Clinicopathologic and endoscopic characteristics of ten patients with gastric hamartomatous inverted polyp: a single center case series.

BACKGROUND: Gastric hamartomatous inverted polyps (GHIPs) are not well characterized and remain diagnostically challenging due to rarity. Therefore, this study aims to investigate the clinicopathologic and endoscopic characteristics of patients with GHIP. METHODS: We retrospectively reviewed clinicopathologic and endoscopic features of ten patients with GHIP who were admitted to Beijing Friendship Hospital from March 2013 to July 2022. All patients were treated successfully by endoscopic resection. RESULTS: GHIPs were usually asymptomatic and found incidentally during gastroscopic examination. They may be sessile or pedunculated, with diffuse or local surface redness or erosion. On endoscopic ultrasonography, the sessile submucosal tumor-type GHIP demonstrated a heterogeneous lesion with cystic areas in the third layer of the gastric wall. Histologically, GHIPs were characterized by a submucosal inverted proliferation of cystically dilated hyperplastic gastric glands accompanied by a branching proliferation of smooth muscle bundles. Inflammatory cells infiltration was observed in the stroma, whereas only one patient was complicated with glandular low-grade dysplasia. Assessment of the surrounding mucosa demonstrated that six patients (60%) had atrophic gastritis or Helicobacter pylori-associated gastritis, and four patients (40%) had non-specific gastritis. Endoscopic resection was safe and effective. CONCLUSIONS: GHIPs often arise from the background of abnormal mucosa, such as atrophic or H.pylori-associated gastritis. We make the hypothesis that acquired inflammation might lead to the development of GHIPs. We recommend to make a full assessment of the background mucosa and H. pylori infection status for evaluation of underlying gastric mucosal abnormalities, which may be the preneoplastic condition of the stomach.

Field study examining the mucosal microbiome in equine glandular gastric disease.

Equine glandular gastric disease (EGGD) is a common disease among athletic horses that can negatively impact health and performance. The pathophysiology of this EGGD remains poorly understood. Previous studies using controlled populations of horses identified differences in the gastric glandular mucosal microbiome associated with disease. The objective of this study was to compare the gastric microbiome in horses with EGGD and those without across multiple barns and differing management practices. We hypothesized that alterations in the microbiome of the gastric glandular mucosa are associated with EGGD. A secondary objective was to perform a risk factor analysis for EGGD using the diet and management data collected. Microbial populations of biopsies from normal pyloric mucosa of horses without EGGD (control biopsies), normal pyloric mucosa of horses with EGGD (normal biopsies) and areas of glandular mucosal disruption in horses with EGGD (lesion biopsies) were compared. Lesion biopsies had a different microbial community structure than control biopsies. Control biopsies had a higher read count for the phylum Actinomycetota compared to lesion biopsies. Control biopsies also had an enrichment of the genera Staphylococcus and Lawsonella and the species Streptococcus salivarius. Lesion biopsies had an enrichment of the genera Lactobacillus and Actinobacillus and the species Lactobacillus equigenerosi. These results demonstrate differences in the gastric glandular microbiome between sites of disrupted mucosa in horses with EGGD compared to pyloric mucosa of horses without EGGD. Risk factor analysis indicated that exercise duration per week was a risk factor for EGGD.

Characterization of gastrointestinal inflammatory cell type in equine glandular gastric disease.

OBJECTIVE: To compare small intestinal inflammation with gastric inflammation in horses with and without equine gastric glandular disease (EGGD), we evaluated endoscopic, macroscopic, and microscopic findings of the glandular stomach and microscopic findings of the small intestine. ANIMALS: 36 horses. METHODS: Horses underwent endoscopy and were scored for EGGD. After euthanasia, stomachs were collected and macroscopically evaluated. Normal pyloric mucosa, glandular lesions, and small intestinal (duodenum, mid-jejunum, and ileum) samples were collected and processed for microscopic examination. Cellular infiltrate was scored. Immunohistochemistry (CD3, CD20, and Iba-1) was performed on the ventral pylorus and small intestine of horses with mild to moderate lymphoplasmacytic infiltrate. A Spearman's correlation coefficient was used to evaluate the relationship of EGGD grade with gastric glandular inflammation, and the relationships of cellular infiltrate type and severity among glandular stomach, duodenum, jejunum, and ileum. RESULTS: Gastrointestinal inflammation was common, with gastric inflammatory infiltrate identified in 92%, duodenal inflammatory infiltrate in 83%, jejunal inflammatory infiltrate in 92%, and ileal inflammatory infiltrate in 92% of horses. Endoscopic evidence of gastric disease (hyperemia or EGGD grade ≥ 2/4) was not associated with the presence or severity of duodenal, jejunal, or ileal inflammation. Gastric lymphoplasmacytic inflammation grade ≥ 2 was associated with duodenal lymphoplasmacytic inflammation grade ≥ 2. This was a convenience sample of horses presenting for euthanasia. Medical history (including deworming history) was unknown. CLINICAL RELEVANCE: Gastric lymphoplasmacytic inflammation is associated with duodenal lymphoplasmacytic inflammation but not more distal small intestinal inflammation. Intestinal inflammation is not associated with endoscopic findings (hyperemia or EGGD grade ≥ 2/4).

Endoscopic Manifestations and Clinical Characteristics of Localized Gastric Light-Chain Amyloidosis.

To determine the endoscopic and clinical features of localized gastric amyloid light-chain (AL) amyloidosis, we retrospectively examined the characteristics of nine patients (eight men and one woman) encountered by the hospitals in our network. Lesions were predominantly flat and depressed with surface vascular dilatation (n=5); others were characterized by subepithelial lesions (n=2), mucosal color change (n=1), and a mass-like morphology with swollen mucosal folds (n=1). Colonoscopy (n=7), video capsule enteroscopy (n=2), serum (n=5) and urine immunoelectrophoresis (n=4), and bone marrow examination (n=3) were performed to exclude involvement of organs other than the stomach. As treatment for gastric lesions of AL amyloidosis, one patient each underwent endoscopic submucosal dissection (n=1) and argon plasma coagulation (n=1), while the remaining seven patients underwent no specific treatment. During a mean follow-up of 4.2 years, one patient died 3.2 years after diagnosis, but the cause of death, which occurred in another hospital, was unknown. The remaining eight patients were alive at the last visit. In conclusion, although localized gastric AL amyloidosis can show various macroscopic features on esophagogastroduodenoscopy, flat, depressed lesions with vascular dilatation on the surface are predominant.

An unusual cause of a protuberant lesion of the gastric antrum.

A 58-year-old man presented to our hospital due to upper abdominal pain for 2 months. Gastroscopy showed a 1.5×1.5×1 cm3 protuberant lesion in the gastric antrum. Magnifying endoscopy with blue laser imaging showed roughly normal micro-surface and micro-vessel structure. Endoscopic ultrasonography showed the lesion originated from the muscularis propria, with low-density irregular cystic echo. Then the patient received treatment of gastrointestinal lesions with endoscopic submucosal dissection. During the operation, it could be seen that the lesion was mainly located in the submucosa, the local depth of which reached the muscularis mucosae. It was tan-white in color, with toughness and cystic tactile sensation. The operation went smoothly and his recovery was good. Pathological studies showed that pancreatic tissue was found in the lesion, which was composed of exocrine acini and ducts. Meanwhile, dilated cystic glands were found in the excised specimens. He was eventually diagnosed as ectopic pancreas in gastric antrum complicated with gastritis cystica profunda (GCP).

Altered Fecal Microbiome and Correlations of the Metabolome with Plasma Metabolites in Dairy Cows with Left Displaced Abomasum.

Left displaced abomasum (LDA) in postpartum dairy cows contributes to significant economic losses. Dairy cows with LDA undergo excessive lipid mobilization and insulin resistance. Although gut dysbiosis is implicated, little is known about the role of the gut microbiota in the abnormal metabolic processes of LDA. To investigate the functional links among microbiota, metabolites, and disease phenotypes in LDA, we performed 16S rDNA gene amplicon sequencing and liquid chromatography-tandem mass spectrometry (LC-MS/MS) of fecal samples from cows with LDA (n = 10) and healthy cows (n = 10). Plasma marker profiling was synchronously analyzed. In the LDA event, gut microbiota composition and fecal metabolome were shifted in circulation with an amino acid pool deficit in dairy cows. Compared with the healthy cows, salicylic acid derived from microbiota catabolism was decreased in the LDA cows, which negatively correlated with Akkermansia, Prevotella, non-esterified fatty acid (NEFA), and ß-hydroxybutyric acid (BHBA) levels. Conversely, fecal taurolithocholic acid levels were increased in cows with LDA. Based on integrated analysis with the plasma metabolome, eight genera and eight metabolites were associated with LDA. Of note, the increases in Akkermansia and Oscillospira abundances were negatively correlated with the decreases in 4-pyridoxic acid and cytidine levels, and positively correlated with the increases in NEFA and BHBA levels in amino acid deficit, indicating pyridoxal metabolism-associated gut dysbiosis and lipolysis. Changes in branched-chain amino acids implicated novel host-microbial metabolic pathways involving lipolysis and insulin resistance in cows with LDA. Overall, these results suggest an interplay between host and gut microbes contributing to LDA pathogenesis. IMPORTANCE LDA is a major contributor to economic losses in the dairy industry worldwide; however, the mechanisms associated with the metabolic changes in LDA remain unclear. Most previous studies have focused on the rumen microbiota in terms of understanding the contributors to the productivity and health of dairy cows; this study further sheds light on the relevance of the lower gut microbiota and its associated metabolites in mediating the development of LDA. This study is the first to characterize the correlation between gut microbes and metabolic phenotypes in dairy cows with LDA by leveraging multi-omics data, highlighting that the gut microbe may be involved in the regulation of lipolysis and insulin resistance by modulating the amino acid composition. Moreover, this study provides new markers for further research to understand the pathogenesis of the disease as well as to develop effective treatment and prevention strategies.

Gastric Histopathologic Findings Are Similar in Portal Hypertension Patients With and Without Endoscopic Portal Hypertensive Gastropathy.

OBJECTIVES: Portal hypertensive gastropathy (PHG) is a diagnosis made based on endoscopic findings in the appropriate clinical setting. Biopsy may be taken during endoscopy for correlation, but the pathologist may encounter a myriad of nonspecific histologic findings. We undertook this study to evaluate contexts where a histologic diagnosis of PHG might be rendered on biopsy. METHODS: Two cohorts were established: stomach biopsy specimens from patients with cirrhosis or undergoing varices screening (n = 188) and stomach biopsy specimens with findings interpreted as PHG in the pathology report (n = 29). RESULTS: In the first cohort, cases with endoscopic varices more frequently displayed foveolar hyperplasia and acute inflammation, with no other histologic differences between cases with and without endoscopic PHG, clinical varices, and clinical cirrhosis. Cases from the second cohort showed no histologic differences when stratified for endoscopic PHG, endoscopic varices, and clinical cirrhosis. Our second cohort displayed the majority of charted histologic findings more frequently than the first. Our results indicate that neither an endoscopic appearance of PHG nor particular clinical diagnoses associated with PHG translate into specific histologic findings. CONCLUSIONS: Although the histologic findings charted displayed increased frequency in pathology reports with an interpretation of PHG, histology should not be used reliably in the diagnosis of PHG.

Effect of melatonin on electrical impedance and biomarkers of damage in a gastric ischemia/reperfusion model.

The damage to the gastrointestinal mucosa induced by ischemia/reperfusion (I/R) is closely related to high mortality in critically ill patients, which is attributable, in part, to the lack of an early method of diagnosis to show the degree of ischemia-induced injury in this type of patients. Electrical Impedance Spectroscopy (EIS) has been shown to be a tool to early diagnose gastric mucosal damage induced by ischemia. A therapeutic alternative to reduce this type of injury is melatonin (MT), which has gastroprotective effects in I/R models. In this work, the effect of treatment with MT on the electrical properties of gastric tissue, biomarkers of inflammatory (iNOS and COX-2), proliferation, and apoptotic process under I/R conditions in male Wistar rats was evaluated through EIS, histological and immunohistochemical analysis. Treatment with MT prevents gastric mucosa damage, causing a decrease in gastric impedance parameters related to the inflammatory process and cellular damage. This suggests that EIS could be used as a tool to diagnose and monitor the evolution of gastric mucosal injury, as well as in the recovery process in critically ill patients.

Mass-Forming Gastric Heterotopia of the Rectum: A Series of 3 Cases from a Single Tertiary Health Center.

BACKGROUND Gastric heterotopia is a benign entity found throughout the gastrointestinal tract but is rarely identified in the rectum. Since 1939, only 94 cases have ever been identified, and it can present as a mass formation with symptomatology that mimics colorectal malignancy. In some instances, malignancy has been shown to arise within rectal gastric heterotopia. Here, we present 3 cases from the past 20-year period of rectal gastric heterotopia at a single tertiary institution. CASE REPORT A 25-year-old man (case 1), a 58-year-old woman (case 2), and a 33-year-old man (case 3) were found to have polypoid mass-like lesions greater than 1.0 cm within the rectum. Following biopsy, pathology showed gastric oxyntic mucosa flanked by colorectal mucosa, thus indicating gastric heterotopia. Presenting symptoms from all patients consisted of unspecified anal pain, hematochezia, or a combination of both. All patients were treated with endoscopic mucosal resection (EMR), which provided relief of symptoms and confirmed no evidence of invasive malignancy. CONCLUSIONS Rectal gastric heterotopia can mimic malignancy and in very rare instances can harbor high-grade dysplasia as well as invasive carcinoma. EMR seems to be a definitive treatment that offers relief to patient symptomatology and reassurance that any dysplasia is identified and removed.

Pattern-based approach to gastritis and gastropathy.

Histological investigation of non-neoplastic endoscopic biopsies of gastric mucosa is one of the most common tasks most pathologists have to face on daily basis. Although the most common clinical question is still being whether Helicobacter organisms are found, pathologists have to bear in mind the whole spectrum of causes and associated morphological patterns of gastritides and gastropathies, governed by characteristic combinations of various types of inflammatory infiltrate, alterative and reactive changes of epithelial component, vascular response, and variability of stromal composition. The association of histopathologic pattern with supposed etiology can be sometimes proved by direct detection of the cause of morphologic changes in the investigated endoscopic sample.

Lymphomatoid gastropathy/NK-cell enteropathy involving the stomach and intestine.

Lymphomatoid gastropathy (LyGa)/natural killer (NK)-cell enteropathy (NKCE) is recognized as a benign NK-cell lymphoproliferative disease. Due to its histological similarity to NK/T cell lymphoma, it is easy to misdiagnose, leading to unnecessary chemotherapy and poor quality of life. This disease is typically observed in the small and large intestines in North America, whereas almost all cases in Japan occur locally in the stomach. Only 11 LyGa/NKCE cases involving both gastric and intestinal lesions have been reported, and there are few reports providing endoscopic images throughout the gastrointestinal tract. We report a case of LyGa/NKCE involving both the stomach and small and large intestines with detailed upper gastrointestinal endoscopy, colonoscopy, capsule endoscopy and pathology images. Its pathogenesis currently remains elusive, but most patients with LyGa/NKCE in Japan have Helicobacter pylori (H. pylori) infection. Our patient was also positive for H. pylori infection at disease onset, but after receiving eradication therapy, ulcerative lesions in both stomach and intestine regressed and no recurrence was observed. This case suggests a link between the pathogenesis of LyGa/NKCE and H. pylori infection.

Role of Gastric Microorganisms Other than Helicobacter pylori in the Development and Treatment of Gastric Diseases.

The microenvironment in the stomach is different from other digestive tracts, mainly because of the secretion of gastric acid and digestive enzymes, bile reflux, special mucus barrier, gastric peristalsis, and so on, which all contribute to the formation of antibacterial environment. Microecological disorders can lead to gastric immune disorders or lead to the decrease of dominant bacteria and the increase of the abundance and virulence of pathogenic microorganisms and then promote the occurrence of diseases. The body performs its immune function through innate and adaptive immunity and maintains microbial balance through the mechanism of immune homeostasis. Microecological imbalance can lead to the invasion of pathogenic microorganisms and damage mucosal barrier and immune system. The coexistence of gastric microorganisms (including viruses and fungi) may play a synergistic or antagonistic role in the pathogenesis of gastric diseases. Probiotics have the ability to compete with intestinal pathogens, increase the secretion of immunoglobulin A (IgA), stimulate the production of mucin, bacteriocin, and lactic acid, regulate the expression and secretion of cytokines, and regulate the growth of microbiota, which all have beneficial effects on the host microbial environment. At present, most studies focused on Helicobacter pylori, ignoring other stomach microbes and the overall stomach microecology. So, in this article, we reviewed advances in human gastric microecology, the relationship between gastric microecology and immunity or gastric diseases, and the treatment of probiotics in gastric diseases, in order to explore new area for further study of gastric microorganisms and treatment of gastric diseases.

Autophagy-lysosome dysfunction is involved in gastric ischemia-reperfusion injury by promoting microglial activation in the paraventricular nucleus.

The hypothalamic paraventricular nucleus (PVN) is a specific center in the brain that regulates gastric mucosal injury following gastric ischemia-reperfusion (GI-R) injury. This study aimed to investigate whether autophagy-lysosome dysfunction in the PVN tissues of GI-R rats is involved in the gastric injury, and the underlying molecular mechanisms. The rat model of GI-R was established by clamping the celiac artery for 30 min and reperfusion for different hours (1, 3, and 6 h). The gastric injury was evaluated by hematoxylin and eosin staining of the stomach and the gastric mucosal index. The autophagy-lysosome dysfunction in the PVN was evaluated by the protein levels of LC3 II and Beclin-1 (markers for autophagosome activity) and the activity of acid phosphatase (a representative lysosomal enzyme). Immunohistochemical staining of ionized calcium-binding adaptor molecule 1 in the PVN was performed to evaluate microglial activation. Reactive oxygen species (ROS) content and phosphorylated γ-aminobutyric acid B receptor (p-GABAB R) expression in the PVN were also examined. The results revealed that, in GI-R rats, the shorter the reperfusion duration, the more severe the gastric mucosal damage. The autophagy-lysosome dysfunction exhibited by GI-R rats further enhanced microglial activation, ROS production, p-GABAB R expression, and gastric injury. In addition, activating microglial cells increased ROS production, p-GABAB R expression, and gastric injury in GI-R rats, while inhibiting microglial activation resulted in the opposite results. Taken together, autophagy-lysosome dysfunction induced by GI-R aggravated the gastric injury by inducing microglia activation.

Lustrous White Erosions Surrounded by an Erythematous Mucosa: A Novel Endoscopic Finding of Gastric Lesions in Patients with Wilson Disease.

Wilson disease is an inherited copper metabolism disorder. We herein report a novel endoscopic finding in three men with Wilson disease. These patients underwent upper endoscopy due to gastrointestinal symptoms or during follow-up. In each case, endoscopy revealed lustrous white erosions surrounded by an erythematous mucosa in the greater curvature of the gastric body. A biopsy of the lesions showed orcein-positive tissue, indicating copper deposition, in the interstitial stroma and fundic glands of the mucosa. All patients had been receiving treatment with zinc acetate. These endoscopic findings might have been related to the cytotoxicity of the accumulated copper and zinc acetate.

Role of the posterior mucosal defense barrier in portal hypertensive gastropathy.

Portal hypertensive gastropathy (PHG) is a complication of cirrhotic or noncirrhotic portal hypertension. PHG is very important in the clinic because it can cause acute or even massive blood loss, and its treatment efficacy and prognosis are poor. Currently, the incidence of PHG in patients with cirrhosis is 20-80%, but its pathogenesis is complicated and poorly understood. Studies have shown that portal hypertension can cause changes in gastric mucosal microcirculation hemodynamics, leading to changes in gastric mucosal histology and function and thereby weakening the mucosal defense barrier. However, no specific drug treatment plans are currently available. This article reviews the current literature to further our understanding of the mechanism underlying PHG and the relationship between PHG and the posterior mucosal defense barrier and to explore new therapeutic targets.

Helicobacter pylori infection disturbs the tumor immune microenvironment and is associated with a discrepant prognosis in gastric de novo diffuse large B-cell lymphoma.

BACKGROUND: Gastric diffuse large B-cell lymphoma (gDLBCL) related to Helicobacter pylori infection exhibits a wide spectrum of prognosis, and the tumor immune microenvironment (TIME) affects tumor progression. However, there are few studies on the correlation between prognosis and changes of TIME induced by H. pylori infection in de novo gDLBCL. METHODS: A retrospective study was performed to determine the prognostic value of TIME related to H. pylori infection in de novo gDLBCL. A total of 252 patients were included and have been treated with standard rituximab to cyclophosphamide, doxorubicin, vincristine, and prednisone chemotherapy or other similar regimens in addition to H. pylori eradication (HPE). All patients were stratified by H. pylori infection, HPE efficacy, and preliminary TIME evaluation using conventional criteria. Statistical analyses were conducted. To assess the mechanism, 30 subjects were assessed for H. pylori infection. The components and spatial distributions of TIME were analyzed. RESULTS: The median follow-up of the 252 patients was 66.6 months (range 0.7-119.2), and the 5-year overall survival (OS) was 78.0%. A total of 109 H. pylori-positive cases with pathological complete remission and high tumor-infiltrating T lymphocytes (cohort 1) had significantly higher 5-year progression-free survival (88.1% vs 70.5%, p<0.001) and OS (89.2% vs 76.6%, p<0.001) than the other 143 patients (cohort 2). Among 30 patients, 19 were cytotoxin-associated gene A-marked as the cohort 1 subset. Compared with cohort 2, cohort 1 exhibited increased inflammatory factors (tumor necrosis factor-α, interferon γ, etc) and decreased immunosuppressive components (PD-L1, PD-1, IL-10, etc). There was reduced NF-kB activation. Cancer-promoting immune cells (PD-1hiTim-3+ CTL, Tregs, M2-like macrophages, etc) occupied a minor spatial distribution, while the antitumor subtypes increased, corresponding to favorable survival. CONCLUSION: H. pylori-evoked inflammatory responses disturb the TIME, causing a differential prognosis in de novo gDLBCL, which can be used to identify patients who could benefit from HPE and immunochemotherapy.