| ObjectiveAssessing the value of the ratio of serum pepsinogen I and II(Pepsinogen I/ Pepsinogen II,PGR),gastrin-17(Gastrin-17,G-17)combined with Helicobacter pylori(Hp)in early screening of gastric cancer,to clear the relationship between serum pepsinogen(PG)or G-17 and the degree or site of gastric mucosal lesions,,and the impact of Helicobacter pylori infection on these indicators,to explore effective screening method for early gastric cancer,and analyze the clinical application value of the method Methods1.Retrospective analysis of 160 patients who underwent gastroscopy in the inpatient department and outpatient department of Qilu Hospital of Shandong University from January to December of 2018.According to the endoscopic pathological diagnosis standard of 2018 version of gastric cancer diagnosis and treatment,160 patients were divided into normal control group without gastric mucosal lesions(or normal gastroscopy)(n=30),non-atrophic gastritis group(n=30),chronic atrophic gastritis group(n=60)and gastric cancer group(n=40).2.3 ml of venous blood of all subjects in the case of an empty stomach were collected in the morning(gastric patients were collected before surgery),and serum was collected for chemiluminescence immunoassay(Chemiluminesent immunoassay assay).CLIA)Determ-ination of serum pepsinogen I(PG),pepsinogen II(PGII),pepsinogen I and II ratio(PGR)and G-17 concentration,detection of H.pylori Ig G antibody Hp-Ig G by immunoblotting.3.To analyze the statistical differences between PG(40),PGII,PGR,G-17 and Helicobacter pylori(HP)infection rates among the groups,and to analyze the impact of Helicobacter pylori infection,site and severity of the lesionson these indicators,using the ROC curve to screen out the best gastric cancer screening indicators.The ABC method of the 2014 gastric cancer screening consensus and the new gastric cancer screening and scoring system of the 2017 Chinese early gastric cancer screening process were used to evaluate the gastric cancer risk in 160 samples,and the high-risk group was screened according to the pathological and gastroscopic results.Analyze the correlation with precancerous diseases and determine the best screening method for gastric cancer.4.Statistical analysis: Statistical analysis was performed using SPSS22.0 statistical software.The measurement data were expressed as mean±standard deviation(sx ±).The comparison between groups was performed by one-way analysis of variance(ANOVA).The comparison between the two groups was performed by LSD-t test.Using the receiver operating characteristics(ROC)to calculate the optimal cut-off value for each variable in the diagnosis of chronic atrophic gastritis The ratio comparison was calculated by Chi-square test.The two standards were compared by Kappa consistency analysis.P <0.05 was considered statistically significant.Results1.The levels of PGII and PGR in the healthy control group(Control),non-atrophic gastritis(NAG),chronic atrophic gastritis(CAG),and gastric cancer(Gastric Cancer,GC)was significantly different(F=22.47,P<0.001,F=40.06,P<0.001),but the levels of PG(40)and G-17 were not significantly different between the above four groups(F=1.61,P=0.139;F =4.40;P=0.05).Although the level of PG(40)in GC group was lower than that in CAG group,there was no significant difference(P = 0.459).The above results suggest that both PG(40)and G-17 have no correlation with the severity of gastric mucosal lesions.However,the infection rates of PGII,PGR and HP are related to the severity of gastric mucosal lesions.2.The results showed that PGI had no significant difference between HP positive and HP negative CAG group and GC group(p>0.05).There was significant difference between the HP negative and the HP positive CAG group(P<0.001).The PGR in the HP negative CAG group was significantly different from the other three groups(P<0.001);There was no significant difference in G-17 between HP positive and HP negative gro CAG and GC groups(P>0.05).The above results indicate that HP infection has no significant effect on PG and G-17,but has significant effects on PGII and PGR.3.In order to determine the effect of lesions site on the secretion levels of PG and G-17,we further analyzed the correlation between PG(40),PGII,PGR,G-17 and other gastric cancer and gastric cancer lesions.The results showed that although PGI was not statistically different between antral atrophic gastritis group and antral gastric cancer group(P=0.74),PGI was significantly decreased in gastric gastric cancer group,and there was significant difference compared with gastric antrum gastric cancer group(P =0.02).PG II was significantly increased in antral atrophic gastritis group and gastric antrum cancer group,which was significantly different from those in gastric body atrophic gastritis group and gastric body cancer group(P<0.001,0.05).PGII was significantly increased in the gastric antral atrophic gastritis group and gastric antrum cancer group,and was significantly differentbetween those in gastric body atrophic gastritis group and gastric body cancer group(P<0.001,0.05);corpus atrophic gastritis compared with the gastric antrum atrophic gastritis group,gastric gastric cancer,and gastric antrum gastric cancer group,the PGR showed a decreasing trend(P<0.001,0.001,0.001).G-17 was significantly lower in the antral atrophic gastritis group and there was significant difference in G-17 level compared with the gastric atrophic gastritis group,gastric antrum gastric cancer group and gastric gastric cancer group(P=0.03,0.001,0.001).The above results indicate that PGI and PGII are affected by the lesion site,PGI is significantly decreased in gastric lesions,and PGII is significantly increased in gastric antrum lesions.G-17 was signifycantly reduced in the atrophy of the antrum,increased in the atrophy of the corpus,and increased significantly in gastric cancer.4.The changes of PG(40),PGII,PGR and G-17 in each group were detected,and it was found that Compared with the moderate atrophic gastritis group,the severe atrophic gastritis group,the early gastric cancer group,and the advanced gastric cancer group,the level of PGII in mild atrophy group were increased with the severity of gastric mucosal lesions,and there was no statistically significant differences(P=0.012,0.01,0.03,0.01),PGR showed a downward trend(P=0.011,0.02,0.02,<0.001);G-17 level gradually increased in early gastric cancer group and advanced gastric cancer group.There were significant differences between the high and mild atrophic gastritis group and the severe atrophic gastritis group(P=0.05,0.01,<0.001,0.01,0.09,<0.001);the above results indicated that with the increase of severityof gastric mucosal lesions,PGR showed a declining trend,PGⅡ levels showed a increasing trend,and the level of G-17 showed a increasing trend in gastric cancer patients.It is indicated that the trend of the above indicators can reflect the degree of gastric mucosal lesions,and all of them have the detection value in the early screening of gastric cancer.5.The ROC curve showed that PGR has the greatest contribution to the diagnosis of chronic atrophic gastritis.The area of ROC curve was AUC=0.827.The combined detection of PGR and G-17 has higher diagnostic value in early screening of gastric cancer.Considering the effect of Helicobacter pylori on PGR,setting different PGR thresholds for HP negative group and HP positive group can significantly improve the diagnosis rate of chronic atrophic gastritis.The results showed that in the Helicobacter pylori-negative group,the ROC curve area of the PGR diagnosis CAG was AUC=0.663,and the sensitivity was 0.91,the specificity was 0.38,and the corresponding cut-off value was 8.21.In the gastric Helicobacter pylori positive group,the ROC curve area of he PGR diagnosis CAG was AUS=0.913,the sensitivity was 0.835,the specificity was 0.72,and the corresponding cut-off value was 4.82.It can be seen that the diagnostic rate of PGR in early gastric cancer screening can be significantly improved by using different PGR thresholds for HP negative and positive patients respectively.6.The new gastric cancer screening and scoring system was significantly higher in sensitivity and specificity than the current ABC method,and the difference was statistical significant(P<0.05).In addition,the high-risk group of gastric cancer determined by the new gastric cancer screening and scoring system was consistent with the optimal threshold of PGR and G-17 determined by this experiment by means of the new scoring system.It is further clarified that the new gastric cancer screening and scoring system can be used as an effective early gastric cancer screening method in local hospitals.Conclusion1.Helicobacter pylori infection can increase PGII butdecreased PGR levels,the impact of HP on the detection of pepsinogen levels should be considered.Therefore,HP-Ig G detection is needed as one of the indicators for early diagnosis of gastric cancer.2.The expression level of PG(40)and PGR is related to the lesion site and pathological stage.With the severity of gastric mucosal lesions,the level of PGII is increased,and the expression level of G-17 is increased in gastric cancer,which is related to the lesion site.Therefore,the variation trends of PG(40),PGR,PGII and G-17 can all reflect the severity of gastric mucosal lesions,and have a detection value in early gastric cancer screening.3.ROC curve shows that PGR has the greatest contribution to the diagnosis of chronic atrophic gastritis.The combined detection of PGR and G-17 has higher diagnostic value in early screening of gastric cancer.Setting different PGR thresholds for HP negative and HP positive groups can significantly improve the diagnostic value of PGR in early gastric cancer screening.4.The new gastric cancer screening and scoring system is significantly better than the previous standard.in sensitivity and specificity.The new gastric cancer screening and scoring system can be used as an effective early gastric cancer screening method in the region. |
