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INTRODUCTION AND AIM Helicobacter pylori (H. pylori) is known to be capable of causing chronic inflammation of the gastric mucosa that slowly progresses through the premalignant stages, reaching localized gastric adenocarcinoma (GAC). Its outcome is closely related to the stage at which diagnosis is made. The aim of the present study was to determine cost-benefit by comparing esophagogastroduodenoscopy, serum pepsinogen detection, and no screening at all. MATERIAL AND METHODS Utilizing Markov chains and Monte Carlo simulation, the costs and effects of various detection modalities were simulated to analyze the cost-benefit of each strategy. For our population, we used the published data of patients with gastric cancer, applicable to the Mexican population. RESULTS The results were reported as incremental cost-effectiveness ratios. The best strategy was serum pepsinogen determination, followed by the strategy of endoscopic examination with continued monitoring every 3 years. CONCLUSIONS The performance of serum pepsinogen serology and directed endoscopic examination (and continued monitoring, if necessary) for GAC screening could be a cost-effective intervention in Mexico, despite the low-to-moderate general prevalence of the disease.

Background Exposed endoscopic full-thickness resection (Eo-EFTR) is emerging as a promising minimally invasive alternative to surgery for the treatment of deep gastric submucosal tumors (G-SMTs). However, literature concerning this subject is heterogeneous and data mostly come from relatively small retrospective studies. Aims We aimed to perform a pooled analysis of published data with regard to gastric Eo-EFTR, providing a pooled estimate of technical and clinical outcomes. Methods The protocol was registered in PROSPERO. MEDLINE and EMBASE databases were searched for studies published from 1998 to 2020. The primary outcomes were complete resection and surgical conversion rates. The secondary outcomes were overall and selected major adverse events rates. The Forest plots on primary and secondary endpoints were produced based on fixed and random effect models. Results Nineteen studies including 952 Eo-EFTR-treated G-SMTs were included. The pooled estimate of the complete resection rate and surgical conversion rates was 99.3% and 0.09%, respectively. The pooled estimate of overall major adverse events, delayed bleeding, delayed perforation and peritonitis, abdominal abscess and/or abdominal infection was 0.29%, 0.14%, 0.14%, and 0.12%, respectively. Conclusion Gastric Eo-EFTR has a high rate of complete resection with a low surgical conversion rate. It appears to be relatively safe and might represent a non-inferior minimally invasive alternative to surgery in selected cases.

Background: Despite the fact that Helicobacter spp. has been detected in equine gastric mucosa, no evidence exists about this infection in Colombian horses affected by equine ulcerative gastric syndrome (EGUS), nor in dental tartar. Objective: To detect Helicobacter spp. DNA in equine gastric mucosa and dental tartar and determine the relationship between the presence of Helicobacter spp. and gastric lesions. Methods: Samples of glandular gastric mucosa and dental tartar were collected from 30 equine slaughterhouses. Macroscopic lesions of the stomachs were classified and the total DNA in all samples was extracted using a commercial extraction kit. A final-point PCR was performed using primers for amplification of a segment of 251 bp of the gene encoding the 16s rRNA region; the amplified fragments were subjected to a second PCR to determine the presence of H. pylori, the VacA gene was typified. The resulting amplicons were sequenced. Results: It was possible to amplify 16s rRNA in several samples but there was no amplification of VacA. Fragments of the sequences were compatible with H. heilmannii. The 23.3 and 10% of gastric and tartar samples were positive for 16s rRNA of Helicobacter spp., respectively. Conclusion: Although genetic material of Helicobacter spp. was found in some animals, there was no relationship with gastric lesions. It is possible that helicobacteriosis has no bearing in EGUS etiology.

The mucosa of the body of the stomach (ie, the gastric corpus) uses 2 overlapping, depth-dependent mechanisms to respond to injury. Superficial injury heals via surface cells with histopathologic changes like foveolar hyperplasia. Deeper, usually chronic, injury/inflammation, most frequently induced by the carcinogenic bacteria Helicobacter pylori, elicits glandular histopathologic alterations, initially manifesting as pyloric (also known as pseudopyloric) metaplasia. In this pyloric metaplasia, corpus glands become antrum (pylorus)-like with loss of acid-secreting parietal cells (atrophic gastritis), expansion of foveolar cells, and reprogramming of digestive enzyme-secreting chief cells into deep antral gland-like mucous cells. After acute parietal cell loss, chief cells can reprogram through an orderly stepwise progression (paligenosis) initiated by interleukin-13-secreting innate lymphoid cells (ILC2s). First, massive lysosomal activation helps mitigate reactive oxygen species and remove damaged organelles. Second, mucus and wound-healing proteins (eg, TFF2) and other transcriptional alterations are induced, at which point the reprogrammed chief cells are recognized as mucus-secreting spasmolytic polypeptide-expressing metaplasia cells. In chronic severe injury, glands with pyloric metaplasia can harbor both actively proliferating spasmolytic polypeptide-expressing metaplasia cells and eventually intestine-like cells. Gastric glands with such lineage confusion (mixed incomplete intestinal metaplasia and proliferative spasmolytic polypeptide-expressing metaplasia) may be at particular risk for progression to dysplasia and cancer. A pyloric-like pattern of metaplasia after injury also occurs in other gastrointestinal organs including esophagus, pancreas, and intestines, and the paligenosis program itself seems broadly conserved across tissues and species. Here we discuss aspects of metaplasia in stomach, incorporating data derived from animal models and work on human cells and tissues in correlation with diagnostic and clinical implications.

Eradication of Helicobacter pylori is the first-line treatment for gastric mucosa-associated lymphoid tissue (MALT) lymphomas; however, lesions may persist in 20% of patients after initial treatment, thereby necessitating the use of an additional therapeutic approach. Other treatment options include radiation therapy, chemotherapy, endoscopic resection, rituximab therapy, or watchful waiting. We present a case of localized gastric MALT lymphoma that did not respond to H. pylori eradication therapy. The patient waited for 12 months but the tumor showed no signs of regression endoscopically. Histologic examination revealed residual MALT lymphoma. The tumor was then successfully treated using endoscopic submucosal dissection and the patient remained disease-free for 4 years. To our knowledge, this is the first case in which a gastric MALT lymphoma was treated with endoscopic submucosal dissection. In conclusion, endoscopic resection may be recommended as second-line therapy for properly selected patients with gastric MALT lymphoma as it is effective and minimally invasive.

У статті наведені результати порівняльної характеристики даних стандартного ендоскопічного дослідження слизової оболонки шлунка у дітей, хворих на хронічний гастрит, асоційований з Helicobacter pylori-інфекцією, з урахуванням цитотоксичності штаму Helicobacter pylori. Визначені характерні ендоскопічні особливості патологічних змін слизової оболонки шлунка при хронічних гастритах, асоційованих з цитотоксичними штамами Helicobacter pylori, у дітей.

Posttreatment evaluation of gastric mucosa-associated lymphoid tissue (MALT) lymphoma currently relies on esophagogastroduodenoscopy with histological assessment of biopsies. Overexpression of the G protein–coupled C-X-C chemokine receptor type 4 (CXCR4) has been previously observed in MALT lymphoma. The aim of this prospective study was to evaluate positron emission tomography (PET) with the novel CXCR4 tracer [68Ga]Pentixafor as a potential alternative to follow up biopsies for assessment of residual disease (noncomplete remission [CR]) after first-line Helicobacter pylori eradication. Forty-six post–H pylori eradication [68Ga]Pentixafor–PET/magnetic resonance imaging (MRI) examinations of 26 gastric MALT lymphoma patients, and 20 [68Ga]Pentixafor–PET/MRI examinations of 20 control group patients without lymphoma, were analyzed. In the MALT lymphoma group, time-matched gastric biopsies were used as reference standard and showed CR in 6 cases. Pooled examination-based accuracy, sensitivity, specificity, and positive and negative predictive values of [68Ga]Pentixafor–PET for detection of residual gastric MALT lymphoma at follow-up were 97.0%, 95.0%, 100.0%, 100.0%, and 92.9%, respectively. Maximum and mean PET standardized uptake values showed moderate correlation with immunohistochemistry-based CXCR4+ cell counts, with correlation coefficients of r = 0.51 and r = 0.52 (P = .008 and P = .006). In summary, CXCR4 imaging with [68Ga]Pentixafor–PET may represent a promising test for assessment of residual gastric MALT lymphomas after H pylori eradication.

Background Although almost all cases of gastric cancer are caused by Helicobacter pylori (HP) infection, there are some rare exceptions. Furthermore, the clinicopathological characteristics of gastric cancer may differ depending on HP infection status. This study aimed to determine the clinicopathological characteristics of undifferentiated-type gastric cancer (UD-GC) according to HP status. Methods The study involved 83 patients with UD-GC who were selected from 1559 patients with gastric cancer who underwent endoscopic resection at our hospital and whose HP infection status was confirmed. Clinicopathological characteristics were evaluated according to HP status (eradicated, n = 28; infected, n = 32; not infected, n = 23). Results In patients without HP infection, UD-GCs were Conclusion The clinicopathological characteristics of UD-GC were similar between HP-infected patients and HP-eradicated patients. Three of four patients with eradicated HP whose UD-GC developed ≥ 10 years after eradication were not eligible for endoscopic treatment and required additional surgery resection. In contrast, UD-GC was curable by endoscopic resection in all patients without HP infection.

Gastrointestinal bleeding is the most frequent major complication of antiplatelet therapy. In patients at low bleeding risk, however, clinically overt gastrointestinal bleeding is relatively uncommon.The authors sought to assess the effects of different antiplatelet regimens on gastrointestinal mucosal injury by means of a novel magnetically controlled capsule endoscopy system in patients at low bleeding risk.Patients (n = 505) undergoing percutaneous coronary intervention in whom capsule endoscopy demonstrated no ulcerations or bleeding (although erosions were permitted) after 6 months of dual antiplatelet therapy (DAPT) were randomly assigned to aspirin plus placebo (n = 168), clopidogrel plus placebo (n = 169), or aspirin plus clopidogrel (n = 168) for an additional 6 months. The primary endpoint was the incidence of gastrointestinal mucosal injury (erosions, ulceration, or bleeding) at 6-month or 12-month capsule endoscopy.Gastrointestinal mucosal injury through 12 months was less with single antiplatelet therapy (SAPT) than with DAPT (94.3% vs 99.2%; P = 0.02). Aspirin and clopidogrel monotherapy had similar effects. Among 68 patients without any gastrointestinal injury at randomization (including no erosions), SAPT compared with DAPT caused less gastrointestinal injury (68.1% vs 95.2%; P = 0.006), including fewer new ulcers (8.5% vs 38.1%; P = 0.009). Clinical gastrointestinal bleeding from 6 to 12 months was less with SAPT than with DAPT (0.6% vs 5.4%; P = 0.001).Despite being at low risk of bleeding, nearly all patients receiving antiplatelet therapy developed gastrointestinal injury, although overt bleeding was infrequent. DAPT for 6 months followed by SAPT with aspirin or clopidogrel from 6 to 12 months resulted in less gastrointestinal mucosal injury and clinical bleeding compared with DAPT through 12 months. (OPT-PEACE [Optimal Antiplatelet Therapy for Prevention of Gastrointestinal Injury Evaluated by Ankon Magnetically Controlled Capsule Endoscopy]; NCT03198741).

Background: With growing incidence of early gastric cancer (EGC), endoscopic submucosal dissection (ESD) is widely performed as a standard treatment for mucosal cancer. Due to the increasing application of ESD, the number of non-curative resection after ESD is also growing, leading to escalating number of patients who require additional gastrectomy with lymph node dissection after non-curative ESD. However, effects of ESD prior to surgery on technical difficulties during operation for EGC remain unclear. Therefore, this study aimed to determine the effect of non-curative ESD on short-term surgical outcomes in patients who underwent additional surgical treatment using propensity score matching method. Methods: To evaluate the effect of ESD on short-term surgical outcomes in patients who underwent additional surgical treatment after a non-curative ESD procedure, patients were divided into two groups: (1) those who underwent additional gastrectomy after non-curative resection of ESD [ESD + Surgery (ES) Group], and (2) those who underwent gastrectomy as the initial treatment [Surgery Only (SO) Group]. To minimize differences in baseline demographic features that could potentially be associated with short-term outcomes, propensity-scored matching analysis was performed. Results: After propensity-scored matching (1:1 matching), 140 patients altogether were selected and analyzed in this study. Complications were experienced by 18 (25.7%) patients in the ES group and 13 (18.6%) patients in the SO group, showing no significant (p

Iron deficiency anaemia is a known complication of a large hiatal hernia in adults. It occurs as a result of erosions on the gastric mucosa secondary to traction at the hiatus during respiration and/or gastric acid-related injuries to the mucosa. Even though anaemia occurs as a result of chronic gastrointestinal blood loss, testing for faecal occult blood is often negative and upper gastrointestinal endoscopy normal as the bleeding is intermittent. In children, a hiatus hernia as a rare cause of iron deficiency anaemia and has been described only in case reports. Here, we describe a 5-year-old boy who presented with severe transfusion-dependent iron deficiency anaemia caused by a paraoesophageal hernia. Surgical repair of the hiatus hernia led to complete resolution of anaemia. One should consider a hiatus hernia as a diagnostic possibility when evaluating a child with refractory iron deficiency anaemia.

OBJECTIVE We sought to investigate the clinical efficacy and safety of a novel endoscopic closure technique in repairing gastric wall defects after endoscopic full-thickness resection (EFTR) of gastric submucosal tumors (SMTs) originating from the muscularis propria layer. METHODS From December 2016 to December 2019, patients with gastric submucosal tumors were enrolled and clinicopathological data were collected. All SMTs were resected by EFTR and gastric wall defects were closed using a novel endoscopic closure technique. The feasibility, efficacy, and safety were evaluated. RESULTS A total of 21 patients with gastric SMTs were included in this study. Among the included SMTs, 15 tumors were located in the fundus of the stomach, and 6 were located in the upper body of the stomach. The average size of the lesions was 2.3 cm (range: 1.9-2.5 cm). All patients underwent EFTR and the gastric wall defect was closed by endoscopic closure. The average endoscopic closure time was 9 min (range: 7-15 min) and the average hospitalization stay length was five days (range: 4-6 days). One patient developed abdominal pain on the first day after the procedure and their body temperature increased; he received treatments such as anti-infection, antacid, and gastrointestinal decompression and was cured and discharged after 4 days. No instance of delayed bleeding, postoperative gastrointestinal fistula, or abdominal infection occurred. No case was transferred to surgery. The postoperative pathology profile included 18 stromal tumors and 3 leiomyomas. During the follow-up period (6-24 months), no case of residual or recurrence was recorded. CONCLUSION The described endoscopic loop ligation technique is feasible, effective, and safe for repairing gastric wall defects after EFTR for gastric submucosal tumors originating from the muscularis propria layer.

Background Since 2006, surgery combined with perioperative chemotherapy is the standard of care for resectable gastric adenocarcinoma in Europe. Specific effects of neoadjuvant chemotherapy remain unknown. The aim was to evaluate the rate of tumor downstaging and its impact on survival in patients undergoing curative resection after neoadjuvant chemotherapy (NeoCT) for gastric adenocarcinoma. Material and Methods All patients treated in a curative intent for gastric or esophagogastric junction adenocarcinomas between 1996 and 2016 in our high-volume center were retrospectively included. Tumor downstaging after NeoCT was defined as ypTN inferior to cTN. The accuracy of clinical staging was evaluated in patients treated by upfront surgery before 2006. Results During the study period, 491 patients were operated for gastric adenocarcinoma, and 449 patients were finally analyzed. Among the 163 (36.3%) patients who received NeoCT, 61 (37.4%) had tumor downstaging. Overall survival and disease-free survival were longer in patients with tumor downstaging compared to patients without it (5-year survival: 84.8% vs 49.7%; P = .002 and 61.7% vs 43.4%; P = .054). In multivariate analysis tumor downstaging was an independent prognosis factor for better overall survival (HR = 5.258; P = .002) and disease-free survival (HR = 2.286; P = .028). Moreover, 45.5% of patients staged cT1-T2N0, in whom upfront surgery was performed, were understaged and ultimately had a more advanced tumor on pathological analysis. Conclusion Response to neoadjuvant chemotherapy constitutes a major prognostic factor for overall and disease-free survival. In the absence of predictive factors for tumor downstaging, the indication for perioperative chemotherapy should remain broad, in particular because of the low accuracy of pretherapeutic staging and therefore the high risk of understaging tumors.

The gastric mucosa is an important endocrine organ, most of which is resected in sleeve gastrectomy (SG). The effect of removing most of the gastric mucosa has not been studied.To assess the effect of ablating the gastric mucosa (an area proportional to that in SG), on obesity and diabetes in a rat model.The Affiliated Hospital of Xuzhou Medical University in Xuzhou Jiangsu, P. R. China.Among 34 fatty Sprague-Dawley rats, 26 randomly received low-dose streptozotocin (STZ) to induce diabetes and then were randomly assigned to gastric mucosa ablation (GMA, n = 10), sleeve gastrectomy (SG, n = 8), and sham (n = 8) groups. The remaining normal fatty rats were assigned to the non-diabetic gastric mucosa ablation (nGMA, n = 8) group. In the GMA groups, the gastric mucosa was thermally ablated using electrocautery. Rats were followed for 8 weeks postoperatively. Preoperative oral glucose tolerance test (OGTT), insulin tolerance test (ITT), and mixed meal tolerance test (MMTT) were repeated at designated time points postoperatively. Changes in body weight, food intake, and fasting blood glucose were also recorded.Fasting ghrelin concentration and area under curve (AUC) decreased significantly (P.05) in the GMA groups and the SG group after surgery. Gastrin concentration remained unchanged in SG but decreased significantly in the GMA groups after surgery. Significantly increased GLP-1 AUC was found in the GMA groups and the SG group postoperatively. The decrease in fasting blood glucose did not differ significantly between the diabetic GMA and SG groups after surgery. Glucose AUC during OGTT in both SG and diabetic GMA groups was decreased significantly from the preoperative level, but the decreased glucose AUC in the SG group was significantly greater (P.05). The decrease in body weight and food intake in the SG group was significantly greater than in the GMA groups.Ablation of most of the gastric mucosa along the greater curvature is effective in weight loss and glycemic control in a rodent model.

We aimed to explore the correlation between P27 expression and Helicobacter pylori (H. pylori) infection in gastric cancer, so as to provide evidence for understanding the pathogenesis of gastric cancer caused by H. pylori infection. A total of 82 samples of gastric cancer tissues and 56 samples of tumor-adjacent normal tissues collected from the gastrectomy were enrolled in this study. Then, 14C-urease breathing test was carried out to evaluate the infection of H. pylori in gastric cancer tissues, the expression of P27 in the tissue samples was detected by the immunohistochemistry staining, and the correlation between the H. pylori infection and P27 expression in gastric cancer was analyzed. Of 82 gastric cancer patients, there were 53 patients with H. pylori infection (64.63%). Among the patients with highly or moderately differentiated gastric cancer, the expression of P27 was much higher than that of patients with poorly differentiated gastric cancer (p 0.01). Besides, comparison of the P27 expression between males and females, among different age groups, tumor sizes, TNM stages, tumor infiltration degrees, or lymph node metastasis, showed no significant differences (p 0.05). Analysis of the correlation revealed that P27 expression was negatively correlated with the infection of H. pylori (p 0.01). Multifactorial logistics regression analysis indicated that tumor differentiation was a risk factor of P27-positive expression in gastric cancer tissues (p 0.01). In addition, P27 expression in the gastric cancer tissues was lower than that in the tumor-adjacent normal tissues (p 0.01). In gastric cancer patients, expression of P27 is correlated with H. pylori infection which, via downregulating P27, can cause the cancerization of gastric mucosa, and P27, for its role in the development and progression of gastric cancer, is a potential auxiliary indicator for clinical diagnosis whether gastric cancer is complicated with H. pylori infection. So, P27 is a key indicator for diagnosis, treatment, and prognostic evaluation of disease in the advanced stage.

Objectives The Kyoto classification of gastritis was established for diagnosing Helicobacter pylori (H. pylori) infection via endoscopic findings. We investigated the role of the Kyoto classification of gastritis in the diagnosis of H. pylori infection and histological gastritis in Japanese individuals. Moreover, the histological findings of gastritis in H. pylori infection were examined based on age and sex differences. Methods We selected 561 patients aged 20-79 years who underwent gastroduodenal endoscopy at our hospital between 2010 and 2018. Endoscopic biopsy specimens from the antrum and corpus were used to investigate H. pylori infection and histology. Endoscopic findings were based on the Kyoto classification of gastritis, and histological findings were based on the updated Sydney System. Results Endoscopic findings based on the Kyoto classification of gastritis (H. pylori positive, 303 patients; H. pylori negative, 258 patients, based on endoscopic findings) had 98.7% sensitivity and 98.4% specificity for histological gastritis. In addition, endoscopic findings in the three age groups (20-39, 40-59, and 60-79 years) had high sensitivity and specificity. Atrophy and intestinal metaplasia were found only in the H. pylori-positive group and progressed with age. Histological inflammation of pyloric mucosa in the younger age group of H. pylori-positive patients was significantly higher than that in the elderly group. Significant inflammation was observed in young women. Conclusions The Kyoto classification of gastritis can not only diagnose H. pylori infection but also detect histological gastritis. Histological gastritis has varying characteristics of inflammation, atrophy, and intestinal metaplasia, depending on age and sex.

Objective: to determine the specifi c number and expression intensity of gelatinase B-positive cells in the gastric surface epithelium and lamina propria (cell component) in the area of the ulcerous defect in rats with experimental acetate ulcer of the stomach.Materials and methods: 18 white Wistar rats were divided into three groups: initial (intact), experimental (modeling of an acetate ulcer) and control (falsely operated) in the experiment. Tissues were obtained from the ulceration zone or the presumed ulceration zone (in the initial and control groups) to asses morphological changes and also indicators, characterizing the activity of gelatinase B 7 days after the simulation of the experiment.Results and Discussion. It was revealed some increase in the specifi c number of gelatinase B-positive cells against the background of moderate accumulation of lymphocytes in the integument epithelium of the gastric mucosa. A signifi cant increase in the specifi c number of gelatinase B-positive cells at the maximum intensity of its expression and a moderate accumulation of eff ector cells of tissue alterations was determined in the cellular component of the lamina propria of the gastric mucosa at the same time.

PURPOSE: Gastric cancers are classified as diffuse-type (DTGC) or intestinal-type (ITGC). DTGCs have distinct clinical and histopathologic features, and carry a worse overall prognosis compared to ITGCs. Atrophic gastritis (AG) and intestinal metaplasia (IM) are known precursors to ITGC. It is unknown if AG and IM increase risk for DTGC. METHODS: We performed a systematic review to identify studies reporting on the association of AG/IM and DTGC. We extracted the odds ratio (OR) of the association from studies, and performed pool analysis. Subgroup analysis was performed on studies reporting histologic severity (using operative link systems) to assess if histologic severity of AG/IM was associated with higher risk. RESULTS: We identified six case-control and eight cohort studies for inclusion. Both AG (pooled OR=1.9, 95% CI 1.5 to 2.4, p

The aim of the present study was to investigate the ability of fish collagen peptides (FCP) from the skin of great hammerhead shark (Sphyrna mokarran) to avert the occurrence of gastric ulcer in experimental rats. FCP treatment prevented the formation of ulcerative lesions on gastric tissues with 86% of inhibition. The histopathology analysis of gastric tissue revealed that the FCP intake prevented the occurrence of hemorrhage and erosion in gastric tissue with formation of mild edema and necrosis, as well as normalized the pH and volume of gastric juice. It also downregulated the expression of pro-inflammatory marker interferon-ɤ (IFN-ɤ) and upregulated the anti-inflammatory marker interleukin-4 (IL-4) in gastric tissue. FCP is capable to modulate the oxidative stress by enhancing the activity of antioxidant defense enzymes superoxide dismutase (SOD) and catalase and by lowering the levels of membrane lipid peroxidation.

Gastric cancer is a malignant tumor that originates from the epithelium of the gastric mucosa. It is the result of a combination of multiple factors, but the current research has not yet clarified its pathogenesis, so further research and exploration are needed. This article is mainly based on the meta-analysis of the improvement of gastrointestinal tumor-related symptoms and prognosis based on medical care and exercise intervention. The control group followed routine care after enrollment. In addition to routine care, patients in the intervention group exercised through assessment, formulation of exercise prescriptions, implementation of supervision, and adjustment. By viewing the subjects' physical examination reports, determine their blood routine, urine routine, blood lipids, blood sugar, liver and kidney function, and electrocardiogram examination. In this experiment, dual-contrast ultrasound in each T staging was greater than 0.8, indicating that the diagnostic method is very accurate in the preoperative diagnosis of gastric cancer T staging. The results show that exercise intervention can improve the pain of patients with gastrointestinal tumors after chemotherapy, relieve cancer-induced fatigue, and improve the quality of life.

We examined the relationship between zonulin and gastric motility in critical care patients and a translational mouse model of systemic inflammation. Gastric motility and haptoglobin (HP) 2 isoform quantification, proxy for zonulin, were examined in patients. Inflammation was triggered by lipopolysaccharide (LPS) injection inC57Bl/6zonulin transgenic mouse (Ztm) and wildtype (WT) mice as controls, and gastro-duodenal transit was examined by fluorescein-isothiocyanate, 6 and 12 h after LPS-injection. Serum cytokines and zonulin protein levels, and zonulin gastric-duodenal mRNA expression were examined. Eight of 20 patients [14 years, IQR (12.25, 18)] developed gastric dysmotility and were HP2 isoform-producing. HP2 correlated with gastric dysmotility (r = − 0.51, CI − 0.81 to 0.003, p = 0.048). LPS injection induced a time-dependent increase in IL-6 and KC-Gro levels in all mice (p

Background:. With the wide application of endoscopic submucosal dissection (ESD) for early gastric neoplasms, metachronous gastric neoplasms (MGN) have gradually become a concern. This study aimed to analyze the characteristics of MGN and evaluate the treatment and follow-up outcomes of MGN patients. Methods:. A total of 814 patients were retrospectively enrolled. All these patients were treated by ESD for early gastric cancer or gastric dysplasia between November 2006 and September 2019 at The First Medical Center of Chinese People's Liberation Army General Hospital. The risk factors for MGN were analyzed using Cox hazard proportional model. Moreover, the cumulative incidence, the correlation of initial lesions and MGN lesions, and the treatment and follow-up outcomes of MGN patients were analyzed. Results:. A total of 4.5% (37/814) of patients had MGN after curative ESD. The 3-, 5-, and 7-year cumulative incidences of MGN were 3.5%, 5.1%, and 6.9%, respectively, and ultimately reaching a plateau of 11.3% at 99 months after ESD. There was no significant correlation between initial lesions and MGN lesions in terms of gross type (P = 0.178), location (long axis: P = 0.470; short axis: P = 0.125), and histological type (P = 0.832). Cox multivariable analysis found that initial multiplicity was the only independent risk factor of MGN (hazard ratio: 4.3, 95% confidence interval: 2.0–9.4, P < 0.001). Seventy-three percent of patients with MGN were treated by endoscopic resection. During follow-up, two patients with MGN died of gastric cancer with lymph node metastasis. The disease-specific survival rate was significantly lower in patients with MGN than that in patients without MGN (94.6% vs. 99.6%, P = 0.006). Conclusions:. The MGN rate gradually increased with follow-up time within 99 months after curative gastric ESD. Thus, regular and long-term surveillance endoscopy may be helpful, especially for patients with initial multiple neoplasms.

Background Myeloid sarcoma (MS) is a rare hematologic malignancy defined as an extramedullary tumor of immature granulocytic cells. It can occur as primary or de novo and be associated with myelodysplasia or myeloproliferative neoplasms. The most frequent locations are the skin, lymph nodes and bones. The case of a patient with a diagnosis of primary granulocytic de novo gastric MS is reported. Case summary A 19-year-old female patient with MS, whose abdominal computed tomography showed a bulky tumor of 16.5 cm in the gastric chamber with infiltration in the retroperitoneal, pancreatic and bile duct region; the histological study showed gastric mucosa diffusely infiltrated by mononucleated cells and the immunohistochemistry expressed myeloperoxidase. After receiving induction chemotherapy based on the 3 + 7 regimen (daunorubicin/cytarabine), the patient developed severe hematological toxicity and neutropenic typhlitis which required a prolonged medical treatment. She presented a rapid disease progression. Although she received supportive treatment, the patient died. Conclusion Gastric primary de novo MS is a rare and aggressive course neoplasm, fostering knowledge is very important to decide its management and to promote more approaches focused on understanding this pathology and its particularities in our population.

Gastric mucosa-associated lymphoid tissue (MALT) lymphoma is a rare disease which is often associated with Helicobacter pylori (H. pylori) infection. First-line treatment of stage IE and IIE localized gastric MALT lymphoma is based on the eradication of H. pylori. The presence of H. pylori resistance factors such as translocation t (11;18), peri-gastric lymph node involvement and the degree of tumor infiltration of the gastric wall; or lack of response to antibiotic therapy are two main indications to treat with definitive radiotherapy (RT). RT is an effective treatment in localized gastric MALT lymphoma. A moderate dose of 30 Gy allows a high cure rate while being well tolerated. After treatment, regular gastric endoscopic follow-up is necessary to detect a potential occurrence of gastric adenocarcinoma.

Background: Braak and others have proposed that Lewy-type α-synucleinopathy in Parkinson’s disease (PD) may arise from an exogenous pathogen that passes across the gastric mucosa and then is retrogradely transported up the vagus nerve to the medulla. Objective: We tested this hypothesis by immunohistochemically staining, with a method specific for p-serine 129 α-synuclein (pSyn), stomach and vagus nerve tissue from an autopsy series of 111 normal elderly subjects, 33 with incidental Lewy body disease (ILBD) and 53 with PD. Methods: Vagus nerve samples were taken adjacent to the carotid artery in the neck. Stomach samples were taken from the gastric body, midway along the greater curvature. Formalin-fixed paraffin-embedded sections were immunohistochemically stained for pSyn, shown to be highly specific and sensitive for α-synuclein pathology. Results: Median disease duration for the PD group was 13 years. In the vagus nerve none of the 111 normal subjects had pSyn in the vagus, while 12/26 ILBD (46%) and 32/36 PD (89%) subjects were pSyn-positive. In the stomach none of the 102 normal subjects had pSyn while 5/30 (17%) ILBD and 42/52 (81%) of PD subjects were pSyn-positive. Conclusion: As there was no pSyn in the vagus nerve or stomach of subjects without brain pSyn, these results support initiation of pSyn in the brain. The presence of pSyn in the vagus nerve and stomach of a subset of ILBD cases indicates that synucleinopathy within the peripheral nervous system may occur, within a subset of individuals, at preclinical stages of Lewy body disease.

Aim. A study of the clinical and morphological traits and cytokine profile of gastritis in schoolchildren with familial history of gastric cancer.Materials and methods. A cross-sectional questionnaire survey was conducted in Siberian regions (Tuva, Even-kiya, Aginskiy Buryat National District, Krasnoyarsk). A total of 3,343 schoolchildren aged 7–17 were surveyed for gastrointestinal complaints and history of gastric cancer in their 1st–2nd degree kindred. Oesophagogastroduo-denoscopy (OGDS) with gastric mucosa biopsy were performed in 463 respondents with complaints. Gastritis was graded in the Sydney classification. Serum cytokine levels (IL-2, IL-4, IL-8, IL-18, IL-1β, IFN-α, TNM-α) were obtained in enzyme immunoassays (ELISA).Results. Schoolchildren with gastritis and familial history of gastric cancer revealed a higher 59.8% rate of dyspeptic complaints vs. 40.8% in negative history (p = 0.001), as well as complaints of weekly heartburn in 14.2 and 8.3% cas-es (p = 0.019), respectively. In positive history and negative H. pylori tests, the cell immune response regulator IL-18 37 was revealed elevated in histology. In histologically verified H. pylori, no cross-cohort differences were observed in serum IL-18 by positive familial history of gastric cancer.Conclusion. Gastritis in schoolchildren with familial predisposition to gastric cancer more often associates with GERD and dyspepsia usually presented in postprandial distress syndrome. The cytokine regulation properties of gastritis in schoolchildren with familial history of gastric cancer have been reported.

Background Gastric pneumatosis indicates the presence of air within the stomach wall. The etiologies included gastric ischemia, gastric intramural infection, gastric mucosal disruption, and secondary to pneumomediastinum. Gastric ischemia is rare because of the rich collateral blood supply to the stomach. Case presentation An 82-year-old man presented to the emergency department with a 2-day history of epigastric fullness, following by fever and low blood pressure. Chest X-ray and abdominal computed tomography revealed gastric pneumatosis at the gastric fundus. The esophagogastroduodenoscopy confirmed the ischemic change of mucosa at the gastric fundus. After antibiotics and medical management, the patient became better and was eventually discharged. Conclusion For the diagnosis of gastric ischemia, physicians should be alert to the hints of gastric pneumatosis from X-ray and computed tomography. It is important to distinguish between gastric ischemia and the other causes of gastric pneumatosis to judge clinical management.

The inflammatory spectrum of gastric diseases includes different clinico-pathological entities, the etiology of which was recently established in the international Kyoto classification. A diagnosis of gastritis combines the information resulting form the gross examination (endoscopy) and histology (microscopy). It is important to consider the anatomical/functional heterogeneity of the gastric mucosa when obtaining representative mucosal biopsy samples. Gastritis includes self-limiting and non-self-limiting (long-standing) inflammatory diseases, and the latter are epidemiologically, biologically and clinically linked to the onset of gastric cancer (i.e. "inflammation-associated cancer"). Different biological models of inflammation-associated gastric oncogenesis have been proposed. Helicobacter pylori (H. pylori) gastritis is the most prevalent worldwide, and H. pylori is classified as a first-class carcinogen. On these bases, eradicating H. pylori is mandatory for the primary prevention of gastric cancer. Non-self-limiting gastritis may also be triggered by the immune-mediated destruction of gastric parietal cells, resulting in autoimmune gastritis. In both H. pylori-related and autoimmune gastritis, the non-self-limiting inflammation results in atrophy of the gastric mucosa, which is the main factor promoting gastric cancer. Long-term follow-up studies consistently demonstrate the prognostic impact of the histological staging of gastritis in gastric cancer secondary prevention strategies.

Aim: To evaluate the prevalence of Helicobacter pylori (H. pylori) and related histopathological lesions in gastric mucosa samples in this single-center study. Methods: Esophagogastroduodenoscopy and endoscopic biopsy reports of 1605 elective cases were retrospectively evaluated. Histopathological examination was evaluated according to the Sydney classification. The data were analyzed according to the prevalence of H. pylori, age, gender, gastric atrophy and intestinal metaplasia rates, and the distribution of the study group in the population below 40 years old and over 40 years old. Results: 584 males (Mean age 51.5 ± 16.5 years) and 1021 females (mean age 49.6 ± 16 years), (p = 0.03), a total of 1605 cases were included in the study. The rate of atrophy, metaplasia and H. pylori positivity in total study population were 0.2%, 16%, 71%, respectively. The rate of atrophy in men and women were 1.2% and 0.8%, respectively (p = 0.006). The rate of metaplasia in men and women were 20.9% and 13.7%, respectively (p

Gastritis is an inflammatory process in the gastric mucosa and gastric mucosa. Gastritis is a state of inflammation or bleeding off the gastric mucosa that is acute, chronic, diffuse, or local. Gastritis or heartburn is an inflammation of the stomach wall, this disease is often found to arise suddenly which is usually characterized by nausea or vomiting, bleeding pain, weakness, decreased appetite or headache. The purpose of this study was to determine the PPI class of drugs most widely used by outpatients with gastric gastritis disorders. Knowing the factors that most often influence of gastric gastritis disorders.To find out the age most often affected by gastric gastritis. This research method used an observational method with the research design used was data collection carried out retrospectively, namely by tracing records at the outpatient installation of Imelda Hospital Medan from January 1 to December 31, 2019. The data obtained at the installation is descriptive and evaluate the use of PPIs with the treatment of gastritis aimed at improving the patient's quality of life, relieving complaints, curing gastritis, preventing recurrences and complications. Besed on the results of the study, the most outpatients with gastritis at the Imleda Hospital Medan were 15 women (17%), 6 men (29%), And the most commonlyused PPI drugs for gastritis patients were lansoprazole in 18 patients (86%), Omeprazole 3 patients (14%).

Ethanol (EtOH) intake is an important global health problem which affects many organs such as the brain, liver and stomach. The aim of the study was to examine the effect of the redox dye methylene blue (MethyB) on oxidative stress and histologic damage to the liver, gastric mucosa, and brain induced high dose ethanol (EtOH). Male rats were treated with EtOH (2 ml/rat, 96%) via intragastric route (for two consecutive days). MethyB (20 or 40 mg/kg, intraperitoneally) was given immediately after EtOH administration. The control group received saline. Rats were euthanized three hours after the last treatment. Brain and liver levels of malondialdehyde (MDA), reduced glutathione (GSH), and paraoxonase-1 (PON-1) as well as brain 5-lipoxygenase (5-LOX) and butyrylcholinesterase (BChE) were determined. Histopathological assessment of brain, liver and gastric damage was done. Results indicated that compared to saline treated animals, EtOH caused significant increase in MDA, along with decreased GSH and PON-1 activity in brain and liver. Additionally, it significantly increased 5-LOX and decreased brain BChE activity. The EtOH group showed the presence of dead and red neurons, and damage of glial cells. The liver exhibited vacuolar degeneration, apoptotic hepatocytes and foci of necrosis. The gastric mucosa showed areas of tissue damage, mucosal atrophy, and loss of normal architecture of glandular cells. The EtOH induced biochemical and histopathological alterations were alleviated after treatment with MethyB at a dose-dependent manner. These results demonstrate that MethyB is able to protect against from acute effects of EtOH on brain, liver and gastric tissue via an antioxidant action. MethyB might be of value in reducing tissue injury in acute EtOH intoxication.

Background. The cytoprotective properties of the gastrointestinal tract in children with chronic gastroduodenitis on the background of food hypersensitivity remain understudied. The purpose is to assess the state of the cytoprotective potential of gastric and duodenal mucosa in adolescents with chronic gastroduodenitis on the background of food hypersensitivity by determining the level of trefoil factor (TFF) 1 in gastric mucosa and TFF-2 — in gastric and duodenal mucosa by immunohistochemistry method. Materials and methods. Fifty adolescents (aged 12 to 17 years) were observed and divided into two groups. The first group consisted of 64 % (n = 32) of patients with chronic gastroduodenitis and food hypersensitivity; the second group included 36 % (n = 18) of children with chronic gastroduodenitis without food hypersensitivity. All children underwent morphological and immunohistochemical studies of biopsy specimens with the determination of TFF-1 and TFF-2. Evaluation of TFF-1 and TFF-2 expression was carried out on a point-scale according to the number of stained epithelial cells of the glands of the antrum and goblet cells in the field of view with a 40-fold magnification: 0 points — no color, 1 point — 30 % of stained cells, 2 points — 30–70 % of stained cells, 3 points — 70–100 % of stained cells. Results. A significant expression of TFF-1 (3 points) in the gastric mucosa occurred in adolescents of both groups. According to the results of the study, 62.5 % (n = 20) of children in the first group and 22 % (n = 4) of adolescents in the second group did not have staining of goblet cells (0 points) in duodenal mucosa, (c 2 = 7.5; p = 0.008). Weak expression (1 point) occurred in 34.5 % (n = 11) of children in the first group and in the majo­rity of children (67 % (n = 12)) in the second group (c 2 = 4.84; p = 0.03). According to the results of statistical analysis, a group of children with food hypersensitivity has 17 times higher risk of atrophic changes in the duodenal mucosa. Conclusions. In children with food hypersensitivity, the cytoprotective properties of the duodenal mucosa are reduced, as evidenced by the absence of TFF-2 expression. In addition, microerosions, a decrease in the number of crypts and Brunner’s glands in the duodenal mucosa are significantly more frequent in the group of children with food hypersensitivity in the absence or weak expression of TFF-2 (p < 0.05).

Proton pump inhibitors (PPIs) are used worldwide to treat of acid-related disorders such as peptic ulcer and gastroesophageal reflux disease and to prevent gastroduodenal injuries due to nonsteroidal anti-inflammatory drugs. PPIs are the most potent inhibitors of gastric acid secretion currently available, and they are one of the most commonly prescribed classes of drugs because of their high efficacy and low toxicity. However, long-term PPI use causes histopathological changes such as parietal cell protrusion into the gland lumen, cystic dilation of gastric fundic glands, and foveolar epithelial hyperplasia. These changes can manifest on endoscopic examination as fundic gland polyps, hyperplastic polyps, multiple white and flat elevated lesions, cobblestone-like mucosa, or black spots. Clinicians must be aware of PPI-induced endoscopic features in patients with chronic long-term PPI use. Conversely, identifying patients with long-term PPI use based on their endoscopic findings is important. Recently, potassium-competitive acid blockers (P-CABs), a new class of acid suppressants that inhibit gastric acid secretion more strongly than PPIs, have recently been introduced clinically. Further long-term prospective studies on these gastric mucosal lesions in patients with either PPI or P-CAB use are required to investigate their association with histopathological changes and to establish the clinical significance of these findings. (Gut Liver 2021;15:-652)

La strongiloidiasis es una infección causada por el parásito strongyloides stercolaris (SS), se asocia con una alta mortalidad en pacientes inmunosuprimidos debido a una diseminación larvaria y síndrome de hiperinfección. El compromiso de la mucosa gástrica es raro, pero cuando se presenta se caracteriza por sangrado digestivo y emesis persistente. Se presenta el caso de un paciente de 27 años con síntomas gastrointestinales, antecedente de infección por HTLV-1 y colitis ulcerativa, quien desarrolló síndrome de hiperinfección por SS. Se describe la presentación clínica, diagnóstico, tratamiento y complicaciones derivadas del cuadro infeccioso.

Background. Helicobacter pylori infection is an important factor in chronic gastritis and duodenal ulcer in children. Over the past decade, different virulence of H.pylori strains has been determined, which depends on its toxicity genes. The purpose was to study the clinical manifestations, endoscopic and histological changes of the gastric mucosa in children with chronic gastritis, induced by H.pylori, with its different toxicity. Materials and methods. One hundred thirty-six children with chronic H.pylori-induced gastritis aged 7–17 years (main group) and 30 healthy children of the same age (control group) were examined clinically and instrumentally. Patients were divided into 2 groups: group IA consisted of 72 children with chronic gastritis, induced by H.pylori CagA “+”, and group IB included 64 children with chronic gastritis, induced by H.pylori CagA “–”, according to the results of determining the total IgG antibodies to CagA antigen in the blood serum or evaluating CagA in gastric mucosal biopsy specimens using polymerase chain reaction. Clinical manifestations, endoscopic and histological changes of the gastric mucosa were analyzed. Statistical processing was performed using the statistical software package Statgra­phics 16.0. Results. In children with chronic gastritis, induced by H.pylori CagA “+” (group IА), the clinical manifestations of pain, abdominal and dyspeptic syndromes were not significantly different from those in patients with chronic gastritis, induced by H.pylori CagA “–” (group IB). There were no significant endoscopic changes in the form of erythematous gastropathy and antral nodularity in children with chronic gastritis, induced by both H.pylori CagA “+” and CagA “–”. Histological changes in groups IA and IB were different: children with chronic gastritis, induced by H.pylori CagA “+”, had inflammatory activity degree II and I and degree II, I, III of gastric contamination by H.pylori, while children with chronic gastritis, induced by H.pylori CagA “–”, had degree I, II activity of the gastric mucosal inflammation and stages II and I of H.pylori contamination. In children with H.pylori-induced chronic gastritis, it is advi­sable to diagnose toxicity of CagA “+” and CagA “–” in order to evaluate H.pylori CagA “–” child’s status. Conclusions. Clinical manifestations of H.pylori-induced chronic gastritis in children are epigastric pain, symptoms of dyspepsia, and chronic intoxication syndrome. Endoscopic manifestations are erythematous gastopathy and/or antral nodularity. In children with chronic gastritis, induced by H.pylori CagA “+” and CagA “–”, there was no significant difference in clinical and endoscopic manifestations. Histological change in gastric mucosa in chronic gastritis, induced by H.pylori, at the stage of exacerbation is diffuse lymphocytic-plasmocytic infiltration of the lamina propria of gastric mucosa with epithelial damage. In the chronic gastritis, induced with H.pylori CagA “+”, II and III degrees of H.pylori contamination predominate, in combination with degrees I and II of inflammation activity. In chronic gastritis, induced by H.pylori CagA “–”, stages II and I of H.pylori contamination predominate. In children with H.pylori-induced chronic gastritis, it is advisable to diagnose its CagA “+”toxicity in order to evaluate H.pylori CagA “–” child’s status., Актуальность. Инфекция Helicobacter pylori является важным фактором хронического гастрита (ХГ) и дуо­денальной язвы у детей. За последнее десятилетие установлена разная вирулентность штаммов H.pylori, которая зависит от его генов токсигенности. Цель: изучить клинические проявления, эндоскопические и гистологические изменения слизистой оболочки желудка (СОЖ) у детей с хроническим гастритом, индуцированным H.pylori, с разной его токсигенностью. Материалы и методы. Проведено клинико-инструментальное обследование 136 детей с хроническим гастритом, индуцированным H.pylori, в возрасте 7–17 лет (основная группа) и 30 здоровых детей этого же возраста (контрольная группа). Пациенты были разделены на 2 группы: IА группу составили 72 ребенка с хроническим гастритом, индуцированным H.pylori CagA «+»; IБ группу — 64 ребенка с хроническим гастритом, индуцированным H.pylori CagA «–», по результатам определения суммарных антител IgG к антигену CagA сыворотки крови и/или определения антигена CagA в биоптатах СОЖ методом полимеразной цепной реакции. Изучали и анализировали клинические проявления, эндоскопические и гистологические изменения слизистой оболочки желудка. Статистическая обработка проводилась с помощью пакета статистических программ Statgrafics 16.0. Результаты. У детей с ХГ, индуцированным H.pylori CagA «+» (IА группа), клинические проявления болевого абдоминального и диспептического синдромов существенно не отличаются от таковых у детей с ХГ, индуцированным H.pylori CagA «–» (ІБ группа). Не выявлены существенные эндоскопические изменения в виде эритематозной гастропатии и антральной нодулярности как у детей с ХГ, индуцированным H.pylori CagA «+», так и у детей с ХГ, индуцированным H.pylori CagA «–». Гистологические изменения в ІА и ІБ группах были разные: детям с ХГ, индуцированным H.pylori CagA «+», свойственны II и I степень активности воспаления и ІІ, І, ІІІ степени обсемененности Н.pylori слизистой оболочки желудка, а детям с ХГ, индуцированным H.pylori CagA «–», свойственны I, II степень активности воспаления слизистой оболочки желудка и II и I степень обсемененности Н.pylori. Выводы. Клиническими проявлениями ХГ, индуцированного H.pylori, у детей в стадии обострения является эпигастральная боль, симптомы диспепсии и хронического интоксикационного синдрома. Эндоскопическими проявлениями являются эритематозная гастропатия и/или антральная нодулярнисть. У детей с ХГ, индуцированным H.pylori СagA «+», и у детей с ХГ, индуцированным H.pylori СagA «–», по клиническим и эндоскопическим проявлениям существенного различия не выявлено. Гистологическим изменением СОШ при ХГ, индуцированном H.pylori, в стадии обострения является диффузная лимфоцитарно-плазмоцитарная инфильтрация собственной пластинки СОЖ с нарушением эпителия. При ХГ, индуцированным H.pylori СagA «+», преобладает II и III степень обсеменения H.pylori в сочетании с I и II степенью активности воспаления СОЖ. При ХГ, индуцированном H.pylori СagA «–», преобладает II и I степень обсеменения H.pylori СОЖ. У детей с ХГ, индуцированным H.pylori, целесообразно диагностировать его токсигенность CagA «+» для оценки H.pylori CagA-статуса ребенка., Актуальність. Інфекція Helicobacter pylori є важливим чинником хронічного гастриту (ХГ) та дуоденальної виразки у дітей. За останнє десятиріччя встановлено різну вірулентність штамів H.pylori, яка залежить від його генів токсигенності. Мета: вивчити клінічні прояви, ендоскопічні та гістологічні зміни слизової оболонки шлунка (СОШ) у дітей з хронічним гастритом, індукованим H.pylori, з різною його токсигенністю. Матеріали та методи. Проведено клініко-інструментальне обстеження 136 дітей з хронічним гастритом, індукованим H.pylori, віком 7–17 років (основна група) та 30 здорових дітей цього ж віку (контрольна група). Пацієнти були розподілені на 2 групи: ІА групу становили 72 дитини з хронічним гастритом, індукованим H.pylori CagA «+»; ІБ групу — 64 дитини з хронічним гастритом, індукованим H.pylori CagA «–», за результатами визначення сумарних антитіл IgG до антигену CagA сироватки крові та/або визначення антигену CagA в біоптатах СОШ методом полімеразної ланцюгової реакції. Вивчали та аналізували клінічні прояви, ендоскопічні та гістологічні зміни слизової оболонки шлунка. Статистична обробка проводилась за допомогою пакета статистичних програм Statgrafics 16.0. Результати. У дітей з ХГ, індукованим H.pylori CagA «+» (ІА група), клінічні прояви больового абдомінального та диспептичного синдромів суттєво не відрізняються від таких у дітей з ХГ, індукованим H.pylori CagA «–» (ІБ група). Не виявлено суттєвих ендоскопічних змін у вигляді еритематозної гастропатії та антральної нодулярності як у дітей з ХГ, індукованим H.pylori CagA «+», так і у дітей з ХГ, індукованим H.pylori CagA «–». Гістологічні зміни в ІА та ІБ групах були різні: дітям з ХГ, індукованим H.pylori CagA «+», властивий ІІ та І ступінь активності запалення і ІІ, І, ІІІ ступені обсіменіння Н.pylori слизової оболонки шлунка, а дітям з ХГ, індукованим H.pylori CagA «–», властивий І та ІІ ступінь активності запалення слизової оболонки шлунка і ІІ та І ступінь обсіменіння Н.pylori. Висновки. Клінічними проявами ХГ, індукованого H.pylori, у дітей в стадії загострення є епігастральний біль, симптоми диспепсії та хронічного інтоксикаційного синдрому. Ендоскопічними проявами є еритематозна гастропатія та/або антральна нодулярність. У дітей з ХГ, індукованим H.pylori СagA «+», та у дітей з ХГ, індукованим H.pylori СagA «–», за клінічними та ендоскопічними проявами суттєвої різниці не виявлено. Гістологічною зміною СОШ при ХГ, індукованому H.pylori, в стадії загострення є дифузна лімфоцитарно-плазмоцитарна інфільтрація власної пластинки СОШ з порушенням епітелію. При ХГ, індукованому з H.pylori СagA «+», переважає II та III ступень обсіменіння H.pylori в поєднанні з I та II ступенем активності запалення СОШ. При ХГ, індукованому H.pylori СagA «–», переважає II та I ступінь обсіменіння H.pylori СОШ. У дітей з ХГ, індукованим H.pylori, доцільно діагностувати його токсигеннісь CagA «+» для оцінки H.pylori CagA-статусу дитини.

Background: Endoscopic treatments for gastric cancers have still been progressing even after the great success of endoscopic submucosal dissection (ESD). Summary: In further advancements of ESD, safe and less-invasive procedures are challenged by managing postoperative bleeding, one of the major adverse events in ESD. Covering the mucosal defect after removal of lesions appears reasonable and effective for preventing delayed bleeding from the post-ESD ulcers. Shielding with biodegradable sheets is attempted on clinical trials, which show equivocal results. Although suturing of the mucosal rims is technically challenging, pilot studies demonstrate favorable outcomes for avoiding post-ESD bleeding even in cases at high risk. In cases after noncurative resection of ESD, the selection of patients who truly require additional gastrectomy with lymph node dissection is important to provide necessary surgery. Risk stratification of lymph node metastases and surgery has been developed, which offers tailor-made management to each patient considering the risks and benefits. In surgery, function-preserving gastrectomy to minimize the resection area in both lymphadenectomy and the primary site is clinically introduced. The sentinel node navigation surgery is promising to realize the minimally invasive gastrectomy, and it should strongly fit ESD as well as laparoscopic endoscopic cooperative surgery or endoscopic full-thickness resection, although nonexposure approaches are desirable. Key Message: Development for less-invasive managements on gastric cancer will be continued in step with the advancement of endoscopic treatments.

The article presents the history of colloidal bismuth subcitrate and considers the basic mechanisms of its effects on the gastric mucosa, both cytoprotective and anti-helicobacter. The recent data of the worldwide researches are given on the use of the bismuth subcitrate as a component of antibacterial therapy in order to improve the effectiveness of the eradication, especially under the resistance to the basic drugs. The results of own researches are also shown, they are dedicated to the dynamics of structural adjustment of the gastric mucosa in patients with chronic atrophic gastritis for 3 years after the eradication of H.pylori. The use of first-line therapy with the addition of the drug De-Nol allowed to achieve eradication in 94.3 % of patients and positive microstructural changes of the gastric mucosa.

Мета: проаналізувати структурні зміни слизової оболонки шлунка та оцінити роль системи оксиду азоту в цих процесах у пацієнтів iз хронічним гастритом та кишковою метаплазією. Матеріали та методи. Морфологічне дослідження проводилося в 38 пацієнтів iз хронічним гастритом та атрофією, локальною (антральний відділ шлунка) або дифузною кишковою метаплазією. Концентрація оксиду азоту була визначена у вмісті шлунка та в крові всіх пацієнтів. Результати. Морфометричне дослідження показало помітне зниження (до (0,12 ± 0,04) %) ядерно-цитоплазматичного співвідношення в пацієнтів iз кишковою метаплазією порівняно з тими, хто мав атрофію. Еліптичність ядер клітин також зменшувалася з розвитком кишкової метаплазії та в пацієнтів без метапластичних змін дорівнювала (0,76 ± 0,04) %, у випадках локальної кишкової метаплазії — (0,65 ± 0,11) %, при дифузнiй метаплазії — (0,41 ± 0,12) %. Встановлено, що у хворих iз кишковою метаплазією, локалiзованою в антральному відділі, рівень оксиду азоту в шлунковому соку збільшується і на 24–65 % перевищує контрольну величину. Розглянуто можливий механізм загибелі клітин слизової оболонки шлунка внаслiдок апоптозу та некрозу в умовах гіперпродукції оксиду азоту. Висновки. Iнгібуючий ефект оксиду азоту на шлункову секрецію реалізується за рахунок його стимулюючого впливу на активність циклооксигенази та синтезу простагландинів.

The aim of the study was to determine of melatonin level in the blood serum in rats of different sexes and age in ulcerative lesions of the stomach. Materials and methods. Using the method of alcohol-prednisolone injury, we have simulated ulcerative lesions of the stomach. The level of melatonin in the blood serum in rats of different age and sexes with ulcerative lesions of the stomach was determined by enzyme-linked immunosorbent assay. Experimental animals were divided into groups by the age, namely 3, 9, 15 and 20 months, corresponding to the human age of 14, 29–30, 43–44, 55–56 years, respectively. Results. In the course of the research, it was found that rats with the ulcerative lesions of the stomach had significant (r ≤ 0.05) reduction of serum melatonin in animals of all experimental groups. In males, the lowest levels of melatonin in ulcerative lesion were in groups of 9 and 20 months — (174.0 ± 12.9) pmol/L and (141.5 ± 21.4) pmol/L, respectively. The level of melatonin in males aged 9 months was significantly lower (p ≤ 0.05), by 26 %, than in rats aged 3 months, and by 16 % — compared with rats aged 15 months (p ≤ 0.05). In rats aged 20 months, melatonin levels were reduced by 40 and 32 % with respect to experimental groups of animals aged 3 and 15 months (p ≤ 0.05). Relatively to the control group, among male rats the greatest reduction also observed in animals ages 20 months — 43 % and 9 months — 39 % (p ≤ 0.05). In male rats aged 3 months, melatonin level was lower by 22 %, and in the age group of 15 months — by 29 % relative to control animals (p ≤ 0.05). In females, reduction of melatonin levels occurred gradually with age: from the highest in females aged 3 months to significantly lowest compared to other age groups — females aged 20 months in the control and experimental groups. The females rats with ulcerative gastric lesions had a decrease in melatonin levels by 21–23 % relative to controls in all age groups (p ≤ 0.05). Discussion. The results indicate that ulcerative lesions of the stomach is likely to result in injury of enterochromaffin cells of the gastric mucosa, accompanied by a significant reduction in levels of melatonin in rats of both sexes and all age groups. Thus, it was found that despite no significant difference between levels of melatonin in males and females on the background of ulcerative lesions of the stomach, the overall level of melatonin reduction in males is 22–43 % higher relative to controls than in females — 21–23 %. The biggest gender differences in melatonin levels decrease were found at the age of 9 months (corresponds to the human age of 29–30 years) — by 39 % in males and by 23 % in females relative to controls and 20 months (corresponds to the human age of 55–56 years) — 43 and 22 %, respectively. The results suggest that in men aged 29–30 and 55–56 years, ulcerative lesions result in significant damage to extrapineal sources of melatonin synthesis and more severe course of the stomach ulcer with the development of complications. Conclusions. 1. Ulcerative lesions of the stomach lead to reduce levels of melatonin in the blood serum in rats of different sexes and age. 2. The greatest reduction in levels of melatonin in experimental gastric ulcer occurs in rat males aged 9 and 20 months corresponding to the human age of 29–30 and 55–56 years.

The feasibility and oncological safety of non-curative endoscopic submucosal dissection (ESD) prior to additional gastrectomy for early gastric cancer (EGC) are still unclear. The aim of this study was to evaluate the impact of non-curative ESD on short- and long-term outcomes of subsequent laparoscopic gastrectomy (LG) for pathological T1 (pT1) EGC. We retrospectively investigated 422 patients who underwent LG for pT1 EGC between January 2007 and December 2017 at our center. Eighty-five of these patients underwent ESD with curative intent before surgery. Using propensity-score matching for sex, age, body mass index, American society of anesthesiologists score, history of previous abdominal surgery, tumor location, mucosal/submucosal infiltration, histology, lymph node metastasis, extent of lymph node dissection, operative method, lymphatic invasion, and venous invasion, the clinicopathologic and survival data of these patients were compared. The median follow-up period was 60 (range 2–168) months. Using propensity-score matching from a total of 422 patients, 75 patients were selected in the Non-ESD and the ESD cohorts each. There were no significant differences in terms of characteristics and clinicopathological findings between the two groups. Furthermore, there were no significant differences in postoperative morbidity (13.3% vs. 17.3%; P = 0.497) and mortality (1.3% vs. 0%; P = 0.316). Both the 5-year overall survival ratio (88.8% vs. 86.9%; P = 0.757) and 5-year disease-specific survival ratio (97.1% vs. 98.4%; P = 0.333) were similar in the two groups. Short- and long-term outcomes of LG in patients with pT1 EGC are not related to preoperative ESD history. Even for non-curative resections, ESD prior to surgery is feasible in terms of oncological and surgical outcomes in pT1 EGC.

Background. Until now, the issue of the correlation between the cytokine balance and the progression of structural changes in the gastric mucosa remain completely uncertain. At the same time, the determination of the role of cytokine ba­lance as a component of gastric carcinogenesis will make it possible to substantiate new approaches to managing patients with atrophic gastritis. The purpose was to assess the level of pro- and anti-inflammatory cytokines, vascular endothelial growth factor (VEGF) at the stages of progression of structural changes in the gastric mucosa of patients with atrophic gastritis. Materials and methods. The study included 79 individuals with atrophic gastritis who underwent narrow band imaging endoscopic examination. The patients were divided into groups taking into account the revealed structural changes in the gastric mucosa: group I — 7 people with gastric mucosal atrophy without intestinal metaplasia (IM); group II — 16 individuals with gastric mucosal atrophy with IM limited by the antrum; group III — 45 people with diffuse IM against the background of gastric mucosal atrophy; group IV — 10 individuals with gastric mucosal dysplasia. In all patients, we assessed the level of interleukins (IL-8, IL-10, IL-18), tumor necrosis factor alpha (TNF-α), VEGF. Results. In patients of group IV, the concentration of IL-8 in the blood serum was 18.6 (11.3; 23.9) pg/ml that was significantly higher than in group I (by 5.0 times, p, Актуальність. До сьогодні питання взаємодії цитокінового балансу та прогресування структурних змін слизової оболонки шлунка (СОШ) залишаються остаточно не визначеними. Водночас визначення ролі цитокінового балансу як складової шлункового канцерогенезу дозволить обґрунтувати нові підходи до тактики ведення пацієнтів з атрофічним гастритом. Мета: оцінити рівень про- та протизапальних цитокінів, васкулоендотеліального фактора росту на етапах прогресування структурних змін СОШ у хворих на атрофічний гастрит. Матеріали та методи. У дослідження включено 79 хворих на атрофічний гастрит, яким проведено ендоскопічне дослідження в режимі NBI. Хворі були розподілені на групи з урахуванням виявлених структурних змін у СОШ: І група — 8 пацієнтів з атрофією СОШ без кишкової метаплазії (КМ); ІІ група — 16 хворих з атрофією СОШ із КМ, обмеженою антральним відділом шлунка; ІІІ група — 45 осіб з дифузною КМ на фоні атрофії СОШ; IV група — 10 пацієнтів з дисплазією СОШ. Усім хворим оцінювали рівень інтерлейкінів (ІЛ-8, ІЛ-10, ІЛ-18), фактора некрозу пухлини альфа (TNF-α), васкулоендотеліального фактора росту (VEGF). Результати. У хворих IV групи концентрація ІЛ-8 в сироватці крові становила 18,6 (11,3; 23,9) пг/мл і була вірогідно вище порівняно з пацієнтами І групи (в 5,0 раза; р

Background. The mechanisms of the functional interaction of the stomach and thyroid gland are based on the biological action of thyroid hormones. According to the European guidelines MAPS II, precancerous conditions of the stomach include atrophy and intestinal metaplasia of the gastric mucosa. The purpose of the work is to evaluate the structural and functional changes in the thyroid parenchyma in patients with precancerous conditions of the stomach. Materials and methods. The study was conducted in 44 patients with precancerous conditions of the stomach: 32 (72.7 %) women and 12 (27.3 %) men aged 33 to 76 years, on average (59.7 ± 1.7) years. Upper endoscopy was performed using the EVIS EXERA III system with an Olympus 190 gastroscope (Japan). According to the results of endoscopic examination, patients were divided into groups: group I — 11 people with atrophy of the gastric mucosa without intestinal metaplasia, group II — 13 individuals with atrophy of the gastric mucosa with intestinal metaplasia, limited by the antrum or body of the stomach, group III — 8 patients with diffuse intestinal metaplasia on the background of the gastric mucosa atrophy. The groups were representative by age and gender. All examined patients underwent a sonological examination of the thyroid gland with the ultrasound scanner Toshiba Xario (Japan) using a multi-frequency linear transducer with a frequency of 5–12 MHz. To assess the functional state of the thyroid gland, the levels of thyroglobulin and thyroid-stimulating hormone in the blood serum were determined by the enzyme immunoassay. Results. A significant increase in the frequency of diffuse and focal changes in the thyroid gland was found in patients with diffuse spread of intestinal metaplasia in the stomach (p < 0.05), which is confirmed by a correlation between the frequency of intestinal metaplasia of the body and antrum of the stomach with the presence of thyroid nodules (r = 0.44, p = 0.003; and r = 0.40, p = 0.006, respectively). At the same time, an increase in the frequency of focal hyperplasia of the gastric mucosa was associated with irregular contours of the thyroid gland (r = 0.41, p = 0.03) and an increase in the density of the thyroid capsule (r = 0.49, p = 0.04) that were the signs of a chronic inflammatory process. The spread of gastric intestinal metaplasia was accompanied by an increase in serum thyroglobulin by more than 3 times (p = 0.0134). Moreover, the level of thyroid-stimulating hormone significantly decreased as the precancerous changes in the gastric mucosa worsened (p = 0.0474), and the correlation between the level of this hormone and the presence of intestinal metaplasia in the stomach body (r = –0.46, p < 0.05) indicates the need for further study of the role of thyroid hormones in the development of precancerous conditions of the stomach. Conclusions. Patients with precancerous conditions of the stomach have a high frequency of structural changes in the thyroid parenchyma (81.8 %) of both diffuse (75.0 % of cases) and focal (43.2 %) nature. The spread of intestinal metaplasia in the gastric mucosa correlates with structural changes in the thyroid parenchyma, which is accompanied by a significant increase in thyroglobulin and a decrease in thyroid-stimulating hormone level in the blood serum. The frequency of structural changes in the thyroid gland increases with the development of precancerous changes in the stomach that is confirmed by a positive correlation between changes in the structure of the thyroid gland and the presence of xanthomas of the gastric mucosa, which are markers of precancerous conditions of the gastric mucosa (r = 0.52, p = 0.03).

Formation of multiple fundic gland polyps or hyperplastic polyps in the gastric mucosa is one of the well-known adverse effects of the long-term acid suppression therapy for peptic ulcer disease. However, similar phenomenon has not been reported to occur in the duodenum. We report a case of duodenal polypoid lesion that developed after the long-term use of acid suppressants and disappeared after the cessation of the treatment. The patient was a 76-year-old man with a history of heavy cigarette smoking and excessive alcohol intake who had been treated with medication of gastric acid suppressants, including proton pump inhibitors and potassium-competitive acid blockers, for refractory gastroesophageal reflux disease. After receiving the acid suppression therapy for 3 years, a polypoid lesion of 10 mm in diameter was found at the portion of the duodenal bulb. This polypoid lesion disappeared 1.5 months after the cessation of treatment. We hypothesized that changes in serum gastrin levels caused by acid suppression therapy might have been associated with the development and regression of the duodenal polypoid lesion.

Gastric cancer is the fourth most common type of cancer worldwide and the second most lethal. Gastric cancer biomarkers can be used for diagnosis, prediction of sensitivity to treatment, and prognosis. The following search terms were applied to PubMed as of December 2020: 'gastric cancer classification', 'gastric cancer epidemiology', 'cancer metastasis' and 'gastric cancer biomarker'. Only experimental studies were reported in the 'biomarkers' section. Some biomarkers can serve as therapeutic targets for antitumoral drugs. The genes analyzed include E-cadherin,Lay abstract Gastric cancer is the fourth most common type of cancer worldwide and the second most lethal. Gastric cancer biomarkers are molecules that have different expressions in tumor cells than in normal body cells, and can be used for diagnosis, prediction of sensitivity to treatment, and prognosis. Biomarkers in gastric cancer can include genes that suppress tumor progression, genes that increase tumor progression by binding to growth molecules, molecules related to the body’s immune response to the tumor, and non-coding RNA molecules (RNA molecules that do not produce proteins but regulate the cell’s genetic material). Some biomarkers can serve as therapeutic targets for anti-tumoral drugs.

Objective: To determine the frequency, demographic and clinical features of the heterotopic gastric mucosa (inlet patch). Methods: This retrospective study involves 244 patients who applied to the gastroenterology outpatient clinic with different symptoms between September 2016 and December 2019, and who were diagnosed with inlet patch in elective esophagogastroduodenoscopy. All endoscopic procedures were performed by the same clinical endoscopist. All medical records of patients including demographic and clinical features and endoscopy findings were reviewed. Results: Considering 2823 patients who underwent elective esophagogastroduodenoscopy in the same study period, inlet patch was detected in 224 (8.6%). The number of male patients was 138 (56.6%) and there was no statistical difference between the two genders. The mean age of the patients was 37.73 ± 13.01 years. Single lesion was detected in 204 (83.6%) patients. The size of the largest lesion was 4.5 cm and the smallest lesion was 0.3 cm. All of the lesions were in the proximal esophagus. 54 patients (22.1%) had at least one supraesophageal or upper esophageal symptom. The most common symptom was globus sensation (64.8%). Patients with large lesions were more likely to experience symptoms (28.2% vs. 13.7%, p=0.008). Conclusion: Careful examination of the proximal esophagus may increase the chance of detecting inlet patch and may explain persistent symptoms in patients without a specific cause. Further understanding of the clinical significance of the disease may also prevent unnecessary diagnostic interventions.

Background/Aims: There are no definite guidelines for the management of gastric lesions diagnosed as indefinite for dysplasia (IND) by endoscopic forceps biopsy (EFB). Therefore, this study aimed to evaluate the clinical outcomes of gastric IND and predictive factors for gastric neoplasm.Methods: This study included 457 patients with a first diagnosis of gastric IND by EFB between January 2005 and December 2013. Patient characteristics and endoscopic and pathological data were reviewed and compared.Results: Of the 457 gastric IND patients, 128 (28%) were diagnosed with invasive carcinoma, 21 (4.6%) with high-grade dysplasia, 31 (6.8%) with low-grade dysplasia, and 277 (60.6%) as negative for dysplasia. Of lesions observed, 180 (39.4%) showed upgraded histology. Multivariate analysis revealed that surface erythema (odds ratio [OR], 2.804; 95% confidence interval [CI], 1.741 to 4.516), spontaneous bleeding (OR, 2.618; 95% CI, 1.298 to 5.279), lesion size ≥ 1 cm (OR, 5.762; 95% CI, 3.459 to 9.597), and depressed morphology (OR, 2.183; 95% CI, 1.155 to 4.124) were significant risk factors for high-grade dysplasia or adenocarcinoma. The ORs associated with 2 and ≥ 3 risk factors were 7.131 and 34.86, respectively.Conclusions: Precautions should be taken in the management of gastric IND patients, especially when risk factors, including surface erythema, spontaneous bleeding, lesion size ≥ 1 cm, and depressed morphology are present. Considering the combined effect of the presence of multiple risk factors on the incidence of high-grade dysplasia or adenocarcinoma, endoscopic resection should be recommended if a gastric IND patient has at two or more of these factors.

Background/aims It is uncertain whether additional endoscopic treatment may be chosen over surgery in patients with positive lateral margins (pLMs) as the only non-curative factor after endoscopic submucosal dissection (ESD) for early gastric cancer (EGC). We aimed to compare the long-term outcomes of additional endoscopic treatments in such patients with those of surgery and elucidate the clinicopathological factors that could influence the treatment selection. Methods A total of 99 patients with 101 EGC lesions undergoing additional treatment after noncurative ESD with pLMs as the only non-curative factor were analyzed. Among them, 25 (27 lesions) underwent ESD, 29 (29 lesions) underwent argon plasma coagulation (APC), and 45 (45 lesions) underwent surgery. Clinicopathological characteristics and long-term outcomes were compared. Results Residual tumor was found in 73.6% of cases. The presence of multiple pLMs was associated with higher risk of residual tumor (p=0.046). During a median follow-up of 58.9 months, recurrent or residual lesions after additional ESD and APC were found in 4% (1/25) and 6.8% (2/29) of patients, respectively. However, all were completely cured with surgery or repeated ESD. There were no extragastric recurrences after additional endoscopic treatment. Lymph node metastasis was identified after additional surgery in one (2.2%) patient with an EGC showing histological heterogeneity. Conclusions Given the favorable long-term outcomes, additional ESD or APC may be an acceptable choice for patients with pLMs as the only non-curative factor after ESD for EGC. However, clincopathological characteristics such as multiple pLMs and histological heterogeneity should be considered in the treatment selection.

BACKGROUND: The Prex2 protein is a member of the Rac family proteins that belongs to small G proteins with a critical role in cell migration, cell proliferation, and apoptosis through its effects on PI3K cell signaling pathway and phosphatase activity of PTEN protein. The effect of PREX2 gene expression has been shown in some cancer cells. A survey of PREX2 gene expression in gastric antral epithelial cells of gastric cancer patients with Helicobacter pylori various genotypes infection can conduct to better understanding H. pylori infection’s carcinogenesis. METHODS: In a case-control study, PREX2 gene expression was evaluated in gastric antral biopsy samples on four groups of patients referred to Sanandaj hospitals, including gastritis with (n=23) and without (n=27) H. pylori infection and gastric cancer with (n=21) and without (n=32) H. pylori infection. Each gastric biopsy sample’s total RNA was extracted and cDNA synthesized by using Kits (Takara Company). The PREX2 gene expression was measured using the relative quantitative real-time RT-PCR method and ΔΔCt formula. RESULTS: The PREX2 gene expression increased in gastric antral biopsy samples of gastritis and gastric cancer patients with H. pylori infection (case groups) than patients without H. pylori infection (control groups) 2.38 and 2.27 times, respectively. The patients with H. pylori vacA s1m1 and sabB genotypes infection showed a significant increase of PREX2 gene expression in gastric cancer antral epithelial cells. CONCLUSION: H. pylori vacA s1m1 and sabB genotypes have the positive correlations with PREX2 gene expression in gastric antral epithelial cells of gastritis and gastric cancer patients. RESUMO CONTEXTO: A proteína Prex2 é membro das proteínas da família Rac que pertencem a pequenas proteínas G com um papel crítico na migração celular, na proliferação celular e na apoptose através de seus efeitos na via de sinalização celular PI3K e atividade fosfatase da proteína PTEN. O efeito da expressão genética PREX2 tem sido mostrada em algumas células cancerosas. Um levantamento da expressão genética PREX2 em células epiteliais antrais gástricas de pacientes infectados com vários genótipos de Helicobacter pylori pode conduzir a um melhor entendimento da carcinogênese da infecção por H. pylori. MÉTODOS: Em estudo de caso-controle, a expressão genética PREX2 foi avaliada em amostras de biópsia antral gástrica em quatro grupos de pacientes encaminhados aos hospitais de Sanandaj, incluindo gastrite com (n=23) e sem (n=27) infecção por H. pylori e de câncer gástrico com (n=21) e sem (n=32) infecção por H. pylori. O RNA total de cada amostra de biópsia gástrica foi extraído e cDNA sintetizado por meio de kits (Takara Company). A expressão genética PREX2 foi medida utilizando-se o método RT-PCR em tempo real quantitativo relativo e a fórmula ΔΔCt. RESULTADOS: A expressão genética PREX2 aumentou em amostras de biópsia antral gástrica de pacientes com gastrite e câncer gástrico com infecção por H. pylori (grupos de casos) em relação aos sem infecção por H. pylori (grupos de controle) 2,38 e 2,27 vezes, respectivamente. Os pacientes com infecção por genótipos H. pylori vacA s1m1 e sabB apresentaram um aumento significativo da expressão genética PREX2 em células epiteliais antrais de câncer gástrico. CONCLUSÃO: Os genótipos H. pylori vacA s1m1 e sabB têm correlações positivas com a expressão genética PREX2 em células epiteliais antrais gástricas de pacientes com câncer gástrico e gastrites.

We herein report a case of intraperitoneal abscess as a postoperative complication of gastric endoscopic submucosal dissection (ESD). A 70-year-old man who underwent ESD for early gastric cancer sought consultation for abdominal pain on postoperative day 28. Abdominal computed tomography revealed intraperitoneal abscess rupture. He underwent image-guided laparoscopic irrigation. His postoperative course was favorable, and he was discharged after 27 days. Intraoperatively, a white plaque adhering to the gastric wall was surrounded by a large pus volume and suspected to be ESD-associated. We present this case with a literature review of the association between intraperitoneal abscess and ESD.

Gastric neuroendocrine tumors (NETs) are rare lesions that arise from enterochromaffin-like cells of the gastric mucosa. Gastric NETs are classified into 3 types of NETs and poorly differentiated neuroendocrine cancers. Most gastric NETs usually present as hemispherical, yellowish, polypoid lesions with a central depression and often as subepithelial tumors (SETs) because they are confined within the submucosal layer. Here, we report a case of gastric NET presenting as SET mimicking a gastrointestinal stromal tumor (GIST). Endoscopy revealed a 2.3-cm-sized SET with intact surface mucosa, and endoscopic ultrasonography showed a homogeneous hypoechoic lesion with a well-circumscribed margin. Typical features of gastric NET, such as yellowish mucosal changes or central ulceration, were not observed. GIST was suspected, and a laparoscopic wedge resection was performed. The final diagnosis was gastric NET with grade 2 differentiation.