Pylori-associated Gastritis Research Articles

Gastritis Stages in Monozygotic and Dizygotic Dyspeptic Twins.

Background The progression of Helicobacter pylori-associated gastritis towards atrophic gastritis is modulated by host-related and environmental factors. Studies that explore the possible involvement of host-related versus environmental factors in the development of gastritis phenotype induced by H. pylori are highly needed. Aims Our study was aimed at investigating the phenotype of H. pylori-associated gastritis in two cohorts of monozygotic and dizygotic twins, using the OLGA/OLGIM gastritis staging system. Methods Two cohorts of monozygotic (14 pairs) and dizygotic (15 pairs) dyspeptic twins prospectively underwent endoscopy with biopsy sampling based on Sydney protocol. H. pylori status and OLGA/OLGIM stages were assessed and compared. Results The mean age of monozygotic and dizygotic twins was 40.4 and 38.6 years, respectively (p = 0.623). The overall prevalence of H. pylori infection was 51.7%. Among the 14 monozygotic twin pairs, five pairs were H. pylori-positive, four were H. pylori-negative, and five were H. pylori-discordant. Among the 15 dizygotic twin pairs, five pairs were H. pylori-positive, five were H. pylori-negative, and five were H. pylori-discordant. Concordance for antrum atrophy in monozygotic twins was 78.6% (11/14 pairs) and in dizygotic twins 73.3% (11/15 pairs) (p = 0.742). Concordance for corpus atrophy in monozygotic versus dizygotic twins was 92.9% (13/14 pairs) and 86.7% (13/15 pairs), respectively (p = 0.584). Concordance for antrum intestinal metaplasia (IM) in monozygotic twins was 85.7% (12/14 pairs) and in dizygotic 73.3% (11/15 pairs) (p = 0.411). Concordance for corpus IM in monozygotic twins was 85.7% (12/14 pairs) and in dizygotic 86.7% (13/15 pairs) (p = 0.941). Among monozygotic and dizygotic subjects, the stage of gastritis was concordant in both H. pylori-positive and H. pylori-negative subjects. Conclusions In conclusion, histological gastric mucosa alterations in monozygotic and dizygotic twins showed high rates of concordance. Furthermore, OLGA/OLGIM gastritis stages were not modulated by the zygosity of the twins.

Expression of ETS1 in gastric epithelial cells positively regulate inflammatory response in Helicobacter pylori-associated gastritis

Gastric epithelial cells (GECs) provide the first point of contact of the host by Helicobacter pylori (H. pylori), and the interaction between H. pylori and GECs plays a critical role in H. pylori-associated diseases. Aberrant expression of transcription factors (TFs) contributes to the pathogenesis of inflammatory disorders, including H. pylori-associated gastritis. ETS (E26 transformation specific) transcription factor family is one of the largest families of evolutionarily conserved TFs, regulating critical functions during cell homeostasis. We screened ETS family gene expression in H. pylori-infected mouse and human GECs and found that ETS1 (ETS proto-oncogene 1, transcription factor) expression was highly affected by H. pylori infection. Then, we reported that ETS1 was induced in GECs by H. pylori via cagA activated NF-κB pathway. Notably, we demonstrated that proinflammatory cytokines IL-1β and TNFα have synergistic effects on ETS1 expression during H. pylori infection in an NF-κB-pathway-dependent manner. RNA-seq assay and Gene-ontology functional analysis revealed that ETS1 positively regulate inflammatory response during H. pylori infection. Increased ETS1 is also detected in the gastric mucosa of mice and patients with H. pylori infection. Collectively, these data showed that ETS1 may play an important role in the pathogenesis of H. pylori-associated gastritis.

Anti-Helicobacter pylori-associated gastritis effect of the ethyl acetate extract of Alpinia officinarum Hance through MAPK signaling pathway

Anti-Helicobacter pylori-associated gastritis effect of the ethyl acetate extract of Alpinia officinarum Hance through MAPK signaling pathway

Increased Production of Matrix Metalloproteinases in Helicobacter pylori Infection that Stimulates Gastric Cancer Stem Cells

Background and aim: Helicobacter pylori (H. pylori) is an incriminated pathogen causing diseases in both animals and humans and considered a zoonotic pathogen. H. pylori infection is considered a cause of gastric cancer, which rests a significant health care challenge. This study analyzes the expression pattern of matrix metalloprotein 2 (MMP-2) in patients with Helicobacter pylori-associated gastritis and the effect of H. pylori on gastric cancer stem cells, as well as study the role of helicon bacteriosis in dog in transmission of H. pylori infection to human. Materials and methods: Fifty-five of each sample (gastric biopsy, blood and stool) were collected from patients suffering from dyspepsia, chronic vomiting and perforated peptic ulcers and also from apparent healthy dogs. The investigation detected H. pylori by serological and histopathological examination. Biopsies were stored in physiological saline for identification of H. pylori by conventional time PCR. MMP-2 and Gastric cancer stem cells were then identified by immunohistochemistry. Results: Serological identification for H. pylori Antigen and Antibodies revealed (63% human, 50% dogs) and (87% human, 90% dogs) respectively were positive. Genotyping of H. pylori based on 16S rRNA gene showed 54.5% of human and 35% of dogs were positive. Immunohistochemistry revealed strong expression of CD44 in H. pylori- associated gastric cancer cases, MMP-2 expression was observed in all neoplastic lesions associated with H. pylori infection. Conclusion: H. pylori infection affects gastric mucosa and induces changes in gastric stem cells altering their differentiation and increased expression of MMP’s and CD44with a resultant potentiation of oncogenic alteration. In addition the up-regulation of both markers could be an instrumental to interpret the origination of gastric cancer.

Anti-parietal cell antibodies seroconversion in patients with autoimmune atrophic gastritis: a prospective study

The purpose of the study was to evaluate the atrophic changes of body and antrum gastric mucosa, the occurrence of Helicobacter pylori infection and the possibility of seroconversion in patients with autoimmune gastritis throughout 10 years.
 Material and methods. 203 Chernobyl nuclear power plant accident recovery workers were included in the prospective study. Blood levels of anti-parietal cell antibodies, basal gastrin-17, pepsinogens I and II were evaluated in all the patients to diagnose autoimmune gastritis and to assess gastric mucosa non-invasively.
 Results. Anti-parietal cell antibodies were found in 34.5% of the patients. Eradication rates were low (32.850.0%) in the patients with atrophy of gastric mucosa in the first 3 years of observation. Statistically significant decrease in pepsinogen I and gastrin-17 serum levels was observed in the patients with H. pylori-associated autoimmune gastritis throughout first 46 years. In the next 710 years pepsinogen I and gastrin-17 serum levels were increasing possibly due to positive effect of H. pylori eradication therapy. Successful eradication leads to disappearance of anti-parietal cell antibodies in 33.4% of the patients by the 10th year of the observation.
 Conclusion. The obtained results show that H. pylori eradication therapy is effective in reducing atrophic changes of gastric mucosa in the patients with autoimmune gastritis. Against the background of successful treatment the levels of pepsinogen I and gastrin-17, the markers of body and antrum gastric mucosa atrophy, were increasing. In the patients with autoimmune gastritis but without H. pylori infection the following trend was not noticed.

Nodularity-like appearance in the cardia: novel endoscopic findings for Helicobacter pylori infection

Background and study aims Helicobacter pylori -associated nodular gastritis, which is associated with follicular lymphoid hyperplasia, is mainly recognized in the antrum. However, we have also observed nodularity-like appearance in the cardia. This study aimed to investigate the clinical significance of cardiac nodularity-like appearance in H. pylori -associated gastritis. Patients and methods Patients who underwent esophagogastroduodenoscopy and were evaluated for H. pylori infection for the first time were enrolled. A nodularity-like appearance in the cardia was defined as a miliary nodular appearance or scattered appearances of small circular whitish coloration. H. pylori infection was diagnosed according to serum anti- H. pylori antibody and the urea breath test or histology. Accuracy of the H. pylori infection diagnoses based on nodularity-like appearance were assessed. Results Among 265 patients, 42 patients (15.8 %) were diagnosed as positive for H. pylori . Cardiac nodularity-like appearance and antral nodularity were recognized in 25 and 15 patients, respectively. In accuracy of predicting H. pylori by cardiac nodularity-like appearance, specificity was 0.996, sensitivity was 0.571, positive predictive value was 0.960, negative predictive value was 0.925, and accuracy was 0.928. The sensitivity of cardiac nodularity-like appearance was significantly higher than that of antral nodularity ( P = 0.0284). Conclusions Cardiac nodularity-like appearance had a high accuracy rate for H. pylori infection diagnosis. Cardiac nodularity-like appearance was found more frequently than antral nodularity.

Association of Helicobacter pylori infection with colorectal polyps and malignancy in China

BACKGROUNDGastric Helicobacter pylori (H. pylori) infection is related to chronic gastritis, gastroduodenal ulcer, and gastric malignancies; whether this infection is related to colorectal polyps and colorectal cancer (CRC), remains debatable.AIMTo investigate the relationship between gastric H. pylori infection and the risk of colorectal polyps and CRC.METHODSWe retrospectively analyzed 3872 patients with colorectal polyps who underwent colonoscopy and pathological diagnosis. We also analyzed 304 patients with primary CRC. The characteristics of these patients were compared with those of the control group, which included 2362 patients with the normal intestinal mucosa. All subjects completed a 14C-urea breath test, bidirectional gastrointestinal endoscopy, and a biopsy on the same day. Data on the number, size, location, and pathology of the polyps, the location, and pathology of the CRC, the detection of H. pylori, and the incidence of H. pylori-associated atrophic gastritis or intestinal metaplasia were obtained. A logistic regression model was used to analyze the relationship between gastric infection due to H. pylori, and the incidence of colorectal polyps and CRC.RESULTSThe prevalence of H. pylori infection was higher in the multiple polyps group than in the solitary polyp group and the control group [95% confidence interval (CI) = 1.02-1.31, P = 0.03; 95%CI: 2.12-2.74, P < 0.001]. The patients with adenomatous polyps had a higher incidence of H. pylori infection than patients with non-adenomatous polyps [59.95% vs 51.75%, adjusted odds ratio (OR) = 1.41, 95%CI: 1.24-1.60, P < 0.01]. Patients with H. pylori-associated atrophic gastritis or intestinal metaplasia were at high risk of CRC (adjusted OR = 3.46, 95%CI: 2.63-4.55, P < 0.01; adjusted OR = 4.86, 95%CI: 3.22-7.34, P < 0.01, respectively). The size and location of the polyps, the histopathological characteristics and the location of CRC were not related to H. pylori infection.CONCLUSIONOur study demonstrates that the incidence of gastric H. pylori infection and H. pylori-associated atrophic gastritis or intestinal metaplasia elevates the risk of colorectal polyps and CRC.

H. pylori-assoziierte Gastritis: Diagnostik, Therapie und Nachsorge

H. pylori-associated gastritis: diagnostic, treatment and surveillance Abstract. Helicobacter pylori infections are limited to the stomach and represent globally the infectious disease with the highest prevalence. H. pylori infection causes in almost 100 % a chronic gastritis and is the main cause of relevant diseases such as atrophic gastritis, peptic ulcer disease and gastric cancer (class I carcinogen according to WHO). Accordingly, a H. pylori associated gastritis signifies a high-impact health economic disease, leading to significant morbidity and mortality. This review summarizes key points regarding diagnosis, treatment and follow-up.

The treatment of helicobacter pylori-associated erosive lesions of gastroduodenal zone with the use of interactive learning technologies and rebamipide in young men

Purpose of the study. To evaluate the effectiveness of interactive teaching technologies and rebamipids in the complex therapy of erosive lesions of the gastroduodenal zone in young men.Material and research methods. Two groups of patients were examined. The observation group included 36 recruits with HP-associated gastritis with erosion (HSE) and duodenitis with erosion (DSE). Comprehensive treatment was used as a treatment: standard first-line triple therapy with the inclusion of rebamipide 100 mg 3 times a day for 14 days and interactive therapeutic training. The comparison group consisted of 18 patients with HP-associated GSE and DsE who received standard triple eradication therapy also for 14 days. The average age of the examined patients in the observation group was 21.0 ± 0.7 years, the comparison group was 20.1 ± 0.7 years.Results. The inclusion of Helicobacter pylori-associated gastritis and duodenitis with erosion of rebamipide and interactive learning technologies into the treatment regimen resulted in more effective relief of pain syndrome and dyspeptic manifestations in conscripts, restoration of mucus-forming and acid-producing functions of the stomach; to lower blood cortisol levels; reduce the degree of morphological activity of inflammation. There is a more effective eradication of Helicobacter pylori (91.7%) and epithelization of erosion (97.2%) in comparison with the standard scheme (88.9% and 94.4%, respectively). The use of interactive teaching technologies allowed to increase the level of medical activity and hygienic literacy (96.0% of recruits changed their diet, the nature of nutrition — 88.0%). The level of psycho-emotional status significantly improved after the treatment.Conclusion Combined therapy using rebamipide and interactive therapeutic training is effective in erosive lesions of the gastroduodenal zone in young men and increases patient adherence to treatment and leads to stabilization of psycho- emotional status.

Helicobacter pylori-induced adrenomedullin modulates IFN-\u03b3-producing T-cell responses and contributes to gastritis

Adrenomedullin (ADM) is a multifunctional peptide that is expressed by many surface epithelial cells, but its relevance to Helicobacter pylori (H. pylori)-induced gastritis is unknown. Here, we found that gastric ADM expression was elevated in gastric mucosa of H. pylori-infected patients and mice. In H. pylori-infected human gastric mucosa, ADM expression was positively correlated with the degree of gastritis; accordingly, blockade of ADM resulted in decreased inflammation within the gastric mucosa of H. pylori-infected mice. During H. pylori infection, ADM production was promoted via PI3K–AKT signaling pathway activation by gastric epithelial cells in a cagA-dependent manner, and resulted in increased inflammation within the gastric mucosa. This inflammation was characterized by the increased IFN-γ-producing T cells, whose differentiation was induced via the phosphorylation of AKT and STAT3 by ADM derived from gastric epithelial cells. ADM also induced macrophages to produce IL-12, which promoted the IFN-γ-producing T-cell responses, thereby contributing to the development of H. pylori-associated gastritis. Accordingly, blockade of IFN-γ or knockout of IFN-γ decreased inflammation within the gastric mucosa of H. pylori-infected mice. This study identifies a novel regulatory network involving H. pylori, gastric epithelial cells, ADM, macrophages, T cells, and IFN-γ, which collectively exert a pro-inflammatory effect within the gastric microenvironment.

High-definition optical magnification with digital chromoendoscopy detects gastric mucosal changes in dyspeptic-patients.

BACKGROUNDAccurate detection of gastric infection by Helicobacter pylori (H. pylori) and premalignant lesions are important for effective provision of treatment, preventing the development of gastric neoplasia. Optical enhancement systems with optical magnification improved the identification of mucosal superficial and vascular patterns in patients with dyspepsia.AIMTo evaluate an optical enhancement system with high-definition magnification, for diagnosis of normal gastric mucosa, H. pylori-associated gastritis, and gastric atrophy.METHODSA cross-sectional, nonrandomized study from November 2015 to April 2016 performed in a single-tertiary academic center from Ecuador. Seventy-two consecutive patients with functional dyspepsia according to the Rome III criteria, were tested for H. pylori using a stool antigen test and were assigned to an Hp+ group or an Hp− control group. Esophagogastroduodenoscopy with high-definition optical magnification and digital chromoendoscopy was performed, and patients were classified into 4 groups, in accordance to the microvascular-architecture pattern of the mucosa. Interobserver and intraobserver agreement among operators were calculated.RESULTSOf the 72 participants, 35 were Hp+ and 37 were Hp−. Among 10 patients with normal mucosal histology in biopsy samples, 90% had a Type I pattern of microvascular architecture by endoscopy. Among participants with type IIa and type IIb patterns, significantly more were Hp+ than Hp− (32 vs 8), and most (31 out of 40) had histological diagnoses of chronic active gastritis. Two of the three participants with a histological diagnosis of atrophy had a type III microvascular pattern. The type I pattern predicted normal mucosa, type IIa–IIb predicted H. pylori infection, and type III predicted atrophy with sensitivities of 90.0%, 91.4%, and 66.7%, respectively. The intraobserver and interobserver agreements had kappa values of 0.91 and 0.89, respectively.CONCLUSIONHigh-definition optical magnification with digital chromoendoscopy is useful for diagnosis of normal gastric mucosa and H. pylori-associated gastritis with high accuracy, but further studies are needed to determine whether endoscopic diagnosis of gastric atrophy is feasible.

Mucosal Th17 Cells Are Increased in Pediatric Functional Dyspepsia Associated with Chronic Gastritis.

Chronic gastritis is a common histologic finding in children with functional dyspepsia (FD). While Th17 cells have been implicated in other forms of gastritis, they have not been evaluated in chronic gastritis. The aim of the current study was to assess Th17 cells in children with FD with and without chronic gastritis. Densities were determined for Th17 cells, eosinophils, and mast cells, respectively, in both the gastric antrum and the duodenum. Densities were compared between five groups: FD with chronic gastritis (N = 20), FD without chronic gastritis (N = 20), Helicobacter pylori-associated gastritis (N = 10), Crohn's gastritis (N = 10), and normal controls (N = 10). Th17 densities were also compared between patients with and without early satiety. FD with chronic gastritis was associated with higher Th17 cell density as compared to normal controls and comparable to both H. pylori-associated gastritis and Crohn's gastritis. Eosinophil and mast cell densities were higher in FD patients with chronic gastritis as compared to either FD without gastritis or normal controls. Th17 density was higher in patients reporting early satiety but not in those with epigastric pain. FD with chronic gastritis is associated with higher Th17 cell, eosinophil, and mast cell density as compared to FD without chronic gastritis or normal controls. Chronic gastritis demonstrated Th17 cell density similar to that seen in other conditions where Th17 cells are believed to play a pathogenic role. Th17 cells may represent another therapeutic target in these patients.

Клиническое наблюдение пациентки с множественными эрозиями пищевода и очагами кислотопродуцирующей желудочной гетеротопии в верхне-, средне- и нижнегрудном отделах пищевода, обсемененными H. pylori, в сочетании с H. pylori-ассоциированным гастритом

Клиническое наблюдение пациентки с множественными эрозиями пищевода и очагами кислотопродуцирующей желудочной гетеротопии в верхне-, средне- и нижнегрудном отделах пищевода, обсемененными H. pylori, в сочетании с H. pylori-ассоциированным гастритом

The use of CNFA lectin in the diagnosis of precancerous changes in the gastric mucosa in patients with Helicobacter pylori-associated chronic gastritis

The use of CNFA lectin in the diagnosis of precancerous changes in the gastric mucosa in patients with Helicobacter pylori-associated chronic gastritis

Dangerous Liaison: Helicobacter pylori, Ganglionitis, and Myenteric Gastric Neurons: A Histopathological Study.

Chronic inflammation induced by Helicobacter pylori (H. pylori) infection plays a major role in development of gastric cancer. However, recent findings suggested that progression of inflammation and neoplastic transformation in H. pylori infection are more complex than previously believed and could involve different factors that modulate gastric microenvironment and influence host-pathogen interaction. Among these factors, gastric myenteric plexus and its potential adaptive changes in H. pylori infection received little attention. This study is aimed at identifying the impact of H. pylori-associated gastritis on number and morphology of nerve cells in the stomach. The distribution of density, inflammation, and programmed cell death in neurons was immunohistochemically assessed in full-thickness archival tissue samples obtained from 40 patients with H. pylori infection who underwent surgery for gastric cancer and were compared with findings on samples collected from 40 age- and sex-matched subjects without bacteria. Overall, significant differences were noted between H. pylori-positive and H. pylori-negative patients. The analysis of tissue specimens obtained from those with infection revealed higher density and larger surface of the myenteric nervous plexus, as well as a significant increase in the number of gastric neuronal cell bodies and glial cells compared to controls. A predominant CD3-immunoreactive T cell infiltrate confined to the myenteric plexus was observed in infected subjects. The presence of mature B lymphocytes, plasma cells, and eosinophils was also noted, but to a lesser extent, within the ganglia. Myenteric ganglionitis was associated with degeneration and neuronal loss. Our results represent the first histopathological evidence supporting the hypothesis that H. pylori-induced gastric inflammation may induce morphological changes in myenteric gastric ganglia. These findings could help gain understanding of some still unclear aspects of pathogenesis of H. pylori infection, with the possibility of having broader implications for gastric cancer progression.

The prevalence of different variants of Helicobacter pylori genotypes in families of patients with helicobacter-associated diseases

The article presents the results of the examination of relatives of the patients with chronic H. pylori-associated gastritis. The genes of H. pylori pathogenicity were investigated by PCR to determine possible intrafamilial transmission of the infection. We established that in families of the patients with chronic gastritis, H. pylori was found in more than 60 % of relatives. The most similar spectrum of the genes of H. pylori pathogenicity was found in the samples of spouses, as well as in the mothers and the children. The study of H. pylori genovariant helps establish the mechanisms and ways of transmission of the infection, identify people infected with the microorganism with the most pronounced pathogenic potential and requiring therapy.

597 Bidirectional Endoscopy in Asymptomatic-Iron Deficiency Anemia (A-IDA)

INTRODUCTION: GI investigation of pts with A-IDA typically begins with both upper (U) and lower (L) GI endoscopy. Guidelines tend to recommend bidirectional endoscopy (BDE) sequencing based on age stratification, or starting with LGI endoscopy. The aim of this study was to determine the most efficient BDE sequence among patients with A-IDA by investigating the relative frequencies of identified associated sources of bleeding by UGI or LGI endoscopy. METHODS: We performed a retrospective chart review of clinical characteristics of pts ≥18 yrs who had BDE performed within 6 months of A-IDA diagnosis between the yrs 2014-2019. Pts were excluded if they had GI tract surgery within 10 yrs, active pregnancy, active GI bleeding, an obvious site of non-GI blood loss or ferritin &gt;100. McNemar's test was used to compare frequency of lesions identified across the general population and stratified for age &lt; 50 and &gt;50 yrs. Bivariate analyses of characteristics associated with UGI and LGI lesions were performed using t-test, Chi-squared test, or Fisher's exact test. Multivariate logistic regression estimated odds ratios. RESULTS: 497 pts were available for analysis (65% female, mean age 63 yrs; Table 1). BDE found IDA-associated lesions in 307 (61.8%) pts comprising 196 (39.4%) exclusively UGI lesions, 66 (13.3%) exclusively LGI lesions, and 45 (9.1%) both UGI and LGI lesions. In our cohort, UGI lesions were more common than LGI lesions [241 (48.5%) vs 111 (22.3%); P &lt; 0.001], regardless of age (P &lt; 0.001) (Table 1). Protective variables against an LGI lesion included female sex [OR 0.51 (0.32-0.86); P = 0.01], BMI [OR 0.96 (0.93-0.99) per unit inc.; P = 0.01] and Hgb [OR 0.88 (0.78-0.98) per unit inc.; P = 0.03]. CKD was associated with LGI lesions [OR 1.99 (1.12-3.48); P = 0.02]. Hgb was higher in pts with only UGI than only LGI lesions (9.4±1.6 vs 8.5±1.5; P = 0.001). PPI use predicted absence of identifiable lesions [OR 0.66 (0.45-0.96); P = 0.03]. The most common UGI lesions were H. pylori-associated (HP-A) gastritis (24.2%) and peptic ulcer disease (17.6%) (Figure 1a). The most common LGI lesions were large polyps (37.7%) and colon CA (16.2%) (Figure 1b). CONCLUSION: Our results indicate 1) pts with A-IDA are more likely to have an UGI than LGI source; thus starting with UGI endoscopy may be prudent; 2) women are less likely to have a LGI source of A-IDA than men; 3) low BMI, low Hgb and CKD predict a LGI source of A-IDA. 4) HP-A UGI lesions account for a significant portion of A-IDA; 5) PPI use predicts the absence of lesions.

1928 A Rare Case of Hematemesis Due to a Large Gastric Pyloric Gland Adenoma

INTRODUCTION: Accounting for less than 3% of all gastric polyps, pyloric gland adenomas (PGAs) are rare tumors that usually arise from the stomach or, less commonly, the esophagus, duodenum, pancreas, or gallbladder. PGAs rarely cause symptoms and hematemesis as the presenting symptom has not been previously described in the literature. We present a rare case of hematemesis secondary to a large gastric PGA. CASE DESCRIPTION/METHODS: A 94 year-old female with a history of hypothyroidism and occasional nonsteroidal anti-inflammatory drug-use presented with hematemesis and hematochezia. She complained of acute-onset nausea, vomiting and diarrhea. Patient was hemodynamically stable at the time of presentation. Admission laboratory studies were significant for a hemoglobin of 7.2 mg/dl compared to 11.4 mg/dl two weeks prior. An esophagogastroduodenoscopy (EGD) was performed and revealed a 4 cm polyp-appearing mass with a short stalk in the mid-greater curvature of the body of the stomach. The tissue was friable and spontaneously bled with minimal friction from the snare, thus likely the etiology for the patient’s symptoms. The polyp was removed in piecemeal fashion using hot snare. Submucosal epinephrine was injected and four DuraClips were deployed over the polypectomy site. The patient declined to undergo a colonoscopy. Following her EGD, patient did not exhibit any additional signs or symptoms of continued bleeding and was discharged home in good condition. Pathology revealed pyloric gland adenoma with high-grade dysplasia. DISCUSSION: This case emphasizes the need for increased awareness regarding the presence of PGAs. These lesions have been shown to arise in chronically damaged mucosa and were associated with autoimmune gastritis in 33.9% of patients, active Helicobacter pylori-associated gastritis in 30.2% of patients, and normal gastric mucosa in only 3.8% of patients. Patients are usually elderly females with an average age of 75 years; though signs and symptoms are variable, laboratory evaluation frequently reveals anemia. This diagnosis is rare but the malignant potential was reported between 12 to 30% of cases in two large studies making improved classification and management necessary.

Beta-defensins and analogs in Helicobacter pylori infections: mRNA expression levels, DNA methylation, and antibacterial activity.

Antimicrobial peptides can protect the gastric mucosa from bacteria, but Helicobacter pylori (H. pylori) can equally colonize the gastric apparatus. To understand beta-defensin function in H. pylori-associated chronic gastritis, we investigated susceptibility, human beta-defensin mRNA expression, and DNA methylation changes to promoters in the gastric mucosa with or without H. pylori infection. We studied the expression of HBD2 (gene name DEFB4A), HBD3 (DEFB103A), and HBD4 (DEFB104) using real-time PCR in 15 control and 10 H. pylori infection patient gastric specimens. This study demonstrates that H. pylori infection is related to gastric enhancement of inducible HBD2, but inducible HBD3 and HBD4 expression levels remained unchanged. HBD2 gene methylation levels were overall higher in H. pylori-negative samples than in H. pylori-positive samples. We also assessed antimicrobial susceptibility using growth on blood agar. The H. pylori strain Tox+ was susceptible to all defensins tested and their analogs (3N, 3NI). These results show that HBD2 is involved in gastritis development driven by H. pylori, which facilitates the creation of an epigenetic field during H. pylori-associated gastric tumorigenesis.

Challenges of Accurate Diagnosis of Helicobacter pylori in Iran

Background: Helicobacter pylori-associated gastritis is regarded as the most prevalent gastrointestinal infection, as well as the major cause of several other diseases. Despite being discovered over 30 years ago, no golden diagnostic method has yet been suggested for this microorganism. Objective: The present study aimed to compare two common diagnostic methods of histology and serology. Materials and Methods: This cross-sectional study began in July, 2016, and was conducted at Imam Jafar Sadegh Hospital (a university hospital) in Maybod, Yazd, Iran, on 70 patients. All the patients underwent endoscopy, and biopsy samples were taken for histology, as well as blood samples for ELISA test. Finally, sensitivity, specificity, NPV (negative predictive values), and PPV (positive predictive values) were calculated and analyzed. Results: The sensitivity, specificity, accuracy, PPV, and NPV of the ELISA method with histology as the gold standard were 87.5%, 36.9%, 54.2%, 42%, and 85%, respectively. Still, the histology method appears to be the most reliable test for the diagnosis of H. pylori in Iran. Conclusion: Regarding the high prevalence of H. pylori in Iran, the present study recommends the use of histology as a diagnostic method in combination with other diagnostic methods for detecting H. pylori infection.