Successful Eradication Therapy Research Articles

Non-improvement of atrophic gastritis in cases of gastric cancer after successful Helicobacter pylori eradication therapy.

Helicobacter pylori (H. pylori) infection is closely related to the development of gastric cancer (GC). However, GC can develop even after H. pylori eradication. Therefore, it would be extremely useful if GC could be predicted after eradication. The Kyoto classification score for gastritis (GA) is closely related to cancer risk. However, how the score for GC changes after eradication before onset is not well understood. To investigate the characteristics of the progression of Kyoto classification scores for GC after H. pylori eradication. Eradication of H. pylori was confirmed in all patients using either the urea breath test or the stool antigen test. The Kyoto classification score of GC patients was evaluated by endoscopy at the time of event onset and three years earlier. In addition, the modified atrophy score was evaluated and compared between the GC group and the control GA group. In total, 30 cases of early GC and 30 cases of chronic GA were evaluated. The pathology of the cancer cases was differentiated adenocarcinoma, except for one case of undifferentiated adenocarcinoma. The total score of the Kyoto classification was significantly higher in the GC group both at the time of cancer onset and three years earlier (4.97 vs 3.73, P = 0.0034; 4.2 vs 3.1, P = 0.0035, respectively). The modified atrophy score was significantly higher in the GC group both at the time of cancer onset and three years earlier and was significantly improved only in the GA group (5.3 vs 5.3, P = 0.5; 3.73 vs 3.1, P = 0.0475, respectively). The course of the modified atrophy score is useful for predicting the onset of GC after eradication. Patients with severe atrophy after H. pylori eradication require careful monitoring.

Incidence and Prediction of Unrelated Mortality After Successful Endoscopic Eradication Therapy for Barrett’s Neoplasia

Background & AimsFollow-up (FU) strategies after endoscopic eradication therapy (EET) for Barrett’s neoplasia do not consider the risk of mortality from causes other than esophageal adenocarcinoma (EAC). We aimed to evaluate this risk during long-term FU, and to assess whether the Charlson Comorbidity Index (CCI) can predict mortality. MethodsWe included all patients with successful EET from the nationwide Barrett registry in the Netherlands. Data were merged with National Statistics for accurate mortality data. We evaluated annual mortality rates (AMRs, per 1000 person-years) and standardized mortality ratio for other-cause mortality. Performance of the CCI was evaluated by discrimination and calibration. ResultsWe included 1154 patients with a mean age of 64 years (±9). During median 59 months (p25–p75 37–91; total 6375 person-years), 154 patients (13%) died from other causes than EAC (AMR, 24.1; 95% CI, 20.5–28.2), most commonly non-EAC cancers (n = 58), cardiovascular (n = 31), or pulmonary diseases (n = 26). Four patients died from recurrent EAC (AMR, 0.5; 95% CI, 0.1–1.4). Compared with the general Dutch population, mortality was significantly increased for patients in the lowest 3 age quartiles (ie, age <71 years). Validation of CCI in our population showed good discrimination (Concordance statistic, 0.78; 95% CI, 0.72–0.84) and fair calibration. ConclusionThe other-cause mortality risk after successful EET was more than 40 times higher (48; 95% CI, 15–99) than the risk of EAC-related mortality. Our findings reveal that younger post-EET patients exhibit a significantly reduced life expectancy when compared with the general population. Furthermore, they emphasize the strong predictive ability of CCI for long-term mortality after EET. This straightforward scoring system can inform decisions regarding personalized FU, including appropriate cessation timing. (NL7039)

The state of psycho-emotional status in adolescent children with chronic gastroduodenitis, associated with Helicobacter pylori infection in the period of exacerbation and remission

Relevance. In the pathogenesis of chronic gastroduodenitis, along with an infectious factor (Helicobacter Pylori infection), an important role is played by the state of the patient’s psycho-emotional status, which is characterized by a high incidence of anxiety and subdepressive states in adolescence. Goals: to assess the state of the psycho-emotional status and quality of life in adolescent children with chronic gastroduodenitis associated with Helicobacter pylori infection in the period of exacerbation, after 1 month and 6 months after successful eradication therapy. Materials and methods. The prospective case-control study included 60 adolescent children with morphologically proven chronic gastroduodenitis associated with Helicobacter pylori infection (main group) in the period of exacerbation, in 1 month. and 6 months. after successful eradication therapy. As a comparison group, 22 schoolchildren with the first health group were taken, comparable in age and gender with the children of the main group. All children underwent psychological testing (Spielberger test to assess the levels of reactive and personal anxiety, Zung test to determine the level of depression) and assessed the quality of life. Results. During the period of remission, more than half of the children with chronic gastroduodenitis had complaints common for asthenic syndrome: weakness, mental exhaustion, and headaches. In the period of exacerbation, the highest rates were noted on the scales of personal and reactive anxiety, depression, followed by improvement during treatment and worsening of indicators after 6 months after eradication therapy. Quality of life indicators, characterized by improvement after eradication therapy, after 6 months. showed a statistically significant decrease on the scales of physical functioning (RP), general health (GH), vitality (VT) and mental health (MH). Conclusion: Adolescent children with chronic gastroduodenitis characterized by changes in the psycho-emotional status in the form of subdepression and increased anxiety, both reactive and personal. These changes are not completely stopped after the use of traditional therapy for chronic gastroduodenitis and persist in the period of remission, worsening the quality of life, increasing the negative perception of the disease and treatment prospects.

Diagnosis and management of Barrett esophagus: European Society of Gastrointestinal Endoscopy (ESGE) Guideline.

MR1 : ESGE recommends the following standards for Barrett esophagus (BE) surveillance:- a minimum of 1-minute inspection time per cm of BE length during a surveillance endoscopy- photodocumentation of landmarks, the BE segment including one picture per cm of BE length, and the esophagogastric junction in retroflexed position, and any visible lesions- use of the Prague and (for visible lesions) Paris classification- collection of biopsies from all visible abnormalities (if present), followed by random four-quadrant biopsies for every 2-cm BE length.Strong recommendation, weak quality of evidence. MR2: ESGE suggests varying surveillance intervals for different BE lengths. For BE with a maximum extent of ≥ 1 cm and < 3 cm, BE surveillance should be repeated every 5 years. For BE with a maximum extent of ≥ 3 cm and < 10 cm, the interval for endoscopic surveillance should be 3 years. Patients with BE with a maximum extent of ≥ 10 cm should be referred to a BE expert center for surveillance endoscopies. For patients with an irregular Z-line/columnar-lined esophagus of < 1 cm, no routine biopsies or endoscopic surveillance are advised.Weak recommendation, low quality of evidence. MR3: ESGE suggests that, if a patient has reached 75 years of age at the time of the last surveillance endoscopy and/or the patient's life expectancy is less than 5 years, the discontinuation of further surveillance endoscopies can be considered. Weak recommendation, very low quality of evidence. MR4: ESGE recommends offering endoscopic eradication therapy using ablation to patients with BE and low grade dysplasia (LGD) on at least two separate endoscopies, both confirmed by a second experienced pathologist.Strong recommendation, high level of evidence. MR5: ESGE recommends endoscopic ablation treatment for BE with confirmed high grade dysplasia (HGD) without visible lesions, to prevent progression to invasive cancer.Strong recommendation, high level of evidence. MR6: ESGE recommends offering complete eradication of all remaining Barrett epithelium by ablation after endoscopic resection of visible abnormalities containing any degree of dysplasia or esophageal adenocarcinoma (EAC).Strong recommendation, moderate quality of evidence. MR7: ESGE recommends endoscopic resection as curative treatment for T1a Barrett's cancer with well/moderate differentiation and no signs of lymphovascular invasion.Strong recommendation, high level of evidence. MR8: ESGE suggests that low risk submucosal (T1b) EAC (i. e. submucosal invasion depth ≤ 500 µm AND no [lympho]vascular invasion AND no poor tumor differentiation) can be treated by endoscopic resection, provided that adequate follow-up with gastroscopy, endoscopic ultrasound (EUS), and computed tomography (CT)/positrion emission tomography-computed tomography (PET-CT) is performed in expert centers.Weak recommendation, low quality of evidence. MR9: ESGE suggests that submucosal (T1b) esophageal adenocarcinoma with deep submucosal invasion (tumor invasion > 500 µm into the submucosa), and/or (lympho)vascular invasion, and/or a poor tumor differentiation should be considered high risk. Complete staging and consideration of additional treatments (chemotherapy and/or radiotherapy and/or surgery) or strict endoscopic follow-up should be undertaken on an individual basis in a multidisciplinary discussion.Strong recommendation, low quality of evidence. MR10 A: ESGE recommends that the first endoscopic follow-up after successful endoscopic eradication therapy (EET) of BE is performed in an expert center.Strong recommendation, very low quality of evidence. B: ESGE recommends careful inspection of the neo-squamocolumnar junction and neo-squamous epithelium with high definition white-light endoscopy and virtual chromoendoscopy during post-EET surveillance, to detect recurrent dysplasia.Strong recommendation, very low level of evidence. C: ESGE recommends against routine four-quadrant biopsies of neo-squamous epithelium after successful EET of BE.Strong recommendation, low level of evidence. D: ESGE suggests, after successful EET, obtaining four-quadrant random biopsies just distal to a normal-appearing neo-squamocolumnar junction to detect dysplasia in the absence of visible lesions.Weak recommendation, low level of evidence. E: ESGE recommends targeted biopsies are obtained where there is a suspicion of recurrent BE in the tubular esophagus, or where there are visible lesions suspicious for dysplasia.Strong recommendation, very low level of evidence. MR11: After successful EET, ESGE recommends the following surveillance intervals:- For patients with a baseline diagnosis of HGD or EAC:at 1, 2, 3, 4, 5, 7, and 10 years after last treatment, after which surveillance may be stopped.- For patients with a baseline diagnosis of LGD:at 1, 3, and 5 years after last treatment, after which surveillance may be stopped.Strong recommendation, low quality of evidence.

Duodenal Eosinophilia in Functional Dyspepsia

Aim: to present observation of a patient diagnosed with functional dyspepsia based on current guidelines, and having increased eosinophil counts in the biopsy specimen of duodenal mucosa. To consider possible causes of duodenal eosinophilia in the light of present-day concepts.Highlights. Patient K., 40 years old, complained of dyspeptic phenomena, the first appearance of which she had noted at the age of 18. The patient noted poor tolerance to canned and fermented foods, which provoked an increase in dyspepsia and sometimes caused watery diarrhea. The examination excluded “symptoms of concern”. Successful antihelicobacter eradication therapy was carried out. Morphological examination of the stomach showed phenomena of mild chronic inflammation without intestinal metaplasia or glandular atrophy. A biopsy of the mucosa of the descending part of the duodenum showed a moderate increase in the levels of mononuclears and eosinophils in its lamina propria without penetration into the epithelium of the villi or formation of clusters. The patient suffers from pollinosis; sensitization to birch pollen was diagnosed by a skin prick test. However, she has no oral allergy symptoms, which does not allow linking duodenal eosinophilia to food allergy. Based on current guidelines, the patient was diagnosed with functional dyspepsia. In addition to dietary restrictions, treatment courses with a proton pump inhibitor, itopride, and S-methylmethionine sulfonium chloride, which has an antihistamine effect, were recommended for periods of worsening dyspepsia.Conclusion. The clinical significance of duodenal eosinophilia and local histamine production in patients with a clinical diagnosis of functional dyspepsia deserves special attention. Triggering factors provoking the worsening of symptoms should be analyzed; in particular, a food diary and exclusion of food allergies are recommended. Histamine-neutralizing drugs may play a role in the treatment of FD with duodenal eosinophilia in the future.

Evaluation of the dynamics of symptoms of dyspepsia after eradication therapy in patients with Helicobacter pylori-associated gastritis

The treatment of functional dyspepsia remains a complex and incompletely resolved issue of gastroenterology. Subjective sensations of the patient, described as a feeling of fullness in the epigastrium after eating, early satiety, pain in the epigastrium, may be a manifestation of dyspepsia associated with Helicobacter pylori (H. pylori) infection. Aim was evaluation of the effectiveness of standard triple eradication therapy enhanced with bismuth tripotassium dicitrate for the relief of symptoms of dyspepsia in patients with H. pylori-associated chronic gastritis. Materials and Methods. The study involved 38 patients with H. pylori-associated chronic gastritis with symptoms of dyspepsia. The Questionnaire “7 × 7” was used to describe the dynamics of symptoms of dyspepsia. Results. At the initial examination, dyspeptic disorders in most patients corresponded the criteria for mild and moderate severity, respectively - 44.7% and 28.9% of patients. The severity of pain in the stomach area on average corresponded to a moderate pain syndrome, and the burning sensation was of low intensity. A feeling of fullness in the stomach after eating and/or early satiety was experienced by 76.3% of patients, pain disorders were observed in 92.1% of individuals. Two months after successful eradication treatment, complete relief of dyspepsia symptoms was noted in 57.9% of patients, and significant relief of symptoms of the combined form of dyspepsia in 23.7% of individuals. Conclusions: Successful standard triple eradication therapy enhanced with bismuth tripotassium dicitrate is effective for the treatment of dyspeptic symptoms in patients with H. pylori-associated chronic gastritis.

Novel histologic score predicts recurrent intestinal metaplasia after successful endoscopic eradication therapy.

Endoscopic eradication therapy (EET) is an effective treatment for Barrett's esophagus (BE); however, disease recurrence remains problematic requiring surveillance post-treatment. While data regarding predictors of recurrence are limited, uncontrolled reflux may play a significant role. Our aim was to develop a scoring system based on histopathologic reflux in surveillance biopsies following EET to identify patients at high risk for recurrence of BE. Patients were identified from two centers in the treatment with resection and endoscopic ablation techniques for BE consortium. Hematoxylin and eosin-stained slides of surveillance biopsies post-EET were assessed for histologic changes associated with reflux from a cohort of patients who also underwent pH-metry (derivation cohort). We developed a novel scoring system (Recurrent Epithelial Changes from Uncontrolled Reflux [RECUR]) composed of dilated intercellular spaces, epithelial ballooning, basal cell hyperplasia, and parakeratosis, to identify patients with abnormal esophageal acid exposure. This scoring system was then used to grade surveillance biopsies from patients with or without recurrence of BE following EET (validation cohort). Of 41 patients in the derivation cohort, 19.5% had abnormal acid exposure times (AET) while on proton pump inhibitor therapy. The mean (SD) RECUR score for patients with AET <4% was 4.0 (1.6), compared with 5.5 (0.9) for AET ≥4% (P = 0.015). In the validation cohort consisting of 72 patients without recurrence and 64 patients with recurrence following EET, the RECUR score was the only significant predictor of recurrence (odds ratio: 1.36, 95% confidence interval: 1.10-1.69, P = 0.005). Histologic grading of surveillance biopsies using the RECUR scoring system correlates with BE recurrence following EET.

Clinical Relevance of Random Biopsies From the Esophagogastric Junction After Complete Eradication of Barrett’s Esophagus is Low

Although random histological sampling from the esophagogastric junction (EGJ) after complete eradication of Barrett's esophagus (BE) is recommended, its clinical relevance is questionable. This study aimed to assess the incidence and long-term outcomes of findings from random EGJ biopsies in a nationwide cohort with long-term follow-up. We included all patients with successful endoscopic eradication therapy (EET), defined as complete endoscopic eradication of all visible BE (CE-BE), for early BE neoplasia from the Dutch registry. Patients were treated and followed-up in 9 expert centers according to a joint protocol. Outcomes included the incidence of intestinal metaplasia (IM) at the EGJ (EGJ-IM) and the association between IM and visible (dysplastic) BE recurrence. A total of 1154 patients were included with a median follow-up of 43 months (interquartile range, 22-69 months). At the time of CE-BE, persisting EGJ-IM was found in 7% of patients (78/1154), which was reproduced during further follow-up in 46% of patients (42/78). No significant association existed between persisting EGJ-IM at CE-BE and recurrent non-dysplastic or dysplastic BE (hazard ratio [HR], 1.15; 95% confidence interval [CI], 0.63-2.13 and HR, 0.73; 95% CI, 0.17-3.06, respectively). Among patients with no EGJ-IM at the time of CE-BE (1043/1154; 90%), EGJ-IM recurred in 7% (72/1043) after a median of 21 months (interquartile range, 15-36 months), and was reproduced during further follow-up in 26% of patients (19/72). No association was found between recurrent EGJ-IM and non-dysplastic or dysplastic recurrence (HR, 1.18; 95% CI, 0.67-2.06 and HR, 0.27; 95% CI, 0.04-1.96, respectively). Because EGJ-IM was not associated with a higher risk for recurrent disease, we recommend to consider abandoning random EGJ sampling after successful EET, under the condition that care is provided in expert centers, and the esophagus, including the EGJ, is carefully inspected (Netherlands Trial Register, NL7309).

H. pylori-associated chronic gastritis: status update on the problem

Chronic gastritis is a group of chronic diseases that are morphologically characterized by persistent inflammatory infiltrate and impaired cellular turnover with the development of intestinal metaplasia, atrophy, and epithelial dysplasia in the gastric mucosa. Numerous studies have shown that Helicobacter pylori (H. pylori) infection is the absolutely dominant etiological factor of CG worldwide. Given this fact, the Expert Council of the latest Maastricht VI 2022 consensus recommended that H. pylori is to be treated as a pathogen, which always results in the development of CG. The prevalence of H. pylori-associated CG is about 44.3–48.5%, however 80–90% of cases are asymptomatic. In H. pylori­infected patients with dyspepsia and no other pathology of the gastroduodenal region, which has been confirmed endoscopically, clinical manifestations can be interpreted as part of H. pylori­associated CG if a long-lasting remission of symptoms has been achieved after successful eradication therapy. While patients with persistent dyspeptic symptoms can be considered as patients with functional dyspepsia, despite successful eradication therapy. Advanced endoscopic techniques (narrow band imaging (NBI) endoscopy, high resolution endoscopy, chromoendoscopy, laser confocal endomicroscopy) are precise and reproducible methods for diagnosing precancerous changes in the mucous membrane. However, the diagnosis of CG requires that inflammatory cells have been histologically detected in the lamina propria. The CG therapy aims to reach a persistent relief of dyspeptic symptoms of the disease (if any), as well as resolution of inflammatory processes and prevention of the progression of precancerous changes in the gastric mucosa. The achievement of these goals is primarily determined by the timely diagnosis of H. pylori infection and successful eradication therapy.

The Resolution of Severe Iron-Deficiency Anemia After Successful Eradication of Helicobacter pylori in Teenagers.

In this case series, 7 H. pylori-infected patients with recurrent and/or refractory IDA (12-16 y old) received successful eradication therapy and were then followed for a median of 20 months (range, 9-76 mo) after oral iron supplementation therapy (1-4 mo) was discontinued. Five patients of our study cohort participated in rigorous sports activities. No visual appearance of ulcerations or erosions was found by esophagogastroduodenoscopy. In all patients studied, the gastric biopsies showed histological evidence of chronic gastritis without significant atrophy and intestinal metaplasia. Compared with the baseline (median values: hemoglobin, 6.3 g/dL; serum iron, 9 μg/dL; serum ferritin, 1.5 ng/mL), values of hemoglobin (P < 0.001), serum iron (P < 0.005), and ferritin (P < 0.001) significantly increased, on average, 2-3 months after eradication therapy and these iron indices were maintained at the same or higher levels at the endpoint of follow-up (median values: 14.2 g/dL, 102 μg/dL, and 29.3 ng/mL, respectively). No patient had recurrence of IDA at the time of final follow-up. H. pylori infection can be closely associated with recurrent or refractory IDA in teenage children. It is speculated that increased iron demands as a result of growth spurt in adolescents may play a synergistic role in combination with H. pylori in the pathogenesis of IDA.

Identification of Helicobacterpylori-related gastric cancer risk using serological gastritis markers and endoscopic findings: a large-scale retrospective cohort study

BackgroundGastric cancer remains a severe public health problem worldwide, particularly in Japan. Recent studies have demonstrated that serum markers are beneficial for risk stratification in gastric cancer development. We aimed to evaluate the usefulness of serum markers either alone or in combination (serum markers plus endoscopy) for effective risk stratification of gastric cancer development.MethodsWe enrolled 22,736 patients aged 20–95 years who underwent blood sampling and endoscopic examination at Hiroshima University Hospital in Japan between 1990 and 2014. The serum pepsinogen (PG) levels and anti-Helicobacter pylori antibody (Hp-Ab) titers were evaluated in each patient. The enrolled patients were matched with the database of the Hiroshima Prefecture Regional Cancer Registry. We processed the medical records and excluded patients with possible confounding factors for PG levels, such as proton pump inhibitor use, prior successful eradication therapy, post-gastrectomy, severe hepatorenal dysfunction, Zollinger–Ellison syndrome, and autoimmune gastritis. Among the remaining 5131 patients, we reviewed records of endoscopic examinations and selected 1507 patients (mean age, 62.5 years; 985 men and 522 women) who underwent endoscopic examination more than three months after blood sampling.First, based on the ABC method, patients were classified as follows: High PG levels and negative Hp-Ab, group A, high PG levels and positive Hp-Ab, group B, low PG levels and positive Hp-Ab, group C, and low PG levels and negative Hp-Ab, group D. Group A was further classified into two subgroups using endoscopic findings: true A without atrophic gastritis and pseudo A with atrophic gastritis. All patients underwent annual endoscopy follow-up.ResultsAmong the 1,507 patients (mean age, 62.5 years; 985 men), 24 were diagnosed with newly developed gastric cancer. No significant difference in cancer development was found between group A (PG negative and Hp-Ab negative) and the other groups. Remarkably, no true A group subjects developed gastric cancer.ConclusionsThe combination of serum markers and endoscopic findings is essential for the risk evaluation of gastric cancer.

Surveillance After Treatment of Barrett's Esophagus Benefits Those With High-Grade Dysplasia or Intramucosal Cancer Most.

Endoscopic eradication therapy with radiofrequency ablation (RFA) and endoscopic mucosal resection is a safe and effective treatment for Barrett's esophagus. Although the outcomes of surveillance endoscopy after successful endoscopic eradication therapy have been described, no previous studies have modeled the natural history or the effect of surveillance endoscopy after successful ablation to prevent progression to invasive esophageal adenocarcinoma. The US RFA Registry is a multicenter registry consisting of patients treated with RFA for Barrett's esophagus at 148 institutions (113 community-based and 35 academic-affiliated). The authors fit models to impute the natural history of recurrence and neoplastic progression after any recurrence or retreatment. Natural history estimates of invasive adenocarcinoma after ablation therapy were compared with as-treated estimates at 5 years to derive the preventive risk difference for surveillance. Natural history estimates for the postablation progression of high-grade dysplasia (HGD) or intramucosal adenocarcinoma to invasive adenocarcinoma after treatment were 6.3% at 5 years compared with 1.3% for low-grade dysplasia (LGD). The natural history model found a much higher preventative risk difference for surveillance for HGD/intramucosal adenocarcinoma (-4.8%), compared with LGD (-1.1%). The numbers needed to surveil at 5 years were 21 and 90 for these groups, respectively, to prevent one case of invasive esophageal adenocarcinoma, making surveillance after successful ablation of baseline HGD more than 4 times as effective at preventing invasive cancer than after successful ablation of baseline LGD. Endoscopic surveillance after successful ablation of baseline HGD or intramucosal cancer is much more effective than surveillance after successful treatment of baseline LGD in averting invasive adenocarcinoma. Although the modest benefits of surveillance for treated LGD may be greater than the risks for patients at average risk for adverse effects of endoscopy, clinicians should concentrate on retaining patients with baseline HGD or cancer in endoscopic surveillance programs.

The Origin of Epithelium with Low-Grade Atypia in Early Gastric Cancer

Introduction: Helicobacter pylori (HP) infection causes chronic inflammation and atrophy of the gastric mucosa and thus a high risk of gastric cancer (GC). With the increasing success of HP infection treatment, a larger number of GCs that develop after eradication can be assessed. Several studies have shown that epithelium with low-grade atypia (ELA) is a frequent characteristic of these GCs, but the origin of this condition is unknown. In this study, we compared the mucin phenotype, cellular proliferation, and p53 staining in ELA and cancerous tissues obtained from patients with GC with and without HP eradication. Methods: The study population consisted of 23 patients with GC that developed after successful HP eradication therapy (eradicated group) and 24 patients with GC and HP infection (infected group). The prevalence of ELA was determined by hematoxylin and eosin staining. Tumor tissue and ELA samples were further analyzed by immunohistochemical staining for Muc5AC, Muc2, p53, and Ki-67. Results: The ELA coverage rate was significantly higher in the eradicated group than in the infected group. Gastric-type mucin was frequently expressed by the ELA, and the mucin phenotypes of ELA and cancerous areas differed in 75% of cases. The Ki-67 labeling index was consistently lower in ELA than in the cancerous mucosa. Fourteen of 21 (66.7%) cancerous lesions, but only 3 ELA samples, were p53-positive. Conclusion: In most cases, ELA on the surfaces of GCs seems to have originated from normal gastric cells, not from cancer cells.

Post-endoscopy Esophageal Neoplasia in Barrett’s Esophagus: Consensus Statements From an International Expert Panel

Post-endoscopy Esophageal Neoplasia in Barrett’s Esophagus: Consensus Statements From an International Expert Panel

Comprehensive Management of Helicobacter pylori Infection

Helicobacter pylori (Hp) infection is a chronic gram-negative bacterial infection, that infects the epithelium of the stomach. This prevalence is very high and varies depending on factors such as geographical location, ethnicity, age, and socioeconomic. The key management of Hp infection is accurate diagnosis and treatment. The H. pylori diagnostic examination consists of non-invasive and invasive tests, the most common non-invasive tests are serological tests, urea breath tests (UBT), and stool antigen tests, while invasive tests are rapid urease tests, histopathology, culture, and PCR. The goal of H. pylori eradication is to heal peptic ulcers and reduce the risk of gastric cancer. Eradication therapy that is recommended worldwide and used in Indonesia is the triple drug combination therapy consisting of a PPI, clarithromycin and amoxicillin or metronidazole for 14 days. The success of eradication therapy is highly dependent on the choice of therapeutic regimen, patient compliance in taking multi-drugs with possible drug side effects, and the sensitivity of H. pylori strains to the antibiotics consumed.

Predictors and timing for the development of symptomatic gastroesophageal reflux disease after successful Helicobactor pylori eradication therapy

Background Helicobacter pylori (H. pylori) eradication success increases the incidence of erosive esophagitis by normalization of gastric acid secretion. The aim of this study is to clarify predictors and timing for the development of symptomatic gastroesophageal reflux disease (GERD) after successful H. pylori eradication based on long-term follow-up. Methods From April 2014 to October 2020, 330 patients with H. pylori infections treated with a standard triple-drug regimen were enrolled, and their records retrospectively reviewed. Development of symptomatic GERD was defined as requiring proton pump inhibitor or vonoprazan therapy to treat symptoms. Results The mean follow-up period was 2.8 years, and symptomatic GERD developed in 41 (12%) patients during the study period. Overall rates of GERD-symptom free patients at 6 months, 1, and 2 years after eradication were 97%, 93%, and 89%, respectively. We evaluated predictors for the development of symptomatic GERD using a Cox proportional hazards regression model. In multivariate analysis, being a current smoker, having functional dyspepsia, hiatal hernia, and severe gastric atrophy were identified as significant predictive factors. The GERD domain score in the Izumo scale was significantly decreased 1 month after vonoprazan therapy consistent with effective treatment of symptomatic GERD. Conclusions The rate of development of symptomatic GERD after successful H. pylori eradication is low over long-term follow-up and is easily controlled by vonoprazan therapy. However, patients with smoking habits, functional dyspepsia, hiatal hernia, or severe gastric atrophy should be followed carefully after eradication.

Prevalence and Risk Factors of Helicobacter Pylori Recurrence in Egyptian Patients with Liver Cirrhosis

Background: Helicobacter pylori (H. pylori) is a worldwide gastrointestinal infection. It is a common risk factor for peptic ulcer disease (PUD), chronic gastritis, and stomach cancer. In patients with cirrhosis, there is a significant association between H. pylori infection and severity of gastropathy due to portal hypertension, chronic stomach upset, frequent upper gastrointestinal bleeding as well as hepatic encephalopathy. Objective: To assess the rate and risk factors of recurrence of H. pylori infection in Egyptian patients with liver cirrhosis after successful eradication therapy. Patients and methods: This study included 500 liver cirrhosis patients who were tested for H. pylori infection. Patients with positive H. pylori infection received proton pump inhibitors (PPI)-based treatment regimen. Successful eradication therapy was assessed 4-8 weeks and repeated over one year after end of treatment using urea breath test (UBT) and stool antigen test (SAT). Results: The prevalence of H. pylori infection in cirrhotic patients was 58%. There were significantly higher serum levels of ammonia and C-reactive protein (CRP) in H. pylori positive patients as well as significantly more gastritis in endoscopy findings in comparison with H. pylori-negative patients. H. pylori recurrence after successful eradication therapy was observed in 22.1% patients of H. pylori-positive cirrhotic patients. Multivariate analysis showed that higher serum ammonia level & receiving multiple treatment courses to achieve H. pylori eradication were independent risk factors for H. pylori recurrence in cirrhotic patients. Conclusion: H. pylori infection is prevalent in liver cirrhosis patients with a significant recurrence rate after eradication therapy. High serum ammonia and the need for multiple treatment courses are risk factors for recurrence.

Risk of Reflux-Related Symptoms and Reflux Esophagitis after Helicobacter pylori Eradication Treatment in the Japanese Population.

Backgrounds: A meta-analysis of reports primarily from Western countries showed no association between Helicobacter pylori eradication and reflux esophagitis development. The risk of reflux esophagitis may differ among different populations based on H. pylori virulence factors and acid secretion ability. We evaluated the prevalence rates of reflux esophagitis in H.-pylori-positive Japanese subjects and assessed risk factors for reflux esophagitis after eradication. Methods: Among 148 H.-pylori-positive subjects who underwent H. pylori eradication from August 2015 to December 2019, we evaluated the prevalence of reflux esophagitis on endoscopy at 12 months after eradication success and the severity of reflux-related symptoms by the F-scale questionnaire at 2 months after treatment and 12 months after eradication success. Results: The prevalence of reflux esophagitis in H.-pylori-positive patients at entry was 2.0% (3/148). At 12 months after eradication success, the prevalence was 10.8% (16/148) (p < 0.01). In the F scale, the median total score before treatment was 4 (range: 0–49), which significantly decreased to 2 (range: 0–22) (p < 0.01) at 2 months after treatment and 3 (range: 0–23) (p < 0.01) at 12 months after eradication success. Following multivariate analysis, the pretreatment total F-scale score was a risk factor for the development of reflux esophagitis (odds ratio: 1.069, 95% confidence interval: 1.003–1.139, p < 0.01). Conclusions: In this H.-pylori-positive Japanese population, eradication therapy was associated with reflux esophagitis in around 10% of patients, particularly in those with severe reflux-related symptoms at baseline. Reflux-related symptoms may improve throughout the 12 months after successful eradication therapy, irrespective of the development of reflux esophagitis.

Armeniaspirol A: a novel anti-Helicobacter pylori agent.

SummaryAntibiotic resistance in Helicobacter pylori has been growing worldwide with current treatment regimens. Development of new compounds for treatment of H. pylori infections is urgently required to achieve a successful eradication therapy in the future. Armeniaspirols, a novel class of natural products isolated from Streptomyces armeniacus, have been previously identified as antibacterial agents against Gram‐positive pathogens. In this study, we found that armeniaspirol A (ARM1) exhibited potent antibacterial activity against H. pylori, including multidrug‐resistant strains, with MIC range values of 4–16 μg ml‐1. The underlying mechanism of action of ARM1 against H. pylori involved the disruption of bacterial cell membranes. Also, ARM1 inhibited biofilm formation, eliminated preformed biofilms and killed biofilm‐encased H. pylori in a dose‐dependent manner. In a mouse model of multidrug‐resistant H. pylori infection, dual therapy with ARM1 and omeprazole showed efficient in vivo killing efficacy comparable to the standard triple therapy, and induced negligible toxicity against normal tissues. Moreover, at acidic pH 2.5, ARM1 exhibited a much more potent anti‐H. pylori activity than metronidazole. Thus, these findings demonstrated that ARM1 is a novel potent anti‐H. pylori agent, which can be developed as a promising drug lead for treatment of H. pylori infections.

Features That Aid Identification of Autoimmune Gastritis in a Background of Active Helicobacter pylori Infection.

Helicobacter pylori-associated and autoimmune gastritis may coexist in a subset of patients who require treatment for both disorders. To delineate findings that identify autoimmune gastritis in the background of H pylori infection. We examined cases of (1) patients with H pylori-associated gastritis who had successful eradication therapy and subsequent biopsies diagnostic of autoimmune gastritis and (2) H pylori-associated gastritis wherein pathologists noted features of autoimmune gastritis during original interpretation. Control patients underwent H pylori eradication but lacked evidence of autoimmune gastritis or H pylori infection after 10 years of follow-up. Eight subjects had H pylori-associated gastritis followed by H pylori-negative sampling that showed autoimmune gastritis. Review of original samples showed full-thickness inflammation of oxyntic mucosa in 8 of 8 and oxyntic gland loss in 7 of 8 cases. Enterochromaffin-like (ECL) cell hyperplasia, pyloric metaplasia, and intestinal metaplasia were present in 4 of 8 (80% of 5 tested cases), 4 of 8, and 3 of 8 cases, respectively. Features of autoimmune gastritis were noted at the time of their original H pylori diagnosis in 11 study subjects. Ten of 11 samples displayed full-thickness inflammation of oxyntic mucosa and/or partial loss of oxyntic glands, 8 of 11 had ECL cell hyperplasia (all tested cases), 6 of 11 showed pyloric metaplasia, and 4 of 11 harbored intestinal metaplasia. Except for full-thickness oxyntic mucosa inflammation, these features were absent in control cases. Full-thickness inflammation combined with oxyntic gland loss and ECL cell hyperplasia may help to identify autoimmune gastritis in patients with concomitant H pylori infection.