Search Results (6)

Objectives: Gastroesophageal reflux disease (GERD) is commonly encountered in adults and children. A subset of patients with GERD are refractory to acid suppressants, implicating other factors in the refluxate. Duodenogastric reflux (DGR) produces similar symptoms through reflux of non-acidic duodenal content and the cytotoxic effect of bile in the esophageal mucosa. Various methods have been utilized to detect DGR using a Bilitec device or Hepatobiliary scintigraphy, amongst the most common, each with their own limitations. We aimed to use combined multichannel intraluminal impedance and pH (MII-pH) monitoring with an additional gastric pH sensor to collect information about acidic and non-acidic gastroesophageal refluxes and to assess whether continuous gastric pH measurement in children provides indirect evidence of DGR for better understanding of the symptoms. Methods: From 2022 through 2023, clinically symptomatic pediatric patients scheduled for esophagogastroduodenoscopy (EGD) and MII-pH at Arnold Palmer Hospital for Children in the United States were included (n = 26). Exclusions included patients taking acid suppressants prior to the start of this study. The data were analyzed for subjects completing at least 18 h of the study protocol. Results: Subjects with a normal pH impedance (n = 5) showed a median non-meal gastric pH of 1.8. Subjects with an abnormal pH impedance (n = 21) showed a median non-meal gastric pH of 2.2. Of the 26 subjects enrolled, the duration of non-meal gastric pH 4.0–7.0 was positively correlated with non-acidic gastroesophageal refluxes. Although all acidic reflux events occurred at gastric pH < 4.0, there was no correlation between the duration of non-meal gastric pH < 4.0 and impedance changes or reflux index. Conclusions: The results showed daily variability in the non-meal gastric pH of pediatric patients and a statistically significant correlation between its duration at pH 4.0 to 7.0 and non-acidic refluxes suggestive of the implication of DGR. Further research is required to assess this association with gastroesophageal reflux and dyspeptic symptoms to investigate the diagnostic tools and therapeutic interventions, including the role of prokinetics and surface protective agents for DGR. Full article

Gastroesophageal reflux disease (GERD) has the highest prevalence among diseases of the digestive system and is characterized by a significant decrease in patients’ quality of life, comparable to arterial hypertension and coronary heart disease. One in every ten cases of reflux esophagitis leads to the formation of Barrett’s esophagus, which is associated with a high risk of esophagus adenocarcinoma. The key factors determining the progression of the disease are the frequency and duration of the reflux of the stomach’s contents. As a result, refluxate, which includes hydrochloric acid, pepsin, and, in the case of concomitant duodeno-gastric reflux, bile acids and lysolecithin, is thrown into the overlying sections of the digestive tract. At the same time, in addition to aggression factors, it is necessary to take into account the state of resistance in the esophageal mucosa to the effects of aggressive refluxate molecules. This review was prepared using systematized data on the protective properties of the esophageal mucosa and modern methods to assess the mucosal barrier in reflux esophagitis. Lesions of the epithelial barrier structure in the esophagus are recognized as the main pathogenetic factor in the development of reflux esophagitis and are a potentially significant therapeutic target in the treatment of GERD and Barrett’s esophagus. This article presents the characteristics of the esophageal mucosal barrier and the protective mechanisms of the esophagus’s mucous membrane in conditions of gastroesophageal reflux. Diagnostic approaches for assessing the course of reflux esophagitis are described for both histological criteria and the possibility of a comprehensive assessment of the state of mucins, tight-junction proteins, and the proliferative activity of the mucosa, including under the conditions of ongoing therapy. Full article

This article systematizes available data from the literature on biliary gastritis (BG) in order to increase the awareness of specialists about the latest possibilities for diagnosing the disease. BG occurs as a result of pathological duodenogastric reflux. In patients with a preserved duodenogastric junction, the dominant factor is represented by motor disorders of the upper digestive tract (primary biliary gastritis), while in patients recovering from surgical interventions it is represented by structural changes (secondary biliary gastritis). Progressive BG can lead to atrophy of the gastric mucosa, intestinal metaplasia, epithelial dysplasia, and eventually to gastric cancer. Diagnostic methods for BG are carried out to identify risk factors, exclude alarm symptoms and identify persistent motor disorders and pathological reflux (24 h pH-impedancemetry, hepatobiliary scintigraphy, 24 h monitoring of bilirubin content in the reflux using a Bilitec 2000 photometer), as well as to diagnose gastritis itself (esophagogastroduodenoscopy, morphological gastrobiopsy examination). The diagnosis of BG should be based on a multidisciplinary approach that combines a thorough analysis of a patient’s complaints, an anamnesis of the disease, and the results of endoscopic and histological research methods. Full article

Duodenogastric reflux (DGR) causes bile reflux gastritis (BRG) and may develop into gastric cancer. DGR is classified as primary in non-operated stomachs or secondary to surgical intervention. Primary DGR and Helicobacter pylori (H. pylori) infection are reportedly related. However, the mechanism is not fully understood. This study aimed to elucidate the relationship between H. pylori infection and pyloric incompetence in a non-operated stomach. A total of 502 non-operated participants who underwent an upper intestinal endoscopy were prospectively enrolled. Endoscopic findings (EAC, endoscopic atrophy classification; nodular gastritis; xanthoma; fundic gland polyp; and incompetence of pylorus), sex, age, gastrin, pepsinogen (PG) I and PG II levels were evaluated. PG I/PG II ratio, anti-H. pylori-Ab positivity, and atrophic gastritis status were significantly different between the normal and incompetent pylori (p = 0.043, <0.001, and 0.001, respectively). Open-type atrophic gastritis was significantly higher in the incompetent pylori. Incompetence of the pylorus and EAC were moderately correlated (Cramer’s V = 0.25). Multivariate analysis revealed that the presence of anti-H. pylori-Ab was the only independent factor associated with the incompetence of the pylorus, with an adjusted odds ratio of 2.70 (95% CI: 1.47–4.94, p = 0.001). In conclusion, pyloric incompetence was associated with H. pylori infection and moderately correlated to the severity of atrophic gastritis in non-operated stomachs. Full article

Epidemiological, clinical, and biological studies convincingly demonstrate that chronic inflammation predisposes to the development of human cancers. In digestive organs, inflammation-associated cancers include colitis-associated colorectal cancers, Helicobacter pylori-associated gastric cancer, as well as Barrett’s esophagus and esophageal adenocarcinoma associated with chronic duodenogastric-esophageal reflux. Cancer is a genomic disease, and stepwise accumulation of genetic and epigenetic alterations of tumor-related genes leads to the development of tumor cells. Recent genome analyses show that genetic alterations, which are evoked by inflammation, are latently accumulated in inflamed epithelial cells of digestive organs. Production of reactive oxygen and aberrant expression of activation-induced cytidine deaminase, a nucleotide-editing enzyme, could be induced in inflamed gastrointestinal epithelial cells and play a role as a genomic modulator of inflammation-associated carcinogenesis. Understanding the molecular linkage between inflammation and genetic alterations will open up a new field of tumor biology and provide a novel strategy for the prevention of inflammation-associated tumorigenesis. Full article

Background and Objectives: Although there are many studies that investigate the relationship between duodenogastric reflux (DGR) and Helicobacter pylori in adult patients, the reported data are contradictory. In addition, there are very few studies in the literature investigating the relationship between DGR and H. pylori in the pediatric age group. In the present study, we investigated the effect of primary DGR on H. pylori and gastritis. Materials and Methods: A total of 361 patients who were referred to the clinic of our hospital with dyspeptic complaints who had an upper gastrointestinal system endoscopy and a gastric biopsy were included in the study. Results: DGR was detected in 45 cases, and 316 cases that did not have DGR were considered as the control group. Comparisons were made between the DGR cases and the control group in terms of risk factors (age, gender), the presence and density of H. pylori, and the presence and severity of gastritis. The average age of the patients who were included in the study was 11.6 ± 4.6 years. A total of 128 (36%) of the cases were male and 233 (64%) were female. DGR was present in 45 (13%) of the cases. The average age of the patients with DGR was 13.9 ± 3.1 years, the average age of the control group was 11.3 ± 4.7, and there were statistically significant differences (p < 0.001). No significant differences were detected in terms of gender between DGR and the control group (p > 0.05). H. pylori (+) was detected in 29 (64%) of patients with DGR, and in 202 (64%) of the control group. No significant differences were detected between H. pylori prevalence (p = 0.947). Gastritis was detected in 37 (82%) of the patients with DGR, and in 245 (77%) of the control group (p = 0.476). No significant differences were detected between the presence and density of H. pylori, gastritis presence, severity and DGR (p > 0.05). Conclusions: The ages of patients with DGR were significantly higher than in the control group, and advanced age was shown to be a risk factor for primary DGR. It was found that the presence of DGR has no effect on the presence and severity of H. pylori. Given this situation, we consider it is important to eradicate H. pylori infection, especially in the case where H. pylori is present together with DGR. Full article