BACKGROUND Gastric cancer(GC)is a highly lethal malignancy with a high incidence and mortality rate globally.Its development follows the Correa model,with intestinal metaplasia(IM)being a critical precursor to GC.Howe...BACKGROUND Gastric cancer(GC)is a highly lethal malignancy with a high incidence and mortality rate globally.Its development follows the Correa model,with intestinal metaplasia(IM)being a critical precursor to GC.However,the mechanisms underlying IM progression to GC remain unclear.This study explored ex-tracellular matrix(ECM)-related gene changes during IM progression to GC,aiming to identify biomarkers that could improve early diagnosis and treatment strategies for GC,ultimately enhancing patient outcomes.AIM To analyze transcriptome sequencing data,molecular biomarkers that can predict GC risk and monitor IM progression can be identified,providing new insights and strategies for preventing IM-GC transformation.METHODS Weighted gene co-expression network analysis served for confirming gene modules.Upregulated ECM-related genes were further tested using univariate Cox regression and least absolute shrinkage and selection operator analysis to select hub genes and construct a survival analysis model.The intestinal cell model was established by stimulating GES-1 cells with chenodeoxycholic acid.RESULTS Weighted gene co-expression network analysis identified 1709 differentially expressed genes from the GSE191275 dataset,while The Cancer Genome Atlas stomach adenocarcinoma revealed 4633 differentially expressed genes.The intersection of these datasets identified 71 upregulated and 171 downregulated genes,which were enriched in ECM-related pathways.Univariate Cox regression analysis identified six genes with prognostic significance,and least absolute shrinkage and selection operator regression pinpointed secreted protein acidic and rich in cysteine(SPARC)and SERPINE1 as non-zero coefficient genes.A prognostic model integrating clinical tumor node metastasis staging,age,SERPINE1,and SPARC was constructed.Immunohistochemistry analysis confirmed an increasing expression of SPARC protein from normal gastric mucosa(-),to IM(+-to+),and to GC(+to++),with significant differences(P<0.05).Western blot analysis demonstrated significantly higher SPARC expression in induced intestinal cells compared to GES-1.Furthermore,after SPARC knockdown in the human GC cell line HGC27,cell counting kit-8 and colony formation assays showed a reduction in cell proliferative ability,while the wound healing assay revealed impaired cell migration capacity.CONCLUSION Comprehensive analysis suggested that a model incorporating clinical tumor node metastasis staging,age,and SPARC/SERPINE1 expression served as a prognostic predictor for GC.Moreover,elevated SPARC expression in IM and GC suggests its potential as a proper biomarker to detect GC in early stage and as a novel therapeutic target,guiding clinical applications.展开更多
BACKGROUND Esophageal epidermoid metaplasia(EEM)is a rare potentially premalignant oesophageal lesion characterized by a dense granular layer with overlying hyperorthokeratosis resembling the epidermis of skin.Given t...BACKGROUND Esophageal epidermoid metaplasia(EEM)is a rare potentially premalignant oesophageal lesion characterized by a dense granular layer with overlying hyperorthokeratosis resembling the epidermis of skin.Given the low prevalence,data to guide management also remains sparse.CASE SUMMARY We highlight a case of a 60-year-old male who presented with gastroesophageal reflux disease symptoms 2 years after an index gastroscopy which showed C0M1 Barrett’s oesophagus.The repeat gastroscopy detected a 15 mm oesophageal epidermoid metaplasia on a background of stable Barrett’s esophagus.This was rather peculiar as the images form his index gastroscopy 2 years prior did not reveal any suspicious oesophageal mucosal abnormality.He underwent a successful endoscopic mucosal resection within 3 months with a surveillance gastroscopy scheduled 6 months later.The cases of confirmed EEM are very low.One study demonstrated out of 1048 consecutive oesophageal biopsies and resections for any indication,only two were EEM(0.19%).It was also noted that the prevalence of epidermoid metaplasia was significantly higher(P<0.05)in the 58 patients with oesophageal squamous neoplasms,two of whom(3.5%)had concurrent epidermoid metaplasia.CONCLUSION This association necessitates careful consideration when determining resection vs surveillance-based management of EEM.展开更多
BACKGROUND Gastric intestinal metaplasia(IM)is a precancerous lesion that is associated with an elevated risk of gastric carcinogenesis.Weiwei Decoction(WWD)is a promising traditional Chinese herbal formula widely emp...BACKGROUND Gastric intestinal metaplasia(IM)is a precancerous lesion that is associated with an elevated risk of gastric carcinogenesis.Weiwei Decoction(WWD)is a promising traditional Chinese herbal formula widely employed in clinical for treating IM.Previous studies suggested the potential involvement of the olfactomedin 4(OLFM4)/nucleotide-binding oligomerization domain 1(NOD1)/caudal-type homeobox gene 2(CDX2)signaling pathway in IM regulation.AIM To verify the regulation of the OLFM4/NOD1/CDX2 pathway in IM,specifically investigating WWD’s effectiveness on IM through this pathway.METHODS Immunohistochemistry for OLFM4,NOD1,and CDX2 was conducted on tissue microarray.GES-1 cells treated with chenodeoxycholic acid were utilized as IM cell models.OLFM4 short hairpin RNA(shRNA),NOD1 shRNA,and OLFM4 pcDNA were transfected to clarify the pathway regulatory relationships.Protein interactions were validated by coimmunoprecipitation.To explore WWD’s pharmacological actions,IM rat models were induced using N-methyl-N’-nitro-N-nitrosoguanidine followed by WWD gavage.Gastric cells were treated with WWD-medicated serum.Cytokines and chemokines content were assessed by enzyme-linked immunosorbent assay and quantitative reverse transcription polymerase chain reaction.RESULTS The OLFM4/NOD1/CDX2 axis was a characteristic of IM.OLFM4 exhibited direct binding and subsequent downregulation of NOD1,thereby sustaining the activation of CDX2 and promoting the progression of IM.WWD improved gastric mucosal histological lesions while suppressing intestinal markers KLF transcription factor 4,villin 1,and MUCIN 2 expression in IM rats.Regarding pharmacological actions,WWD suppressed OLFM4 and restored NOD1 expression,consequently reducing CDX2 at the mRNA and protein levels in IM rats.Parallel regulatory mechanisms were observed at the protein level in IM cells treated with WWD-medicated serum.Furthermore,WWD-medicated serum treatment strengthened OLFM4 and NOD1 interaction.In case of antiinflammatory,WWD restrained interleukin(IL)-6,interferon-gamma,IL-17,macrophage chemoattractant protein-1,macrophage inflammatory protein 1 alpha content in IM rat serum.WWD-medicated serum inhibited tumor necrosis factor alpha,IL-6,IL-8 transcriptions in IM cells.CONCLUSION The OLFM4/NOD1/CDX2 pathway is involved in the regulation of IM.WWD exerts its therapeutic efficacy on IM through the pathway,additionally attenuating the inflammatory response.展开更多
Objective: To study the expression of cyclooxygenase-2 (COX-2) protein in different subtypes of intestinal metaplasia (IM) and gastric carcinoma, evaluate the possibility of COX-2 forecasting the risk of malignant pot...Objective: To study the expression of cyclooxygenase-2 (COX-2) protein in different subtypes of intestinal metaplasia (IM) and gastric carcinoma, evaluate the possibility of COX-2 forecasting the risk of malignant potential of IM, and the relationship between COX-2 expression and gastric carcinogenesis. Methods: Forty cases of chronic atrophic gastritis (CAG) with IM, 40 cases of gastric carcinoma and corresponding paracancerous tissues were selected to construct a tissue microarray. High iron diamine/alcian blue (HID/AB) staining and Hematoxylin and Eosin (HE) staining was used to classify IM and gastric carcinoma, and the expression of COX-2 protein detected in different subtypes of IM and gastric cancer by using immunohistochemistry. Results: The positive expression rate of COX-2 was 45.65%, 59.38% and 77.27% in IM foci in CAG, IM foci in paracancerous tissues, and intestinal-type gastric carcinoma, respectively, significantly higher than in diffuse-type gastric cancer (16.67%)(P<0.05, 0.005 and 0.005, respectively), and the expression intensity of COX-2 protein showed a increased tendency gradually in the sequence of IM foci in CAG→IM foci in paracancerous tissues→intestinal-type gastric carcinoma (P<0.005). The positive expression rate of COX-2 protein in type Ⅲ IM was significantly higher than in type Ⅰ and type Ⅱ IM (P<0.005 and 0.05, respectively), and the expression intensity also showed a increased tendency gradually from type Ⅰ to type Ⅲ IM (P<0.005). Conclusion: The expression level of COX-2 was increased gradually along with the increase of the risk of malignancy of IM, and its expression level may be a useful index to forecast the risk of malignant potential of IM. COX-2 expression was associated with intestinal-type gastric carcinoma, but it might also have some role in the carcinogenesis of diffuse-type gastric carcinoma.展开更多
AIM:To compare two types of classification of intestinal metaplasia(IM)of the stomach and to explore their relationship to gastric carcinoma.METHODS:Forty-seven cases of gastric IM were classified into type or typeacc...AIM:To compare two types of classification of intestinal metaplasia(IM)of the stomach and to explore their relationship to gastric carcinoma.METHODS:Forty-seven cases of gastric IM were classified into type or typeaccordingto mucin histochemical staining and compared with a novel classification in which the specimens were classif ied into simple IM(SIM)or atypical IM according to polymorphism in terms of atypical changes of the metaplastic epithelium.Forty-seven IM and thirty-seven gastric carcinoma samples were stained for p53,c-erbB-2 and Ki67 proteins by Envision immunohistochemical technique.RESULTS:There were no significant differences in the expression of p53 and c-erbB-2 among type type,typeIM and gastric carcinomas.The positive expression rate of Ki67 was significantly higher in gastric carcinomas than in type IM while no signif icant Ki67 expression differences were observed among type,typeIM and gastric carcinomas.The expression ofp53,c-erbB-2 and Ki67 proteins in 20 SIM,27 Atypical IM and 37 gastric carcinomas showed significant differences between SIM and gastric carcinomas while no significant differences were observed between Atypical IM and gastric carcinomas.CONCLUSION:Atypical IM may better reveal the pre-cancerous nature of IM and could be a helpful indicator in the clinical follow up of patients.展开更多
AIM:To compare the reliability of gastritis staging sys-tems in ranking gastritis-associated cancer risk in a large series of consecutive patients.METHODS:Gastric mucosal atrophy is the precancer-ous condition in whic...AIM:To compare the reliability of gastritis staging sys-tems in ranking gastritis-associated cancer risk in a large series of consecutive patients.METHODS:Gastric mucosal atrophy is the precancer-ous condition in which intestinal-type gastric cancer(GC)most frequently develops.The operative link for gas-tritis assessment(OLGA)staging system ranks the GC risk according to both the topography and the severity of gastric atrophy(as assessed histologically on the ba-sis of the Sydney protocol for gastric mucosal biopsy).Both cross-sectional and long-term follow-up trials have consistently associated OLGA stages Ⅲ-Ⅳ with a higher risk of GC.A recently-proposed modification of the OLGA staging system(OLGIM)basically incorporates the OLGA frame,but replaces the atrophy score with an assessment of intestinal metaplasia(IM)alone.A series of 4552 consecutive biopsy sets(2007-2009)was re-trieved and reassessed according to both the OLGA and the OLGIM staging systems.A set of at least 5 biopsy samples was available for all the cases considered.RESULTS:In 4460 of 4552 cases(98.0%),both the high-risk stages(Ⅲ + Ⅳ)and the low-risk stages(0 +Ⅰ + Ⅱ)were assessed applying the OLGA and OL-GIM criteria.Among the 243 OLGA high-risk stages,14(5.8%)were down-staged to a low risk using OLGIM.The 67(1.5%)incidentally-found neoplastic lesions(intraepithelial or invasive)were consistently associated with high-risk stages,as assessed by both OLGA and OLGIM(P < 0.001 for both).Two of 34 intestinal-type GCs coexisting with a high-risk OLGA stage(stage Ⅲ)were associated with a low-risk OLGIM stage(stage Ⅱ).CONCLUSION:Gastritis staging systems(both OLGA and OLGIM)convey prognostically important informa-tion on the gastritis-associated cancer risk.Because of its clinical impact,the stage of gastritis should be included as a conclusive message in the gastritis histol-ogy report.Since it focuses on IM alone,OLGIM staging is less sensitive than OLGA staging in the identif ication of patients at high risk of gastric cancer.展开更多
BACKGROUND Chronic atrophic gastritis(AG)with intestinal metaplasia(IM)significantly increases the risk of gastric cancer.Some medicines have showed definite therapeutic effects in AG and IM regression.AIM To validate...BACKGROUND Chronic atrophic gastritis(AG)with intestinal metaplasia(IM)significantly increases the risk of gastric cancer.Some medicines have showed definite therapeutic effects in AG and IM regression.AIM To validate the efficacy of Lamb’s tripe extract and vitamin B12 capsule(LTEVB12)initial therapy and celecoxib rescue therapy for IM and AG.METHODS A total of 255 patients were included to receive LTEVB12 initial therapy(2 capsules each time,three times daily for 6 mo)in hospital in this study.The patients with failure of IM regression continued to receive celecoxib rescue therapy(200 mg,once daily for 6 mo).After each therapy finished,the patients underwent endoscopy and biopsy examination.The regression efficiency was assessed by the operative link on gastritis assessment(OLGA)and the operative link on the gastric intestinal metaplasia assessment(OLGIM)staging system.Logistic regression analysis was applied to identify factors associated with the curative effect.RESULTS For LTEVB12 initial therapy,the reversal rates of IM and AG were 52.95%and 48.24%,respectively.Analogously,for celecoxib rescue therapy,the effective rates for IM and AG were 56.25%and 51.56%,respectively.The IM regression rate of complete therapy was up to 85.03%.In different OLGA and OLGIM stages of IM patients,therapeutic efficiency showed a significant difference in each group(P<0.05).For both therapies,patients with high stages(III or IV)of both the OLGA and OLGIM evaluation systems showed a higher IM or AG regression rate than those with low stages(I or II).Among patients with high stages(OLGIM III and IV),the IM regression rate was above 70%for each therapy.Eating habits,fresh vegetable intake,and high-salt diet were identified as independent factors for the IM reversal effect of LTEVB12 therapy,especially high-salt diet(odds ratio=1.852,P<0.05).CONCLUSION Monotherapy could reverse IM and AG.LTEVB12 initial therapy and celecoxib rescue therapy significantly increase the regression effect.IM may not be the point of no return among gastric precancerous lesions.展开更多
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...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.展开更多
Heliobacter pylori(H. pylori), a group 1 human gastric carcinogen, is significantly associated with chronic gastritis, gastric mucosal atrophy, and gastric cancer.Approximately 20% of patients infected with H. pylori ...Heliobacter pylori(H. pylori), a group 1 human gastric carcinogen, is significantly associated with chronic gastritis, gastric mucosal atrophy, and gastric cancer.Approximately 20% of patients infected with H. pylori develop precancerous lesions, among which metaplasia is the most critical. Except for intestinal metaplasia(IM), which is characterized by goblet cells appearing in the stomach glands, one type of mucous cell metaplasia, spasmolytic polypeptide-expressing metaplasia(SPEM), has attracted much attention. Epidemiological and clinicopathological studies suggest that SPEM may be more strongly linked to gastric adenocarcinoma than IM. SPEM, characterized by abnormal expression of trefoil factor 2, mucin 6, and Griffonia simplicifolia lectin II in the deep glands of the stomach, is caused by acute injury or inflammation. Although it is generally believed that the loss of parietal cells alone is a sufficient and direct cause of SPEM, further in-depth studies have revealed the critical role of immunosignals.There is controversy regarding whether SPEM cells originate from the transdifferentiation of mature chief cells or professional progenitors. SPEM plays a functional role in the repair of gastric epithelial injury. However, chronic inflammation and immune responses caused by H. pylori infection can induce further progression of SPEM to IM, dysplasia, and adenocarcinoma. SPEM cells upregulate the expression of whey acidic protein 4-disulfide core domain protein 2 and CD44 variant 9, which recruit M2 macrophages to the wound. Studies have revealed that interleukin-33, the most significantly upregulated cytokine in macrophages, promotes SPEM toward more advanced metaplasia. Overall, more effort is needed to reveal the specific mechanism of SPEM malignant progression driven by H.pylori infection.展开更多
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 consecuti...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.展开更多
Gastric cancer remains the second most frequent cause of cancer-related mortality in the world. Screening programs in some Asian countries are impractical in the majority of other countries worldwide. Therefore, follo...Gastric cancer remains the second most frequent cause of cancer-related mortality in the world. Screening programs in some Asian countries are impractical in the majority of other countries worldwide. Therefore, follow-up of precancerous lesions is advisable for secondary gastric cancer prevention. Intestinal metaplasia (IM) is recognized as a precancerous lesion for gastric cancer, increasing the risk by 6-fold. IM is highly prevalent in the general population, being detected in nearly 1 of every 4 patients undergoing upper endoscopy. The IM prevalence rate is significantly higher in patients with Helicobacter pylori (H. pylori) infection, in first-degree relatives of gastric cancer patients, in smokers and it increases with patient age. IM is the "breaking point" in the gastric carcinogenesis cascade and does not appear to regress following H. pylori eradication, although the cure of infection may slow its progression. Gastric cancer risk is higher in patients with incomplete-type IM, in those with both antral and gastric body involvement, and the risk significantly increases with IM extension over 20% of the gastric mucosa. Scheduled endoscopic control could be cost-effective in IM patients, depending on the yearly incidence of gastric cancer in IM patients, the stage of gastric cancer at diagnosis discovered at surveillance, and the cost of endoscopy. As a pragmatic behavior, yearly endoscopic control would appear justified in all IM patients with at least one of these conditions: (1) IM extension > 20%; (2) the presence of incomplete type IM; (3) first-degree relative of gastric cancer patients; and (4) smokers. In the remaining IM patients, a less intensive (2-3 years) could be proposed.展开更多
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 gast...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 Hpylori-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 pylon 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.展开更多
AIM: To investigate the effects of interleukin-8 (IL-8 ), macrophage migration inhibitory factor (MIF ) gene polymorphisms, Helicobacter pylori (H. pylori ) infection, on the risk of developing severe chronic atrophic...AIM: To investigate the effects of interleukin-8 (IL-8 ), macrophage migration inhibitory factor (MIF ) gene polymorphisms, Helicobacter pylori (H. pylori ) infection, on the risk of developing severe chronic atrophic gastritis (SCAG) and intestinal metaplasia (IM). METHODS: A total of 372 cases were selected from a cohort study in Linqu County, a high risk area for gastric cancer (GC) in northern China. To obtain a sufficient group size, patients with normal or superficial gastritis were included. Based on an average follow-up period of 56 mo, the 372 cases were divided into no progres-sion group (no histological progression from normal or superficial gastritis, n = 137), group Ⅰ (progressed from normal or superficial gastritis to SCAG, n = 134) and group Ⅱ (progressed from normal or superficial gastritis to IM, n = 101). IL-8 , MIF gene polymorphisms were detected by polymerase chain reaction-based denaturing high-performance liquid chromatography analysis and DNA sequencing. RESULTS: An increased risk of SCAG was found in subjects with IL-8-251 AA genotype [odds ratio (OR) = 2.62, 95% CI: 1.23-5.72] or IL-8-251 A allele carriers (AA + AT) (OR = 1.81, 95% CI: 1.06-3.09). An elevated risk of IM was found in subjects with IL-8-251 AT genotype (OR = 2.27, 95% CI: 1.25-4.14) or IL-8-251 A allele carriers (OR = 2.07, 95% CI: 1.16-3.69). An increased risk of SCAG was found in subjects with MIF-173 GC genotype (OR = 2.36, 95% CI: 1.38-4.02) or MIF-173 C allele carriers (GC + CC) (OR = 2.07, 95% CI: 1.21-3.55). An elevated risk of IM was found in subjects with MIF-173 CC genotype (OR = 2.27, 95% CI: 1.16-4.46) or MIF-173 C allele carriers (OR = 3.84, 95% CI: 1.58-9.34). The risk of SCAG and IM was more evident in subjects carrying IL-8-251 A allele (OR = 6.70, 95% CI: 1.29-9.78) or MIF-173 C allele (OR = 6.54, 95% CI: 2.97-14.20) and positive for H. pylori infection. CONCLUSION: IL-8-251 and MIF-173 gene polymorphisms are significantly associated with the risk of SCAG and IM in a population with a high risk of GC in Linqu County, Shandong Province, China.展开更多
AIM: To investigate the effect of H pylori eradication on atrophic gastritis and intestinal metaplasia (IM).METHODS: Two hundred and fifty-nine patients with atrophic gastritis in the antrum were included in the study...AIM: To investigate the effect of H pylori eradication on atrophic gastritis and intestinal metaplasia (IM).METHODS: Two hundred and fifty-nine patients with atrophic gastritis in the antrum were included in the study, 154 patients were selected for H pylori eradication therapy and the remaining 105 patients served as untreated group. Gastroscopy and biopsies were performed both at the beginning and at the end of a 3-year follow-up study. Gastritis was graded according to the updated Sydney system.RESULTS: One hundred and seventy-nine patients completed the follow-up, 92 of them received H pylori eradication therapy and the remaining 87 H pyloriinfected patients were in the untreated group. Chronic gastritis, active gastritis and the grade of atrophy significantly decreased in H pylori eradication group (P＜0.01). However, the grade of IM increased in H pylori -infected group (P＜0.05).CONCLUSION: H pylori eradication may improve gastric mucosal inflammation, atrophy and prevent the progression of IM.展开更多
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-section...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）.CONCLUSION： -765C carrier status should be considered as another susceptibility marker for gastric adenocarcinoma development in patients with atrophy or intestinal metaplasia.展开更多
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-c...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.展开更多
AIM:To examine how the expression of caudal type homebox transcription factor 2(Cdx2) is regulated in the development of malignancy in Barrett's esophagus.METHODS:Cdx2,mucin(MUC) series(MUC2,MUC5AC and MUC6),p53 a...AIM:To examine how the expression of caudal type homebox transcription factor 2(Cdx2) is regulated in the development of malignancy in Barrett's esophagus.METHODS:Cdx2,mucin(MUC) series(MUC2,MUC5AC and MUC6),p53 and E-cadherin expression in Barrett's esophagus and adenocarcinoma specimens were examined by immunostaining.Isolated clusters of cells from(1) MUC2 and Cdx2-positive intestinal metaplastic mucosa;(2) MUC5AC and MUC6-positive,and MUC2 and Cdx2-negative high-grade dysplasia(HD),or intramucosal adenocarcinoma(IMC);and(3) MUC5AC,MUC6 and Cdx2-positive poorly-differentiated invasive adenocarcinoma(PDA) were analyzed by methylationspecific polymerase chain reaction using sets of primers for detecting methylation status of the Cdx2 gene.RESULTS:Most of the non-neoplastic Barrett's esophageal mucosa showing intestinal-type metaplasia with or without low-grade dysplasia was positive for E-cadherin,MUC series and Cdx2,but negative for p53.A portion of the low-grade to HD was positive for E-cadherin,MUC5AC,MUC6 and p53,but negative for MUC2 and Cdx2.The definite IMC area was strongly positive for MUC5AC,MUC6 and p53,but negative for MUC2 and Cdx2.Methylation of the Cdx2 promoter was not observed in intestinal metaplasia,while hypermethylation of part of its promoter was observed in hot dipped and IMC.Hypermethylation of a large fraction of the Cdx2 promoter was observed in PDA.CONCLUSION:Cdx2 expression is restored irrespective of the methylation status of its promoter.Apparent positive immunohistochemical results can be a molecular mark for gene silencing memory.展开更多
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 muco...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.展开更多
AIM:To describe the clinical presentation and complications of portal hypertension (PH) secondary to myelofibrosis with myeloid metaplasia (MMM).METHODS: Medical records for 123 patients with MMM were reviewed.RESULTS...AIM:To describe the clinical presentation and complications of portal hypertension (PH) secondary to myelofibrosis with myeloid metaplasia (MMM).METHODS: Medical records for 123 patients with MMM were reviewed.RESULTS: Thirteen patients with PH secondary to MMM were identified. Median ages at time of MMM and PH diagnosis were 61 and 66 years, respectively. The interval from MMM diagnosis to presentation with one of the PH features ranged from 1 to 11 years. Variceal bleeding and ascites were the most common presentations. Of the eight patients who presented with variceal bleeding, six patients underwent endoscopic variceal ligation (EVL) with no variceal recurrence or hematological worsening during a 12-mo follow up period.CONCLUSION: Patients with MMM might develop PH. Exact mechanisms leading to PH in MMM are still controversial. As in other etiologies, variceal bleeding and ascites are the most common presentations. Anemia may correlate with, and/or predict, the severity of the PH presentation in these patients. EVL can successfully control variceal bleeding in MMM. Further clinical studies are required.展开更多
Objective To evaluate the gastric microbiome in patients with chronic superficial gastritis(CSG)and intestinal metaplasia(IM)and investigate the influence of Helicobacter pylori(H.pylori)on the gastric microbiome.Meth...Objective To evaluate the gastric microbiome in patients with chronic superficial gastritis(CSG)and intestinal metaplasia(IM)and investigate the influence of Helicobacter pylori(H.pylori)on the gastric microbiome.Methods Gastric mucosa tissue samples were collected from 54 patients with CSG and IM,and the patients were classified into the following four groups based on the state of H.pylori infection and histology:H.pylori-negative CSG(n=24),H.pylori-positive CSG(n=14),H.pylori-negative IM(n=11),and H.pylori-positive IM(n=5).The gastric microbiome was analyzed by 16S rRNA gene sequencing.Results H.pylori strongly influenced the bacterial abundance and diversity regardless of CSG and IM.In H.pylori-positive subjects,the bacterial abundance and diversity were significantly lower than in H.pylori-negative subjects.The H.pylori-negative groups had similar bacterial composition and bacterial abundance.The H.pylori-positive groups also had similar bacterial composition but different bacterial relative abundance.The relative abundance of Neisseria,Streptococcus,Rothia,and Veillonella were richer in the I-HP group than in G-HP group,especially Neisseria(t=175.1,P<0.001).Conclusions The gastric microbial abundance and diversity are lower in H.pylori-infected patients regardless of CSG and IM.Compared to H.pylori-positive CSG group and H.pylori-positive IM,the relative abundance of Neisseria,Streptococcus,Rothia,and Veillonella is higher in H.pylori-positive patients with IM than in H.pylori-positive patients with CSG,especially Neisseria.展开更多
基金Supported by the Inner Mongolia Autonomous Region Health Science and Technology Program,No.202201441Qingmiao Plan of Baotou Medical College,No.BYJJ-ZRQM202230。
文摘BACKGROUND Gastric cancer(GC)is a highly lethal malignancy with a high incidence and mortality rate globally.Its development follows the Correa model,with intestinal metaplasia(IM)being a critical precursor to GC.However,the mechanisms underlying IM progression to GC remain unclear.This study explored ex-tracellular matrix(ECM)-related gene changes during IM progression to GC,aiming to identify biomarkers that could improve early diagnosis and treatment strategies for GC,ultimately enhancing patient outcomes.AIM To analyze transcriptome sequencing data,molecular biomarkers that can predict GC risk and monitor IM progression can be identified,providing new insights and strategies for preventing IM-GC transformation.METHODS Weighted gene co-expression network analysis served for confirming gene modules.Upregulated ECM-related genes were further tested using univariate Cox regression and least absolute shrinkage and selection operator analysis to select hub genes and construct a survival analysis model.The intestinal cell model was established by stimulating GES-1 cells with chenodeoxycholic acid.RESULTS Weighted gene co-expression network analysis identified 1709 differentially expressed genes from the GSE191275 dataset,while The Cancer Genome Atlas stomach adenocarcinoma revealed 4633 differentially expressed genes.The intersection of these datasets identified 71 upregulated and 171 downregulated genes,which were enriched in ECM-related pathways.Univariate Cox regression analysis identified six genes with prognostic significance,and least absolute shrinkage and selection operator regression pinpointed secreted protein acidic and rich in cysteine(SPARC)and SERPINE1 as non-zero coefficient genes.A prognostic model integrating clinical tumor node metastasis staging,age,SERPINE1,and SPARC was constructed.Immunohistochemistry analysis confirmed an increasing expression of SPARC protein from normal gastric mucosa(-),to IM(+-to+),and to GC(+to++),with significant differences(P<0.05).Western blot analysis demonstrated significantly higher SPARC expression in induced intestinal cells compared to GES-1.Furthermore,after SPARC knockdown in the human GC cell line HGC27,cell counting kit-8 and colony formation assays showed a reduction in cell proliferative ability,while the wound healing assay revealed impaired cell migration capacity.CONCLUSION Comprehensive analysis suggested that a model incorporating clinical tumor node metastasis staging,age,and SPARC/SERPINE1 expression served as a prognostic predictor for GC.Moreover,elevated SPARC expression in IM and GC suggests its potential as a proper biomarker to detect GC in early stage and as a novel therapeutic target,guiding clinical applications.
文摘BACKGROUND Esophageal epidermoid metaplasia(EEM)is a rare potentially premalignant oesophageal lesion characterized by a dense granular layer with overlying hyperorthokeratosis resembling the epidermis of skin.Given the low prevalence,data to guide management also remains sparse.CASE SUMMARY We highlight a case of a 60-year-old male who presented with gastroesophageal reflux disease symptoms 2 years after an index gastroscopy which showed C0M1 Barrett’s oesophagus.The repeat gastroscopy detected a 15 mm oesophageal epidermoid metaplasia on a background of stable Barrett’s esophagus.This was rather peculiar as the images form his index gastroscopy 2 years prior did not reveal any suspicious oesophageal mucosal abnormality.He underwent a successful endoscopic mucosal resection within 3 months with a surveillance gastroscopy scheduled 6 months later.The cases of confirmed EEM are very low.One study demonstrated out of 1048 consecutive oesophageal biopsies and resections for any indication,only two were EEM(0.19%).It was also noted that the prevalence of epidermoid metaplasia was significantly higher(P<0.05)in the 58 patients with oesophageal squamous neoplasms,two of whom(3.5%)had concurrent epidermoid metaplasia.CONCLUSION This association necessitates careful consideration when determining resection vs surveillance-based management of EEM.
基金Supported by National Natural Science Foundation of China,No.82104747 and No.82305133Basic and Applied Basic Research Foundation of Guangdong Province,China,No.2020A1515110947+1 种基金General Project of Shenzhen Science and Technology Innovation Commission,No.JCYJ20230807094659030,No.JCYJ20230807094805012,No.JCYJ20210324111602007,and No.JCYJ20220531091815034the Scientific Research Project of Guangdong Provincial Bureau of Traditional Chinese Medicine,No.20221349.
文摘BACKGROUND Gastric intestinal metaplasia(IM)is a precancerous lesion that is associated with an elevated risk of gastric carcinogenesis.Weiwei Decoction(WWD)is a promising traditional Chinese herbal formula widely employed in clinical for treating IM.Previous studies suggested the potential involvement of the olfactomedin 4(OLFM4)/nucleotide-binding oligomerization domain 1(NOD1)/caudal-type homeobox gene 2(CDX2)signaling pathway in IM regulation.AIM To verify the regulation of the OLFM4/NOD1/CDX2 pathway in IM,specifically investigating WWD’s effectiveness on IM through this pathway.METHODS Immunohistochemistry for OLFM4,NOD1,and CDX2 was conducted on tissue microarray.GES-1 cells treated with chenodeoxycholic acid were utilized as IM cell models.OLFM4 short hairpin RNA(shRNA),NOD1 shRNA,and OLFM4 pcDNA were transfected to clarify the pathway regulatory relationships.Protein interactions were validated by coimmunoprecipitation.To explore WWD’s pharmacological actions,IM rat models were induced using N-methyl-N’-nitro-N-nitrosoguanidine followed by WWD gavage.Gastric cells were treated with WWD-medicated serum.Cytokines and chemokines content were assessed by enzyme-linked immunosorbent assay and quantitative reverse transcription polymerase chain reaction.RESULTS The OLFM4/NOD1/CDX2 axis was a characteristic of IM.OLFM4 exhibited direct binding and subsequent downregulation of NOD1,thereby sustaining the activation of CDX2 and promoting the progression of IM.WWD improved gastric mucosal histological lesions while suppressing intestinal markers KLF transcription factor 4,villin 1,and MUCIN 2 expression in IM rats.Regarding pharmacological actions,WWD suppressed OLFM4 and restored NOD1 expression,consequently reducing CDX2 at the mRNA and protein levels in IM rats.Parallel regulatory mechanisms were observed at the protein level in IM cells treated with WWD-medicated serum.Furthermore,WWD-medicated serum treatment strengthened OLFM4 and NOD1 interaction.In case of antiinflammatory,WWD restrained interleukin(IL)-6,interferon-gamma,IL-17,macrophage chemoattractant protein-1,macrophage inflammatory protein 1 alpha content in IM rat serum.WWD-medicated serum inhibited tumor necrosis factor alpha,IL-6,IL-8 transcriptions in IM cells.CONCLUSION The OLFM4/NOD1/CDX2 pathway is involved in the regulation of IM.WWD exerts its therapeutic efficacy on IM through the pathway,additionally attenuating the inflammatory response.
基金This study was supported by the Key Clinical Project of the Chinese Ministry of Health (No. 20012130)
文摘Objective: To study the expression of cyclooxygenase-2 (COX-2) protein in different subtypes of intestinal metaplasia (IM) and gastric carcinoma, evaluate the possibility of COX-2 forecasting the risk of malignant potential of IM, and the relationship between COX-2 expression and gastric carcinogenesis. Methods: Forty cases of chronic atrophic gastritis (CAG) with IM, 40 cases of gastric carcinoma and corresponding paracancerous tissues were selected to construct a tissue microarray. High iron diamine/alcian blue (HID/AB) staining and Hematoxylin and Eosin (HE) staining was used to classify IM and gastric carcinoma, and the expression of COX-2 protein detected in different subtypes of IM and gastric cancer by using immunohistochemistry. Results: The positive expression rate of COX-2 was 45.65%, 59.38% and 77.27% in IM foci in CAG, IM foci in paracancerous tissues, and intestinal-type gastric carcinoma, respectively, significantly higher than in diffuse-type gastric cancer (16.67%)(P<0.05, 0.005 and 0.005, respectively), and the expression intensity of COX-2 protein showed a increased tendency gradually in the sequence of IM foci in CAG→IM foci in paracancerous tissues→intestinal-type gastric carcinoma (P<0.005). The positive expression rate of COX-2 protein in type Ⅲ IM was significantly higher than in type Ⅰ and type Ⅱ IM (P<0.005 and 0.05, respectively), and the expression intensity also showed a increased tendency gradually from type Ⅰ to type Ⅲ IM (P<0.005). Conclusion: The expression level of COX-2 was increased gradually along with the increase of the risk of malignancy of IM, and its expression level may be a useful index to forecast the risk of malignant potential of IM. COX-2 expression was associated with intestinal-type gastric carcinoma, but it might also have some role in the carcinogenesis of diffuse-type gastric carcinoma.
基金Supported by The Health Department of Shandong Province,No.T 47
文摘AIM:To compare two types of classification of intestinal metaplasia(IM)of the stomach and to explore their relationship to gastric carcinoma.METHODS:Forty-seven cases of gastric IM were classified into type or typeaccordingto mucin histochemical staining and compared with a novel classification in which the specimens were classif ied into simple IM(SIM)or atypical IM according to polymorphism in terms of atypical changes of the metaplastic epithelium.Forty-seven IM and thirty-seven gastric carcinoma samples were stained for p53,c-erbB-2 and Ki67 proteins by Envision immunohistochemical technique.RESULTS:There were no significant differences in the expression of p53 and c-erbB-2 among type type,typeIM and gastric carcinomas.The positive expression rate of Ki67 was significantly higher in gastric carcinomas than in type IM while no signif icant Ki67 expression differences were observed among type,typeIM and gastric carcinomas.The expression ofp53,c-erbB-2 and Ki67 proteins in 20 SIM,27 Atypical IM and 37 gastric carcinomas showed significant differences between SIM and gastric carcinomas while no significant differences were observed between Atypical IM and gastric carcinomas.CONCLUSION:Atypical IM may better reveal the pre-cancerous nature of IM and could be a helpful indicator in the clinical follow up of patients.
基金Supported by An AIRC grant from the Veneto Regional Authorities,2009the"Guido Berlucchi"Foundation+1 种基金the"Morgagni"Association for Oncological Research (PadovaPD)
文摘AIM:To compare the reliability of gastritis staging sys-tems in ranking gastritis-associated cancer risk in a large series of consecutive patients.METHODS:Gastric mucosal atrophy is the precancer-ous condition in which intestinal-type gastric cancer(GC)most frequently develops.The operative link for gas-tritis assessment(OLGA)staging system ranks the GC risk according to both the topography and the severity of gastric atrophy(as assessed histologically on the ba-sis of the Sydney protocol for gastric mucosal biopsy).Both cross-sectional and long-term follow-up trials have consistently associated OLGA stages Ⅲ-Ⅳ with a higher risk of GC.A recently-proposed modification of the OLGA staging system(OLGIM)basically incorporates the OLGA frame,but replaces the atrophy score with an assessment of intestinal metaplasia(IM)alone.A series of 4552 consecutive biopsy sets(2007-2009)was re-trieved and reassessed according to both the OLGA and the OLGIM staging systems.A set of at least 5 biopsy samples was available for all the cases considered.RESULTS:In 4460 of 4552 cases(98.0%),both the high-risk stages(Ⅲ + Ⅳ)and the low-risk stages(0 +Ⅰ + Ⅱ)were assessed applying the OLGA and OL-GIM criteria.Among the 243 OLGA high-risk stages,14(5.8%)were down-staged to a low risk using OLGIM.The 67(1.5%)incidentally-found neoplastic lesions(intraepithelial or invasive)were consistently associated with high-risk stages,as assessed by both OLGA and OLGIM(P < 0.001 for both).Two of 34 intestinal-type GCs coexisting with a high-risk OLGA stage(stage Ⅲ)were associated with a low-risk OLGIM stage(stage Ⅱ).CONCLUSION:Gastritis staging systems(both OLGA and OLGIM)convey prognostically important informa-tion on the gastritis-associated cancer risk.Because of its clinical impact,the stage of gastritis should be included as a conclusive message in the gastritis histol-ogy report.Since it focuses on IM alone,OLGIM staging is less sensitive than OLGA staging in the identif ication of patients at high risk of gastric cancer.
基金Shaanxi Foundation for Innovation Team of Science and Technology,No.2018TD-003Project from State Key Laboratory of Cancer Biology,No.2019CBSKL2019ZZ07.
文摘BACKGROUND Chronic atrophic gastritis(AG)with intestinal metaplasia(IM)significantly increases the risk of gastric cancer.Some medicines have showed definite therapeutic effects in AG and IM regression.AIM To validate the efficacy of Lamb’s tripe extract and vitamin B12 capsule(LTEVB12)initial therapy and celecoxib rescue therapy for IM and AG.METHODS A total of 255 patients were included to receive LTEVB12 initial therapy(2 capsules each time,three times daily for 6 mo)in hospital in this study.The patients with failure of IM regression continued to receive celecoxib rescue therapy(200 mg,once daily for 6 mo).After each therapy finished,the patients underwent endoscopy and biopsy examination.The regression efficiency was assessed by the operative link on gastritis assessment(OLGA)and the operative link on the gastric intestinal metaplasia assessment(OLGIM)staging system.Logistic regression analysis was applied to identify factors associated with the curative effect.RESULTS For LTEVB12 initial therapy,the reversal rates of IM and AG were 52.95%and 48.24%,respectively.Analogously,for celecoxib rescue therapy,the effective rates for IM and AG were 56.25%and 51.56%,respectively.The IM regression rate of complete therapy was up to 85.03%.In different OLGA and OLGIM stages of IM patients,therapeutic efficiency showed a significant difference in each group(P<0.05).For both therapies,patients with high stages(III or IV)of both the OLGA and OLGIM evaluation systems showed a higher IM or AG regression rate than those with low stages(I or II).Among patients with high stages(OLGIM III and IV),the IM regression rate was above 70%for each therapy.Eating habits,fresh vegetable intake,and high-salt diet were identified as independent factors for the IM reversal effect of LTEVB12 therapy,especially high-salt diet(odds ratio=1.852,P<0.05).CONCLUSION Monotherapy could reverse IM and AG.LTEVB12 initial therapy and celecoxib rescue therapy significantly increase the regression effect.IM may not be the point of no return among gastric precancerous lesions.
文摘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.
基金Supported by the Guangdong Basic and Applied Basic Research Foundation,No.2020A1515110947the National Natural Science Foundation of China,No.82104747+1 种基金the Scientific Research Project of Guangdong Bureau of Traditional Chinese Medicine,No.20231303the Guangdong Provincial Key Research and Development Plan,No.2020B1111100011.
文摘Heliobacter pylori(H. pylori), a group 1 human gastric carcinogen, is significantly associated with chronic gastritis, gastric mucosal atrophy, and gastric cancer.Approximately 20% of patients infected with H. pylori develop precancerous lesions, among which metaplasia is the most critical. Except for intestinal metaplasia(IM), which is characterized by goblet cells appearing in the stomach glands, one type of mucous cell metaplasia, spasmolytic polypeptide-expressing metaplasia(SPEM), has attracted much attention. Epidemiological and clinicopathological studies suggest that SPEM may be more strongly linked to gastric adenocarcinoma than IM. SPEM, characterized by abnormal expression of trefoil factor 2, mucin 6, and Griffonia simplicifolia lectin II in the deep glands of the stomach, is caused by acute injury or inflammation. Although it is generally believed that the loss of parietal cells alone is a sufficient and direct cause of SPEM, further in-depth studies have revealed the critical role of immunosignals.There is controversy regarding whether SPEM cells originate from the transdifferentiation of mature chief cells or professional progenitors. SPEM plays a functional role in the repair of gastric epithelial injury. However, chronic inflammation and immune responses caused by H. pylori infection can induce further progression of SPEM to IM, dysplasia, and adenocarcinoma. SPEM cells upregulate the expression of whey acidic protein 4-disulfide core domain protein 2 and CD44 variant 9, which recruit M2 macrophages to the wound. Studies have revealed that interleukin-33, the most significantly upregulated cytokine in macrophages, promotes SPEM toward more advanced metaplasia. Overall, more effort is needed to reveal the specific mechanism of SPEM malignant progression driven by H.pylori infection.
文摘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.
文摘Gastric cancer remains the second most frequent cause of cancer-related mortality in the world. Screening programs in some Asian countries are impractical in the majority of other countries worldwide. Therefore, follow-up of precancerous lesions is advisable for secondary gastric cancer prevention. Intestinal metaplasia (IM) is recognized as a precancerous lesion for gastric cancer, increasing the risk by 6-fold. IM is highly prevalent in the general population, being detected in nearly 1 of every 4 patients undergoing upper endoscopy. The IM prevalence rate is significantly higher in patients with Helicobacter pylori (H. pylori) infection, in first-degree relatives of gastric cancer patients, in smokers and it increases with patient age. IM is the "breaking point" in the gastric carcinogenesis cascade and does not appear to regress following H. pylori eradication, although the cure of infection may slow its progression. Gastric cancer risk is higher in patients with incomplete-type IM, in those with both antral and gastric body involvement, and the risk significantly increases with IM extension over 20% of the gastric mucosa. Scheduled endoscopic control could be cost-effective in IM patients, depending on the yearly incidence of gastric cancer in IM patients, the stage of gastric cancer at diagnosis discovered at surveillance, and the cost of endoscopy. As a pragmatic behavior, yearly endoscopic control would appear justified in all IM patients with at least one of these conditions: (1) IM extension > 20%; (2) the presence of incomplete type IM; (3) first-degree relative of gastric cancer patients; and (4) smokers. In the remaining IM patients, a less intensive (2-3 years) could be proposed.
文摘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 Hpylori-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 pylon 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.
基金Supported by The Grants from Beijing Municipal Science Foundationthe Key Technology Research and Development Program, No. 2002BA711A06+1 种基金the National 973 Project, No.1998051203863 Project, No. 2006A402
文摘AIM: To investigate the effects of interleukin-8 (IL-8 ), macrophage migration inhibitory factor (MIF ) gene polymorphisms, Helicobacter pylori (H. pylori ) infection, on the risk of developing severe chronic atrophic gastritis (SCAG) and intestinal metaplasia (IM). METHODS: A total of 372 cases were selected from a cohort study in Linqu County, a high risk area for gastric cancer (GC) in northern China. To obtain a sufficient group size, patients with normal or superficial gastritis were included. Based on an average follow-up period of 56 mo, the 372 cases were divided into no progres-sion group (no histological progression from normal or superficial gastritis, n = 137), group Ⅰ (progressed from normal or superficial gastritis to SCAG, n = 134) and group Ⅱ (progressed from normal or superficial gastritis to IM, n = 101). IL-8 , MIF gene polymorphisms were detected by polymerase chain reaction-based denaturing high-performance liquid chromatography analysis and DNA sequencing. RESULTS: An increased risk of SCAG was found in subjects with IL-8-251 AA genotype [odds ratio (OR) = 2.62, 95% CI: 1.23-5.72] or IL-8-251 A allele carriers (AA + AT) (OR = 1.81, 95% CI: 1.06-3.09). An elevated risk of IM was found in subjects with IL-8-251 AT genotype (OR = 2.27, 95% CI: 1.25-4.14) or IL-8-251 A allele carriers (OR = 2.07, 95% CI: 1.16-3.69). An increased risk of SCAG was found in subjects with MIF-173 GC genotype (OR = 2.36, 95% CI: 1.38-4.02) or MIF-173 C allele carriers (GC + CC) (OR = 2.07, 95% CI: 1.21-3.55). An elevated risk of IM was found in subjects with MIF-173 CC genotype (OR = 2.27, 95% CI: 1.16-4.46) or MIF-173 C allele carriers (OR = 3.84, 95% CI: 1.58-9.34). The risk of SCAG and IM was more evident in subjects carrying IL-8-251 A allele (OR = 6.70, 95% CI: 1.29-9.78) or MIF-173 C allele (OR = 6.54, 95% CI: 2.97-14.20) and positive for H. pylori infection. CONCLUSION: IL-8-251 and MIF-173 gene polymorphisms are significantly associated with the risk of SCAG and IM in a population with a high risk of GC in Linqu County, Shandong Province, China.
基金Supported by the Scientific Research Fund of the Health Bureau of Zhejiang Province, No. 2001QN012
文摘AIM: To investigate the effect of H pylori eradication on atrophic gastritis and intestinal metaplasia (IM).METHODS: Two hundred and fifty-nine patients with atrophic gastritis in the antrum were included in the study, 154 patients were selected for H pylori eradication therapy and the remaining 105 patients served as untreated group. Gastroscopy and biopsies were performed both at the beginning and at the end of a 3-year follow-up study. Gastritis was graded according to the updated Sydney system.RESULTS: One hundred and seventy-nine patients completed the follow-up, 92 of them received H pylori eradication therapy and the remaining 87 H pyloriinfected patients were in the untreated group. Chronic gastritis, active gastritis and the grade of atrophy significantly decreased in H pylori eradication group (P＜0.01). However, the grade of IM increased in H pylori -infected group (P＜0.05).CONCLUSION: H pylori eradication may improve gastric mucosal inflammation, atrophy and prevent the progression of IM.
基金Supported by the Portuguese League Against Cancer (Liga Portuguesa Contra o Cancro-Núcleo Regional do Norte) and AstraZeneca Foundation
文摘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）.CONCLUSION： -765C carrier status should be considered as another susceptibility marker for gastric adenocarcinoma development in patients with atrophy or intestinal metaplasia.
文摘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.
基金Supported by Grant-in Aid from Ministry of Education,Sports and Culture (GP Program for Basic Science),Japan
文摘AIM:To examine how the expression of caudal type homebox transcription factor 2(Cdx2) is regulated in the development of malignancy in Barrett's esophagus.METHODS:Cdx2,mucin(MUC) series(MUC2,MUC5AC and MUC6),p53 and E-cadherin expression in Barrett's esophagus and adenocarcinoma specimens were examined by immunostaining.Isolated clusters of cells from(1) MUC2 and Cdx2-positive intestinal metaplastic mucosa;(2) MUC5AC and MUC6-positive,and MUC2 and Cdx2-negative high-grade dysplasia(HD),or intramucosal adenocarcinoma(IMC);and(3) MUC5AC,MUC6 and Cdx2-positive poorly-differentiated invasive adenocarcinoma(PDA) were analyzed by methylationspecific polymerase chain reaction using sets of primers for detecting methylation status of the Cdx2 gene.RESULTS:Most of the non-neoplastic Barrett's esophageal mucosa showing intestinal-type metaplasia with or without low-grade dysplasia was positive for E-cadherin,MUC series and Cdx2,but negative for p53.A portion of the low-grade to HD was positive for E-cadherin,MUC5AC,MUC6 and p53,but negative for MUC2 and Cdx2.The definite IMC area was strongly positive for MUC5AC,MUC6 and p53,but negative for MUC2 and Cdx2.Methylation of the Cdx2 promoter was not observed in intestinal metaplasia,while hypermethylation of part of its promoter was observed in hot dipped and IMC.Hypermethylation of a large fraction of the Cdx2 promoter was observed in PDA.CONCLUSION:Cdx2 expression is restored irrespective of the methylation status of its promoter.Apparent positive immunohistochemical results can be a molecular mark for gene silencing memory.
文摘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.
文摘AIM:To describe the clinical presentation and complications of portal hypertension (PH) secondary to myelofibrosis with myeloid metaplasia (MMM).METHODS: Medical records for 123 patients with MMM were reviewed.RESULTS: Thirteen patients with PH secondary to MMM were identified. Median ages at time of MMM and PH diagnosis were 61 and 66 years, respectively. The interval from MMM diagnosis to presentation with one of the PH features ranged from 1 to 11 years. Variceal bleeding and ascites were the most common presentations. Of the eight patients who presented with variceal bleeding, six patients underwent endoscopic variceal ligation (EVL) with no variceal recurrence or hematological worsening during a 12-mo follow up period.CONCLUSION: Patients with MMM might develop PH. Exact mechanisms leading to PH in MMM are still controversial. As in other etiologies, variceal bleeding and ascites are the most common presentations. Anemia may correlate with, and/or predict, the severity of the PH presentation in these patients. EVL can successfully control variceal bleeding in MMM. Further clinical studies are required.
基金supported by the Medicine and Health,Science and Technology Plan Project of Zhejiang(2020KY1009).
文摘Objective To evaluate the gastric microbiome in patients with chronic superficial gastritis(CSG)and intestinal metaplasia(IM)and investigate the influence of Helicobacter pylori(H.pylori)on the gastric microbiome.Methods Gastric mucosa tissue samples were collected from 54 patients with CSG and IM,and the patients were classified into the following four groups based on the state of H.pylori infection and histology:H.pylori-negative CSG(n=24),H.pylori-positive CSG(n=14),H.pylori-negative IM(n=11),and H.pylori-positive IM(n=5).The gastric microbiome was analyzed by 16S rRNA gene sequencing.Results H.pylori strongly influenced the bacterial abundance and diversity regardless of CSG and IM.In H.pylori-positive subjects,the bacterial abundance and diversity were significantly lower than in H.pylori-negative subjects.The H.pylori-negative groups had similar bacterial composition and bacterial abundance.The H.pylori-positive groups also had similar bacterial composition but different bacterial relative abundance.The relative abundance of Neisseria,Streptococcus,Rothia,and Veillonella were richer in the I-HP group than in G-HP group,especially Neisseria(t=175.1,P<0.001).Conclusions The gastric microbial abundance and diversity are lower in H.pylori-infected patients regardless of CSG and IM.Compared to H.pylori-positive CSG group and H.pylori-positive IM,the relative abundance of Neisseria,Streptococcus,Rothia,and Veillonella is higher in H.pylori-positive patients with IM than in H.pylori-positive patients with CSG,especially Neisseria.
