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The pathogenesis of eosinophilic esophagitis involves immunoglobulin G4 (IgG4) deposition. However, the relationship between IgG4 and eosinophilic gastroenteritis (EGE) is unclear. To investigate gastrointestinal deposition of IgG4 in EGE. Biopsies of the esophagus, stomach, and small intestine were evaluated in patients with and without EGE. Immunohistochemical staining for IgG4 was performed, and the proportions of the stained areas were compared. Sera from patients with EGE were assayed for food-specific IgG4, including egg white, wheat, rice, soy, and cow milk. Seventeen patients were included in this study (EGE group, n = 10; control group, n = 7). Compared with the control group, the proportion of IgG4-stained area in the EGE group was approximately threefold higher (40.2% [32.3–49.5]) vs. 12.1% [4.0–21.9], p = 0.014) in the esophagus, fivefold higher in the stomach (17.3% [11.1–26.2] vs. 3.7% [1.5–5.2], p = 0.014), and sixfold higher in the small intestine (28.0% [15.0–33.2] vs. 4.5% [2.6–9.8], p = 0.019). There was no significant association between the proportion of IgG4-stained area and the number of infiltrating eosinophils. Serum egg white-specific IgG4 levels were correlated with the proportion of IgG4-stained areas in the small intestine (R = 0.7, p = 0.035). IgG4 accumulated within the gastrointestinal mucosa in EGE. The positive correlation between serum egg white-specific IgG4 levels and the proportion of IgG4-stained areas in the small intestine suggests a role for IgG4 in the disease pathophysiology.

The incidence of eosinophilic esophagitis (EoE), a Th2-type allergic disease of the esophagus, has increased with the higher prevalence of gastroesophageal reflux disease (GERD). Both conditions are chronic inflammatory diseases with similar clinical presentations, yet their pathogenesis is thought to differ. Recent evidence indicates that forkhead box P3 (FOXP3)-positive regulatory T cells (Tregs) play a critical role in immune tolerance and control of Th2-biased responses in various allergic diseases.This study aimed to investigate differences in Treg induction between EoE and GERD and clarify whether this difference was related to the clinicopathological findings of patients with EoE.Thirty patients (15 men, 15 women) with EoE and 30 patients (15 men, 15 women) with GERD were included. Patient characteristics, including endoscopic and pathological findings, were compared between the two groups. Immunohistochemistry staining was used to identify T lymphocytes and Tregs. Tregs were identified by CD3 + FOXP3 + staining, and T cells were defined as CD3 + cells. The number of T cells and Tregs in the epithelium was counted, and the average of Tregs/T cells was calculated.The ratio of Tregs/CD3 + T cells in the esophageal epithelium was significantly lower in the EoE group than in the GERD group (9.9% vs. 23.6%, P = 0.0000012). Comparison of the ratio of Tregs/CD3 + T cells by age, gender, endoscopic findings, and histological findings in patients with EoE revealed a significant difference in gender.Treg induction was impaired, and this effect was more pronounced in male adult patients with EoE than those with GERD.

Mycophenolate Mofetil (MMF) is routinely used immunosuppressant in solid organ transplantation is commonly associated with several gastrointestinal (GI) side effects. Here we present a case of giant gastric ulcer of 5 cm from MMF use post cardiac transplant. Case Description A 56-year-old male with history of severe ischemic cardiomyopathy post heart transplant was on immunosuppression with MMF, tacrolimus and prednisone for 5 months. He presented with severe epigastric pain and intermittent episodes of melena for 1 month. His pain radiated to back that is worsened with eating. Associated with loss of appetite, vomiting and 16-pound weight loss in 3 months. He never smoked, drank alcohol or used over the counter pain medications. He was profoundly anemic requiring blood transfusions. EGD performed demonstrated very large clean-based ulcer of 5 cm diameter in the body, smaller ulcer of 8 mm diameter in pre-pyloric region and 5–10 small aphthous ulcers in the gastric body and fundus. Gastric biopsies taken from the ulcer were negative for Helicobacter pylori, cytomegalovirus and malignancy. Flexible sigmoidoscopy revealed non-bleeding inflamed internal hemorrhoids. Consequently, MMF was discontinued and switched to azathioprine. He was treated with twice daily proton pump inhibitor therapy with resolution of abdominal pain, improved appetite and weight gain. Discussion MMF is well known for common GI side-effects such as nausea, diarrhea, vomiting, ulcers, abdominal pain and rarely gastrointestinal bleeding. Few studies reported 3 to 8% incidence of ulcer perforation and GI bleeding within 6 months. Risk of gastroduodenal erosions is nearly 1.83 times for MMF, with the highest lesions associated with MMF-tacrolimus-corticosteroid combination treatment as seen in our patient. Hypothesis is that GI tract is vulnerable because of dependence of enterocytes on de novo synthesis of purines, which is disrupted by MMF. Typically, upper GI mucosal injuries of mucosal irritation leading to esophagitis, gastritis and/or ulcers are seen. Endoscopy is both diagnostic and therapeutic if bleeding gastric ulcers are noted. Minor complications improve with reduction of drug dose or use of enteric coated preparation if feasible. Discontinuation of the drug is main stay in the management of MMF related ulcer disease. Simple medical treatment with either H2-receptor antagonists, proton-pump inhibitors, coating agents, prostaglandins or combination has proven effective in most cases. Considering excellent results with medical management of ulcer, role of surgery is limited.

How gastric cancer (GC) incidence is associated with changes in the gastric microbiome has not been firmly established. The present study therefore aims to investigate the microbial communities present within the gastric mucosa of patients with superficial gastritis (SG) or GC. Paired tumor and paracancerous samples of the gastric mucosa were collected from 18 patients being surgically treated for GC and from 32 patients with SG being treated via gastroscopy. The gastric microbiome in these samples was then profiled via 16S rRNA sequencing, with a linear discriminant analysis effect size (LEfSe) approach used to identify and compare different bacteria, and with PICRUSt used for predictive functional analyses. GC patients exhibited a distinct gastric microbiota profile from that observed in SG patients. These changes were evident in both tumor and paracancerous tissues from GC patients. Specifically, we found that 6 bacterial genera were specifically enriched in GC tissue samples relative to SG samples, while 18 genera were depleted in these same samples. Based on the differential abundance of these bacteria, we were able to calculate microbial dysbiosis index (MDI) values, which were significantly higher in GC patients than in SG patients. In addition, MDI values were negatively correlated with gastric Shannon index and were positively correlated with relative Helicobacter spp. abundance. Importantly, these MDI values were readily able to discriminate between GC and SG patient samples. Functional analysis suggested that GC patients were more likely to harbor a nitrosating microbial community. GC patients exhibited a gastric microbiome profile distinct from that observed in SG patients, with these differences being evident in both tumor and paracancerous tissues. Differences in the relative abundance of Helicobacter spp. may be the primary driver of gastric dysbiosis in GC patients.

Suppurative gastritis is an uncommon lesion and often an occult cause of upper abdominal pain without florid signs of a septic focus. There are two main phenotypic forms: (1) localized, also referred to as gastric abscess; and (2) diffuse, in which the differential diagnosis includes a more diverse range of benign and malignant lesions. Cross-section imaging such as CT allows for rapid diagnosis and demonstrates the location and extent, but not the specific etiology, of the lesion. High-frequency endoscopic ultrasound (EUS) and fine needle aspiration (FNA) have greatly improved the safety and diagnostic accuracy of suppurative gastritis. EUS/FNA provides an opportunity to arbitrate among infectious and malignant or benign tumors, to identify specific pathogens, and in cases of localized gastric abscesses, for resolution by decompression. More advanced endoscopic procedures are rapidly emerging to supplement EUS/FNA, which already demonstrate the promise of improved, minimally-invasive diagnosis and effective management for the diverse range of lesions causing suppurative gastritis.

The causes for the occurrence of goblet cells at the gastroesophageal junction (GEJ-GC) are unknown. The aim of our study was to compare the concurrent histologic changes of the stomach in (1) patients with GEJ-GC, but without Barrett’s esophagus (BE) to those in (2) patients with BE and in (3) controls without GEJ-GC or BE. We used an electronic database of histopathologic records from 1.3 million individual patients, who underwent esophago-gastro-duodenoscopy (EGD) in 2009–2018. We compared the prevalence of Helicobacter pylori-positive gastritis (HpG), gastric intestinal metaplasia (G-IM), chronic inactive gastritis (CIG), and reactive gastropathy (RG) among the 3 patient groups, using odds ratios and their 95% confidence intervals. Of all EGD patients, 4.0% harbored BE and 2.4% GEJ-GC. The average age of patients with GEJ-GC (60 ± 14) was significantly younger than the age of patients with BE (63 ± 12) and significantly older than the age of controls (55 ± 17). Female subjects were more common among GEJ-GC (54%) than BE (37%), but less common than among controls (63%). The 3 gastric histopathology changes associated with H. pylori were significantly more common in GEJ-GC than BE (for HpG 2.42, 2.29–2.56; for G-IM 1.82, 1.73–1.92; for CIG 1.31, 1.22–1.41). The corresponding differences between GEJ-GC and controls were less striking (for HpG 0.97, 0.93–1.01; for G-IM 1.15, 1.11–1.19; for CIG 0.90, 0.85–0.95). RG was slightly less common in GEJ-GC than BE (0.89, 0.86–0.92) and controls (0.94, 0.91–0.96). With respect to its demographic and histopathologic features, GEJ-GC likely represents gastric intestinal metaplasia as opposed to BE and should prompt gastric intestinal metaplasia screening and management.

Early diagnosis of gastric cancer is difficult in China due to the lack of a valid method for endoscopic screening. Early gastric cancer, especially flat gastric cancer, lacks specific endoscopic features. Many cases appear to be similar to ordinary gastritis cases under normal white light endoscopy, which can lead to misdiagnosis. In order to find a new method to improve detection rate of early gastric cancer in China, we designed a trial to validate linked color imaging (LCI) for screening of early gastric cancer in a high-risk population, as compared to white light imaging (WLI). Subjects were randomly allocated to either the LCI + WLI or WLI group and then subjected to gastroscopy and all endoscopies were made after special preparation. All endoscopists had knowledge of this experiment. The main indicator was the rate of detection of gastric neoplastic lesions. The difference in the detection rate between the two groups is reported. The detection rate was 4.31% in the WLI group and 8.01% in the LCI + WLI group. This is a difference of 3.70% with a P value

The late 1800s Louis Pasteur and Robert Koch introduced and popularized the germ theory of disease. At that time, gastric cancer was the most common cause of cancer deaths in most countries making the stomach an early site of microbial research with a focus on gastric luminal and mucosal bacteria and the role of Boas-Oppler bacillus (Lactobacillus) in the diagnosis of gastric cancer. In the 1970s, the research focus evolved to studies of the gastric microbiome in the production of nitrosamines and included development of the Correa cascade. Interest in nitrosamine production peaked in the late 1980s and was replaced by studies of the newly described Helicobacter pylori and studies of its role in gastritis, gastric atrophy, and gastric cancer. The last decade has witnessed a rebirth in interest in the gastric microbiota as part of worldwide interest in the human microbiome. Although fungi were prominent in the studies of gastric microbiology in the nineteenth century, their potential role in disease pathogenesis has yet to be addressed using modern techniques. Overall, current studies of the gastric bacterial microbiome do not provide convincing evidence to expand the role of the gastric microbiome in cancer pathogenesis beyond what is directly attributable to the oncogenic potential of H. pylori and its role in persisting acute-on-chronic inflammation.

Eosinophilic esophagitis (EoE) is a chronic disease, but the extent of patient loss to follow-up (LTFU) and health care utilization has not been fully investigated.To determine frequency and predictors of LTFU and health care utilization in EoE patients.In this retrospective cohort study, we extracted data from patients with a new diagnosis of EoE. Follow-up time for each patient was calculated as the time from the first diagnostic endoscopy to the last GI-related contact date in the medical record. Patients with and without LTFU were compared, and the volume of EoE-related health care interactions was recorded.Of 944 EoE cases, 249 (26%) met the definition for LTFU. Major reasons for LTFU were never being scheduled (45%) and inability to contact patients (40%). Factors independently associated with regular follow-up were having insurance (aOR 2.89; 95% CI 1.85-4.50), white race (aOR 2.16; 95% CI 1.37-3.41), and longer symptom length (aOR 1.04 per year; 95% CI 1.01-1.08). At the time of last contact, patients with follow-up had better symptom response (55% vs. 12%; p 0.001), improved esophageal caliber (14.3 vs. 12.4 mm; p = 0.005), and more histologic response (45% vs. 4% at 15 eos/hpf; p 0.001). Health care utilization was high, with an average of 4.6 endoscopies and 4.0 clinic visits over the follow-up period.LTFU of newly diagnosed EoE cases was common and associated with lack of insurance, non-white race, and shorter symptom duration. Those who followed up had high health care utilization but improved response rates. Strategies are needed to help decrease LTFU in EoE.

Evidence regarding the association between sleep disturbance and functional dyspepsia (FD) remains limited in the young population. This study aimed to investigate the association between sleep disturbance and FD including subgroups among Japanese young people. Study subjects were 8923 university students. FD was defined according to the Rome III criteria. Subjects with FD were further categorized as having postprandial distress syndrome (PDS) or epigastric pain syndrome (EPS). Subjects completed a self-reported questionnaire assessing self-reported sleep duration, sleep disturbance, difficulty falling asleep, deep sleep disorder, nocturnal awakening, early awakening, and daytime sleepiness. The prevalence of FD was 1.9%. After adjustment, all types of sleep disturbances were independently positively associated with FD (total sleep disturbance: OR 4.11 [95% CI: 2.89–5.78], difficulty falling asleep: OR 3.97 [95% CI: 2.53–6.01], deep sleep disorder: OR 4.85 [95% CI: 3.06–7.40], nocturnal awakening: OR 4.35 [95% CI: 1.90–8.67], early awakening: OR 4.50 [95% CI: 1.97–8.97], and daytime sleepiness: OR 2.83 [95% CI: 1.25–5.56]). While nocturnal awakening and daytime sleepiness were not associated with EPS, the other types of sleep disturbance were independently positively associated with EPS and PDS. No association between self-reported sleep duration and FD was found. Sleep disturbance may be independently positively associated with the prevalence of FD among Japanese young people. Nocturnal awakening and daytime sleepiness were not associated with EPS; the other types of sleep disturbance were independently positively associated with EPS and PDS.

BACKGROUND: Helicobacter pylori infection is an established causal factor for non-cardia gastric cancer. H. pylori negative gastric cancer prevalence among U.S. patients is unclear. METHODS: This retrospective cohort study examined H. pylori prevalence among consecutive patients with incident non-cardia gastric adenocarcinoma at the Houston VA Hospital (11/2007–10/2018). H. pylori positivity was defined by H. pylori on histopathology, positive antibody serology, stool antigen, or urea breath testing. We examined for trends in H. pylori negative gastric cancer based on year of diagnosis. Associations between histopathologic and cancer-related outcomes with H. pylori positivity were determined using regression models. RESULTS: Of 91 patients with gastric adenocarcinoma, most were men (N=87, 95.6%), black (N=47, 51.6%), with mean age at diagnosis of 68.0 years (SD 10.8). In addition to gastric cancer biopsy histopathology, 74 patients (81.3%) had ≥1 testing for H. pylori, including antibody serology (n=34), non-cancer gastric biopsy histopathology (n=63), or stool antigen (n=1). The overall prevalence of H. pylori infection was 38.5% and 45.9% among patients with ≥2 H. pylori tests. The proportions of H. pylori positive gastric cancer decreased from 50.0% (2007–2010) to 43.4% (2011–2014) and 29.3% (2015–2018) (p=0.096). Active/acute gastritis (adjOR 3.74), atrophic gastritis (adjOR 15.30), and gastric intestinal metaplasia (adjOR 3.65) were associated with H. pylori positive gastric cancer. DISCUSSION: The prevalence of H. pylori infection among patients with non-cardia gastric adenocarcinoma is relatively low (38.5–45.9%) and decreasing over time. This finding suggests there may be other important causal factors apart from H. pylori for gastric adenocarcinoma.

Early detection of early gastric cancer (EGC) allows for less invasive cancer treatment. However, differentiating EGC from gastritis remains challenging. Although magnifying endoscopy with narrow band imaging (ME-NBI) is useful for differentiating EGC from gastritis, this skill takes substantial effort. Since the development of the ability to convolve the image while maintaining the characteristics of the input image (convolution neural network: CNN), allowing the classification of the input image (CNN system), the image recognition ability of CNN has dramatically improved. To explore the diagnostic ability of the CNN system with ME-NBI for differentiating between EGC and gastritis. A 22-layer CNN system was pre-trained using 1492 EGC and 1078 gastritis images from ME-NBI. A separate test data set (151 EGC and 107 gastritis images based on ME-NBI) was used to evaluate the diagnostic ability [accuracy, sensitivity, positive predictive value (PPV), and negative predictive value (NPV)] of the CNN system. The accuracy of the CNN system with ME-NBI images was 85.3%, with 220 of the 258 images being correctly diagnosed. The method’s sensitivity, specificity, PPV, and NPV were 95.4%, 71.0%, 82.3%, and 91.7%, respectively. Seven of the 151 EGC images were recognized as gastritis, whereas 31 of the 107 gastritis images were recognized as EGC. The overall test speed was 51.83 images/s (0.02 s/image). The CNN system with ME-NBI can differentiate between EGC and gastritis in a short time with high sensitivity and NPV. Thus, the CNN system may complement current clinical practice of diagnosis with ME-NBI.

Nodular gastropathy (NG) is an inflammatory condition of the gastric mucosa characterized by the endoscopic detection of multiple millimeter protrusions. A strong association between NG and Helicobacter pylori and a possible role of NG as a risk factor for undifferentiated gastric cancer have been described. The aim of this study was to characterize the pathogenic and inflammatory profile of patients with NG. Adult patients referred for upper gastrointestinal endoscopy were prospectively enrolled in this study. H. pylori infection status was determined by rapid urease test. Biopsies were stained with hematoxylin–eosin. Sydney and OLGA scores were used to assess gastritis characteristics and gastric cancer risk. PCR analysis was performed to determine bacterial load and virulence factors CagA (and its EPIYA motifs) and VacA alleles. Finally, gastric mucosa cytokine gene expression (IL-8, IL-1β, and TNF-α) was determined by real-time RT-PCR. Forty-eight patients, mean age of 36 years, were recruited. All NG patients were infected by H. pylori. OLGA score was similar in both groups (NG patients and non-NG patients). NG patients had higher bacterial load in the gastric corpus (p = 0.01) and significantly less pro-inflammatory cytokine levels than non-NG infected patients (p = 0.01). In our study, NG is not associated with preneoplastic lesions. An increase in bacterial load without a concomitant increase in mucosal inflammatory cytokine responses in H. pylori-infected subjects with NG may represent a general dampening of immune responses or an additional mechanism of H. pylori active immune evasion.

In Japan, laser light source (Laser) endoscopy is widely available, and the characteristics of light-emitting diode light source (LED) endoscopy have not been clarified. We assessed the visibility of early gastric cancers (EGCs) and Helicobacter pylori (H. pylori)-associated gastritis for LED endoscopy compared with laser endoscopy using white-light imaging (WLI) and linked color imaging (LCI). We assessed 99 lesions between February 2019 and March 2020. The visibility was scored from four (excellent visibility) to one (poor visibility) by evaluating videos including EGCs and gastric mucosa captured using WLI and LCI with LED endoscopy (LED-WLI and LED-LCI, respectively) and laser endoscopy (Laser-WLI and Laser-LCI, respectively). The primary end point was the non-inferiority of the visibility of EGCs and H. pylori-associated gastritis between LED-/Laser-WLI and LED-/Laser-LCI. The visibility scores of EGCs for LED-/Laser-WLI and LED-/Laser-LCI were 3.14/2.97 and 3.39/3.35, respectively. The visibility scores of H. pylori-associated gastritis [intestinal metaplasia (IM), diffuse redness (DR), regular arrangement of collecting venules (RAC) and map-like redness (MR)] for LED-/Laser-WLI and LED-/Laser-LCI were 3.05/2.85 and 3.60/3.50 (IM), 2.76/2.50 and 2.96/2.86 (DR), 2.69/2.44 and 2.77/2.62 (RAC) and 2.97/2.75 and 3.39/3.27 (MR). Non-inferiority was demonstrated for visualizing EGCs and H. pylori-associated gastritis. LED-WLI and LED-LCI can be used to visualize EGCs and H. pylori-associated gastritis with non-inferiority to Laser-WLI and Laser-LCI. Furthermore, even with LED, LCI was more effective than WLI for evaluating EGCs and H. pylori-associated gastritis. Therefore, LED endoscopy can be used to detect EGCs and evaluate H. pylori-associated gastritis accurately.

Limited data are available to support current guidelines recommendations on obtaining gastric and duodenal biopsies of patients with clinical and histologic manifestations consistent with eosinophilic esophagitis (EoE) to rule out eosinophilic gastritis (EG) or duodenitis (EoD). Our study examined the prevalence of concomitant extraesophageal, gastrointestinal pathology to better characterize the diagnostic yield of additional biopsies. This was a single-center, retrospective study which utilized ICD 9 codes (530.13) and search queries of pathology reports (“Eosinophilic esophagitis,” “EoE”) to identify EoE patients. Patient endoscopy reports, pathology reports, and office notes were manually reviewed to characterize cases. The electronic health record search yielded 1,688 EoE adults. In those who had extra-esophageal biopsies obtained, EG was identified in 34 (3.4%), H. pylori in 45 (4.6%), EoD in 27 (3.3%), and histology consistent with celiac disease in 20 (2.5%). Endoscopic abnormalities were found in the stomach of 92% of patients with EoE and EG and in the duodenum of 50% of patients with EoE and EoD. Symptoms of dyspepsia and/or abdominal pain occurred in a significantly greater proportion of patients with extraesophageal disease (64% vs. 19% in EoE group, p

Functional nausea and vomiting syndromes and gastroparesis, collectively grouped as nausea and vomiting syndromes (NVS), are overlapping conditions with incompletely understood pathophysiology. Gastric slow wave abnormalities are thought to contribute.This study aimed to systematically review and meta-analyze the prevalence of slow wave abnormalities measured by electrogastrography (EGG) in patients with NVS.MEDLINE, EMBASE, EMBASE classic, and CENTRAL databases were systematically searched for articles using EGG in adults (≥ 18 years) with NVS. EGG metrics of interest were percentage time in bradygastria, normogastria, and tachygastria as well as dominant frequency and dominant power. Outcomes were also compared with functional dyspepsia (FD), gastroesophageal reflux disease (GORD), and control cohorts.Seven hundred and sixty NVS patients and 308 controls were included from 24 studies. Overall, 64% of patients had EGG abnormalities. Average percent time in normogastria was low during fasting (50%; 95% CI 40-63%) and fed (53%; 95% CI 41-68%) states in patients, with substantial periods in fasting bradygastria (34.1%; 95% CI 25-47%) and postprandial tachygastria (21%; 95% CI 17-26%). Across gastric disorders, pooling of 84 studies showed a comparably high prevalence of EGG abnormalities in NVS (24 studies; n = 760) and GORD (13 studies; n = 427), compared to FD (47 studies; n = 1751) and controls (45 studies; n = 1027).Frequency-based gastric slow wave abnormalities are prominent in NVS. The strength and consistency of these associations across many studies suggests that gastric dysrhythmia may be an important factor in NVS, motivating the development of more reliable methods for their clinical assessment.

Quinolone-containing triple therapy has been considered as the second-line therapy for eradication of Helicobacter pylori (H. pylori). At present, there are no data to show the efficacy and safety of antofloxacin-based rescue therapy for the eradication of H. pylori, and this pilot clinical trial was designed.A total of 196 patients who failed H. pylori eradication using the clarithromycin-based or metronidazole-based triple or bismuth quadruple therapy were randomly allocated to one of the following rescue eradication therapy groups: AEA group (antofloxacin 200 mg once daily, esomeprazole 20 mg + amoxicillin 1000 mg twice daily) for 14 days, or LEA group (levofloxacin 500 mg once daily, esomeprazole 20 mg + amoxicillin 1000 mg twice daily) for 14 days. The minimal inhibitory concentrations were tested by the E-test method. The gyrA mutation was analyzed by sequencing. Follow-upA total of 178 eligible patients were included in this study. The eradication rate was significantly higher in AEA group than in LEA group according to both ITT (87.6% vs. 68.5%; P = 0.002) and PP analyses (90.7% vs. 70.1%; P = 0.001). ITT analyses indicated that the eradication rate was significantly higher in AEA group than in LEA group with Asn87 mutation (78.9% vs. 31.3%; P = 0.005) and levofloxacin-resistant strains (76.9% vs. 44.2%; P = 0.003). Two groups exhibited similar adverse event rates (AEA 14.6% vs. LEA 20.2%, P = 0.323).The findings showed that antofloxacin may be a promising candidate in rescue therapy for H. pylori eradication failure in China.

As one of the most prevalent infections globally, Helicobacter pylori (H. pylori) continues to present diagnostic and therapeutic challenges for clinicians worldwide. Diagnostically, the "test-and-treat" strategy is the recommended approach for healthcare practitioners when managing this potentially curable disease. The choice of testing method should be based on several factors including patient age, presenting symptoms, and medication use, as well as test reliability, availability, and cost. With rising antibiotic resistance, particularly of macrolides, care must be taken to ensure that therapy is selected based on regional resistance patterns and prior antibiotic exposure. In the USA, macrolide antibiotic resistance rates in some areas have reached or exceeded a generally accepted threshold, such that clarithromycin triple therapy may no longer be an appropriate first-line empiric treatment. Instead, bismuth quadruple therapy should be considered, while levofloxacin-based or alternative macrolide-containing therapies are also options. Once treated, it is essential to test for eradication as untreated H. pylori is associated with serious complications including peptic ulcer disease, mucosa-associated lymphoid tissue lymphoma, and gastric cancer. This review article aims to consolidate current knowledge of H. pylori infection with a particular emphasis on diagnostic and treatment strategies.

International audience; Background: GATA factors, which constitute a family of transcription regulatory proteins, participate in gastrointestinal development. Trefoil factor 1 (TFF1) plays a crucial role in mucosal defense and healing, and evidence suggests that GATA-5 mediated its regulation. Gastric cancer is a multiple-step process triggered by Helicobacter pylori and is characterized by accumulation of molecular and epigenetic alteration. The aim of this study was to evaluate the effect of H. pylori infection on the regulation of GATA-5 and TFF1 in vitro and in vivo.Results: Infected cells exhibited upregulation of GATA-5 and TFF1 after 48 h. An increase in GATA-5 and TFF1 mRNA levels was also found in mice samples after 6 and 12 months of infection, respectively. In human samples, we found an association between H. pylori infection and GATA-5 upregulation. In fact, among H. pylori-infected patients, hypermethylation was observed in 45.5% of pediatric samples, in 62.6% of chronic gastritis samples, and in 63% of gastric cancer samples. Regarding TFF1, the expression levels were similar in pediatrics and adults patients, and were independent of H. pylori infection, and the expression of these factors was downregulated in gastric cancer samples. GATA-5 promoter methylation was associated with a decrease in TFF1 mRNA levels.Conclusions: Our results suggest that the upregulation of GATA-5 and TFF1 observed in vitro and in vivo may be correlated with a protective effect of the mucosa in response to infection. The epigenetic inactivation of GATA-5 observed in human biopsies from infected patients may suggest that this alteration is an early event occurring in association with H. pylori infection.

Aim To observe the therapeutic effect of low-dose amitriptyline (AMT) on epigastric pain syndrome (EPS) in patients with functional dyspepsia. Methods Sixty patients with EPS were randomly divided into the following two groups for a four-week clinical trial: routine treatment with pantoprazole (RT group) and the AMT group. The RT group was treated with 40 mg of pantoprazole once daily. The AMT group received 25 mg of AMT once daily before bedtime. The Nepean Dyspepsia Index (NDI) checklist, Hamilton Rating Scale of Anxiety/Depression (HAMA/HAMD), and Pittsburgh Sleep Quality Index (PSQI) were employed to evaluate dyspepsia symptoms, psychological distress, and sleep, respectively. Results All items were similar between the two groups before treatment (0 week). After 4 weeks of treatment, the NDI–symptom checklist score as well as the severity and bothersomeness of EPS in the AMT group was significantly decreased compared with those in the RT group (p

Background MicroRNAs, targeting mRNAs of cancer-associated genes, are often aberrantly expressed in human gastric cancer (GC). Aim We have examined the possible role and mechanisms of miRNA regulation of Prdx-6 in the development and progression of H. pylori-related gastric mucosal lesions. Methods First, miR-24-3p was predicted to target Prdx-6, and this negative regulation was validated by luciferase reporter analyses, Western blot, and quantitative RT-PCR. Next, immunohistochemistry and in situ hybridization were performed to detect the Prdx-6 and miR-24-3p expression in tissue microarrays of gastric mucosal lesions. Finally, the miR-24-3p function in GC cell line N87 was examined by MTT, Annexin V-FITC, PI, transwell migration, and Matrigel invasion assays. Results In our study, Prdx-6 expression was negatively regulated by miR-24-3p expression and miR-24-3p interacted with the 3′-untranslated region of Prdx-6 to down-regulate its expression level. In addition, miR-24-3p expression gradually decreased in human gastric specimens from chronic superficial gastritis (CSG) to dysplasia and was upregulated in GC tissues compared with adjacent normal tissues. Contrary to this, Prdx-6 expression showed inverse tendency in the same tissue. More so, expression of miR-24-3p was reduced in samples with H. pylori infection, especially in CSG. Moreover, miR-24-3p was associated with GC lymph nodes and liver metastasis. Gain- or loss-of-function experiments showed that miR-24-3p significantly inhibited N87 cell growth, migration, and invasion and promoted apoptosis, while Prdx-6 reversed these miR-24-3p effects. Conclusions miR-24-3p was identified as a regulator of development and progression of H. pylori-related gastric mucosal lesions.

Gastroparesis (GP) is a disabling chronic gastroenterologic disorder with high morbidity that severely impacts patients’ quality of life. GP can present acutely after a viral-like gastrointestinal illness resulting in speculation that in some patients, neurologic damage caused by the infection might underlie the pathogenesis of idiopathic gastroparesis (IGP). The aim of this study is to document case reports of Enterovirus (EV) infection as a possible cause of IGP. Eleven patients referred with a diagnosis of GP underwent workup to exclude known causes of GP. Those with a history of flu-like symptoms or gastroenteritis prior to onset of GP symptoms had gastric biopsies taken during upper endoscopy to assess for the presence of gastric mucosal EV infection. Data on presenting symptoms, extra-intestinal symptoms and conditions, prior nutritional support requirements, upper endoscopy findings, and response to therapy were cataloged. Eleven patients were diagnosed as IGP. Nine had active EV infection on gastric biopsies and were included (7/9 female, mean age 43 years). Eight out of nine received EV treatment with antivirals and/or immune therapies, with a wide degree of variability in treatment regimens. Four out of eight who received EV treatment had symptomatic improvement. One patient had stable symptoms. Three patients are currently undergoing therapy. Gastric EV infection was frequently detected (82 %) in patients undergoing investigation for IGP. Antiviral and/or immune therapies against EV seem to be favorable, as most of our patients had resolution of their GP symptoms after treatment. This is the first study to identify EV as a possible infectious etiology of IGP.