| Objective: The etiology of chronic gastritis is complex, and thedamage of oxidative stress may play an important role in its occurrence anddevelopment. Long-term heavy drinking not only damages the liver, butalso has a certain damage on the esophagus, stomach, pancreas and otherdigestive organs. An epidemiological investigation showed that thedrinkers had more frequency suffering from esophageal cancer, cardiaccancer, gastric cancer, and rectal cancer than the non-drinkers. So far therelationship between moderate alcohol consumption and gastrointestinaldamage is unclear. Some people thought that appropriate ethanol couldproduce metabolites which couldn’t do damage to the body. Even the freeradicals produced were beneficial to stress mechanism of the body, whichhad a protective effect on the gastric mucosa by increasing the level ofgastric prostaglandin. That might be an adaptive protective effect on thebody. While others believed that the drinking did not have any beneficialeffect on the esophagus, stomach, pancreas and other digestive organs. Asurvey of abroad about alcohol and health showed that a small amount ofalcohol couldn’t do damaged to the human body. Therefore, It is believedthat the propaganda which moderate drinking was healthy to the publicmight be misleading. By the comparison among three groups about serumSOD activity, MDA content and the expression intensity of gastric mucosaliNOS, this study explored the relationship between the drinking and thedevelopment of chronic gastritis, and the role of free radical damage mayplayed in.Methods:87patients of chronic gastritis diagnosed by electronicgastroscope were selected, which were divided into three groups: group I______________________________________________________________________________________________ (no alcohol group)52cases, group II (moderate alcohol group)25cases,group III (heavy alcohol group)10cases. when the patients were taken thetest of electronic gastroscope, three pieces of tissue in gastric antrum andone piece at stomach corner, totally four specimens were collected. onepiece of tissue in the gastric antrum was prepared for rapid urease test todetect Helicobacter pylori. If the result of rapid urease test was negative,the patients should been taken14C breath test. Either one of the resultpositive was Helicobacter pylori positive,and both negative was H. pylorinegative. The remaining specimens were fixed in4%formaldehydesolution for HE staining and immunohistochemistry to detect theexpression intensity of iNOS. Take3-5ml of vein blood in every patient,centrifugal, collect the serum into1ml EP tube, and then store them in arefrigerator at-80℃for the determination of the activity of SOD andMDA content. The data was analyzed by SPSS16.0statistical software. Weused chi-square test to compare the rate, and dealt with level data usingnon-parametric test. If the data met the normal distribution we usedvariance analysis, or else we used non-parametric test. We took α=0.05asthe level of significance.Results:1The relationship between Drinking and chronic atrophic gastritis: theincidence of the three groups of patients with chronic atrophic gastritis was40.4%(21/52) for group I,56%(14/25) for group II, and group III70%(7/10), respectively. The incidence of chronic atrophic gastritis presented atrend of increases, but the difference was not significant (P>0.05).2The results of comparison among the three groups about the activityof SOD was that there was no significant difference between group I withGroup II, and the activity of SOD in group I with II were significantlyhigher than that of group III, but the difference was not significant (P>0.05).3MDA content of group I, group II, group III increased gradually, butthe difference was not significant (P>0.05). 4There was no significant difference among the there groups aboutexpression intensity of iNOS (P>0.05).5Chronic atrophic gastritis had lower activity of SOD than chronicnon-atrophic gastritis (P<0.05), had higher MDA content than chronicnon-atrophic gastritis (P<0.05), had higher iNOS expression than chronicnon-atrophic gastritis (P <0.05).6There was no significant difference (P>0.05) in the incidence ofchronic atrophic gastritis among the three groups with H. pylori positive,and the incidence had a trend of increases.Conclusions:1With the increasing of alcohol consumption, the incidence of chronicatrophic gastritis showed a rising trend. Drinking may play an importantrole in the incidence and the development of chronic atrophic gastritis.2Comparing with non-atrophic gastritis, chronic atrophic gastritis hadlower activity of SOD, higher MDA content and larger iNOS expressionintensity, suggesting that oxidative stress might play an important role inthe development of chronic atrophic gastritis.3Moderate drinking had no significant effect on the incidence ofchronic atrophic gastritis, but heavy drinking could increase the incidenceof chronic atrophic gastritis.4There was no significant relationship between drinking and H. pyloriinfection rate, but the two factors might exist synergies in the occurrenceand development of atrophic gastritis. |
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