 234 and 271 controls. There were significant differences in the genotype and allele frequencies of rs11845632 and rs2196447 between the DEACMP group and controls group (all P-values <0.05). This study describes a positive association between Neurexin 3 and controls in the Han Chinese population, and provides genetic evidence to support the susceptibility of DEACMP, which may be the resulting interaction of environmental and genetic factors.
| S-EPMC3827149 | biostudies-literature
Project description:BackgroundWe explored the association of leucine-rich repeats and calponin homology domain containing 1 (LRCH1) gene polymorphisms with genetic susceptibility to delayed encephalopathy after acute carbon monoxide poisoning (DEACMP), which might provide a theoretical basis for the pathogenesis, diagnosis, and prognosis research of DEACMP.MethodsFour single nucleotide polymorphisms, rs1539177 (G/A), rs17068697 (G/A), rs9534475 (A/C), and rs2236592 (T/C), of LRCH1, selected as candidate genes through genome-wide association analysis, were genotyped in 661 patients (DEACMP group: 235 cases; ACMP group: 426 cases) using Sequenom Massarray®. The association analysis of four SNPs and LRCH1 was performed under different genetic models.ResultsLRCH1 polymorphisms (rs1539177, rs17068697, rs9534475) under additive and dominant genetic models were significantly associated with an increased risk of DEACMP, but no significant association under allele and recessive models was found. The LRCH1 rs2236592 polymorphism was susceptible to DEACMP only under the dominant model (TT/TC + CC, OR = 1.616, 95% CI: 1.092-2.390, P = 0.015784). In addition, the A allele gene of rs9534475 polymorphism in LRCH1 might increase the risk for DEACMP (OR = 1.273, 95% CI: 1.013-1.601, P = 0.038445).ConclusionsWe found a significant association between the four LRCH1 polymorphisms and DEACMP. The allelic A of rs9534475 polymorphism in LRCH1 might be a risk factor for DEACMP.
| S-EPMC6916040 | biostudies-literature
Project description:ObjectiveDelayed neurological sequelae (DNS) is a serious complication that occurs after acute carbon monoxide (CO) intoxication. The study identified factors for predicting DNS development for the purpose of improving CO intoxication treatment strategies.MethodsThe medical records of 65 patients admitted to Shizuoka Saiseikai General Hospital between 2004 and 2020 due to CO poisoning were retrospectively reviewed. Univariate and multivariate logistic regression analyses were performed, using a range of evaluated items as explanatory variables and the development of DNS as the response variable.ResultsPatients who developed DNS were found to have higher peak creatine kinase (CK) (odds ratio, 1.0003; 95% CI, 1.0001-1.0005; P<0.001), and experienced a greater number of days during which walking was impossible in the acute stage following intoxication (odds ratio, 1.011; 95% CI, 1.005-1.018; P<0.001) according to the univariate analysis. Multivariate analyses indicated that DNS development was related to the score, peak CK (U/L) + 40 × the number of days in which walking was impossible. The model demonstrated an area under the receiver operating characteristic curve (AUC) of 0.96 (95% CI, 0.91-1.00), and DNS was predicted with 100% sensitivity and 82% specificity.ConclusionAn indicator that incorporates the number of days that walking is impossible for a patient could be useful in planning therapeutic strategies.
| S-EPMC8011735 | biostudies-literature
Project description:ObjectiveThe 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 methodsA 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.ResultsWe 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).ConclusionsCadherin gene SNPs (rs1944294, rs2513796) are associated with an increased risk of DEACMP in the Chinese population.
| S-EPMC8818434 | biostudies-literature