The Influence Of Inflammation And Oxidative Stress On Carotid Artery Intima And Plaques In Patients With Helicobacter Pylori Infection And Alcoholic Fatty Liver Disease

ObjectiveThe aim of this study is to explore whether or not “the phenomenon of second hit” withAtherosclerosis for Helicobacter pylori infection and Alcoholic fatty liver disease, to furtherexplain the mechanism of atherosclerosis on inflammation and oxidative stress and providetheory guide for the clinical treatment of Atherosclerosis.MethodsA study of carotid intima-media thickness and plaques on both sides by carotid arterycolor ultrasound was conducted in146eligible patients with/without Helicobacter pyloriinfection and/or Alcoholic fatty liver disease from January2013to December2013. C13breath test to detect Helicobacter pylori infection and ALT, AST, γ-GT, TC, TG, LDL,ApoA1, ApoB, GLU, HCY, IL–6, CRP, MDA and SOD in venous blood were examined.Results1. There were no significant differences among groups for age, sex and drinking age,P>0.05.2. The serum levels of ALT, AST, γ-GT, TC, TG, ApoA1, ApoB, GLU, IL-6, CRP,MDA and SOD were different among groups(P<0.05), while there were no significantdifferences on the serum levels of LDL, HDL, HCY (P>0.05).3. The serum levels of AST, γ-GT, TG, IL-6in patients with Helicobacter pyloriinfection and Alcoholic fatty liver disease group were elevated than those of the Hpinfection group (P<0.05), while contrast in two groups, the serum levels of ALT, TC, ApoA1,ApoB, GLU, CRP, MDA and SOD were no significant statistical difference (P>0.05).4. Only the serum levels of GLU in patients with Helicobacter pylori infection and Alcoholic fatty liver disease group was elevated than that of the Alcoholic liver diseasegroup (P<0.05).while comparison in two groups,the serum levels of ALT, AST, γ-GT, TC,TG, ApoA1, ApoB, IL-6, CRP, MDA and SOD were no significant statistical difference(P>0.05).5. The serum levels of ALT, AST, γ-GT, TC, TG, ApoB, GLU, IL-6, CRP, MDA, SODand MDA/SOD ratio in patients with Helicobacter pylori infection and Alcoholic fatty liverdisease group were higher than those of the control group (P<0.05), only the serum level ofApoA1was no significant statistical difference in two groups (P>0.05).6. There were statistically difference on the serum levels of CRP, SOD in Hp infectiongroup than those of the control group (P<0.05), while the serum levels of ALT, AST, γ-GT,TC, TG, ApoA1, ApoB, GLU, IL-6, MDA had no obvious statistical significance in twogroups(P>0.05).7. The serum levels of ALT, AST, γ-GT, TC, TG, ApoB, CRP, MDA and SOD inalcoholic fatty liver disease group were higher than those of the control group (P<0.05),while the serum levels of ApoA1, GLU, IL-6level had no statistical difference (P>0.05).8. The thickening rate of the carotid intima-media thickness and the incidence ofcarotid plaques in the patients with Helicobacter pylori infection and Alcoholic fatty liverdisease group were significantly higher than those of the control group, presented asignificant statistical difference (=11.423, P<0.01and=8.423, P<0.01, respectively).To compared with the rest groups, the changes of thickening rate of the carotid intima-mediathickness and the incidence of carotid plaques were not difference(P>0.05).Conclusion1. The influence on carotid intima in two coexist risk factors of Helicobacter pyloriinfection and Alcoholic fatty liver disease had more obvious than the exist alone,and theatherosclerosis was aggravated,“the phenomenon of second hit” was confirmed.2. Helicobacter pylori infection and/or Alcoholic fatty liver disease can lead to theimbalance of the blood lipid, glucose, blood uric acid, inflammatory mediators, oxidationand antioxidant, while the changes were more obvious when the two risk factors coexist.Carotid artery intima thickness and Atherosclerosis were more serious.3. The increase of carotid artery intima thickness and the formation of Atheroscleroticplaques caused by Helicobacter pylori infection and Alcoholic fatty liver disease，theaggravated and progression of Atherosclerosis, which were through interfering with lipidand uric acid metabolism, was by initiatting the endometrium inflammation and oxidativestress process.