Determinación de Helicobacter spp. en mucosa gástrica glandular de muías a través de la prueba de la actividad de la ureasa e histopatología / Determination of Helicobacter spp. in glandular gastric mucosa of mules through the test of urease activity and histopathology

RESUMEN La información sobre la presentación y los factores predisponentes del síndrome de úlcera gástrica en mulas (SUGM) es escasa en comparación con el síndrome de úlcera gástrica en equinos (SUGE) y asnales. Debido a la naturaleza multifactorial de este síndrome, la helicobacteriosis ha sido estudiada en otras especies. El objetivo de este trabajo fue establecer la presencia de Helicobacter spp. en mucosa gástrica de mulas a través de la prueba rápida de la ureasa (PRU) y de análisis histopatológico. Menos del 27% de las muestras reaccionaron a la PRU, con tiempos prolongados de reacción, y al Agar Urea (prueba de oro), con menor porcentaje de positividad. La histopatología reveló procesos inflamatorios crónicos, sin presencia de bacterias curvoespiraladas. Las PRU no fueron conclusivas en la determinación de Helicobacter spp., comportamiento similar reportado en equinos. Se requieren exámenes diagnósticos más específicos y procedimientos complementarios orientados a explorar por regiones del estómago en la consideración del número de muestras representativas.

ABSTRACT Information on the presentation and predisposing factors of Mule Gastric Ulcer Syndrome (MGUS) is scarce, compared to Equine Gastric Ulcer Syndrome (EGUS) and donkeys. Within the multifactorial nature of this syndrome, helicobacteriosis has been studied in other species. The objective of this work was to establish the presence of Helicobacter spp. in gastric mucosa of mules, through the rapid urease test (RUT) and histopathological analysis. Less than 27% of the samples reacted to RUTs, with prolonged reaction times, and Urea Agar (gold test), with a lower percentage of positivity. Histopathology revealed chronic inflammatory processes, without the presence of curved-spiral bacteria. The RUTs were not conclusive in the determination of Helicobacter spp., a similar behavior reported in horses. More specific diagnostic tests and complementary procedures are required to explore the regions of the stomach in consideration of the number of representative samples.

Associação de alterações anatomopatológicas com o Helicobacter spp. por meio de análise imuno-histoquímica em estômagos de leitões / Association of anatomopathological changes with the Helicobacter spp. through immunohistochemical analysis in piglets stomachs

O objetivo deste trabalho foi relacionar os achados anatomopatológicos das lesões gástricas subclínicas de ocorrência natural em leitões com a presença, ou não, de Helicobacter spp. por meio da imuno-histoquímica. Foram utilizados 48 leitões de linhagem genética comercial. Os animais foram adquiridos em uma granja comercial, com peso médio de 34 Kg e idade média de 79 dias; após o abate, seus estômagos foram coletados e avaliados. Avaliações histopatológicas e imuno-histoquímicas foram realizadas em amostras das regiões anatômicas aglandular e glandular. Macroscopicamente, 34 (70,83%) leitões apresentaram lesões na região aglandular, enquanto que em 14 animais (29,17%) não foram encontradas alterações nesta região. Dos estômagos com lesão, 14 foram classificados como grau 1, seis como grau 2 e 14 como grau 3. Microscopicamente, 44 amostras (91,66%) apresentaram paraqueratose. Deste total, 22 apresentaram a forma discreta, 20 a moderada e dois a acentuada. Na avaliação macroscópica da porção glandular, 41 (85,4%) animais apresentaram alteração em pelo menos uma das três regiões, e em somente sete (14,6%) não foram encontradas lesões em nenhuma delas. Em 14 deles, houve aumento da atividade mucípara, em dois, houve erosão e, em cinco, hiperemia. As lesões na região glandular do estômago foram mais extensas no antro e no cárdia, seguidas do fundo. Em relação à análise imuno-histoquímica, 21 (43,8%) amostras tiveram resultados negativos em todas as regiões, e 24 (50%) foram positivas em pelo menos uma delas, sendo que nenhuma foi positiva em todas. Os achados anatomopatológicos demonstraram relação estatística com a bactéria e, sua imunomarcação não associada à lesão em certas regiões gástricas, demonstra seu caráter saprofítico e oportunista.

The aim of this study was to relate the anatomopathological findings of naturally occurring subclinical gastric lesions in piglets, with or without Helicobacter spp. through immunohistochemistry. Forty-eight piglets of commercial genetic lineage were used. The animals were acquired in a commercial farm, with an average weight of 34 kg and an average age of 79 days, and after slaughter, their stomachs were collected and evaluated. Samples from the glandular and aglandular anatomical regions were evaluated. Macroscopically, 34 (70.83%) samples had lesions on aglandular region, while 14 (29.17%) nothing had. Of the injured stomachs, 14 were classified as grade 1, six as grade 2 and 14 as grade 3. Microscopically, 44 samples (91.66%) showed parakeratosis. Of these, 22 showed a discreet manner, 20 moderate and two severe. In the glandular region, in 41 (85.4%) samples there was a change in at least one of the three regions, and only seven animals (14.6%) showed no change in any of the three. Fourteen samples showed increased muciparous activity, two showed erosion and five hyperemia. The lesions were higher in antral regions and cardic, followed the fundus. In relation to immunohistochemistry, 21(43.8%) samples were negative in all areas, 24 (50%) were positive in at least one, and none were positive in all. The anatomopathological findings showed a statistical relationship with the bacteria, and its immunostaining, not associated with gastric lesions in certain regions, demonstrates its saprophytic and opportunistic character.

Helicobacter pylori testing in a population of Korean patients with pernicious anemia

No abstract available.

Evaluating Diagnostic Tests for Helicobacter pylori Infection Without a Reference Standard: Use of Latent Class Analysis

Evaluation of diagnostic tests requires reference standards, which are often unavailable. Latent class analysis (LCA) can be used to evaluate diagnostic tests without reference standards, using a combination of observed and estimated results. Conditionally independent diagnostic tests for Helicobacter pylori infection are required. We used LCA to construct a reference standard and evaluate the capability of non-invasive tests (stool antigen test and serum antibody test) to diagnose H. pylori infection compared with the conventional method, where histology is the reference standard. A total of 96 healthy subjects with endoscopy histology results were enrolled from January to July 2016. Sensitivity and specificity were determined for the LCA approach (i.e., using a combination of three tests as the reference standard) and the conventional method. When LCA was used, sensitivity and specificity were 83.8% and 99.4% for histology, 80.0% and 81.9% for the stool antigen test, and 63.6% and 89.3% for the serum antibody test, respectively. When the conventional method was used, sensitivity and specificity were 75.8% and 71.1% for the stool antigen test and 77.7% and 60.7% for the serum antibody test, respectively. LCA can be applied to evaluate diagnostic tests that lack a reference standard.

Comparison of 7- and 14-Day Eradication Therapy for Helicobacter pylori with First- and Second-Line Regimen: Randomized Clinical Trial

Influence of Helicobacter pylori Infection on Endoscopic Findings of Gastric Adenocarcinoma of the Fundic Gland Type

PURPOSE: Gastric adenocarcinoma of the fundic gland type (chief cell predominant type) (GA-FG-CCP) was first reported as a rare adenocarcinoma found in the normal fundic mucosa. Recent studies have proposed the possibility that GA-FG-CCPs were also generated in the atrophic mucosa after Helicobacter pylori (HP) eradication therapy. However, little is known on the endoscopic findings of GA-FG-CCP generated in the atrophic mucosa due to its extreme rarity. MATERIALS AND METHODS: A total of 8 patients who underwent endoscopic submucosal resection and were diagnosed with GA-FG-CCP generated in the HP-uninfected mucosa (4 cases, HP-uninfected group) or HP-eradicated atrophic mucosa (4 cases, HP-eradicated group) were retrospectively analyzed, and their endoscopic findings, including magnifying endoscopy with narrow band imaging (M-NBI), and pathological features were compared. RESULTS: While GA-FG-CCPs in the 2 groups displayed similar macroscopic appearance, M-NBI demonstrated that characteristic microvessels (tapered microvessels like withered branches) were specifically identified in the HP-eradicated group. Pathological investigation revealed that a decreasing number of fundic glands and thinned foveolar epithelium covering tumor ducts were thought to lower the thickness of the covering layer over tumor ducts in the HP-eradicated group. Moreover, dilation of vessels just under the surface of the lesions contributed to the visualization of microvessels by M-NBI. CONCLUSIONS: The change in background mucosa due to HP infection influenced the thickness of the covering layer over the tumor ducts and M-NBI finding of GA-FG-CCP.

β-carotene Inhibits Expression of c-Myc and Cyclin E in Helicobacter pylori-infected Gastric Epithelial Cells

BACKGROUND: Helicobacter pylori infection is a major risk factor in the development of gastric cancer. H. pylori infection of gastric epithelial cells increases the levels of reactive oxygen species (ROS), activates oncogenes, and leads to β-catenin-mediated hyper-proliferation. β-Carotene reduces ROS levels, inhibits oxidant-mediated activation of inflammatory signaling and exhibits anticancer properties. The present study was carried out to determine if β-carotene inhibits H. pylori-induced cell proliferation and the expression of oncogenes c-myc and cyclin E by reducing the levels of β-catenin and phosphorylated glycogen synthase kinase 3β (p-GSK3β). METHODS: Gastric epithelial AGS cells were pre-treated with β-carotene (5 and 10 μM) for 2 hours prior to H. pylori infection and cultured for 6 hours (for determination of the levels of p-GSK3β, GSK3β, and β-catenin) and 24 hours (for determination of cell viability and protein levels of c-myc and cyclin E). Cell viability was determined by the MTT assay and protein levels were determined via western blot-based analysis. RESULTS: β-Carotene inhibited H. pylori-induced increases in the percentage of viable cells, phosphorylated GSK3β (p-GSK3β), and the levels of β-catenin, c-myc and cyclin E. CONCLUSIONS: β-Carotene inhibits H. pylori-induced hyper-proliferation of gastric epithelial cells by suppressing β-catenin signaling and oncogene expression.

Astaxanthin Prevents Decreases in Superoxide Dismutase 2 Level and Superoxide Dismutase Activity in Helicobacter pylori-infected Gastric Epithelial Cells

BACKGROUND: Helicobacter pylori increases production of reactive oxygen species (ROS), which activates inflammatory and carcinogenesis-related signaling pathways in gastric epithelial cells. Therefore, reducing ROS, by upregulating antioxidant enzyme, such as superoxide dismutase (SOD), may be a novel strategy to prevent H. pylori-associated gastric diseases. Astaxanthin is an antioxidant carotenoid that prevents oxidative stress-induced cell injury. The present study was aimed to determine whether H. pylori decreases SOD activity by changing the levels of SOD1/SOD2 and whether astaxanthin prevents changes in SOD levels and activity in H. pylori-infected gastric epithelial AGS cells. METHODS: AGS cells were pre-treated with astaxanthin for 3 hours prior to H. pylori infection and cultured for 1 hour in the presence of H. pylori. SOD levels and activity were assessed by Western blot analysis and a commercial assay kit, respectively. Mitochondrial ROS was determined using MitoSOX fluorescence. RESULTS: H. pylori decreased SOD activity and the SOD2 level, but increased mitochondrial ROS in AGS cells. The SOD1 level was not changed by H. pylori infection. Astaxanthin prevented H. pylori-induced decreases in the SOD2 level and SOD activity and reduced mitochondrial ROS in AGS cells. CONCLUSIONS: Consumption of astaxanthin-rich food may prevent the development of H. pylori-associated gastric disorders by suppressing mitochondrial oxidative stress.

Prevalence of Helicobacter pylori Infection in Patients with Chronic Kidney Disease

No abstract available.

Helicobacter pylori Infection in Patients with Chronic Kidney Disease: A Systematic Review and Meta-Analysis

BACKGROUND/AIMS: Insufficient systematic reviews were conducted in the previous meta-analyses about the prevalence of Helicobacter pylori infection in patients with chronic kidney disease (CKD). The aim of this study was to evaluate the prevalence of H. pylori infection in patients with CKD. METHODS: A systematic review of studies that evaluated the prevalence of H. pylori infection in patients with CKD compared to a control group was performed. Only studies with adult patients were included, and studies with renal transplant recipients or diabetic nephropathy patients were excluded. Random-effects model meta-analyses with sensitivity analyses and subgroup analyses were conducted to confirm the robustness of the main result. A meta-regression analysis was conducted to explore the influence of potential heterogeneity on the outcomes. The methodological quality of the included publications was evaluated using the Risk of Bias Assessment tool for Nonrandomized Studies. Publication bias was also assessed. RESULTS: In total, 47 studies were identified and analyzed. The total prevalence of H. pylori infection was 48.2% (1,968/4,084) in patients with CKD and 59.3% (4,097/6,908) in the control group. Pooled analysis showed a significantly lower prevalence of H. pylori infection in patients with CKD (vs control group: odds ratio, 0.64; 95% confidence interval, 0.52 to 0.79). Sensitivity analyses revealed consistent results, and meta-regression analysis showed no significant confounders. No publication bias was detected. CONCLUSIONS: The results of this study suggest a lower prevalence of H. pylori infection in patients with CKD.

Management of Antibiotic-Resistant Helicobacter pylori Infection: Perspectives from Vietnam

Antibiotic resistance is the most important factor leading to the failure of eradication regimens. This review focuses on the prevalence of Helicobacter pylori primary and secondary resistance to clarithromycin, metronidazole, amoxicillin, levofloxacin, tetracycline, and multidrug in Vietnam. We searched the PubMed, EMBASE, Vietnamese National Knowledge Infrastructure, and Vietnamese Biomedical databases from January 2000 to December 2016. The search terms included the following: H. pylori infection, antibiotic (including clarithromycin, metronidazole, amoxicillin, levofloxacin, tetracycline, and multidrug) resistance in Vietnam. The data were summarized in an extraction table and analyzed manually. Finally, Excel 2007 software was used to create charts. Ten studies (three studies in English and seven in Vietnamese) were included in this review. A total of 308, 412, 523, 408, 399, and 268 H. pylori strains were included in this review to evaluate the prevalence of H. pylori primary resistance to amoxicillin, clarithromycin, metronidazole, levofloxacin, tetracycline, and multidrug resistance, respectively. Overall, the primary resistance rates of amoxicillin, clarithromycin, metronidazole, levofloxacin, tetracycline, and multidrug resistance were 15.0%, 34.1%, 69.4%, 27.9%, 17.9% and 48.8%, respectively. Secondary resistance rates of amoxicillin, clarithromycin, metronidazole, levofloxacin, tetracycline, and multidrug resistance were 9.5%, 74.9%, 61.5%, 45.7%, 23.5% and 62.3%, respectively. In Vietnam, primary and secondary resistance to H. pylori is increasing over time and affects the effectiveness of H. pylori eradication.

Effect of Citric Acid on Accuracy of ¹³C-Urea Breath Test after Helicobacter pylori Eradication Therapy in a Region with a High Prevalence of Atrophic Gastritis

BACKGROUND/AIMS: The validity of ¹³C-urea breath test (¹³C-UBT) for Helicobacter pylori detection is influenced by atrophic gastritis. The aim of this study was to evaluate the effect of citric acid on the accuracy of ¹³C-Urea breath test after H. pylori eradication therapy in a region where atrophic gastritis is common. METHODS: In this prospective study, H. pylori-positive patients received ¹³C-UBT after H. pylori eradication regimen. They were classified into citric acid group and control group. To determine diagnostic accuracy of ¹³C-UBT, patients were offered invasive methods. RESULTS: A total of 1,207 who successfully took H. pylori-eradication regimen received UBT. They were assigned into the citric acid group (n=562) and the control group (n=645). The mean ¹³C-UBT value of the citric acid group was 10.3±26.4‰, which was significantly (p<0.001) higher than that of that control group (5.1‰±12.6‰). Of these patients 122 patients were evaluated by endoscopic biopsy methods. Based on invasive tests, the accuracy, sensitivity, specificity, positive predictive value, and negative predictive value of ¹³C-UBT for the citric acid group were 83.3%, 91.7%, 81.3%, 55.0%, and 97.5%, respectively. Those of the control group were 87.7%, 90.9%, 88.2%, 62.5%, and 97.8%, respectively. They were not significantly different between the two groups. Although the presence of gastric atrophy and intestinal metaplasia (IM) decreased the accuracy, the decrease was not significant. CONCLUSIONS: In a country with high prevalence of atrophic gastritis or IM, false positivity remained common despite the use of citric acid in ¹³C-UBT.

Ten-Day Concomitant, 10-Day Sequential, and 7-Day Triple Therapy as First-Line Treatment for Helicobacter pylori Infection: A Nationwide Randomized Trial in Korea

BACKGROUND/AIMS: This nationwide, multicenter prospective randomized controlled trial aimed to compare the efficacy and safety of 10-day concomitant therapy (CT) and 10-day sequential therapy (ST) with 7-day clarithromycin-containing triple therapy (TT) as first-line treatment for Helicobacter pylori infection in the Korean population. METHODS: Patients with H. pylori infection were assigned randomly to 7d-TT (lansoprazole 30 mg, amoxicillin 1 g, and clarithromycin 500 mg twice daily for 7 days), 10d-ST (lansoprazole 30 mg and amoxicillin 1 g twice daily for the first 5 days, followed by lansoprazole 30 mg, clarithromycin 500 mg, and metronidazole 500 mg twice daily for the remaining 5 days), or 10d-CT (lansoprazole 30 mg, amoxicillin 1 g, clarithromycin 500 mg, and metronidazole 500 mg twice daily for 10 days). The primary endpoint was eradication rate by intention-to-treat (ITT) and per-protocol (PP) analyses. RESULTS: A total of 1,141 patients were included. The 10d-CT protocol achieved a markedly higher eradication rate than the 7d-TT protocol in both the ITT (81.2% vs 63.9%) and PP analyses (90.6% vs 71.4%). The eradication rate of the 10d-ST protocol was superior to that of the 7d-TT protocol (76.3% vs 63.9%, ITT analysis; 85.0% vs 71.4%, PP analysis). No significant differences in adherence or serious side effects were found among the three treatment arms. CONCLUSIONS: The 10d-CT and 10d-ST regimens were superior to the 7d-TT regimen as standard first-line treatment in Korea.

Association between Body Mass Index and Gastric Cancer Risk According to Effect Modification by Helicobacter pylori Infection / Journal of the Korean Cancer Association, 대한암학회지

PURPOSE: Few studies investigated roles of body mass index (BMI) on gastric cancer (GC) risk according to Helicobacter pylori infection status. This study was conducted to evaluate associations between BMI and GC risk with consideration of H. pylori infection information. MATERIALS AND METHODS: We performed a case-cohort study (n=2,458) that consists of a subcohort, (n=2,193 including 67 GC incident cases) randomly selected from the Korean Multicenter Cancer Cohort (KMCC) and 265 incident GC cases outside of the subcohort. H. pylori infection was assessed using an immunoblot assay. GC risk according to BMI was evaluated by calculating hazard ratios (HRs) and their 95% confidence intervals (95% CIs) using weighted Cox hazard regression model. RESULTS: Increased GC risk in lower BMI group (< 23 kg/m²) with marginal significance, (HR, 1.32; 95% CI, 0.98 to 1.77) compared to the reference group (BMI of 23-24.9 kg/m²) was observed. In the H. pylori non-infection, both lower (< 23 kg/m²) and higher BMI (≥ 25 kg/m²) showed non-significantly increased GC risk (HR, 10.82; 95% CI, 1.25 to 93.60 and HR, 11.33; 95% CI, 1.13 to 113.66, respectively). However, these U-shaped associations between BMI and GC risk were not observed in the group who had ever been infected by H. pylori. CONCLUSION: This study suggests the U-shaped associations between BMI and GC risk, especially in subjects who had never been infected by H. pylori.

Helicobacter pylori inhibited cell proliferation in human periodontal ligament fibroblasts through the Cdc25C/CDK1/cyclinB1 signaling cascade

PURPOSE: Several studies have shown that the oral cavity is a secondary location for Helicobacter pylori colonization and that H. pylori is associated with the severity of periodontitis. This study investigated whether H. pylori had an effect on the periodontium. We established an invasion model of a standard strain of H. pylori in human periodontal ligament fibroblasts (hPDLFs), and evaluated the effects of H. pylori on cell proliferation and cell cycle progression. METHODS: Different concentrations of H. pylori were used to infect hPDLFs, with 6 hours of co-culture. The multiplicity of infection in the low- and high-concentration groups was 10:1 and 100:1, respectively. The Cell Counting Kit-8 method and Ki-67 immunofluorescence were used to detect cell proliferation. Flow cytometry, quantitative real-time polymerase chain reaction, and western blots were used to detect cell cycle progression. In the high-concentration group, the invasion of H. pylori was observed by transmission electron microscopy. RESULTS: It was found that H. pylori invaded the fibroblasts, with cytoplasmic localization. Analyses of cell proliferation and flow cytometry showed that H. pylori inhibited the proliferation of periodontal fibroblasts by causing G2 phase arrest. The inhibition of proliferation and G2 phase arrest were more obvious in the high-concentration group. In the low-concentration group, the G2 phase regulatory factors cyclin dependent kinase 1 (CDK1) and cell division cycle 25C (Cdc25C) were upregulated, while cyclin B1 was inhibited. However, in the high-concentration group, cyclin B1 was upregulated and CDK1 was inhibited. Furthermore, the deactivated states of tyrosine phosphorylation of CDK1 (CDK1-Y15) and serine phosphorylation of Cdc25C (Cdc25C-S216) were upregulated after H. pylori infection. CONCLUSIONS: In our model, H. pylori inhibited the proliferation of hPDLFs and exerted an invasive effect, causing G2 phase arrest via the Cdc25C/CDK1/cyclin B1 signaling cascade. Its inhibitory effect on proliferation was stronger in the high-concentration group.

The Effect of Trimebutine and/or Helicobacter pylori Eradication on the Gastroesophageal Reflux Disease, Irritable Bowel Syndrome, and Functional Dyspepsia Overlapping Disorders

No abstract available.

Common Locations of Gastric Cancer: Review of Research from the Endoscopic Submucosal Dissection Era

Detection of early-stage gastric cancer improves the prognosis of patients. Endoscopic submucosal dissection (ESD) is a curative and stomach-preserving treatment for early gastric cancer (EGC) associated with a low risk of lymph node metastasis. However, several studies have reported missed diagnosis of gastric cancer. Therefore, endoscopists are required to learn accurate diagnostic skills to eliminate endoscopic blind spots. A systematic screening protocol to map the entire stomach without blind spots reduces the risk of missed lesions. Knowledge of the features of EGC or dysplasia is essential to identify suspicious lesion. Information of the common sites of occurrence of EGC can also enable a detailed endoscopic examination to improve detection rates. Previous reports investigating the location of gastric cancers resected by ESD or surgery showed that the antrum and lesser curvature of stomach were predominantly affected. Helicobacter pylori-induced atrophic changes advance from the antrum to the corpus along the lesser curvature, predominantly affecting these areas. Gastric cancers in the antrum and the lower corpus are also commonly missed during screening examination. Therefore, a careful examination of the lower third stomach is warranted to avoid missing synchronous and metachronous gastric lesions. Knowledge of the location of EGC enables accurate endoscopic examination and detection of EGC in early stage.

Changes in Helicobacter pylori Immunoglobulin G Levels and Gastric Mucosal Atrophy after Successful Eradication of Helicobacter pylori

BACKGROUND/AIMS: Limited information is available about the relationship between Helicobacter pylori (H. pylori) immunoglobulin (Ig) G and serum pepsinogen (pepsinogen [PG], a marker of gastric mucosal atrophy) concentrations after H. pylori eradication. MATERIALS AND METHODS: Eligible patients who underwent endoscopic submucosal dissection (ESD) for early gastric cancer from August 2007 to March 2013 in a tertiary-referral center, and whose serum H. pylori IgG and PG concentrations were measured at the time of performing ESD and one year post-ESD, were selected. Successful H. pylori eradication was achieved after ESD in all the patients. According to the decrease in serum H. pylori IgG concentration after bacterial eradication, the patients were categorized as group 1 (IgG concentration decreased by <50%), and group 2 (IgG concentration decreased by ≥50%). RESULTS: Of the 106 patients, 25 (23.6%) were classified into group 1 and 81 (76.4%) into group 2. One year after H. pylori eradication, the serum PG II concentration was significantly decreased in group 2 (12.46±8.18 vs. 8.28±6.11, P=0.024). Although the serum PG I/II ratio of group 2 was higher than that of group 1 (8.32±4.52 ng/mL vs. 6.39±4.04 ng/mL), the difference was not significant (P=0.058). One year after successful eradication, elevated serum PG I/II ratio was observed in 21 patients (84%) in group 1 and in 77 patients (95.1%) in group 2 (P=0.087). The mean serum PG I/II ratio was also elevated in both groups. Serum PG II concentration was significantly decreased in group 2. CONCLUSIONS: A notable decrease in the concentration of H. pylori IgG antibody after bacterial eradication might reflect gastric mucosal atrophy. However, our study showed no statistically significant difference.

Can Eradication of Helicobacter pylori Improve the Symptoms of Functional Dyspepsia?

No abstract available.

Helicobacter pylori Infection and the Kyoto Classification of Gastritis

Estimating the risk of Helicobacter pylori (H. pylori)-induced gastric cancer during endoscopic examination is important. Owing to recent advances in gastrointestinal endoscopy, the gross appearance of the background gastric mucosa has enabled discrimination of subjects with active, chronic, and past H. pylori infection from those with no history of infection. To provide subjective criteria for H. pylori infection-related endoscopic findings with increased risk of gastric cancer, the Kyoto classification of gastritis was proposed at the 85th annual meeting of the Japanese Society for Gastrointestinal Endoscopy in May 2013 in Kyoto. The main contents focus on determining the gastric cancer risk by scoring the endoscopic findings of the background gastric mucosa from 0 to 8. These important findings are not described in the Kyoto Global Consensus Conference proceedings published in English. To better estimate the gastric cancer risk during screening endoscopy in an H. pylori-prevalent population, knowledge of the Japanese version of the Kyoto classification is important. This new classification emphasizes the discrimination of subjects with H. pylori infection by assessing 19 endoscopic findings (presence of atrophy, intestinal metaplasia, diffuse redness, spotty redness, mucosal swelling, enlarged folds, sticky mucus, chicken skin-like nodularity, foveolar-hyperplastic polyp, xanthoma, depressed erosion, regular arrangement of collecting venules, fundic gland polyp, linear red streak, raised erosion, hematin deposit, multiple white and flat-elevated lesions, patchy redness, and map-like redness). In this review, the validity of the Kyoto classification is summarized in conjunction with several suggestions to resolve emerging H. pylori infection-related problems in Korea.