| Objective:Comparing the levels of blood lipid,inflammation marker and intestinal mucosal barrier related indicator between elderly patient with carotid atherosclerosis and the elderly person without arctoid atherosclerosis,and analysis the change of intestinal mucosal barrier in elderly patients with carotid atherosclerosis,investigating whether intestinal mucosal barrier damage are associated with the incidence of atherosclerosis.Methods:We selected 80 cases of elderly patient with carotid atherosclerosis from 2017.1 to 2017.10 in our hospital as case group,and choose 20 cases of elderly persons without carotid atherosclerosis as control group in our hospital physical examination center.We collected the general demographic data,blood lipid levels,inflammatory markers,lipopolysaccharide(LPS)levels,results of stool routine and fecal flora analysis of our study subjects,calculate the serum levels of D-lactic acid(D-Lac)and secretory immunoglobulin A(SIg A).Compared the baseline con dition,blood lipid levels,chronic low inflammation,and the degree of intestinal mucosal barrier injury between the two groups.SPSS 22.0 was used for statistical analysis,the measurement data were expressed as the means±SD,and the independ ent sample t-test was used to analysis the measurement date,the counting data was represented by the number of cases and percentages,and the c2 test was used for comparing proportions.Carotid artery atherosclerosis risk factors were analyzed by binary classification logistic regression analysis,the correlation analysis between the levels of blood lipid,inflammation maker,LPS,D-Lac and SIg A were used based on spearman correlation analysis.A P value of 0.05 or less was considered to indicate statistical significance.Results:1.The number of smokers in the case group accounted for 62.5%,and the proportion of patients with hypertension and diabetes in the case group were higher than the control group(P<0.05).2.The average age(74.90±11.98years)and BMI(24.37±3.07 kg/m2)of the case group were higher than that of the control group(69.75±8.55 years;22.78±2.90 kg/m2).The difference was statistically significant(P<0.05).3.There were significant differences in the levels of TCHO?LDL-C?HDL-C and CRP between the case group and the control group,and the levels of TCHO?LDL-C?CRP were significantly higher in the cases group,but the level of HDLC was significantly higher in the control group(P<0.05).4.The levels of LPS and D-Lac in the case group were significantly higher than that in the control group,while the SIg A level in the control group was significantly higher than that in the case group(P<0.01).5.According to the results of logistic regression analysis,diabetes and high serum level of LPS were the independent risk factors for carotid atherosclerosis,and high serum levels of HDL-C and SIg A were the protection factors for carotid atherosclerosis.6.Spearman correlation analysis results showed that HDL-C was negatively correlated with CRP and LPS level(r =-0.499,P = 0.000;r =-0.247,P = 0.013),while positively correlated with SIg A level(r = 0.358,P = 0.000);and the correlations between TCHO and the levels of D-Lac were significantly positive(r = 0.207,P = 0.039);the correlation between CRP and level of LPS were positive(r = 0.244,P = 0.014),and the correlation between the CRP and level of SIg A were positive(r = 0.289,P = 0.004).Conclusions:1.Age,smoking,hypertension,diabetes,BMI,TCHO,LDL-C?HDL-C are the influencing factors for carotid atherosclerosis.2.Patients with carotid atherosclerosis may have a significantly low chronic inflammatory state.The function of intestinal mucosal barrier in patients with carotid atherosclerosis are impaired.3.Diabetes and high LPS level are the independent risk factors for carotid atherosclerosis,and higher levels of HDL-C and SIg A are the protection factors for car otid atherosclerosis.4.Gut microbiota can translocate from gut when intestinal mucosal barrier damage,and the microbiota may release LPS or other metabolic products,which may cause low degree chronic inflammation reaction in our body,promote the development of atherosclerosis. |
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