Нейроэндокринные опухоли желудка и инфекция Н. pylori: особенности ведения пациентов на примере клинического случая

Helicobacter pylori infection in children: recommendations for diagnosis and treatment.

To evaluate the accuracy of several methods aimed to detect Helicobacter pylori stool antigens in patients with upper gastrointestinal bleeding. Thirty-four patients with upper gastrointestinal bleeding because of peptic ulcer were included. The first stool sample during hospitalization was collected, and stool antigens were determined with: polyclonal enzyme-linked immunosorbent assay (Premier-Platinum-HpSA); monoclonal enzyme-linked immunosorbent assay (Amplified-IDEIA-HpStAR); and rapid monoclonal immunochromatographic test (ImmunoCard-STAT HpSA). A patient was considered infected when H. pylori was diagnosed with invasive tests (rapid urease test or histology) or with (13)C-urea breath test. When all tests were negative, a new breath test was repeated after stopping proton pump inhibitors. All patients were infected and, therefore, only sensitivity of the tests could be calculated: polyclonal enzyme-linked immunosorbent assay (74%), monoclonal enzyme-linked immunosorbent assay (94%), and rapid monoclonal immunochromatographic test (60%; concordance between the two observers was high, kappa = 0.9). Neither the presence of maelena nor the delay in obtaining stool samples explained false negatives. Neither the polyclonal enzyme-linked immunosorbent assay stool antigen test nor the rapid immunochromatographic stool antigen test can be recommended to diagnose H. pylori infection in patients with upper gastrointestinal bleeding. However, the monoclonal enzyme-linked immunosorbent assay stool antigen test is highly sensitive for detecting the infection in patients with this complication, although more studies are necessary to evaluate the specificity of the method.

Helicobacter pylori infection has been considered to play significant role in gastric carcinogenesis, but only a minority of people who harbor this organism will develop gastric cancer. H. pylori infection first causes chronic non atrophic gastritis. Chronic non atrophic gastritis may evolve to atrophic gastritis and intestinal metaplasia and finally to dysplasia and adenocarcinoma. To estimate the prevalence of H. pylori infection and the precancerous gastric lesions and their relationship, in patients with dyspeptic symptoms who underwent upper gastrointestinal endoscopy at a reference center in the central region of Rio Grande do Sul state, Brazil. We analyzed gastric biopsies taken from corpus and antrum of patients who underwent upper gastrointestinal endoscopy for H. pylori detection, between 1994 and 2003. According to Sydney system, chronic non atrophic gastritis, atrophic gastritis and intestinal metaplasia were diagnosed by histological examination (H-E stain). The histological diagnoses were related to H. pylori infection status. Biopsies from 2,019 patients were included in the study. Patients mean age was 52 (+/-15) and 59% were female. Seventy six percent had H. pylori infection. Normal mucosa, chronic non atrophic gastritis, atrophic gastritis and intestinal metaplasia were diagnosed in 5%, 77%, 3% and 15%, respectively. The OR for any degree of gastric mucosa lesion in infected patients was 10 (CI95% 6.50 - 17%). The OR for infected patients had chronic non atrophic gastritis was 3 (CI95% 2,2 - 3,4). The OR for infected patients had atrophic gastritis or intestinal metaplasia was less than 1. The prevalence of H. pylori infection in this population was high (76%) and infected individuals had the probability 10 folds greater than non infected individuals to have any lesion of gastric mucosa. The prevalence of precancerous lesions was 77% for non atrophic chronic gastritis, 3% for atrophic gastritis and 15% for intestinal metaplasia. Infected patients had risk 3 folds greater than non-infected for the occurrence of non atrophic chronic gastritis. H. pylori infection did not show risk for occurrence of atrophic gastritis and intestinal metaplasia, suggesting that other risk factors should be involved in the carcinogenesis process.

Background: Although the pathogenesis of gastric xanthoma (GX) remains unclear, an association of GX with atrophic gastritis has been reported. Helicobacter pylori is closely related to atrophic gastritis. The aim of this study was to investigate the relationship among GX, H. pylori, and atrophic gastritis. Methods: Sixty-seven patients with GX were assessed for H. pylori infection by serum anti-H. pylori IgG antibody, in addition to the rapid urease test, culture, and histologic examination using biopsy specimens of the antrum and corpus. The findings were compared with 67 age- and sex-matched control subjects without GX. The distribution of atrophic gastritis was assessed endoscopically. The severity of atrophic gastritis was determined endoscopically and histologically. Serum pepsinogen (PG) levels were also measured. Immunohistochemical staining of GX samples for H. pylori antigen was performed. H. pylori clinical isolates from patients with GX and controls were assessed for cagA by means of polymerase chain reaction. Results: The prevalence of H. pylori was significantly higher in patients with GX than in controls (94% and 72%, respectively). A significantly more extensive atrophic gastritis was present in patients with GX, as determined endoscopically and histologically, than in controls. Serum PG-I levels and the PG-I/PG-II ratio were significantly lower in the GX group than in the control group. H. pylori antigens were frequently identified in the cytoplasm of xanthoma cells in H. pylori-positive specimens of GX (54 of 63 specimens, 86%), whereas no immunoreactivity for H. pylori antigens was detected in H. pylori-negative specimens of GX. There was no significant difference in the positive rate of cagA between the two groups. Conclusions: Our results identified a close relationship among H. pylori infection, GX, and atrophic gastritis. A proportion of GXs may be provoked by H. pylori infection.

Helicobacter pylori ( H. pylori ) infection and autoimmune inflammation of the gastric mucosa are recognized as the leading etiologic factors of chronic atrophic gastritis. At the same time, the mechanisms of the development and progression of gastric mucosal atrophy associated with a risk of gastric cancer in these types of gastritis are highly heterogeneous, and need a more detailed study of this issue to work out a follow-up personalized approach to the management of patients. In recent years, there have been reports confirming that autoimmune gastritis (AIG) without concurrent H. pylori infection and without signs of significant inflammation of other etiologies has a relatively benign course and a low risk of neoplastic transformation of the gastric mucosa into gastric cancer. However, the emergence of reports that H. pylori infection may elicit autoimmunity toward parietal cells, which results in the atrophy of the gastric body mucosa makes the issue of management and identification of carcinogenesis risks in patients with chronic gastritis of mixed etiology more urgent. This scientific review aims to systematize the available data on AIG, the mechanisms of development of atrophy and atrophy-associated risks of carcinogenesis, both in isolated autoimmune inflammation and in persistent or previous H. pylori (“pure” AIG), persistent H. pylori infection, or in the post-eradication therapy period. Special attention is paid to the phenomenon of molecular mimicry between H. pylori antigens and epitopes of gastric parietal cells during the development of gastritis of mixed-etiology.

Aim. Determination of the prevalence of Helicobacter pylori (H. pylori) infection among the population of the Ryazan region. Materials and Methods. 833 individuals (809 adults and 24 children) were examined for presence of IgG class antibodies using the enzyme immunoassay (2017-2018). The criteria for inclusion into the study were: a desire of a patient to undergo examination for the presence of antibodies to H. pylori in blood. Criteria for exclusion: past treatment for helicobacteriosis. The presence of helicobacteriosis was determined by enzyme immunoassay for quantitative detection of IgG class antibodies (anti-H. pylori IgG) using BCM Diagnostics Helicobacter pylori IgG (USA) test system and for qualitative determination of IgG antibodies to H. pylori in blood serum on IMMULITE 2000 (Germany; test IMMULITE 2000 H. pylori IgG). Sensitivity of the used test systems was 95.0%, specificity 98.0%. Results. High contamination of adult residents of Ryazan with H. pylori 65.6% was found (70.6% of males, 64.4% of females). Prevalence of H. pylori infection among adults in 2017 was 64.4% and in 2018 70.2%, however, the observed increase in the number of infected individuals was not statistically significant (p0.05). The highest prevalence of H. pylori infection was observed in individuals 40 years of age (67.2%). Gender-related differences in the prevalence of Helicobacter pylori infection were revealed in individuals of 40 years and older. H. pylori infection in males of 40 years was 75.2%, against 65.5% in females of the same age (p0.05). In children of 4-16 years, the share of individuals with positive serological test with anti-H. pylori IgG reached 20.8%. All H. pylori infected children were above 9 years of age. Individuals with positive serological tests received consultation of a gastroenterologist, and on indications underwent additional examination with administration of eradication treatment. In patients with indefinite results the examination was repeated after a week and/or the presence of H. pylori antigen in feces was determined. Conclusion. The data obtained indicate a high level of infection with H. pylori in the adult population in the Ryazan region 65.6%. The incidence of detection of anti-H. pylori IgG in the population was maximal in individuals 40 years (67.2%).

Helicobacter Pylori Infection and Vitamin B12 Deficiency During Early Pregnancy in an Urban Slum in Bangladesh (P24-035-19)

BACKGROUNDAtrophic gastritis has been shown to be one of the long term sequelae ofHelicobacter pylori infection.AIMSTo determine the prevalence of atrophic gastritis in outpatients, to study the accuracy of serological...

There is an increasing interest in noninvasive tests for detecting Helicobacter pylori (H. pylori) infection. Unlike serological and urea breath tests, the possibility of searching for H. pylori in feces has been scarcely investigated. The aim of this prospective pilot study was to evaluate the usefulness of a new enzyme immunoassay for detecting H. pylori antigens in feces, as a predictor of H. pylori status in the pre- and posttreatment settings. One hundred and fifty-four symptomatic, anti-H. pylori untreated patients (Group A) and 116 anti-H. pylori treated patients (Group B) underwent gastroscopy with biopsies of the antrum and corpus for histology (H) and rapid urease test (RUT). In the anti-H. pylori treated group, a 13C-urea breath test (UBT) was also performed. In Group A, H. pylori status was defined as positive or negative when both H and RUT gave concordant positive or negative results. In Group B, the patients were considered eradicated if all three tests were negative. A stool specimen was collected from all patients the day after gastroscopy, and tested by using an enzyme immunoassay commercial kit for detecting H. pylori antigens in feces (HpSAT). Eighty-five patients in Group A (55%) and 44 in Group B (38%) were H. pylori infected. On the whole, HpSAT showed a sensitivity of 94% and specificity of 86%. In Group A and Group B, sensitivity and specificity were 94% versus 93%, and 90% versus 82%, respectively (p < 0.05). HpSAT seems to be a reliable method for predicting H. pylori status in anti-H. pylori untreated patients. Conversely, the test appears less suitable to evaluate the outcome of the eradicating treatment. Consequently, it is likely to be accepted for the primary diagnosis of H. pylori status, particularly in dyspeptic young patients.

Evaluation of a new enzyme immunoassay for detecting Helicobacter pylori in feces: a prospective pilot study

Effects of Helicobacter pylori and Nonsteroidal Anti-Inflammatory Drugs on Peptic Ulcer Disease: A Systematic Review

Autoimmune gastritis (AIG) is a chronic inflammatory condition characterized by immune-mediated destruction of gastric parietal cells, leading to oxyntic atrophy, achlorhydria and hypergastrinemia. While AIG was historically linked to gastric adenocarcinoma and type I neuroendocrine tumors (NETs), recent evidence suggests the risk of adenocarcinoma in AIG is lower than previously believed, particularly in Helicobacter pylori (H. pylori)-negative patients. The increased cancer risk in AIG is mainly attributed to concurrent or past H. pylori infection. The incidence of gastric adenocarcinoma in AIG ranges from 0.12% to 0.5% per year, with cumulative risks over 10 years reported at 1-3%. In contrast, type I NETs are more commonly associated with AIG, with an annual incidence of 0.68-2.8% and cumulative rates as high as 15.3% over 5years. Adenomatous polyps, which can progress to malignancy, have been reported in 4.6-13.6% of AIG patients. This review examines the immune and molecular mechanisms underlying AIG's pathogenesis, positioning it as a model of immune-mediated epithelial injury with limited carcinogenic potential. AIG is associated with reparative metaplastic phenotypes, such as pseudopyloric and complete intestinal metaplasia, which contrast with the more aggressive incomplete intestinal metaplasia observed in H. pylori-induced gastritis. The reduced risk of adenocarcinoma in AIG is attributed to the absence of H. pylori, a T cell-dominated microenvironment, minimal macrophage infiltration and protective factors such as altered gastric microbiota, epigenetic modifications, increased CD3+ intraepithelial cytotoxic T lymphocytes and reduced interleukin-33/interleukin-13 signaling. Although AIG is linked to preneoplastic changes, its primary neoplastic risks include the development of type I NETs and adenomatous polyps, which carry a potential for malignant transformation, necessitating long-term surveillance in patients with hypergastrinemia, extensive atrophy and associated gastric lesions. Challenges persist in distinguishing AIG from other atrophic gastritis types due to limitations in serological and histological markers, but emerging diagnostic tools, such as lymphocyte profiling and molecular assays, promise improved accuracy. This review underscores the importance of tailored surveillance and management strategies to address the distinct neoplastic risks associated with AIG, while advocating for further research into its immune landscape and molecular pathways.

Objective: Autoimmune gastritis (AIG) is characterized by the loss of acid-secreting glands, resulting in hypochlorhydria and hypergastrinemia, conditions that significantly increase the risk of developing gastric neuroendocrine tumors (NETs) and gastric adenocarcinoma. In recent years, AIG has garnered increasing attention in both clinical and research settings. However, comprehensive studies on the clinical and endoscopic characteristics of AIG particularly cases complicated by gastric neoplastic lesions remain limited in China. This study aims to comprehensively summarize the clinical and endoscopic features of AIG and its associated gastric neoplastic lesions. Methods: A retrospective analysis was conducted using medical records from patients with AIG diagnosed at Sichuan Provincial People's Hospital between 2019 and 2024. Data collected included demographic information, medical history, serological test results, imaging findings, and endoscopic observations. The clinical and endoscopic features of AIG patients with gastric NETs or epithelial-derived tumors were compared to those without gastric neoplastic lesions to identify potential risk factors and diagnostic indicators for tumor development in AIG. Results: A total of 72 patients with AIG were included, of whom 62.5% (45/72) were female, with an age range of 30 to 79 years old (mean age: 57±11 years). Parietal cell antibody (PCA) positivity was observed in 93.1% (67/72), intrinsic factor antibody (IFA) positivity in 45.8% (33/72), and Helicobacter pylori (H. pylori) co-infection in 48.6% (35/72). Endoscopically, 84.7% (61/72) showed prominent corpus-dominant advanced atrophy; 47.2% (34/72) had sticky adherent mucus; and 41.7% (30/72) displayed residual oxyntic mucosa in the gastric body or fundus. Only 23.6% (17/72) had normal antrum mucosa, and just 16.7% (12/72) showed a circular wrinkle-like pattern. Gastric neoplastic lesions were identified in 35 patients (48.6%), including 15 cases (20.8%) with NETs and 20 cases (27.8%) with epithelial-derived tumors (four adenocarcinomas, three adenomas, and 13 cases of intraepithelial neoplasia). No significant differences were found between tumor and non-tumor groups in terms of age, gender, PCA/IFA positivity, gastrin levels, anemia status, folic acid, or serum iron levels. However, patients with NETs had significantly lower vitamin B12 levels compared to those without tumors (183±111 ng/L vs. 323±159 ng/L, t=2.47, P=0.042). Additionally, AIG patients with NETs were more likely to be H. pylori-negative compared to both the non-tumor group (66.7% vs. 35.1%, χ2=5.26, P=0.072) and the epithelial-derived tumor group (66.7% vs. 30.0%, χ2=5.80, P=0.055). The incidence of reverse atrophy in the epithelial-derived tumor group was significantly lower than that in the non-tumor group (65.0% vs. 91.9%, χ2=6.49, P=0.011) and the NETs group (65.0% vs. 93.3%, χ2=3.90, P=0.048).​ Conclusion: In AIG patients with NETs, serum vitamin B12 levels are significantly reduced, suggesting that vitamin B12 deficiency may be a key risk factor or clinical indicator for NET development in AIG. Furthermore, NETs are more frequently observed in AIG patients without H. pylori infection, while epithelial-derived tumors are more commonly associated with H. pylori co-infection.

AGA Clinical Practice Update on the Diagnosis and Management of Atrophic Gastritis: Expert Review

Objective: We investigated the risk of gastric cancer among men with Helicobacter pylori (H. pylori) infection or atrophic gastritis (AG) in a 15-year follow-up.Materials and methods: Study population consists of 12,016 men aged 50–65 years at the beginning of the follow-up in 1994–1996. Serum levels of pepsinogen I (SPGI) and antibodies (IgG) to H. pylori (HpAb) were assayed from serums collected in 1994–1996. Incidence of gastric cancer in the study population was assessed in follow-up from 1994 to 2011 by data from the nationwide cancer registry. Based on SPGI and HpAb values, standardized incidence ratios (SIRs) of gastric cancer were calculated in three subgroups, that is, in those with a healthy stomach, those with H. pylori infection but without AG and those with AG. Risk ratios (RR) of gastric cancer were calculated using SIR of subgroups.Results: During 15 years, seven gastric cancers appeared per 79,928 person years among men with healthy stomachs, 50 cancers per 92,533 person years in men with H. pylori infection but without AG, and 8 per 8658 person years in men with AG. Risk ratio (RR) of stomach cancer in men with H. pylori infection was 5.8 (95%CI: 2.7–15.3) compared to men with healthy stomachs, and 9.1 (95%CI: 2.9–30.0) in men with AG. There were no differences in cancer risk between cardia and distal stomach.Conclusions: Risk of gastric cancer is low in men with healthy stomachs. It is significantly increased in those with H. pylori infection and more in those with AG.