Deformity of duodenal bulb, gastric metaplasia of duodenal regenerating mucosa and recurrence of duodenal ulcer: A correlated study

AIM: To investigate the correlation among the presence and degree of gastric metaplasia of duodenal regenerating mucosa, the deformity of bulb and the recurrence of duodenal ulcer.METHODS: A total of 99 patients with duodenal ulcer were treated with H2-antagonist with or without antimicrobial therapy. All patients received follow-up endoscopic examinations 6 wk after treatment. When the ulcer(s) were noted to be healed, two biopsies were taken from the ulcer scar for histological study of gastric metaplasia, and 4 biopsies were taken from antrum for Helicobacter pylori(H pylori) study. Out of these cases,44 received further follow-up endoscopic examinations after 3, 6 and 12 mo respectively for studying the recurrence rate of duodenal ulcers. The correlation among ulcer recurrence, degree of gastric metaplasia of regenerating mucosa, bulbar deformity, and colonization of Hpylori in the stomach was then studied.RESULTS: The results showed that there was a strong correlation between the deformity of duodenal bulb and the degree of gastric metaplasia of regenerating duodenal mucosa. The recurrence rate of duodenal ulcer had a significant difference between patients with and without Hpyloricolonization in the stomach (P＜0.001). The greater the degree of gastric metaplasia of duodenal regenerating mucosa, the higher the recurrence rate of duodenal ulcer (P= 0.021). The more deformed the duodenal bulb, the higher the incidence of recurrence of duodenal ulcer (P = 0.03).CONCLUSION: There is a correlation among deformity of duodenal bulb, gastric metaplasia of duodenal regenerating mucosa and recurrence of duodenal ulcer.A more severely deformed duodenal bulb is closely related to a greater extent of gastric metaplasia. Both factors contribute to the recurrence of duodenal ulcer.

Role of digital chromoendoscopy and confocal laser endomicroscopy for gastric intestinal metaplasia and cancer surveillance

In Japan and countries such as South Korea and Tai-wan, China, the standard technique for detecting earlygastric cancer (EGC) is chromoendoscopy. This technique involves a magnified endoscope and the use ofan indigo-carmine spray to distinguish between EGCand non-EGC areas. However, this technique is notwidely adopted in many parts of the world. One important reason for limited use is that this technique needsan experienced endoscopist to interpret the imagesduring the procedure. In addition, the sensitivity for detecting gastric intestinal metaplasia (GIM), a precancerous lesion of EGC, is graded as suboptimal. Moreover,the requirement of a cumbersome spraying method isinconvenient and needs preparation time. Easier digitalchromoendoscopy techniques, such as Narrow-bandImaging and Flexible spectral Imaging Color Enhancement, have been reported to facilitate targeted GIM and EGC biopsy. They provide higher sensitivities over conventional white light endoscopy. Recently, the noveltechnology of confocal laser endomicroscopy has been introduced as a high-magnification (1000 ×) real-time evaluation for many early gastrointestinal (GI) cancersand precancerous GI lesions, including colonic polyp,Barrett's esophagus, and GIM. The advantage of this technique is that it can be used as an in vivo confirmation of the presence of GIM and EGC during endoscopic surveillance. This review aims to explain the current information on the usefulness of digital chromoendos-copy and confocal laser endomicroscopy for evaluating GIM and EGC during endoscopic surveillance and the possible future role of these techniques for GI cancerscreening programs.

Non-sequential narrow band imaging for targeted biopsy and monitoring of gastric intestinal metaplasia

AIM: To evaluate the efficacy of non-sequential narrow band imaging (NBI) for a better recognition of gastric intestinal metaplasia (GIM). METHODS: Previously diagnosed GIM patients underwent targeted biopsy from areas with and without GIM, as indicated by NBI, twice at an interval of 1 year. The authors compared the endoscopic criteria such as light blue crest (LBC), villous pattern (VP), and large long crest (LLC) with standard histology. The results from two surveillance endoscopies were compared with histology results for sensitivity, specif icity, positive predic-tive value (PPV), negative predictive value (NPV), and likelihood ratio of positive test (LR+). The number of early gastric cancer cases detected was also reported. RESULTS: NBI targeted biopsy was performed in 38 and 26 patients during the first and second surveillance endoscopies, respectively. There were 2 early gastric cancers detected in the first endoscopy. No cancer was detected from the second study. Surgical and endoscopic resections were successfully performed in each patient. Sensitivity, specifi city, PPV, NPV, and LR+ of all 3 endoscopic criteria during the first/second surveillances were 78.8%/91.3%, 82.5%/89.1%, 72.8%/77.8%, 86.8%/96.1, and 4.51/8.4, respectively. LBC provided the highest LR+ over VP and LLC. CONCLUSION: Non-sequential NBI is useful for GIM targeted biopsy. LBC provides the most sensitive reading. However, the optimal duration between two surveillances requires further study.

Narrow-band imaging with magnifying endoscopy is accurate for detecting gastric intestinal metaplasia

AIM:To investigate the predictive value of narrowband imaging with magnifying endoscopy (NBI-ME) for identifying gastric intestinal metaplasia (GIM) in unselected patients. METHODS:We prospectively evaluated consecutive patients undergoing upper endoscopy for various indications, such as epigastric discomfort/pain, anaemia, gastro-oesophageal reflux disease, suspicion of peptic ulcer disease, or chronic liver diseases. Patients underwent NBI-ME, which was performed by three blinded, experienced endoscopists. In addition, five biopsies (2 antrum, 1 angulus, and 2 corpus) were taken and examined by two pathologists unaware of the endoscopic findings to determine the presence or absence of GIM. The correlation between light blue crest (LBC) appearance and histology was measured. Moreover, we quantified the degree of LBC appearance as less than 20% (+), 20%-80% (++) and more than 80% (+++) of an image field, and the semiquantitative evaluation of LBC appearance was correlated with IM percentage from the histological findings. RESULTS:We enrolled 100 (58 F/42 M) patients who were mainly referred for gastro-esophageal reflux disease/dyspepsia (46%), cancer screening/anaemia (34%), chronic liver disease (9%), and suspected celiac disease (6%); the remaining patients were referred for other indications. The prevalence of Helicobacter pylori (H. pylori ) infection detected from the biopsies was 31%, while 67% of the patients used proton pump inhibitors. LBCs were found in the antrum of 33 patients (33%); 20 of the cases were classified as LBC+, 9 as LBC++, and 4 as LBC+++. LBCs were found in the gastric body of 6 patients (6%), with 5 of them also having LBCs in the antrum. The correlation between the appearance of LBCs and histological GIM was good, with a sensitivity of 80% (95%CI:67-92), a specificity of 96% (95%CI:93-99), a positive predictive value of 84% (95%CI:73-96), a negative predictive value of 95% (95%CI:92-98), and an accuracy of 93% (95%CI:90-97). The NBI-ME examination overlooked GIM in 8 cases, but the GIM was less than 5% in 7 of the cases. Moreover, in the 6 false positive cases, the histological examination showed the presence of reactive gastropathy (4 cases) or H. pylori active chronic gastritis (2 cases). The semiquantitative correlation between the rate of LBC appearance and the percentage of GIM was 79% (P < 0.01). CONCLUSION:NBI-ME achieved good sensitivity and specificity in recognising GIM in an unselected population. In routine clinical practice, this technique can reliably target gastric biopsies.

Helicobacter pylori associated gastric intestinal metaplasia:Treatment and surveillance

Gastric cancer(GC) is one of the leading causes of cancer related death in the world, particularly in East Asia. According to the Correa's cancer cascade, noncardia GC is usually developed through a series of mucosal changes from non-atrophic gastritis to atrophic gastritis(AG), intestinal metaplasia(IM), dysplasia and adenocarcinoma. Atrophic gastritis and IM are therefore generally considered to be pre-neoplastic gastric lesions. Helicobacter pylori(H. pylori) infection is an important initiating and promoting step of this gastric carcinogenesis cascade. Emerging long-term data showed that eradication of H. pylori reduced the risk of subsequent cancer development. It however remains confusing whether eradication of the bacterium in individuals with pre-neoplastic gastric lesions could regress these changes as well as in preventing cancer. Whilst H. pylori eradication could likely regress AG, the presence of IM may be a point of no return in this cascade. Hence, surveillance by endoscopy may be indicated in those with extensive IM or those with incomplete IM, particularly in populations with high GC risk. The optimal interval and the best tool of surveillance endoscopy remains to be determined in future studies.

Histochemical studies on intestinal metaplasia adjacent to gastric cardia adenocarcinoma in subjects at high-incidence area in Henan, north China

AIM: To characterize the histochemical type and pattern of intestinal metaplasia (IM) adjacent to gastric cardia adenocarcinoma (GCA) and distal gastric cancer (GC) in Linzhou, Henan Province, China.METHODS: Alcian-blue-periodic acid Schiff and high iron diamine-Alcian blue histochemical methods were performed on 142 cases of IM, including 49 cases of GCA and 93 cases of GC. All the patients were from Linzhou, Henan Province, China, the highest incidence area for both GCA and squamous cell carcinoma. Radio- or chemotherapy was not applied to these patients before surgery.RESULTS: The detection rate of IM in tissues adjacent to GCA tissues was 44.9%, which was significantly lower than that in GC tissues (80.64%, P<0.01). The rates of both incomplete small intestinal and colonic IM types identified by histochemistry in GCA tissues (31.82% and 63.64%, respectively) were significantly higher than those in GC (5.33% and 21.33%, respectively, P<0.01).CONCLUSION: IM in GCA and GC should be considered as a separate entity. Further research is needed to evaluate whether neoplastic progression of IM is related to its mucin profile in GCA.

Comparison of operative link for gastritis assessment, operative link on gastric intestinal metaplasia assessment, and TAIM stagings among men with atrophic gastritis

BACKGROUND Gastric cancer is the world’s third most lethal malignancy. Most gastric cancers develop through precancerous states of atrophic gastritis and intestinal metaplasia. Two staging systems, operative link for gastritis assessment(OLGA)and operative link on gastric intestinal metaplasia assessment(OLGIM), have been developed to detect high gastric cancer risk. European guidelines recommend surveillance for high-risk OLGA/OLGIM patients(stages Ⅲ–Ⅳ),and for those with advanced stage of atrophic gastritis in the whole stomach mucosa. We hypothesize, that by combining atrophy and intestinal metaplasia into one staging named TAIM, more patients with increased gastric cancer risk could be detected.AIM To evaluate the clinical value of the OLGA, OLGIM, and novel TAIM stagings as prognostic indicators for gastric cancer.METHODS In the Helsinki Gastritis Study, 22346 elderly male smokers from southwestern Finland were screened for serum pepsinogen I(PGI). Between the years 1989 and1993, men with low PGI values(PGI < 25 μg/L), were invited to undergo an oesophagogastroduodenoscopy. In this retrospective cohort study, 1147 men that underwent gastroscopy were followed for gastric cancer for a median of 13.7 years, and a maximum of 27.3 years. We developed a new staging system, TAIM,by combining the topography with the severity of atrophy or intestinal metaplasia in gastric biopsies. In TAIM staging, the gastric cancer risk is classified as low or high.RESULTS Twenty-eight gastric cancers were diagnosed during the follow-up, and the incidence rate was 1.72 per 1000 patient-years. The cancer risk associated positively with TAIM [Hazard ratio(HR) 2.70, 95%CI: 1.09–6.69, P = 0.03]. The risk increased through OLGIM stages 0-Ⅳ(0 vs Ⅳ: HR 5.72, 95%CI: 1.03–31.77, P for trend = 0.004), but not through OLGA stages 0–Ⅳ(0 vs Ⅳ: HR 5.77, 95%CI:0.67–49.77, P for trend = 0.10). The sensitivities of OLGA and OLGIM stages Ⅲ–Ⅳ were low, 21% and 32%, respectively, whereas that of TAIM high-risk was good, 79%. On the contrary, OLGA and OLGIM had high specificity, 85% and81%, respectively, but TAIM showed low specificity, 42%. In all three staging systems, the high-risk men had three-to four-times higher gastric cancer risk compared to the general male population of the same age.CONCLUSION OLGIM and TAIM stagings show prognostic value in assessing gastric cancer risk in elderly male smokers with atrophic gastritis.

Helicobacter pylori infection, glandular atrophy and intestinal metaplasia in superficial gastritis, gastric erosion, erosive gastritis, gastric ulcer and early gastric cancer

AIM: To evaluate the histological features of gastric mucosa, including Helicobacter pylori infection in patients with early gastric cancer and endoscopically found superficial gastritis, gastric erosion, erosive gastritis,gastric ulcer.METHODS: The biopsy specimens were taken from the antrum, corpus and upper angulus of all the patients.Giemsa staining, improved toluidine-blue staining, and H pylori-specific antibody immune staining were performed as appropriate for the histological diagnosis of H pylori infection. Hematoxylin-eosin staining was used for the histological diagnosis of gastric mucosa inflammation, gastric glandular atrophy and intestinal metaplasia and scored into four grades according to the Updated Sydney System.RESULTS: The overall prevalence of H pylori infection in superficial gastritis was 28.7%, in erosive gastritis 57.7%,in gastric erosion 63.3%, in gastric ulcer 80.8%, in early gastric cancer 52.4%. There was significant difference (P＜0.05), except for the difference between early gastric cancer and erosive gastritis. H pylori infection rate in antrum, corpus, angulus of patients with superficial gastritis was 25.9%, 26.2%, 25.2%, respectively; in patients with erosive gastritis 46.9%, 53.5%, 49.0%,respectively; in patients with gastric erosion 52.4%, 61.5%,52.4%, respectively; in patients with gastric ulcer 52.4%,61.5%, 52.4%, respectively; in patients with early gastric cancer 35.0%, 50.7%, 34.6%, respectively. No significant difference was found among the different site biopsies in superficial gastritis, but in the other diseases the detected rates were higher in corpus biopsy (P＜0.05). The grades of mononuclear cell infiltration and polymorphonuclear cell infiltration, in early gastric cancer patients, were significantly higher than that in superficial gastritis patients, lower than that in gastric erosion and gastric ulcer patients (P＜0.01);however, there was no significant difference compared with erosive gastritis. The grades of mucosa glandular atrophy and intestinal metaplasia were significantly highest in early gastric cancer, lower in gastric ulcer, the next were erosive gastritis, gastric erosion, the lowest in superficial gastritis (P＜0.01). Furthermore, 53.3% and 51.4% showed glandular atrophy and intestinal metaplasia in angular biopsy specimens, respectively; but only 40.3%and 39.9% were identified in antral biopsy, and 14.1%and 13.6% in corpus biopsy; therefore, the angulus was more reliable for the diagnosis of glandular atrophy and intestinal metaplasia compared with antrum and corpus (P＜0.01). The positivity rate of glandular atrophy and intestinal metaplasia of superficial gastritis with H pyloripositivity was 50.7%, 34.1%; of erosive gastritis 76.1%,63.0%; of gastric erosion 84.8%, 87.8%; of gastric ulcer 80.6%, 90.9%; and of early gastric cancer 85.5%, 85.3%,respectively. The positivity rate of glandular atrophy and intestinal metaplasia of superficial gastritis with H pylorinegativity was 9.9%, 6.9%; of erosive gastritis 42.5%,42.1%; of gastric erosion 51.1%, 61.9%; of gastric ulcer 29.8%, 25.5%; and of early gastric cancer 84.0%,86.0%,respectively. The positivity rate of glandular atrophy and intestinal metaplasia of superficial gastritis, erosive gastritis, gastric erosion, and gastric ulcer patients with H pylori positivity was significantly higher than those with H pylori negativity (P＜0.01); however, there was no significant difference in patients with early gastric cancer with or without H pylori infection.CONCLUSION: The progression of the gastric pre-cancerous lesions, glandular atrophy and intestinal metaplasia in superficial gastritis, gastric erosion, erosive gastritis and gastric ulcer was strongly related to H pylori infection. In depth studies are needed to evaluate whether eradication of H pylori infection will really diminish the risk of gastric cancer.

Prevalence of Helicobacter pylori infection and intestinal metaplasia in subjects who had undergone surgery for gastric adenocarcinoma in Northwest Italy

AIM: To investigate the seroprevalence of Helicobacter pylori(H pylorri) infection and its more virulent strains as well as the correlation with the histologic features among patients who had undergone surgery for gastric cancer (GC).METHODS: Samples from 317 (184 males, 133females, mean age 69±3.4 years) consecutive patients who had undergone surgery for gastric non-cardia adenocarcinoma were included in the study. Five hundred and fifty-five (294 males, 261 females, mean age 57.3±4.1 years) patients consecutively admitted to the Emergency Care Unit served as control. Histological examination of tumor, lymph nodes and other tissues obtained at the time of surgery represented the diagnostic 'gold standard'. An enzyme immunosorbent assay was used to detect serum anti-H pylori(IgG)antibodies and Western blotting technique was utilized to search for anti-CagA protein (IgG).RESULTS: Two hundred and sixty-one of three hundred and seventeen (82.3%) GC patients and 314/555 (56.5%)controls were seropositive for anti-H pylori (P＜0.0001;OR, 3.58; 95%CI, 2.53-5.07). Out of the 317 cases, 267(84.2%) were seropositive for anti-CagA antibody vs 100 out of 555 (18%) controls (P＜0.0001; OR, 24.30;95%CI, 16.5-35.9). There was no difference between the frequency of H pyloriin intestinal type carcinoma (76.2%) and diffuse type cancer (78.8%). Intestinal metaplasia (IM) was more frequent but not significant in the intestinal type cancer (83.4% vs 75.2% in diffuse type and 72.5% in mixed type). Among the patients examined for IM, 39.8% had IM type Ⅰ, 8.3% type Ⅱ and 51.9% type Ⅲ (type Ⅲ vs others, P = 0.4).CONCLUSION; This study confirms a high seroprevalence of H pyloriinfection in patients suffering from gastric adenocarcinoma and provides further evidence that searching for CagA status over H pylori infection might confer additional benefit in identifying populations at greater risk for this tumor.

Gastric intestinal metaplasia is associated with gastric dysplasia but is inversely correlated with esophageal dysplasia

AIM To determine which clinical factors might be associated with gastric intestinal metaplasia(IM) in a North American population.METHODS Pathology and endoscopy databases at an academicmedical center were reviewed to identify patients with and without gastric IM on biopsies for a retrospective cohort study. Patient demographics, insurance status, and other clinical factors were reviewed.RESULTS Four hundred and sixty-eight patients with gastric IM(mean age: 61.0 years ± 14.4 years, 55.5% female) and 171 without gastric IM(mean age: 48.8 years ± 20.8 years, 55.0% female) were compared. The endoscopic appearance of atrophic gastritis correlated with finding gastric IM on histopathology(OR = 2.05, P = 0.051). Gastric IM was associated with histologic findings of chronic gastritis(OR = 2.56, P < 0.001), gastric ulcer(OR = 6.97, P = 0.015), gastric dysplasia(OR = 6.11, P = 0.038), and gastric cancer(OR = 6.53, P = 0.027). Histologic findings of Barrett's esophagus(OR = 0.28, P = 0.003) and esophageal dysplasia(OR = 0.11, P = 0.014) were inversely associated with gastric IM. Tobacco use(OR = 1.73, P = 0.005) was associated with gastric IM.CONCLUSION Patients who smoke or have the endoscopic finding of atrophic gastritis are more likely to have gastric IM and should have screening gastric biopsies during esophagogastroduodenoscopy(EGD). Patients with gastric IM are at increased risk for having gastric dysplasia and cancer, and surveillance EGD with gastric biopsies in these patients might be reasonable.

-765G > C COX-2 polymorphism may be a susceptibility marker for gastric adenocarcinoma in patients with atrophy or intestinal metaplasia

AIM: To investigate the relationship between the -765G > C COX-2 polymorphism and the development of different gastric lesions: atrophy or intestinal metaplasia and gastric adenocarcinoma. METHODS: A cross-sectional study was performed involving 320 Portuguese individuals (210 without evidence of neoplastic disease, 73 patients with gastric adenocarcinomas and 37 with atrophy or intestinal metaplasia) using a PCR-RFLP method. RESULTS: -765C allele was overrepresented in the patients with gastric adenocarcinoma (51%) when compared either with the control group (38%) or patients with atrophy or intestinal metaplasia (27%). Callele was found to be very common in our population (0.22), and a multivariate logistic regression analysis revealed nearly 3-fold increased risk for the progression to gastric adenocarcinoma in patients with atrophy or intestinal metaplasia carrying the -765C allele (OR = 2.67, 95% CI = 1.03-6.93; P = 0.04).considered as another susceptibility marker for gastric adenocarcinoma development in patients with atrophy or intestinal metaplasia.

Comparison of white-light endoscopy,optical-enhanced and aceticacid magnifying endoscopy for detecting gastric intestinal metaplasia:A randomized trial

BACKGROUND Gastric intestinal metaplasia(GIM)is a precancerous lesion of the stomach,which severely affects human life and health.Currently,a variety of endoscopic techniques are used to screen/evaluate GIM.Traditional white-light endoscopy(WLE)and acetic-acid chromoendoscopy combined with magnifying endoscopy(MEAAC)are the interventions of choice due to their diagnostic efficacy for GIM.Optical-enhanced magnifying endoscopy(ME-OE)is a new virtual chromoendoscopy technique to identify GIM,which combines bandwidth-limited light and image enhancement processing technology to enhance the detection of mucosal and vascular details.We hypothesized that ME-OE is superior to WLE and MEAAC in the evaluation of GIM.AIM To directly compare the diagnostic value of WLE,ME-AAC,and ME-OE for detection of GIM.METHODS A total of 156 patients were subjected to consecutive upper gastrointestinal endoscopy examinations using WLE,ME-AAC,and ME-OE.Histopathological findings were utilized as the reference standard.Accuracy,sensitivity,specificity,and positive and negative predictive values of the three endoscopy methods in the diagnosis of GIM were evaluated.Moreover,the time to diagnosis with MEAAC and ME-OE was analyzed.Two experts and two non-experts evaluated the GIM images diagnosed using ME-OE,and diagnostic accuracy and intra-and inter-observer agreement were analyzed.RESULTS GIM was detected in 68 of 156 patients(43.6%).The accuracy of ME-OE was highest(91.7%),followed by ME-AAC(86.5%),while that of WLE(51.9%)was lowest.Per-site analysis showed that the overall diagnostic accuracy of ME-OE was higher than that of ME-AAC(P=0.011)and WLE(P<0.001).The average diagnosis time was lower in ME-OE than in ME-AAC(64±7 s vs 151±30 s,P<0.001).Finally,the inter-observer agreement was strong for both experts(k=0.862)and non-experts(k=0.800).The internal consistency was strong for experts(k=0.713,k=0.724)and moderate for non-experts(k=0.667,k=0.598).CONCLUSION For endoscopists,especially experienced endoscopists,ME-OE is an efficient,convenient,and time-saving endoscopic technique that should be used for the diagnosis of GIM.

A squamous metaplasia in a gastric ulcer scar of the antrum

An 81-year-old man presented with epigastric pain and weight loss for one month. He had a past history of pulmonary tuberculosis, 10 years ago. We performed a gastroscopy, which showed a linear depressed whitish gastric ulcer scar (0.8 cm in length) in the posterior wall of the prepyloric antrum. The result of biopsy was reported as squamous epithelium. Immunohistochemical staining using an antibody to high molecular weight cytokeratin (HMC) revealed positive staining in the squamous epithelium. Two years later, the lesion was followed up. The lesion remained at same site endoscopically, but no squamous epithelium could be seen microscopically.

Gastric intestinal metaplasia development in African American predominant United States population

BACKGROUND Gastric cancer significantly contributes to cancer mortality globally.Gastric intestinal metaplasia(GIM)is a stage in the Correa cascade and a premalignant lesion of gastric cancer.The natural history of GIM formation and progression over time is not fully understood.Currently,there are no clear guidelines on GIM surveillance or management in the United States.AIM To investigate factors associated with GIM development over time in African American-predominant study population.METHODS This is a retrospective longitudinal study in a single tertiary hospital in Washington DC.We retrieved upper esophagogastroduodenoscopies(EGDs)with gastric biopsies from the pathology department database from January 2015 to December 2020.Patients included in the study had undergone two or more EGDswith gastric biopsy.Patients with no GIM at baseline were followed up until they developed GIM or until the last available EGD.Exclusion criteria consisted of patients age<18,pregnancy,previous diagnosis of gastric cancer,and missing data including pathology results or endoscopy reports.The study population was divided into two groups based on GIM status.Univariate and multivariate Cox regression was used to estimate the hazard induced by patient demographics,EGD findings,and Helicobacter pylori(H.pylori)status on the GIM status.RESULTS Of 2375 patients who had at least 1 EGD with gastric biopsy,579 patients were included in the study.138 patients developed GIM during the study follow-up period of 1087 d on average,compared to 857 d in patients without GIM(P=0.247).The average age of GIM group was 64 years compared to 56 years in the non-GIM group(P<0.001).In the GIM group,adding one year to the age increases the risk for GIM formation by 4%(P<0.001).Over time,African Americans,Hispanic,and other ethnicities/races had an increased risk of GIM compared to Caucasians with a hazard ratio(HR)of 2.12(1.16,3.87),2.79(1.09,7.13),and 3.19(1.5,6.76)respectively.No gender difference was observed between the study populations.Gastritis was associated with an increased risk for GIM development with an HR of 1.62(1.07,2.44).On the other hand,H.pylori infection did not increase the risk for GIM.CONCLUSION An increase in age and non-Caucasian race/ethnicity are associated with an increased risk of GIM formation.The effect of H.pylori on GIM is limited in low prevalence areas.

Gastric Intestinal Metaplasia Is the Most Common Histopathological Phenotype among Endoscopically Diagnosed Atrophic Gastritis Patients in North-East China

Background: Gastric cancer and gastric precancerous lesions are highly prevalent in China. However, prevalence of the different precancerous lesions has not been reported from the north-east region of China. Detection of precancerous gastric lesions at an early stage complemented with a follow-up strategy for high risk groups would probably aid in declining the mortality rate in patients with gastric cancer. Helicobacter pylori infection, salt intake, smoking, alcohol, family history of gastric cancer, atrophic gastritis and intestinal metaplasia are established risk factors of gastric cancer. The aim of this study was to evaluate the frequency of various histopathological phenotypes among atrophic gastritis patients in this region and to report if gender and increasing age carry risk in the development of these lesions. Methods: This retrospective study was conducted on 518 patients with endoscopic diagnosis of atrophic gastritis. Using the patient number in database, histopathological diagnosis of the biopsy specimen of all patients was recorded. All biopsy specimens were assessed for the presence of inflammation, atrophic gastritis, metaplasia and/or dysplasia. Results: Intestinal metaplasia was observed in 67.38% of patients. Dysplasia and atrophy were present in 9.46% and 3.67% patients, respectively. Gender and increasing age were not found to be risk factors for intestinal metaplasia, dysplasia and atrophic gastritis (p-values 0.08, 0.43, 0.297 and 0.98, 0.20, 0.54;respectively). 19.49% subjects showed inflammatory activity which was significantly associated with female gender (P = 0.0008). Conclusion: Intestinal metaplasia was the most histopathological phenotype among endoscopically diagnosed atrophic gastritis patients. Large-population based on prospective studies should be designed to determine prevalence of precancerous lesions and the risk factors involved in the progression of these lesions in our region.

Long-term Follow-up Study on Gastric Intestinal Metaplasia Subtype and Its Relation to Expression of P53,Bcl-2 and PCNA

Objective： To investigate the correlation of typies of gastric intestinal metaplasia（IM）, expression of p53, bcl-2 and the proliferating cell nuclear antigen（PCNA）, with the lesion＇s evolution. Methods： A total of 80 patients with IM（53 male and 27 female, 35-64 years old） from an area with high-risk of gastric cancer（GC） in China were enrolled into this prospective study, including 28 cases of type Ⅰ （complete）, 25 cases of type Ⅱ （incomplete） , and 27 cases of type Ⅲ （incomplete）. Of the 80 cases, 62 cases including 19 cases of type Ⅰ, 22 type Ⅱ and 21 type Ⅲ, were followed up for 5-14 years（49 cases for 14 years, 6 for 10 years, and 7 for 5 years）. All of the 80 cases were studied immunohistochemically for the expression of p53, bcl-2 and PCNA. Results： The rate of p53-expressing cases was higher in type Ⅲ（25.9%） than in type Ⅰ（10.7%） and type Ⅱ （12.0%）, but without statistical significance（P=0.3070）. The positive rate of bcl-2 was obviously lower in type Ⅰ （21.4%） and type Ⅱ （24.0%） than in type Ⅲ（37.0%）, but not statistically significant（P=0.4223）. We observed difference in PCNA labelling index （LI） between type Ⅱ and type Ⅲ（P=0.0037）, and the difference was particularly significant in type Ⅰ as compared with type Ⅲ（P〈0.0001）. There was no statistical significance between type I and type II （P=0.0616）. Evolution into GC was detected in 0%, 4.5%, and 14.3% of type Ⅰ, type Ⅱ, and type Ⅲ IM cases, respectively. Progression to dysplasia was detected in 31.6%, 18.2%, and 14.3% of type Ⅰ, type Ⅱ, and type Ⅲ IM cases, respectively. Persistence of IM was documented in 31.6%, 45.5%, and 42.9% of type Ⅰ, type Ⅱ, and type Ⅲ IM cases, respectively. Regression of IM was documented in 36.8%, 31.8%, and 28.6% of type Ⅰ, type Ⅱ, and type ⅢIM cases, respectively. In progressive, persistent and regressive groups, the positive rates of p53 were 17.6%, 16.0% and 15.0%, bcl-2 were 29.4%, 36.0% and 25.0%, and PCNA LIs were 24.953±14.477, 23.752±12.934 and 25.105±10.055, respectively. There were no significant differences between the groups. Conclusion： The present follow-up study indicated that type Ⅲ had a higher risk for development of cancer than type Ⅰ or Ⅱ. PCNA LI was significantly higher in type Ⅲthan in type Ⅰ and Ⅱ, suggesting that cell proliferation in type Ⅲwas more active. Our data also indicated that the expression of p53 and bcl-2 had no apparent association with the particular type and the expression of p53, bcl-2 and PCNA had no apparent correlation with evolution of IM. Further studies with a larger sample size are needed to verify present observation.

Microsatellite Instability in Intestinal Metaplasia and Gastric Cancer

Objective: To investigate the changeable patterns of microsatellite instability(MSI)in intestinal metaplasia(IM)and gastric cancer(GC)and the role of MSI in gastric carcinogenesis. Methods: Silver staining single strand conformation polymorphism-polymeriase chain reaction(PCR-SSCP)was used to screen MSI markers at 5 loci in formalin-fixed,paraffin-embedded tissues of GC(n=30),IM(n=40)and corresponding normal gastric tissues. Results: The abnormal shifting of the single-strand DNA was identified in 7(23.3%)out of GC and in 8(20%)out of IM samples.Three(10%)tumors and one(2.5%)IM displayed high-frequency MSI(two or more loci altered).Low-frequency MSI(one loci altered)was detected in 4(13.3%)of the tumors and in 7(17.5%)IM samples.GC with MSI was associated with distal location of the tumors but age,sex,differentiation,lymph nodes metastasis and TNM stage(P=0.044).MSI was more likely detected in moderate-grade IM than in mild-grade IM tissues(34.8% versus 0; P=0.013); and MSI had a tendency to be easily detected in female with IM. Conclusion: The progressive accumulation of MSI in areas of IM may contribute to GC development,representing an important molecular event in the multistep gastric carcinogenesis.

Gastric Atrophy, Intestinal Metaplasia in Helicobacter pylori Gastritis: Prevalence and Predictors Factors

Gastric atrophy and intestinal metaplasia represent the most important premalignant lesions in gastric carcinogenesis. The severity of gastric mucosal inflammation depends on the bacterium Helicobacter pylori (HP), on the host and on environmental factors. The aim of our study is to determine the prevalence and factors associated with Gastric atrophy and intestinal metaplasia in patients infected with Helicobacter pylori. Methods: This is a prospective study over a period of 4 years (May 2009 - January 2015) conducted in the service of Hepatology and Gastroenterology in hospital university Hassan II of Fez in collaboration with microbiology and molecular biology laboratory and epidemiology service of Faculty of Medicine and Pharmacy Fes. We included in our study all patients aged over 15 years, having ulcerative dyspepsia, peptic ulcer disease, gastritis or esophagitis. Results: During the study period, 1190 patients were included of which 70% had HP infection (N = 833). The average age was 48.21 years [16 - 99 years], sex ratio M/F was 1, 11. 60% of patients were older than 45 years. Chronic smoking was found in 12% of patients. Gastric atrophy was observed in 84% (N = 699) of patients infected with HP. Gastric atrophy was localized in 70% in the antrum and 30% in the fundus and 24% in both. The activity of gastritis (p = 0.0001) and the density of the HP (p = 0.005) were factors associated with atrophy. Intestinal metaplasia was observed in 13.5% of patients (N = 112). The density of HP (p = 0.037) and severe atrophy (p = 0.001) were factors associated with metaplasia. Other factors studied: age, sex, smoking, CagA+ genotype were not associated with either gastric atrophy or intestinal metaplasia. Conclusion: In our study, the prevalence of atrophic gastritis and intestinal metaplasia in patients infected with Helicobacter pylori was 84% and 13.5% respectively, which was a high prevalence. The activity of gastritis, and density of HP were factors associated with atrophy. The density of HP and severe atrophy were factors associated with metaplasia.

窄带成像放大内镜分级系统在慢性萎缩性胃炎实时诊断及危险分层中的价值研究

目的探讨窄带成像放大内镜(narrow band imaging magnification endoscopy,NBI-ME)分级系统在慢性萎缩性胃炎(chronic atrophic gastritis,CAG)实时诊断及危险分层中的价值。方法收集40岁以上接受NBI-ME检查患者的内镜和病理资料,评估NBI-ME分级系统和组织病理学金标准—OLGA/OLGIM(operative link for gastritis assessment/operative link for gastric intestinal metaplasia assessment)分期系统的相关性及一致性。结果共纳入63例患者,男41例,女22例,胃窦和胃体部的NBI-ME评分和组织学评分的一致性均为73.0%,总体一致性显著(Kappa=0.695,P<0.05;加权Kappa=0.907,P<0.05),其中胃窦的一致性良好(Kappa=0.604,P<0.05),胃体的一致性中等(Kappa=0.487,P<0.05);Cochran-Mantel-Haenszel分析表明,高危NBI-ME分级(Ⅱ~Ⅳ级)的患者诊断为高危OLGA/OLGIM分期的可能性更高(P<0.0001),NBI-ME分级诊断高危CAG/GIM的敏感性为81.8%(95%CI:59.7%~94.8%),特异性为95.1%(95%CI:83.5%~99.4%)。结论NBI-ME评分与组织病理学评分具有较高一致性,它是一种简便、经济并实时诊断CAG及识别胃癌高危人群的检查及随访方式。

MEX3A、CDX2、MUC2与MUC5AC判断可癌变胃肠化生的应用价值

目的 探讨MEX3A与胃癌和肠上皮化生(以下简称肠化生)分化特性的相关性及其联合尾型同源盒转录因子2(caudal-related homeobox transcription factor 2,CDX2)、黏蛋白2(mucin 2,MUC2)和黏蛋白5AC(mucin 5AC,MUC5AC)判断可癌变肠化生的作用。方法 选取2010年1月至2014年12月沈阳医学院附属中心医院、沈阳医学院附属第二医院外科手术切除的胃癌及癌旁石蜡包埋组织样本410例,根据病理诊断将其分为对照组(轻度浅表性胃炎,79例)、肠化生组(149例)和胃癌组(182例)。免疫组织化学检测各组MEX3A、CDX2、MUC2和MUC5AC的表达。结果 MEX3A高表达于胃癌组及肠化生组,特别是弥漫型胃癌、低分化胃癌和Ⅲ型肠化生(P<0.05);CDX2和MUC2高表达于胃癌组和肠化生组,特别是肠型胃癌、高中分化胃癌、Ⅰ型和Ⅱ型肠化生(P<0.05);MUC5AC高表达于对照组,低表达于胃癌组和肠化生组,特别是肠型胃癌、Ⅰ型和Ⅲ型肠化生(P<0.05)。胃癌和肠化生分化程度与MEX3A和MUC5AC表达均呈负相关,与CDX2和MUC2表达呈正相关(P<0.05)。胃癌组织中MEX3A与CDX2、MUC2表达呈负相关,与MUC5AC表达呈正相关(P<0.05);肠化生组织中MEX3A与CDX2、MUC2表达呈负相关(P<0.05),CDX2与MUC2表达呈正相关(P<0.05)。结论 MEX3A与胃癌和肠化生分化程度呈负相关,胃癌具有MEX3A高表达、CDX2和MUC2低表达的特点。