The Association Research Of Parkin Gene Polymorphism And Delayed Encephalopathy After Acute Carbon Monoxide Poisoning

BackgroundDelayed encephalopathy after of acute carbon monoxide poisoning(DEACMP) is a group of central nervous system damage, by acute dementia and extrapyramidal symptoms as the main manifestation of neuropsychiatric symptoms, its pathogenesis is still not clear, recently the research about DEACMP stays in the cerebrospinal fluid and blood biochemical level, there is no report about molecular genetic research. Studying the genes concerning DEACMP and investigate the genetic predisposition will help to elucidate its pathogenesis and provide genetics basis to prevent and treat this disease.ObjectiveTo investigate the association of Parkin gene (rs1784594andrs1893895) polymorphism with delayed encephalopathy after acute carbon monoxide poisoning and to explore the DEACMP gene susceptibility.Method1. The diagnostic criteria was based on the book of "Internal Medicine, sixth Edition" and Zhao Xiangzhi’s criteria on delayed encephalopathy after acute carbon monoxide poisoning (DEACMP).180DEACMP patients (118male and62female) and262patients (120male and142female) without delayed encephalopathy after carbon monoxide poisoning (ACMP) as control from Han ethnic group in Northern Henan province were recruited into rs1784594group; and217DEACMP patients (120male and97female) and226ACMP patients (107male and119female) as control from Han in Northern Henan province were recruited into rs1893895group. The acute carbon monoxide poisoning patients were all in compliance with "National Occupational Standard for Acute Carbon Monoxide Poisoning Diagnosis GB8781-88". All patients were over40years old.2.5ml ulnar vein blood was collected into tubes with EDTA anticoagulant respectively from fasting DECAMP patients at6:00-8:00am, and from ACMP patients within1d after they fully consciously recovered. Then the blood samples were stored at-70℃followed by DNA extraction with TIANGEN’s blood genomic DNA extraction kit.3. The Parkin gene rs1784594, rs1893895SNPs were detected with PCR restriction fragment length polymorphism (PCR-RFLP) technology.4. Data analysis was conducted with SPSS13.0statistical software, using the goodness-of-fit of the chi-square test to check the conformity of genotype distribution to the Hardy-Weinderg equilibrium and the chi-square test for correlation analysis.Results1. There is significant difference of Parkin gene rsl784594distribution between the DEACMP group and the ACOP group (P<0.05). After separated by gender, there is no difference between male and female group in all patients of DEACMP and ACOP groups or in either DEACMP or ACOP respectively (all P>0.05).2. There is no significant difference of Parkin gene rs1893895distribution between the DEACMP group and the ACOP group (P>0.05). After separated by gender, there is no difference between male and female group in all patients of DEACMP and ACOP groups or in either DEACMP or ACOP respectively (all P>0.05).Conclusions1. No supportive evidence has been found on the association of DEACMP with Parkin gene rsl893895polymorphism for rsl893895being the susceptibility gene of DEACMP.2. There was association between rs1784594polymorphism and DEACMP indicating that polymorphism might be the molecular genetic basis of DEACMP pathogenesis.3. When two groups were stratified by sex, the Parkin gene rsl784594allele frequencies in female participants in both groups were significantly different (χ2=3.985, P=0.046, OR=1.483,95%CI=1.006-2.186).4. The interaction between different genotypes of rsl893895and rs1784594loci showed an increased risk of DEACMP in patients with the A/G and A/A genotype in above both loci simultaneously (OR=2.52,95%CI=1.09-5.80).