Association between regular arrangement of collecting venules and Helicobacter pylori status in routine endoscopy

Background The sensitivity of regular arrangement of collecting venules (RAC)-positive pattern for predicting Helicobacter pylori (H. pylori)-negative status greatly altered from 93.8 to 48.0% in recent two decades of various studies, while the reason behind it remained obscure. The aim of this study was to investigate the value of RAC as an endoscopic feature for judging H. pylori status in routine endoscopy and reviewed the underlying mechanism. Methods A prospective study with high-definition non-magnifying endoscopy was performed. RAC-positive and RAC-negative patients were classified according to the collecting venules morphology of the lesser curvature in gastric corpus. Gastric biopsy specimens were obtained from the lesser and greater curvature of corpus with normal RAC-positive or abnormal RAC-negative mucosal patterns. Helicobacter pylori status was established by hematoxylin and eosin staining and immunohistochemistry. Results 41 RAC-positive and 124 RAC-negative patients were enrolled from June 2020 to September 2020. The prevalence of H. pylori infection in patients with RAC-positive pattern and RAC-negative pattern was 7.3% (3/41) and 71.0% (88/124), respectively. Among all 124 RAC-negative patients, 36 (29.0%) patients were H. pylori-negative status. Ten patients (32.3%) demonstrated RAC-positive pattern in 31 H. pylori-eradicated cases. The sensitivity, specificity, positive predictive value, and negative predictive value of RAC-positive pattern for predicting H. pylori-negative status were 51.4% (95% CI, 0.395–0.630), 96.7% (95% CI, 0.900–0.991), 92.7% (95% CI, 0.790–0.981), and 71.0% (95% CI, 0.620–0.786), respectively. Conclusions RAC presence can accurately rule out H. pylori infection of gastric corpus, and H. pylori-positive status cannot be predicted only by RAC absence in routine endoscopy. Trial registration The present study is a non-interventional trial.

A Rare case of Menetrier’s disease presenting with Protein Losing Gastropathy Mimicking Carcinoma Stomach

Ménétrier's disease (MD) (also known as giant hypertrophic gastritis or hypoproteinemic hypertrophic gastropathy) is a rare premalignant entity characterized by markedly hypertrophied mucosal folds of the fundus and the gastric corpus typically associated with , hypochlorhydria, protein losing enteropathy causing hypoalbuminemia and anemia. However, the natural history of MD in adults remains unclear and is rarely reported in the literature. Its constellation of classic symptoms includes nausea, vomiting, abdominal pain and peripheral edema, and it is associated with increased risk of gastric cancer. Nevertheless, its pathophysiology is not yet fully understood and clinical and endoscopic diagnosis can be difficult to establish. Malignant transformation in MD should not be overlooked, and regular monitoring of the gastric mucosa via endoscopy is necessary.

Alterations in mucosa-associated microbiota in the stomach of patients with gastric cancer

Purpose The purpose of this study was to characterize alterations in mucosa-associated microbiota in different anatomical locations of the stomach during gastric cancer progression and to identify associations between Helicobacter pylori infection and gastric microbial changes in patients with gastric cancer. Methods Twenty-five H. pylori negative subjects with chronic gastritis and thirty-four subjects with gastric cancer were recruited, including H. pylori negative and positive patients with tumors in the antrum and the corpus. Gastric mucosa-associated microbiota were determined by 16S ribosomal RNA gene sequencing using a 454 sequencing platform. Results We found that individuals with chronic gastritis from three different anatomical sites exhibited different microbiota compositions, although the microbial alpha diversity, richness and beta diversity were similar. Compared to patients with chronic gastritis, the gastric microbiota compositions were significantly different at the order level in the antrum and the corpus of patients with gastric cancer, which was dependent on the H. pylori infection status. Microbial alpha diversity and species richness, however, were similar between chronic gastritis and gastric cancer cases and independent of H. pylori status. The microbial community structure in patients with gastric cancer was distinct from that in patients with chronic gastritis. In addition, we found that the presence of H. pylori markedly altered the structure in gastric corpus cancer, but only mildly affected the antrum. Conclusion Our data revealed distinct niche-specific microbiota alterations during the progression from gastritis to gastric cancer. These alterations may reflect adaptions of the microbiota to the diverse specific environmental habitats in the stomach, and may play an important, as yet undetermined, role in gastric carcinogenesis.

Association Between Regular Arrangement of Collecting Venules and Helicobacter Pylori Status in Routine Endoscopy

Background: The sensitivity of regular arrangement of collecting venules (RAC)-positive pattern for predicting Helicobacter pylori (H. pylori)-negative status greatly altered from 93.8% to 48.0% in recent two decades of various studies, while the reason behind it remained obscure. The aim of this study was to investigate the value of RAC as an endoscopic feature for judging H. pylori status in routine endoscopy and reviewed the underlying mechanism.Methods: A prospective study with high-definition non-magnifying endoscopy was performed. RAC-positive and RAC-negative patients were classified according to the collecting venules morphology of the lesser curvature in gastric corpus. Gastric biopsy specimens were obtained from the lesser and greater curvature of corpus with normal RAC-positive or abnormal RAC-negative mucosal patterns. H. pylori status was established by hematoxylin and eosin staining and immunohistochemistry. Results: 41 RAC-positive and 124 RAC-negative patients were enrolled from June 2020 to September 2020. The prevalence of H. pylori infection in patients with RAC-positive pattern and RAC-negative pattern was 7.3% (3/41) and 71.0% (88/124), respectively. Among all 124 RAC-negative patients, 36 (29.0%) patients were H. pylori-negative status. Ten patients (32.3%) demonstrated RAC-positive pattern in 31 H. pylori-eradicated cases. The sensitivity, specificity, positive predictive value, and negative predictive value of RAC-positive pattern for predicting H. pylori negative status were 51.4% (95%CI, 0.395-0.630), 96.7% (95%CI, 0.900-0.991), 92.7% (95%CI, 0.790-0.981), and 71.0% (95%CI, 0.620-0.786), respectively.Conclusions: RAC presence can accurately rule out H. pylori infection of gastric corpus, and H. pylori-positive status cannot be predicted only by RAC absence in routine endoscopy.Trial registrationThe present study is a non-interventional trial.

Proteomics signature of autoimmune atrophic gastritis: towards a link with gastric cancer

Background Autoimmune atrophic gastritis (AAG) is a chronic disease that can progress to gastric cancer (GC). To better understand AAG pathology, this proteomics study investigated gastric proteins whose expression levels are altered in this disease and also in GC. Methods Using two-dimensional difference gel electrophoresis (2D-DIGE), we compared protein maps of gastric corpus biopsies from AAG patients and controls. Differentially abundant spots (|fold change|≥ 1.5, P < 0.01) were selected and identified by LC–MS/MS. The spots were further assessed in gastric antrum biopsies from AAG patients (without and with Helicobacter pylori infection) and from GC patients and unaffected first-degree relatives of GC patients. Results 2D-DIGE identified 67 differentially abundant spots, with 28 more and 39 less abundant in AAG-corpus than controls. LC–MS/MS identified these as 53 distinct proteins. The most significant (adjusted P < 0.01) biological process associated with the less abundant proteins was “tricarboxylic acid cycle”. Of the 67 spots, 57 were similarly differentially abundant in AAG-antrum biopsies irrespective of H. pylori infection status. The differential abundance was also observed in GC biopsies for 14 of 28 more abundant and 35 of 39 less abundant spots, and in normal gastric biopsies of relatives of GC patients for 6 and 25 spots, respectively. Immunoblotting confirmed the different expression levels of two more abundant proteins (PDIA3, GSTP gene products) and four less abundant proteins (ATP5F1A, PGA3, SDHB, PGC). Conclusion This study identified a proteomics signature of AAG. Many differential proteins were shared by GC and may be involved in the progression of AAG to GC.

Changes in Gastric Corpus Microbiota With Age and After Helicobacter pylori Eradication: A Long-Term Follow-Up Study

Helicobacter pylori infection changes gastric microbiota profiles. However, it is not clear whether H. pylori eradication can restore the healthy gastric microbiota. Moreover, there has been no study regarding the changes in gastric microbiota with aging. The objective of this study was to investigate the changes in gastric corpus microbiota with age and following H. pylori eradication. Changes in corpus mucosa-associated microbiota were evaluated in 43 individuals with endoscopic follow-up &gt; 1 year, including 8 H. pylori-uninfected and 15 H. pylori-infected subjects with no atrophy/metaplasia by histology and pepsinogen I/II ratio &gt; 4.0; 17 H. pylori-infected subjects with atrophy/metaplasia and pepsinogen I/II ratio &lt; 2.5; and 3 subjects with atrophy/metaplasia, no evidence of active H. pylori infection, negative for anti-H. pylori immunoglobulin G (IgG) antibody testing, and no previous history of H. pylori eradication. Successful H. pylori eradication was achieved in 21 patients. The gastric microbiota was characterized using an Illumina MiSeq platform targeting 16S ribosomal DNA (rDNA). The mean follow-up duration was 57.4 months (range, 12–145 months), and median follow-up visit was 1 (range, 1–3). Relative abundance of Lactobacillales and Streptococcus was increased with atrophy/metaplasia. In H. pylori-uninfected subjects (n = 8), an increase in Proteobacteria (Enhydrobacter, Comamonadaceae, Sphingobium); a decrease in Firmicutes (Streptococcus, Veillonella), Fusobacteria (Fusobacterium), Nocardioidaceae, Rothia, and Prevotella; and a decrease in microbial diversity were observed during the follow-up (p trend &lt; 0.05). In 10 of 21 subjects (47.6%), H. pylori eradication induced restoration of microbial diversity; however, a predominance of Acinetobacter with a decrease in microbial diversity occurred in 11 subjects (52.3%). The presence of atrophy/metaplasia at baseline and higher neutrophil infiltration in the corpus were associated with the restoration of gastric microbiota after successful eradication, whereas a higher relative abundance of Acinetobacter at baseline was associated with the predominance of Acinetobacter after H. pylori eradication (p &lt; 0.05). To conclude, in H. pylori-uninfected stomach, relative abundance of Proteobacteria increases, relative abundance of Firmicutes and Fusobacteria decreases, and microbial diversity decreases with aging. H. pylori eradication does not always restore gastric microbiota; in some individuals, gastric colonization by Acinetobacter species occurs after anti-Helicobacter treatment.

Differences in image-enhanced endoscopic findings between Helicobacter pylori-associated and autoimmune gastritis

Background and study aims The aim of this study was to elucidate the differences in image-enhanced endoscopy (IEE) findings between Helicobacter-pylori-associated and autoimmune gastritis. Patients and methods Seven H. pylori-naïve, 21 patients with H. pylori-associated gastritis and seven with autoimmune gastritis were enrolled. Mucosal atrophy in the corpus was evaluated using autofluorescence imaging and classified into small, medium and large. In a 2 × 2-cm area of the lesser curvature of the lower corpus, micromucosal pattern was evaluated by magnifying narrow band imaging and proportion of foveola (FV)- and groove (GR)-type mucosa was classified into FV > 80 %, FV 50 % to 80 %, GR 50 % to 80 %, and GR > 80 %, then a biopsy specimen was taken. Results Fifteen of 21 (71 %) H. pylori-associated gastritis patients exhibited medium-to-large atrophic mucosa at the corpus lesser curvature. All autoimmune gastritis patients had large atrophic mucosa throughout the corpus (P < 0.001). All H. pylori-naïve patients had the FV > 80 % micromucosal pattern. Nineteen of 21 (90 %) H. pylori-associated gastritis patients had varying proportions of GR- and FV-type mucosae and five of seven (71 %) autoimmune gastritis patients showed FV > 80 % mucosa (P < 0.001). Compared with patients who were H. pylori-naïve, patients with H. pylori-associated and autoimmune gastritis exhibited a higher grade of atrophy (P < 0.001), but only patients with H. pylori-associated gastritis showed a higher grade of intestinal metaplasia (P = 0.022). Large mucosal atrophy with FV > 80 % micromucosal pattern had sensitivity of 71 % (95 % CI: 29 %–96 %) and specificity of 100 % (95 % CI: 88 % to 100 %) for diagnosis of autoimmune gastritis. Conclusions IEE findings of the gastric corpus differed between H. pylori-associated and autoimmune gastritis, suggesting different pathogenesis of the two diseases.