Intestinal Metaplasia Of Gastric Mucosa Research Articles

A New Diagnosis of Intestinal Metaplasia in Gastric Mucosa: Convolutional Neural Network Based on Visual Auxiliary Method

Abstract Introduction/Objective Intestinal metaplasia (IM) is a common lesion observed in chronic gastric disease and is thought to be associated with the development of gastric cancer. One of the characteristics of IM is the presence of goblet cells. However, differentiating these inconspicuous goblet cells from glandular cavities and gastric mucus cells using traditional algorithms is inefficient. This paper proposes an interpretable auxiliary diagnosis method for gastric mucosal intestinal metaplasia based on a convolutional neural network(CNN). Methods/Case Report The overall flow chart of the algorithm is shown in Figure 1A. The self-constructed gastric mucosa dataset is utilized in this paper for IM. To improve performance, some modifications are applied to the U-Net. The auxiliary diagnosis process incorporates R34W and R34U for segmenting the glands and IM regions. The R34W represents a dual-resolution input network structure (Figure 1B). For the initial stage of the auxiliary diagnosis, the convolutional neural network calculates patches with both large and small fields for gland region segmentation. Then, the IM glands segmentation network is used to classify regions with and without IM lesions. Results (if a Case Study enter NA) The result of the WSI level mask generated after post-processing is shown in Figure 2A. R34W Net offers significant advantages in differentiating open epithelial structures and proper glands. This network effectively differentiates between proper glands and epithelial regions while maintaining precise segmentation, leveraging high-resolution features in a small visual field. The quantitative indexes of gland segmentation networks are shown in Figure 2B. As part of auxiliary diagnosis, the classification of proper glands with intestinal metaplasia achieves the highest accuracy of 0.95 and AUC of 0.975 in the test datasets (Figure 2C). The area proportion of IM regions generated by CNN is shown in Figure 2D. Conclusion This paper provides a visual auxiliary method based on a CNN for the pathological diagnosis of intestinal metaplasia. The goal is to enhance the speed and accuracy of pathologists in performing this diagnosis. Additionally, we propose a CNN with a dual-resolution input structure, which is utilized for segmenting gastric proper glands.

Weierning, a Chinese patent medicine, improves chronic atrophic gastritis with intestinal metaplasia.

Weierning tablet (WEN) is a traditional Chinese patent medicine widely used in clinical for chronic atrophic gastritis (CAG) therapy for years. However, the underlying mechanisms of WEN on anti-CAG are still unveiled. The present study aimed to elucidate the characteristic function of WEN on anti-CAG and to illuminate its potential mechanism. The CAG model was established by gavage rats with a modeling solution (consisting of 2% sodium salicylate and 30% alcohol) with irregular diets and free access to 0.1% ammonia solution for two months on end. An enzyme-linked immunosorbent assay was used to measure the serum levels of gastrin, pepsinogen, and inflammatory cytokines. qRT-PCR was applied to measure mRNA expressions of IL-6, IL-18, IL-10, TNF-α, and γ-IFN in gastric tissue. Pathological changes and the ultrastructure of gastric mucosa were examined by hematoxylin and eosin staining and transmission electron microscopy, respectively. AB-PAS staining was applied to observe the intestinal metaplasia of gastric mucosa. Immunohistochemistry and Western blot were used to measure the expression levels of mitochondria apoptosis-related proteins and Hedgehog pathway-related proteins in gastric tissues. Expressions of Cdx2 and Muc2 protein were determined by immunofluorescent staining. WEN could dose-dependently lower the serum level of IL-1β and the mRNA expressions of IL-6, IL-8, IL-10, TNF-α, and γ-IFN in gastric tissue. Also, WEN significantly alleviated the collagen deposition in gastric submucosa, regulated the expressions of Bax, Cleaved-caspase9, Bcl2, and Cytochrome c to reduce the apoptosis of gastric mucosa epithelial cells, and maintained the integrity of the gastric mucosal barrier. Moreover, WEN could reduce protein expressions of Cdx2, Muc2, Shh, Gli1, and Smo, and reverse intestinal metaplasia of gastric mucosa to block the progress of CAG. This study demonstrated a positive effect of WEN on improving CAG and reverse intestinal metaplasia. These functions were related to the suppression of gastric mucosal cells' apoptosis and the inhibition of Hedgehog pathways' activation.

Preparation, optimization and in vivo study of gastric floating tablets of constunolide and dehydrocostus lactone with ideal therapeutic effect on gastric diseases

Costunolide (COS) and dehydrocostus lactone (DEH), as natural phytochemical components, mainly originated from Aucklandiae radix (AR) and Vladimiriae radix (VR) used in the treatment of gastric diseases in traditional Chinese medicine. The α-methylene-γ-butyrolactone ring structure is the same active part of COS and DEH, and shows good curative effects, such as breast cancer, leukemia and gastric related diseases. Furthermore, the previous research of the lab team found that the combination of COS and DEH promoted the repair of gastric ulcer and effectively alleviated intestinal metaplasia of gastric mucosa. Nevertheless, the rapid gastric emptying process and inefficient gastrointestinal absorption resulted in low oral bioavailability of COS and DEH. Based on floating and swelling technology, this study developed a gastric floating drug delivery system for prolonging gastric residence time to delay the drug release in the stomach and enhance the bioavailability of COS and DEH. The gastric floating tablets of COS and DEH were prepared by the direct powder compression method, and the optimized formulation contained 30% HPMC K15 M and 10% NaHCO3. The results of response variable showed that the floating lag time was 13.50 ± 1.87 s, total floating time was 11.83 ± 0.41 h, 2 h and 12 h cumulative drug release was 29.87 ± 2.22%, 70.89 ± 4.27%, respectively. Additionally, the physicochemical properties of the floating tablets were characterized by friability, hardness, weight variation, Fourier transform infrared spectrum (FT-IR), differential scanning calorimeter (DSC) and X-ray diffraction (X-RD). The study on release kinetics showed that the drug release mechanism of gastric floating tablets of COS and DEH was both diffusion and matrix erosion. Moreover, scanning electron microscope (SEM), swelling and erosion indexes studies further explained the release mechanism. Furthermore, in vivo X-ray imaging of male New Zealand rabbits proved the gastric retention effect of the gastric floating tablets in the stomach (10 ± 3.46 h). The results of these experiments demonstrated that the gastric floating tablets of COS and DEH had the potential for a good gastric residence time and sustained release effect.

Helicobacter pylori Pathogenicity Islands and Giardia lamblia Cysteine Proteases in Role of Coinfection and Pathogenesis.

Helicobacter pylori is a well-known human-specific stomach pathogen that infects more than half of the world’s population. The infection with this bacterium can cause a variety of gastrointestinal problems, including chronic gastritis, peptic ulcers, and even cancer. H. pylori is a highly infectious bacterium. H. pylori causes an increase in gastric mucosa pH or gastric mucosa intestinal metaplasia. These modifications in the stomach environment are necessary for G. lamblia colonization to occur. Giardia lamblia is a flagellate protozoan parasite that can cause giardiasis in humans and other mammals. It dwells in the duodenum and upper jejunum. Globally, over 280 million cases of human giardiasis are predicted to occur each year. Simultaneous human colonization by G. lamblia and H. pylori is a typical occurrence since the viruses’ predisposing factors are similar in both groups. Giardiasis is a parasitic infection that affects both children and adults worldwide. Infection with Giardia is more common in underdeveloped countries. Globally, more than 200 million cases of giardiasis are detected each year. In contrast, the presence of G. lamblia in the host body triggers an immunological response comparable to that of H. pylori, with lymphocytes strongly polarized towards Th1. As a result, their combined presence exacerbates host tissue damage. The major goal of this seminar is to describe the pathophysiology, immunology, and clinical aspects of G. lamblia and H. pylori coinfection using a comprehensive search of PubMed, Lancet, and Google Scholar sources. Upper gastrointestinal problems such as upper abdominal pain, abdominal bloating, nausea, vomiting, epigastric pain/burning, and belching are all caused by both organisms. Differentiation by physical examination is impossible in people infected with both bacteria. For this coinfection distinction, a laboratory diagnosis is required. G. lamblia and H. pylori, when present together, have a synergistic effect on the host and can cause serious damage. As a result, researchers should delve deeper into the mechanics underlying this potential microbial interaction.

Helicobacter pylori-Related Metabolic Parameters and Premalignant Gastric Mucosa Histological Lesions in Swiss Bariatric Patients.

Obesity, as a major risk factor of metabolic syndrome (MetS), represents a pandemic, especially in Western societies, and is considered a risk factor for malignancies. Helicobacter pylori (Hp), is a definite carcinogen with global distribution. We aimed to investigate, for the first time in Switzerland, the main gastric mucosa premalignant histological lesions of bariatric patients in correlation with MetS components and Hp Infection (Hp-I). By reviewing retrospectively 94304 patient cases, a total of 116 eligible patients having undergone bariatric surgery were identified. The mean patient age was 48.66 years. Hp(+) patients were 24% (28/116). Presence of gastric mucosa atrophy was documented in 8/28 Hp(+) patients (29%) and (2/88) Hp(−) ones (2%) (p = 0.006). Gastric mucosa intestinal metaplasia was observed in 14/28 (50%) Hp(+) patients versus 3/88 (3.4%) of Hp(-) group (p < 0.0001). Hp(+) patients exhibited statistically higher arterial hypertension (p = 0.033). The homeostatic model of assessment insulin resistance was also statistically significantly higher for the Hp(+) group (p < 0.001). In a multivariate analysis, including arterial hypertension, gastric mucosa atrophy, and intestinal metaplasia as variables, statistical significance remained only for intestinal metaplasia (p = 0.001). In conclusion, Hp-I is associated with premalignant gastric mucosa histologic lesions and MetS components, including arterial hypertension and IR. Further large-scale prospective studies are required to confirm these findings.

ENHANCED ENDOSCOPY FOR THE DIAGNOSIS OF GASTRICANTRALINTESTINAL METAPLASIA

Background: The detection of early gastric cancer may improve survival and avoid major gastric surgeries. Gastric Intestinal Metaplasia (GIM) is a precancerous lesion of the stomach. Screening for GIM may therefore lead to early detection of gastric neoplastic lesions. Objective: This study was designed to determine the effect of conventional Narrow Band Image (NBI) in combination with acetic acid (AA-NBI) on the diagnosis of antral GIM. Patients and Methods: The present study was performed in 100 consecutive adults who required endoscopic examination at AL Hussein University Hospital, Department of Internal Medicine, Endoscopy Unit, Conventional white-light endoscopy (WLE), NBI and AA-NBI was performed in all patients by the same endoscopist during a single procedure with a GIF Q290 endoscope (Olympus Medical Systems, Tokyo, Japan), All suspicious antral gastric lesions was photographed. Any abnormal mucosal change, such as localized discoloration and rough areas, was considered indicative of GIM lesions. Results: Fifty-six (56.0%) out of the 100 individuals examined were found to have GIM (by biopsy), of which 34 (60.7%) were diagnosed correctly by NBI (sensitivity 66.7% and specificity 68.2%) and 42 (75%) were correctly identified by AA–NBI (sensitivity 75% and specificity 73.91%), as compared to only 24 (42.86%) by WLE (sensitivity 42.86% and specificity 37.5%). Therefore, the sensitivity of AA–NBI in the diagnosis of GIM was significantly higher than NBI (p < 0.05) and WLE (p < 0.001). Our study indicates that AA-NBI can improve the accuracy of endoscopy-targeted biopsies for GIM. Conclusion: Acetic acid staining combined with NBI was of a higher sensitivity and specificity in the diagnosis of intestinal metaplasia in gastric mucosa, which was in good consistency with the pathological diagnosis. Compared with the normal NBI, it was more capable to detect lesions of intestinal metaplasia in gastric mucosa, improved the accuracy of targeted biopsy to intestinal metaplasia, and has an important significance in the early detection and treatment of tumors.

ENHANCED ENDOSCOPY FOR THE DIAGNOSIS OF GASTRICANTRALINTESTINAL METAPLASIA

Background: The detection of early gastric cancer may improve survival and avoid major gastric surgeries. Gastric Intestinal Metaplasia (GIM) is a precancerous lesion of the stomach. Screening for GIM may therefore lead to early detection of gastric neoplastic lesions. Objective: This study was designed to determine the effect of conventional Narrow Band Image (NBI) in combination with acetic acid (AA-NBI) on the diagnosis of antral GIM. Patients and Methods: The present study was performed in 100 consecutive adults who required endoscopic examination at AL Hussein University Hospital, Department of Internal Medicine, Endoscopy Unit, Conventional white-light endoscopy (WLE), NBI and AA-NBI was performed in all patients by the same endoscopist during a single procedure with a GIF Q290 endoscope (Olympus Medical Systems, Tokyo, Japan), All suspicious antral gastric lesions was photographed. Any abnormal mucosal change, such as localized discoloration and rough areas, was considered indicative of GIM lesions. Results: Fifty-six (56.0%) out of the 100 individuals examined were found to have GIM (by biopsy), of which 34 (60.7%) were diagnosed correctly by NBI (sensitivity 66.7% and specificity 68.2%) and 42 (75%) were correctly identified by AA–NBI (sensitivity 75% and specificity 73.91%), as compared to only 24 (42.86%) by WLE (sensitivity 42.86% and specificity 37.5%). Therefore, the sensitivity of AA–NBI in the diagnosis of GIM was significantly higher than NBI (p < 0.05) and WLE (p < 0.001). Our study indicates that AA-NBI can improve the accuracy of endoscopy-targeted biopsies for GIM. Conclusion: Acetic acid staining combined with NBI was of a higher sensitivity and specificity in the diagnosis of intestinal metaplasia in gastric mucosa, which was in good consistency with the pathological diagnosis. Compared with the normal NBI, it was more capable to detect lesions of intestinal metaplasia in gastric mucosa, improved the accuracy of targeted biopsy to intestinal metaplasia, and has an important significance in the early detection and treatment of tumors.

Potential role of chromatin remodeling factor genes in atrophic gastritis/gastric cancer risk.

Atrophic gastritis (AG), intestinal metaplasia (IM), and Helicobacter pylori (HP) are the risk factors for the development of gastric cancer (GC). Chromatin remodeling is one of the epigenetic mechanisms involved in the carcinogenesis of GC. The purpose of this study was to investigate the expression profiles of defined chromatin remodeling genes in gastric mucosal samples and their values as gastric carcinogenesis biomarkers. In total, 95 patients were included in the study. Patients were divided into 3 groups as: GC group (n=34), AG group (n=36), and control group (n=25). AG group was further divided into subgroups based on the presence of HP and IM in gastric mucosa. Chromatin remodeling gene expressions were analyzed using real-time PCR (RT-PCR) array in all groups. Data were evaluated using the RT-qPCR primer assay data analysis software. EED, CBX3, and MTA1 were more overexpressed, whereas ARID1A, ING5, and CBX7 were more underexpressed in the AG and GC groups compared with the controls. No significant differences were observed between the AG and GC groups concerning the expression of these 6 genes, although the fold change levels of these genes in the GC group were well above than in the AG group. EED, CBX3, and MTA1 were significantly more overexpressed in HP- and IM-positive AG subgroup compared with the HP- or IM-negative AG subgroup. In conclusion, our results provide an evidence of epigenetic alterations in AG. Expressions of EED, CBX3, MTA1, ARID1A, ING5, and CBX7 may be considered as promising markers to be used in GC screening for patients with AG.

Diagnostic value of endoscopic acetic acid staining combined with narrow band imaging in the diagnosis of intestinal metaplasia in gastric mucosa

Early detection and diagnosis of intestinal metaplasia in gastric mucosa will be of great significance to delay or reverse the occurrence of gastric carcinoma. Acetic acid staining combined with narrow band imaging (NBI) was applied to this study, to investigate its value in the diagnosis of intestinal metaplasia in gastric mucosa.

Diagnostic value of endoscopic acetic acid staining combined with narrow band imaging in the diagnosis of intestinal metaplasia in gastric mucosa

Diagnostic value of endoscopic acetic acid staining combined with narrow band imaging in the diagnosis of intestinal metaplasia in gastric mucosa

Helicobacter pylori as a crucial factor in intestinal metaplasia development of gastric mucosa

&lt;p class="BodyText1"&gt;&lt;em&gt;Helicobacter pylori&lt;/em&gt; (&lt;em&gt;H. pylori&lt;/em&gt;) is detected on the surface of gastric epithelium and in goblet cells, predominantly in patients with chronic atrophic gastritis and incomplete intestinal metaplasia (IM). &lt;em&gt;H. pylori&lt;/em&gt; infection persistence leads to the formation of gastrointestinal phenotype of IM. &lt;em&gt;H. pylori&lt;/em&gt; can be considered as an etiological factor of IM. It inhibits the expression of SOX2 in gastric epithelial cells, hence activating transcription factor CDX2 as a counterpart to &lt;em&gt;MUC5AC&lt;/em&gt; gene inhibition and &lt;em&gt;MUC2&lt;/em&gt; gene induction. Thus, in metaplastic cells, programming differentiation after intestinal phenotype will develop. The role of &lt;em&gt;H. pylori&lt;/em&gt; in the origin of intestinal metaplasia of gastric mucosa was defined in this study to elucidate the probable mechanism of cell reprogramming. The activation of CDX2, with simultaneous inactivation and decreased number of genes (&lt;em&gt;e.g.&lt;/em&gt;, &lt;em&gt;SHH&lt;/em&gt;, &lt;em&gt;SOX2&lt;/em&gt;, and &lt;em&gt;RUNX3&lt;/em&gt;) responsible for gastric differentiation, was identified to cause the appearance of IM. &lt;/p&gt;

Inactivation of NKX6.3 in the stomach leads to abnormal expression of CDX2 and SOX2 required for gastric-to-intestinal transdifferentiation

Intestinal metaplasia in gastric mucosa is considered a preneoplastic lesion that progresses to gastric cancer. However, the molecular networks underlying this lesion formation are largely unknown. NKX6.3 is known to be an important regulator in gastric mucosal epithelial differentiation. In this study, we characterized the effects of NKX6.3 that may contribute to gastric intestinal metaplasia. NKX6.3 expression was significantly reduced in gastric mucosae with intestinal metaplasia. The mRNA expression levels of both NKX6.3 and CDX2 predicted the intestinal metaplasia risk, with an area under the receiver operating characteristic curve value of 0.9414 and 0.9971, respectively. Notably, the NKX6.3 expression level was positively and inversely correlated with SOX2 and CDX2, respectively. In stable AGSNKX6.3 and MKN1NKX6.3 cells, NKX6.3 regulated the expression of CDX2 and SOX2 by directly binding to the promoter regions of both genes. Nuclear NKX6.3 expression was detected only in gastric epithelial cells without intestinal metaplasia. Furthermore, NKX6.3-induced TWSG1 bound to BMP4 and inhibited BMP4-binding activity to BMPR-II. These data suggest that NKX6.3 might function as a master regulator of gastric differentiation by affecting SOX2 and CDX2 expression and the NKX6.3 inactivation may result in intestinal metaplasia in gastric epithelial cells.

Endoscopic and morphological features of chronic subatrophic gastroduodenitis in children

Aim. To identify the pecularities of clinical, functional features and morphological characteristics in children with subatrophic gastroduodenitis after eradication treatment.Methods. Gastrointestinal tract condition was examined in 26 children with subatrophic gastroduodenitis. Esophagogastroduodenoscopy with morphological analysis of biopsy specimens, esophageal pH test and urea breath test were performed.Results. 16 (60.7%) children reported low-grade pain, severe pain occurred in 3 (11.5%) patients, no abdominal pain was reported in 7 (27.6%) patients. A biopsy specimen was gained in 22 patients; moderate contamination with H. pylori was detected in 13 (59%) patients, severe - in 9 (41%) patients. Breath test was positive in all patients (n=26). Morphological study revealed fibrotic changes in 14 (63.6%) patients, atrophy and sclerosis lesions - in 7 (31.8%) and 17 (77.3%) patients, respectively, in addition to clear signs of inflammation. Intestinal metaplasia of the gastric mucosa was discovered in 4 (18.2%) children. Candidiasis of the stomach and duodenum was diagnosed in 7 (31.8%) children. All patients were administered standard eradication treatment. Repeated breath test after 4 weeks was positive in 9 (41%) patients, including 7 (31.8%) who were diagnosed with candidiasis by biopsy test. At 12 months, the control endoscopy performed in 19 patients: 5 patients, who failed to follow the recommendation, had marked clinical and endoscopic signs of relapse, no patients with good treatment compliance (n=14, 73.6%) had any clinical manifestations, although endoscopic signs of inflammation preserved in 9 (47.4%) children. Biopsy with histological examination was repeated in 9 patients. Signs of inflammation were significantly reduced in 6 (66.7%) patients, while the foci of atrophy, sclerosis and intestinal metaplasia retained in 2 out of 9 children. Contamination with H. pylori had significantly decreased.Conclusion. Endoscopic signs of gastroduodenal chronic inflammation correspond to the severity of morphological characteristics in the acute stage of gastroduodenitis. Children with preserved signs of intestinal metaplasia of gastric and duodenal mucosa require intensive treatment and prolonged follow-up.

The association between Helicobacter pylori gastritis and lymphoid aggregates, lymphoid follicles and intestinal metaplasia in gastric mucosa of children.

The aim of the study was to determine the topographic prevalence of lymphoid follicles, lymphoid aggregates, gastric glandular atrophy and intestinal metaplasia among children with chronic abdominal pain. The association between these lesions and age, type of gastritis and Helicobacter pylori density was also assessed. A total of 358 patients (mean age: 10, 18 ± 3, 26 years; male : female ratio: 0.92) with chronic abdominal pain who had upper gastrointestinal endoscopy were included in the study. The endoscopic and histopathological findings were documented. The prevalence of lymphoid follicles, lymphoid aggregates, atrophy and intestinal metaplasia according to the type of gastritis and their relation with H. pylori density were determined. H. pylori was detected in 214 (59.8%) patients. H. pylori- positive patients were found to be significantly older than H. pylori-negative patients (P < 0.01). The endoscopy revealed that the most common finding observed was antral nodularity in H. pylori-positive patients and normal mucosal appearance in H. pylori-negative patients. Panmucosal gastritis both in the corpus and antrum and the prevalence of lymphoid follicles and lymphoid aggregates were more frequent in the H. pylori-positive group (P < 0.01). None of the patients had atrophy, whereas 11 patients had intestinal metaplasia. Although positive correlation was obtained between lymphoid lesions and H. pylori density, no significant relation was established between intestinal metaplasia, lymphoid lesions and H. pylori density. Lymphoid follicles and lymphoid aggregates in gastric mucosa involving both antrum and corpus significantly correlated with H. pylori infection, H. pylori density and type of gastritis in children.

Prognostic factors for metastatic colorectal cancer after first-line chemotherapy with FOLFOX-4 or FOLFIRI regimen.

Information on prognostic factors for metastatic colorectal cancer is an important basis for planning the treatment and predicting the outcomes of the patients; however, it has not been well established. The aim of this study was to identify factors that predict results of chemotherapy and to establish a plan for treatment of patients whose tumors are inoperable due to metastatic colorectal cancer. We conducted a retrospective review of records from 75 patients treated for colorectal cancer in Kosin University Gospel Hospital, from October 2004 to September 2008. Patients with inoperable tumors due to metastasis at the time of diagnosis who were treated with oxaliplatin or irinotecan as the first-line treatment were included in this study. We investigated the factors that might have an effect on overall survival. A total of 75 patients were included in this study. Results of univariate analysis showed that hemoglobin (Hb) ≥10 g/dL at the time of diagnosis, no increase in CEA on the follow-up examination after chemotherapy, chemotherapy plus surgery, and better response to chemotherapy were significant prognostic factors. Results of multivariate analysis showed that Hb ≥10 g/dL at the time of diagnosis (p<0.001), surgery after chemotherapy (p=0.001), and better response to chemotherapy (p=0.014) were significant prognostic factors. In this study, Hb ≥10 g/dL at the time of diagnosis, surgery after chemotherapy, and better response to chemotherapy were significant prognostic factors for metastatic colorectal cancer.

The co-expression of functional gastric proteins in dynamic gastric diseases and its clinical significance

BackgroundPepsinogen C (PGC) and mucin1 (MUC1) are important physiologically functional gastric proteins; Mucin2 (MUC2) is an “ectopic” functional protein in intestinal metaplasia of gastric mucosa. We analyzed the co-expression of the above-mentioned three proteins in dynamic gastric diseases {superficial gastritis (SG)-atrophic gastritis (AG)--gastric cancer (GC)} as well as different histological types of gastric cancer in order to find molecular phenotypes of gastric cancer and precancerous disease and further explore the potential co-function of PGC, MUC1 and MUC2 in the occurrence and development of gastric cancer.MethodsThe SG-AG-GC sequence was 57-57-70 cases in this case–control study, respectively. Different histological types of GC were 28 cases of highly and moderately differentiated aden ocarcinoma (HMDA)、30 of poorly differentiated adenocarcinoma (PDA) and 12 of mucinous adenocarcinoma (MA) or signet ring cell carcinoma (SRCC). PGC, MUC1 and MUC2 expression in situ were detected in all 184 cases using immunohistochemistry.ResultsBoth PGC and MUC1 had a significantly decreased expression in GC than in SG and AG (P < 0.0001 and P < 0.01, respectively); While MUC2 had a significant increased expression in AG than in SG and GC (P < 0.0001). Seven phenotypes of PGC, MUC1 and MUC2 co-expression were found in which PGC+/MUC1+/MUC2- phenotype took 94.7%(54/57) in SG group; PGC+/MUC1+/MUC2+ and PGC-/MUC1+/MUC2+ phenotype took 43.9% (25/57) and 52.6% (30/57) in AG; the phenotypes in GC group appeared variable; extraordinarily, PGC-/MUC1-/MUC2+ phenotype took 100% (6/6) in MA or SRCC group and had a statistical significance compared with others (P < 0.05).ConclusionsPhenotypes of PGC, MUC1 and MUC2 co-expression in dynamic gastric diseases are variable. In SG group it always showed PGC+/MUC1+/MUC2- phenotype and AG group showed two phenotypes (PGC+/MUC1+/MUC2+ and PGC-/MUC1+/MUC2+); the phenotypes in GC group appeared variable but the phenotype of PGC-/MUC1-/MUC2+ may be a predictive biomarker for diagnosing MA or SRCC, or distinguishing histological MA or SRCC from tubular adenocarcinoma accompanied by mucinous secretion or signet ring cell scattered distribution.

Correlations among Helicobacter pylori infection and the expression of cyclooxygenase‐2 and vascular endothelial growth factor in gastric mucosa with intestinal metaplasia or dysplasia

To examine the rate of Helicobacter pylori infection and the expression of cyclooxygenase-2 (COX-2) and vascular endothelial growth factor (VEGF) in gastric mucosa with intestinal metaplasia or dysplasia, and explore their correlations in precancerous gastric lesions. A total of 172 patients were included in the study. H. pylori infection was evaluated by hematoxylin-eosin and modified Giemsa staining. The expression of COX-2 and VEGF proteins was detected by immunohistochemistry. The rates of H. pylori infection in gastric mucosal dysplasia (DYS), intestinal metaplasia in gastric mucosa (IM), chronic atrophic gastritis (CAG) and chronic superficial gastritis (CSG) patients were significant differences (P = 0.001). The average optical density (AOD) values of COX-2 staining in CSG, CAG, IM and DYS patients were 13.81 +/- 5.53, 45.28 +/- 21.44, 73.67 +/- 26.02 and 91.23 +/- 45.11, respectively, with significant differences among CSG, CAG and IM patients (P = 0.037, 0.001 and 0.047 for CSG vs CAG, CSG vs IM and CAG vs IM, respectively). The expression level of VEGF in DYS patients was significantly higher than those in other patients (P = 0.001, 0.001 and 0.001 for DYS vs CSG, DYS vs CAG and DYS vs IM, respectively). The expression levels of COX-2 in H. pylori-positive IM, CAG and DYS patients were significantly higher than those in H. pylori-negative counterparts (P = 0.043, 0.009, 0.001, respectively). Additionally, the expression level of COX-2 was positively correlated with that of VEGF with the aggravation of gastric mucosal lesions (r = 0.640, P = 0.006). H. pylori infection might be able to induce the expression of COX-2 in precancerous gastric lesions, which in turn upregulates the expression of VEGF.

Incomplete Intestinal Metaplasia as an Indicator for Early Detection of Gastric Carcinoma in The Events of Helicobacter Pylori Positive Chronic Atrophic Gastritis

The aim of the study was to ascertain the existence of intestinal metaplasia in gastric mucosa of patients with gastric carcinoma coupled with H. pylori positive chronic atrophic gastritis and possible connection of IM with the development of gastric carcinoma. The paper presents prospective study that included 50 patients with gastric carcinoma and 50 patients with chronic atrophic H. pylori positive gastritis. All the patients were subjected to gastroscopy as well as biopsy targeted at antrum, lesser curvature and corpus and at the area 1-2 cm removed from tumor lesion. Biopsy samples were sliced by microtome and stained. We analyzed presence, frequency and severity of inflammatory-regenerative, metaplastic and dysplastic changes in the mucosa and evaluated their prognostic value. We typed IM immunohistochemically. This study confirmed responsibility of H. pylori for inflammatory events in gastric mucosa in patients with gastric carcinoma. According to our findings incomplete IM of types IIa and IIb as precancerous lesion is responsible for the development of gastric carcinoma and is associated with chronic atrophic gastritis grade I and II (92% of subjects, p=0.0097, h=1, p=0.01). Thus, the finding of incomplete intestinal metaplasia may be used as an indicator for early gastric carcinoma detection. Patients with patho-histologically verified incomplete intestinal metaplasia associated with active chronic atrophic gastritis of levels I and II represent risk group for the development of gastric carcinoma of intestinal type.

Frequent and Rapid Progression of Atrophy and Intestinal Metaplasia in Gastric Mucosa of Patients with MALT Lymphoma

Association of gastric mucosa-associated lymphoid tissue (MALT) low-grade lymphoma and adenocarcinoma has repeatedly been reported. The aim of this study was to evaluate the frequency and the spreading of atrophy and intestinal metaplasia in gastric mucosa of patients with gastric MALT lymphoma followed after conservative treatment. Forty-five patients (mean age 45 +/- 2.1 yr) with gastric MALT lymphoma, treated by Helicobacter pylori eradication, chemotherapy with per os single alkylating agents, or both treatments have been followed by gastroscopy with biopsies in antrum and corpus at least once a year. Univariate and multivariate analysis evaluated the association between the appearance of atrophy and intestinal metaplasia in antrum or corpus and different factors related to patients, H. pylori status, lymphoma features, and treatment. In addition, histological aspects of gastric biopsies at the diagnosis period and at the end of follow-up were compared with those of two control groups of age-matched patients with H. pylori gastritis. At the diagnosis time, only intestinal metaplasia in corpus was more frequent in patients with gastric MALT lymphoma than in patients with nonulcer dyspepsia. Within median follow-up of 54.4 months (range 9-196), the percentage of patients with gastric atrophy and intestinal metaplasia increased significantly and became significantly higher than in age-matched nonulcer dyspepsia patients. Multivariate analysis showed significant association between corpus intestinal metaplasia and corpus atrophy, intestinal metaplasia in antrum, and duration of the follow-up. Conservative management of gastric MALT lymphoma including H. pylori eradication is associated with progression of gastric atrophy and intestinal metaplasia with frequent involvement of the corpus which is known to be a precancerous condition. These findings show that long-term endoscopic monitoring should be recommended in such patients.

Histopathologic characteristics of intestinal metaplasia in gastric mucosa of children

一、材料和方法 1.材料:对1990-2004年我科及浙江大学附属儿童医院病理科共12 746例胃镜活检胃黏膜组织进行回顾性研究,其中诊断胃炎伴胃黏膜肠上皮化生55例,男性23例,女性32例,年龄最小者3岁,最大16岁,平均年龄(9.1±2.8)岁.随机抽取200例经病理诊断胃炎不伴肠化患儿作为对照组。