Revealing the pathogenesis of gastric intestinal metaplasia based on the mucosoid air-liquid interface.

BACKGROUND: Gastric intestinal metaplasia (GIM) is an essential precancerous lesion. Although the reversal of GIM is challenging, it potentially brings a state-to-art strategy for gastric cancer therapeutics (GC). The lack of the appropriate in vitro model limits studies of GIM pathogenesis, which is the issue this work aims to address for further studies. METHOD: The air-liquid interface (ALI) model was adopted for the long-term culture of GIM cells in the present work. This study conducted Immunofluorescence (IF), quantitative real-time polymerase chain reaction (qRT-PCR), transcriptomic sequencing, and mucoproteomic sequencing (MS) techniques to identify the pathways for differential expressed genes (DEGs) enrichment among different groups, furthermore, to verify novel biomarkers of GIM cells. RESULT: Our study suggests that GIM-ALI model is analog to the innate GIM cells, which thus can be used for mucus collection and drug screening. We found genes MUC17, CDA, TRIM15, TBX3, FLVCR2, ONECUT2, ACY3, NMUR2, and MAL2 were highly expressed in GIM cells, while GLDN, SLC5A5, MAL, and MALAT1 showed down-regulated, which can be used as potential biomarkers for GIM cells. In parallel, these genes that highly expressed in GIM samples were mainly involved in cancer-related pathways, such as the MAPK signal pathway and oxidative phosphorylation signal pathway. CONCLUSION: The ALI model is validated for the first time for the in vitro study of GIM. GIM-ALI model is a novel in vitro model that can mimic the tissue micro-environment in GIM patients and further provide an avenue for studying the characteristics of GIM mucus. Our study identified new markers of GIM as well as pathways associated with GIM, which provides outstanding insight for exploring GIM pathogenesis and potentially other related conditions.

UMobileNetV2 model for semantic segmentation of gastrointestinal tract in MRI scans.

Gastrointestinal (GI) cancer is leading general tumour in the Gastrointestinal tract, which is fourth significant reason of tumour death in men and women. The common cure for GI cancer is radiation treatment, which contains directing a high-energy X-ray beam onto the tumor while avoiding healthy organs. To provide high dosages of X-rays, a system needs for accurately segmenting the GI tract organs. The study presents a UMobileNetV2 model for semantic segmentation of small and large intestine and stomach in MRI images of the GI tract. The model uses MobileNetV2 as an encoder in the contraction path and UNet layers as a decoder in the expansion path. The UW-Madison database, which contains MRI scans from 85 patients and 38,496 images, is used for evaluation. This automated technology has the capability to enhance the pace of cancer therapy by aiding the radio oncologist in the process of segmenting the organs of the GI tract. The UMobileNetV2 model is compared to three transfer learning models: Xception, ResNet 101, and NASNet mobile, which are used as encoders in UNet architecture. The model is analyzed using three distinct optimizers, i.e., Adam, RMS, and SGD. The UMobileNetV2 model with the combination of Adam optimizer outperforms all other transfer learning models. It obtains a dice coefficient of 0.8984, an IoU of 0.8697, and a validation loss of 0.1310, proving its ability to reliably segment the stomach and intestines in MRI images of gastrointestinal cancer patients.

Accuracy of artificial intelligence-assisted endoscopy in the diagnosis of gastric intestinal metaplasia: A systematic review and meta-analysis.

BACKGROUND AND AIMS: Gastric intestinal metaplasia is a precancerous disease, and a timely diagnosis is essential to delay or halt cancer progression. Artificial intelligence (AI) has found widespread application in the field of disease diagnosis. This study aimed to conduct a comprehensive evaluation of AI's diagnostic accuracy in detecting gastric intestinal metaplasia in endoscopy, compare it to endoscopists' ability, and explore the main factors affecting AI's performance. METHODS: The study followed the PRISMA-DTA guidelines, and the PubMed, Embase, Web of Science, Cochrane, and IEEE Xplore databases were searched to include relevant studies published by October 2023. We extracted the key features and experimental data of each study and combined the sensitivity and specificity metrics by meta-analysis. We then compared the diagnostic ability of the AI versus the endoscopists using the same test data. RESULTS: Twelve studies with 11,173 patients were included, demonstrating AI models' efficacy in diagnosing gastric intestinal metaplasia. The meta-analysis yielded a pooled sensitivity of 94% (95% confidence interval: 0.92-0.96) and specificity of 93% (95% confidence interval: 0.89-0.95). The combined area under the receiver operating characteristics curve was 0.97. The results of meta-regression and subgroup analysis showed that factors such as study design, endoscopy type, number of training images, and algorithm had a significant effect on the diagnostic performance of AI. The AI exhibited a higher diagnostic capacity than endoscopists (sensitivity: 95% vs. 79%). CONCLUSIONS: AI-aided diagnosis of gastric intestinal metaplasia using endoscopy showed high performance and clinical diagnostic value. However, further prospective studies are required to validate these findings.

Epigenetic Modulation of GPER Expression in Gastric and Colonic Smooth Muscle of Male and Female Non-Obese Diabetic (NOD) Mice: Insights into H3K4me3 and H3K27ac Modifications.

Type 1 diabetes (T1D) affects gastrointestinal (GI) motility, favoring gastroparesis, constipation, and fecal incontinence, which are more prevalent in women. The mechanisms are unknown. Given the G-protein-coupled estrogen receptor's (GPER) role in GI motility, we investigated sex-related diabetes-induced epigenetic changes in GPER. We assessed GPER mRNA and protein expression levels using qPCR and Western blot analyses, and quantified the changes in nuclear DNA methyltransferases and histone modifications (H3K4me3, H3Ac, and H3K27Ac) by ELISA kits. Targeted bisulfite and chromatin immunoprecipitation assays were used to evaluate DNA methylation and histone modifications around the GPER promoter by chromatin immunoprecipitation assays in gastric and colonic smooth muscle tissues of male and female control (CTR) and non-obese diabetic (NOD) mice. GPER expression was downregulated in NOD, with sex-dependent variations. In the gastric smooth muscle, not in colonic smooth muscle, downregulation coincided with differences in methylation ratios between regions 1 and 2 of the GPER promoter of NOD. DNA methylation was higher in NOD male colonic smooth muscle than in NOD females. H3K4me3 and H3ac enrichment decreased in NOD gastric smooth muscle. H3K4me3 levels diminished in the colonic smooth muscle of NOD. H3K27ac levels were unaffected, but enrichment decreased in NOD male gastric smooth muscle; however, it increased in the NOD male colonic smooth muscle and decreased in the female NOD colonic smooth muscle. Male NOD colonic smooth muscle exhibited decreased H3K27ac levels, not female, whereas female NOD colonic smooth muscle demonstrated diminished enrichment of H3ac at the GPER promoter, contrary to male NOD. Sex-specific epigenetic mechanisms contribute to T1D-mediated suppression of GPER expression in the GI tract. These insights advance our understanding of T1D complications and suggest promising avenues for targeted therapeutic interventions.

Ovarian serous carcinoma with stomach metastasis: a rare case report and literature review.

Ovarian cancer is a common tumor among women. It is often asymptomatic in the early stages, with most cases already at stage III to IVE at the time of diagnosis. Direct spread and lymphatic metastasis are the primary modes of metastasis, whereas hematogenous spread is rare. An initial diagnosis of ovarian cancer that has metastasized to the stomach is also uncommon. Therefore, clear treatment methods and prognostic data for such metastasis are lacking. In our hospital, we encountered a patient with an initial imaging diagnosis of a gastric tumor and a history of an ovarian tumor with endoscopic abdominal metastasis. Based on the characteristics of the case, the two tumors were considered to be the same. After chemotherapy, a partial response was observed in the stomach and pelvic lesions, suggesting the effectiveness of the treatment. Through three treatments of recurrence, gastroscopy confirmed the stomach to be a metastatic site. Therefore, determining the primary source of advanced tumors is crucial in guiding treatment decisions. Clinicians must approach this comprehensively, relying on thorough evaluation and personal experience.

Helicobacter pylori glycan biosynthesis modulates host immune cell recognition and response.

Introduction: The pathogenic bacterium Helicobacter pylori has evolved glycan-mediated mechanisms to evade host immune defenses. This study tests the hypothesis that genetic disruption of H. pylori glycan biosynthesis alters immune recognition and response by human gastric epithelial cells and monocyte-derived dendritic cells. Methods: To test this hypothesis, human cell lines were challenged with wildtype H. pylori alongside an array of H. pylori glycosylation mutants. The relative levels of immune response were measured via immature dendritic cell maturation and cytokine secretion. Results: Our findings indicate that disruption of lipopolysaccharide biosynthesis diminishes gastric cytokine production, without disrupting dendritic cell recognition and activation. In contrast, variable immune responses were observed in protein glycosylation mutants which prompted us to test the hypothesis that phase variation plays a role in regulating bacterial cell surface glycosylation and subsequent immune recognition. Lewis antigen presentation does not correlate with extent of immune response, while the extent of lipopolysaccharide O-antigen elaboration does. Discussion: The outcomes of this study demonstrate that H. pylori glycans modulate the host immune response. This work provides a foundation to pursue immune-based tailoring of bacterial glycans towards modulating immunogenicity of microbial pathogens.

Are there new biomarkers of the gastroduodenal microbiota useful in the diagnosis of coeliac disease in children? A pilot study.

The changing of microbiome could precede the development of coeliac disease (CeD). We compared the bacterial profile of microbiota of tissues collected simultaneously from the stomach and duodenum in newly diagnosed patients with CeD. Biopsies were collected from 60 children and adolescents aged 2-18 years: (1) 40 patients with CeD; (2) 20 children as control group. The evaluation of the bacterial microbiota was carried out by sequencing the V3-V4 regions of the 16S rRNA subunit, using next-generation sequencing (NGS). The composition of bacterial microbiota was correlated with clinical and blood parameters. The beta diversity analysis revealed a significant dissimilarity in the gastric samples between the CeD and control group (Bray-Curtis index, P = 0.008, and weighted UniFrac distance, P = 0.024). At L2 (phylum level), Campylobacterota was only present in the stomach of the CeD group. A comparison of the abundance of bacteria between the stomach and duodenum showed significant differences in 10 OTUs (operational taxonomic units) in the control and 9 OTUs in the CeD group at L6 (genus) and in 8 OTUs and in 6 OTUs, respectively, at L7 (species). A significant correlation was observed between the genus Novosphingobium in stomach of CeD group and possession of the DQ2.5 and DQ 8 allele, and in the duodenum - between the DQ 8 allele and the species Blautia wexlerae. Significant differences in selected, little-known genera of bacteria suggest their potential role as new biomarkers in the development of CeD. To fully understand the mechanism of CeD development in genetically predisposed individuals, it is necessary to take into account not only the abundance of a given genus or species of bacteria, but also the anatomical location of its occurrence.

Predictors of anastomotic leak and conduit necrosis after oesophagectomy: Results from the oesophago-gastric anastomosis audit (OGAA).

BACKGROUND: Both anastomotic leak (AL) and conduit necrosis (CN) after oesophagectomy are associated with high morbidity and mortality. Therefore, the identification of preoperative, modifiable risk factors is desirable. The aim of this study was to generate a risk scoring model for AL and CN after oesophagectomy. METHODS: Patients undergoing curative resection for oesophageal cancer were identified from the international Oesophagogastric Anastomosis Audit (OGAA) from April 2018-December 2018. Definitions for AL and CN were those set out by the Oesophageal Complications Consensus Group. Univariate and multivariate analyses were performed to identify risk factors for both AL and CN. A risk score was then produced for both AL and CN using the derivation set, then internally validated using the validation set. RESULTS: This study included 2247 oesophagectomies across 137 hospitals in 41 countries. The AL rate was 14.2% and CN rate was 2.7%. Preoperative factors that were independent predictors of AL were cardiovascular comorbidity and chronic obstructive pulmonary disease. The risk scoring model showed insufficient predictive ability in internal validation (area under the receiver-operating-characteristic curve [AUROC] = 0.618). Preoperative factors that were independent predictors of CN were: body mass index, Eastern Cooperative Oncology Group performance status, previous myocardial infarction and smoking history. These were converted into a risk-scoring model and internally validated using the validation set with an AUROC of 0.775. CONCLUSION: Despite a large dataset, AL proves difficult to predict using preoperative factors. The risk-scoring model for CN provides an internally validated tool to estimate a patient's risk preoperatively.

Bisphenol A and selenium deficiency exposure induces pyroptosis and myogenic differentiation disorder in chicken muscle stomach.

Bisphenol A (BPA), which is commonly found in the environment due to its release from the use of plastics and food overpacks, has become a major stressor for environmental sustainability and livestock and poultry farming health. Selenium (Se) deficiency causes structural damage and inflammatory responses to the digestive system and muscle tissue, and there is a potential for concurrent space-time exposure to nutritional deficiency diseases and environmental toxicants in livestock and poultry. The mechanisms of damage to chicken muscular stomach from BPA or/and Se deficiency treatment are still not known. Here, we established a chicken model of BPA (20 mg/kg) or/and Se deficiency (0.039 mg/kg) exposure, and detected histopathological changes in the muscular stomach tissue, the levels of iNOS/NO pathway, IL-6/JAK/STAT3 pathway, pyroptosis, and myogenic differentiation by H&E staining, immunofluorescence staining, real-time quantitative PCR, and western blot methods. The data revealed that BPA or Se deficiency exposure caused gaps between muscle fibers with inflammatory cell infiltration; up-regulation of the iNOS/NO pathway and IL-6/JAK/STAT3 pathway; up-regulation of NLRP3/Caspase-1-dependent pyroptosis related genes; down-regulation of muscle-forming differentiation (MyoD, MyoG, and MyHC) genes. The combination of BPA and Se deficiency was associated with higher toxic impairment than alone exposure. In conclusion, we discovered that BPA and Se deficiency caused myogastric pyroptosis and myogenic differentiation disorder. These findings provide a theoretical basis for the co-occurrence of animal nutritional deficiency diseases and environmental toxicant exposures in livestock and poultry farming, and may provide important insights into limiting the production of harmful substances.

Comparison of gastric inflammation and metaplasia induced by Helicobacter pylori or Helicobacter felis colonization in mice.

Gastric cancer is the fifth most diagnosed cancer in the world. Infection by the bacteria Helicobacter pylori (HP) is associated with approximately 75% of gastric cancer cases. HP infection induces chronic gastric inflammation, damaging the stomach and fostering carcinogenesis. Most mechanistic studies on gastric cancer initiation are performed in mice and utilize either mouse-adapted strains of HP or the natural mouse pathogen Helicobacter felis (HF). Here, we identified the differences in gastric inflammation, atrophy, and metaplasia associated with HP and HF infection in mice. PMSS1 HP strain or the CS1 HF strain were co-cultured with mouse peritoneal macrophages to assess their immunostimulatory effects. HP and HF induced similar cytokine production from cultured mouse peritoneal macrophages revealing that both bacteria exhibit similar immunostimulatory effects in vitro. Next, C57BL/6J mice were infected with HP or HF and were assessed 2 months post-infection. HP-infected mice caused modest inflammation within both the gastric corpus and antrum, and did not induce significant atrophy within the gastric corpus. In contrast, HF induced significant inflammation throughout the gastric corpus and antrum. Moreover, HF infection was associated with significant atrophy of the chief and parietal cell compartments and induced the expression of pyloric metaplasia (PM) markers. HP is poorly immunogenic compared to HF. HF induces dramatic CD4+ T cell activation, which is associated with increased gastric cancer risk in humans. Thus, HP studies in mice are better suited for studies on colonization, while HF is more strongly suited for studies on the effects of gastric inflammation on tumorigenesis. . IMPORTANCE: Mouse infection models with Helicobacter species are widely used to study Helicobacter pathogenesis and gastric cancer initiation. However, Helicobacter pylori is not a natural mouse pathogen, and mouse-adapted H. pylori strains are poorly immunogenic. In contrast, Helicobacter felis is a natural mouse pathogen that induces robust gastric inflammation and is often used in mice to investigate gastric cancer initiation. Although both bacterial strains are widely used, their disease pathogenesis in mice differs dramatically. However, few studies have directly compared the pathogenesis of these bacterial species in mice, and the contrasting features of these two models are not clearly defined. This study directly compares the gastric inflammation, atrophy, and metaplasia development triggered by the widely used PMSS1 H. pylori and CS1 H. felis strains in mice. It serves as a useful resource for researchers to select the experimental model best suited for their studies.

Stomach size in anorexia nervosa: A new challenge?

BACKGROUND & AIMS: Changes in stomach size may impact eating behaviour. A recent study showed gastric dilatation in restrictive eating disorders using computed tomography scans. This study aimed to describe stomach size in the standing position in women with anorexia nervosa (AN). METHODS: Women treated for AN at our institution were retrospectively included if they had undergone upper gastrointestinal radiography (UGR) after the diagnosis of AN. Two control groups (CG1 and CG2) were included, both comprising female patients: CG1 patients were not obese and underwent UGR for digestive symptoms of other aetiologies, and CG2 comprised obese individuals who had UGR before bariatric surgery. A UGR-based Stomach Size Index (SSI), calculated as the ratio of the length of the stomach to the distance between the upper end of the stomach and the top of the iliac crests, was measured in all three groups. Gastromegaly was defined as SSI >1.00. RESULTS: 45 patients suffering from AN (28 with restrictive and 17 with binge/purge subtype), 10 CG1 and 20 CG2 subjects were included in this study. Stomach Size Index was significantly higher in AN (1.27 ± 0.24) than in CG1 (0.80 ± 0.11) and CG2 (0.68 ± 0.09); p < 0.001, but was not significantly different between patients with the restrictive and binge/purge subtypes. Gastromegaly was present in 82.2% of patients with AN and not present in the control groups. In patients with AN, gastromegaly was present in 12/15 patients without digestive symptoms (80.0%) and in 25/30 patients with digestive complaints (83.3%) at time of UGR (p = 0.99). In the AN group, no significant relationship was found between SSI and body mass index. CONCLUSION: Gastromegaly is frequent in AN and could influence AN recovery. This anatomical modification could partially explain the alterations of gastric motility previously reported in AN.

Metaplastic regeneration in the mouse stomach requires a reactive oxygen species pathway.

In pyloric metaplasia, mature gastric chief cells reprogram via an evolutionarily conserved process termed paligenosis to re-enter the cell cycle and become spasmolytic polypeptide-expressing metaplasia (SPEM) cells. Here, we use single-cell RNA sequencing (scRNA-seq) following injury to the murine stomach to analyze mechanisms governing paligenosis at high resolution. Injury causes induced reactive oxygen species (ROS) with coordinated changes in mitochondrial activity and cellular metabolism, requiring the transcriptional mitochondrial regulator Ppargc1a (Pgc1α) and ROS regulator Nf2el2 (Nrf2). Loss of the ROS and mitochondrial control in Ppargc1a-/- mice causes the death of paligenotic cells through ferroptosis. Blocking the cystine transporter SLC7A11(xCT), which is critical in lipid radical detoxification through glutathione peroxidase 4 (GPX4), also increases ferroptosis. Finally, we show that PGC1α-mediated ROS and mitochondrial changes also underlie the paligenosis of pancreatic acinar cells. Altogether, the results detail how metabolic and mitochondrial changes are necessary for injury response, regeneration, and metaplasia in the stomach.

Biomarker discovery and validation for gastrointestinal tumors: A comprehensive review of colorectal, gastric, and liver cancers.

Gastrointestinal (GI) malignancies, encompassing gastric, hepatic, colonic, and rectal cancers, are prevalent forms of cancer globally and contribute substantially to cancer-related mortality. Although there have been improvements in methods for diagnosing and treating GI cancers, the chances of survival for these types of cancers are still extremely low. According to the World Cancer Research International Fund's most recent figures, stomach cancer was responsible for roughly one million deaths worldwide in 2020. This emphasizes the importance of developing more effective tools for detecting, diagnosing, and predicting the outcome of these cancers at an early stage. Biomarkers, quantitative indications of biological processes or disease states, have emerged as promising techniques for enhancing the diagnosis and prognosis of GI malignancies. Recently, there has been a considerable endeavor to discover and authenticate biomarkers for various GI cancers by the utilization of diverse methodologies, including genomics, proteomics, and metabolomics. This review provides a thorough examination of the current state of biomarker research in the field of gastrointestinal malignancies, with a specific emphasis on colorectal, stomach, and liver cancers. A thorough literature search was performed on prominent databases such as PubMed, Scopus, and Web of Science to find pertinent papers published until November, 2023 for the purpose of compiling this review. The diverse categories of biomarkers, encompassing genetic, epigenetic, and protein-based biomarkers, and their potential utility in the fields of diagnosis, prognosis, and treatment selection, are explored. Recent progress in identifying and confirming biomarkers, as well as the obstacles that persist in employing biomarkers in clinical settings are emphasized. The utilization of biomarkers in GI cancers has significant potential in enhancing patient outcomes. Ongoing research is expected to uncover more efficient biomarkers for the diagnosis and prognosis of these cancers.

Histopathologic evaluation of gastric intestinal metaplasia in non-neoplastic biopsy specimens: Accuracy and interobserver reliability among general pathologists and pathology residents.

OBJECTIVES: This study aimed to evaluate the accuracy and interobserver reliability of diagnosing and subtyping gastric intestinal metaplasia (IM) among general pathologists and pathology residents at a university hospital in Thailand, focusing on the challenges in the histopathologic evaluation of gastric IM for less experienced practitioners. METHODS: The study analyzed 44 non-neoplastic gastric biopsies, using a consensus diagnosis of gastrointestinal pathologists as the reference standard. Participants included 6 general pathologists and 9 pathology residents who assessed gastric IM and categorized its subtype (complete, incomplete, or mixed) on digital slides. After initial evaluations and receiving feedback, participants reviewed specific images of gastric IM, as agreed by experts. Following a one-month washout period, a reevaluation of the slides was conducted. RESULTS: Diagnostic accuracy, interobserver reliability, and time taken for diagnosis improved following training, with general pathologists showing higher accuracies than residents (median accuracy of gastric IM detection: 100 % vs. 97.7 %). Increased years of experience were associated with more IM detection accuracy (p-value<0.05). However, the overall median accuracy for diagnosing incomplete IM remained lower than for complete IM (86.4 % vs. 97.7 %). After training, diagnostic errors occurred in 6 out of 44 specimens (13.6 %), reported by over 40 % of participants. Errors involved omitting 5 slides with incomplete IM and 1 with complete IM, all showing a subtle presence of IM. CONCLUSIONS: The study highlights the diagnostic challenges in identifying incomplete gastric IM, showing notable discrepancies in accuracy and interobserver agreement. It underscores the need for better diagnostic protocols and training to enhance detection and management outcomes.

Spectrum of endoscopic gastric subepithelial lesions encountered on EUS-FNA: A single center experience.

BACKGROUND AND OBJECTIVES: Endoscopic ultrasound guided fine needle aspiration (EUS-FNA) is a minimally invasive and reliable non-surgical technique for the diagnosis of gastrointestinal lesions. The present study aimed to evaluate the spectrum of lesions encountered in the gastric subepithelium on EUS-FNA at a tertiary care center. MATERIALS AND METHODS: Archival data of all patients undergoing EUS-FNA for gastric submucosal lesions over a period of 5 years was retrieved. Patient demographics, clinical presentation, and EUS findings were recorded along with the FNA results. RESULTS: A total of 78 EUS-FNA samples were analyzed. Material was adequate in 62 cases (79.48%) and inadequate in 16 cases (12.82%) patients due to scant cellularity. Of the adequate samples, 34 (43.5%) were reported as neoplastic while 20 (25.64%) were non-neoplastic, and 8 (10.25%) were reported as suspicious of a neoplasm. In the neoplastic category, the predominant diagnosis was of spindle cell neoplasm comprising gastrointestinal stromal tumor (13), benign neural tumor (03), leiomyoma (02), and spindle cell tumors (03). The latter could not be categorized further due to a lack of IHC material. The next common diagnosis was adenocarcinoma (06) followed by neuroendocrine tumor (02) and poorly differentiated carcinoma (01). The non-neoplastic lesions included non-specific pathology (15), inflammatory lesions (08), and one case each of tuberculosis, pancreatic rest, and Brunner gland hamartoma. Cell blocks for ancillary testing were available in 54 cases (65.23%) and follow-up was available in 42 cases (53.84%). CONCLUSION: EUS-FNA is a good modality for the diagnosis of gastric submucosal lesions with a high diagnostic yield.

Corrosive induced esophageal and gastric injury: Histopathological evaluation of surgically resected specimens over a decade in a tertiary care center.

BACKGROUND: Caustic ingestion is associated with long-term sequelae like esophageal stricture, gastric cicatrization, and long-term risk of dysplasia or even carcinoma. However, only a few small studies have explored histopathological aspects of caustic-induced esophageal/gastric injury. MATERIALS AND METHODS: We retrospectively evaluated specimens of patients undergoing surgery due to caustic ingestion-related complications from 2008 to 2020. Pathological examination was conducted by two independent gastro-pathologists to evaluate the extent and depth of the caustic injury, presence or absence of tissue necrosis, type and degree of inflammation, or presence of any dysplastic cells. RESULTS: A total of 54 patients underwent surgical exploration during the inclusion period and complete details of 39 specimens could be retrieved. The mean age of the included patients was 28.66 ± 9.31 years and 25 (64.1%) were male. The majority of patients (30; 76.9%) had a history of caustic ingestion more than three months before the surgery and the presence of long or refractory stricture was the most common indication for the surgery (20; 51.28%). In the resected specimen, a majority of patients had superficial esophageal or gastric ulcer (90.6%; 60.0%), transmural inflammation (68.8%; 65.6%), transmural fibrosis (62.5%; 34.4%), and hypertrophied muscularis mucosa (78.13%; 53.3%). However, none of the patients had dysplasia in the resected esophageal or gastric specimens. CONCLUSION: Caustic ingestion leads to mucosal ulceration, transmural inflammation, and transmural fibrosis which might be the reason for refractory stricture in such patients.

Primary extranodal NK/T cell lymphoma of stomach: A case report and review of literature.

ABSTRACT: Extranodal Natural killer/T (NK/T) cell lymphoma nasal type is an aggressive non-Hodgkin lymphoma and has a constant association with Epstein-Barr virus (EBV) infection. Approximately more than 75% cases are located in upper aero-digestive tract, of which stomach is a very rare site. Very few cases of gastric extranodal NK/T cell lymphoma have been reported in the literature. A 22-year-old male patient presented with complaints of abdominal pain and hematemesis. Endoscopy showed a large ulcer in the stomach. Partial gastrectomy done and histopathology showed transmural infiltration by intermediate size atypical lymphoid cells which are immunopositive for CD3, CD56, TIA, EBV-encoded RNA (EBER) and negative for CD4, CD8, CD20. A diagnosis of extranodal NK/T cell lymphoma nasal type was made.

Endoscopic Kyoto and Kimura-Takemoto Classifications Are Comparable in Predicting High-Risk Gastric Precancerous Lesions.

INTRODUCTION: Severe and extensive gastric atrophy, extensive or incomplete gastric intestinal metaplasia, and gastric dysplasia are considered high-risk gastric precancerous lesions (HGPLs). Endoscopic findings based on the endoscopic Kyoto classification (EKC) and the Kimura-Takemoto classification (KTC) have been reported to be significantly associated with HGPLs. This study aimed to compare these two classifications in predicting active Helicobacter pylori (H. pylori) infection and HGPLs. METHODS: This is a cross-sectional study conducted on naïve dyspeptic patients who underwent upper gastrointestinal endoscopy at a tertiary hospital. Endoscopic findings were scored according to the EKC and KTC. Mapping biopsies were taken, and H. pylori infection was determined using a locally validated rapid urease test and histology. The performance of EKC was compared with that of KTC using the area under the receiver operating characteristic curve (AUC) in predicting active H. pylori infection and HGPLs. RESULTS: There were 292 patients with a median age of 46 and a male-to-female ratio of 1:1. The rates of active H. pylori infection and HGPLs were 61.3% and 14.0%, respectively. The EKC was better than the KTC in predicting active H. pylori infection (AUC: 0.771 vs. 0.658, respectively; p < 0.001). However, these two classifications had comparable performance in predicting HGPLs (AUC: 0.792 vs. 0.791, respectively; p = 0.956). CONCLUSION: Compared to EKC, KTC is inferior in predicting active H. pylori infection but has comparable performance in predicting HGPLs.

A surgical case of inflammatory pseudotumor by hepatic anisakiasis.

Anisakiasis is a parasitic infection caused by the ingestion of raw or undercooked seafood infected with Anisakis larvae. It generally affects the gastrointestinal tract, particularly the stomach, but very rare cases have been reported in which infection of the liver leads to the formation of inflammatory pseudotumors. We herein report an extremely rare case of an inflammatory pseudotumor induced by hepatic anisakiasis that was laparoscopically resected for the purpose of both diagnosis and treatment. A 51-year-old woman underwent a routine medical checkup by ultrasound examination, which incidentally detected a 15-mm mass on the surface of S6 of the liver. Because a malignant tumor could not be ruled out on several preoperative imaging studies, laparoscopic partial resection of the liver was performed. Histopathological examination revealed Anisakis larva in the inflammatory pseudotumor, suggesting hepatic anisakiasis. This report describes an extremely rare case of an inflammatory pseudotumor induced by hepatic anisakiasis. Because the preoperative diagnosis could not be obtained by several imaging modalities, laparoscopic liver resection with a sufficient margin might be suitable for diagnosis and treatment of this disease.