| Objective: Chronic atrophic gastritis (Chronic atrophic gastritis, theCAG) is a common disease of digestive system, in1978the world healthorganization (who) will it as a cancer of the stomach before state, especiallywith IM and (or) ATP, the cancer is more likely.Glutathione peroxidase(GSH-Px) and superoxide dismutase (SOD) and malondialdehyde (MDA) asindicators of oxidatie stress, and jointly participate in the regulation ofmucosal tissue oxidation reaction to achieve the role of protecting gastricmucosa, the surfactant content in peripheral blood from reaction inside thestomach, to a certain extent the oxidative stress state in the blood, so thedetection of serum SOD, MDA, GSH-Px oxidation can be found early gastricmucosa damage status, treatment as soon as possible, thereby preventing themucosa atrophy.Studied in this paper by observing the CAG turbidity toxinintrinsic syndrome in patients with gastric mucosa pathological changes, Hpinfection, the activity of serum SOD, GSH-Px and content of MDA, turbidpoison intrinsic card and inflammatory changes and the relationship betweenHp infection and turbid poison connotation hou justification of the essence, tofurther explore the application of theory of turbidity toxin in the CAG,turbidity toxin theory of modern medical research provides an objective basis.Methods:1In the research literature and consult this professional experts, on thebasis of in accordance with the unified standards to make chronic atrophicgastritis clinical questionnaire.2According to the Chinese medicine new medicine clinical researchguiding principles of diagnostic criteria to dialectical analysis of clinic patients,the satisfactory patients were divided into two groups, including turbiditytoxin intrinsic group of47cases, liver stomach with group of36cases. 3In February2012-October2013in hebei province hospital outpatientand ward clear the CAG patients diagnosed by epidemiological investigation.Collect the patient’s age, gender, family history, course of diseases, clinicalsymptoms, gastroscopy and pathological manifestations, such as information,fill in the questionnaire, and the integrated quantitative according to uniformstandard, using descriptive statistical method to find out incidence with age,sex, duration, the relationship between family history.4Detecting Hp by14C breath test, observe gastric mucosa under theelectronic gastroscope, observe the tissue pathology of gastric mucosa undermicroscope after HE staining.5The activity of serum SOD, gsh-px and content of MDA wererespectively tested through the WST-1, colorimetric method and associatesmethod.6anxiety and depression scores are reference to Hamilton anxiety anddepression scale (Hamilton).Results:1Endoscopy results: turbid poison intrinsic group under gastroscope isgiven priority to with gastric mucosa rough, erosion and uplift nodules, liverstomach with group with erythema oozy, bleeder, bile reflux.2Hp infection: turbidity toxin intrinsic group of47cases, Hp infectionwas32cases, liver stomach with group was for12cases, two groups hassignificant difference in Hp infection, turbidity toxin intrinsic group Hpinfection rate is higher than liver stomach with group (P<0.05).3Gastric mucosa pathological aspects: compared with the liver stomachwith group, turbidity toxin relation between intrinsic group of gastric mucosaatrophy, intestinal and atypical hyperplasia degree increased significantly, thedifference had statistical significance (P<0.05).4Hp infection gastric mucosa pathological changes: Compared with Hpinfection negative, Hp infection was moderately severe atrophy, intestinal andatypical hyperplasia degree increased significantly, the difference wasstatistically significant (P<0.05). 5The activity of serum SOD, GSH-Px and content of MDA: Turbiditytoxin intrinsic syndrome patients’ serum activity of SOD, gsh-px was lowerthan that in group liver stomach discord, the difference was statisticallysignificant (P<0.05), the content of MDA is higher than that of liver stomachwith group, the difference was statistically significant (P<0.05).6Hp infection and activity of SOD, GSH-Px and content of MDA: theactivity of serum SOD, GSH-Px in Hp infection group was significantly lowerthan the negative, the difference was statistically significant (P<0.05), thecontent of MDA was significantly higher than the negative, the difference wasstatistically significant (P<0.05).7In47patients with turbid poison intrinsic group has4cases of severedepression, depression in14cases, certainly may depression have19cases, nodepression in10cases,12cases with severe anxiety, anxiety in19cases,certainly may be anxious in10cases, no anxiety in6cases, and liver stomachcompared with group, two groups of patients in terms of anxiety anddepression scores have no obvious difference (P>0.05).Conclusions:1The CAG among the elderly, long course of disease, more in5~10years, and has a certain tendency of familial aggregation and genetic.2The CAG patients more emotional psychological barriers, payattention to the factors in clinical patients of modern to enhance therapeuticeffect.3"Turbid poison" and HP infection and gastric mucosal atrophy,intestinal and atypical hyperplasia is closely related, is one of the importantpathogenic factors cause the CAG.4Hp infection can increase the gastric mucosal atrophy, intestinal andchances of atypical hyperplasia, its mechanism is probably influences theactivity of serum SOD, gsh-px and MDA content, leading to gastric mucosadysfunction oxidative stress and cause gastric mucosal injury.5The activity of serum SOD, gsh-px of Turbidity toxin intrinsic groupreduced significantly and the content of MDA increased significantly, this suggests "turbid poison" may be the oxygen free radicals produced by externalfactors and the internal environment can survive,"Turbid poison" may havecontributed to the mechanism of gastric mucosal atrophy caused imbalance ofoxygen free radical metabolism in peripheral blood, and from a certain extent,affect the stomach level of oxygen free radicals in the blood circulation, thuscaused to the gastric mucosa injury, aggravating gastric mucosal atrophy,formed by the oxidation reaction. |
PDF Full Text Request