Gastric Metabolomics Detects Helicobacter pylori Correlated Loss of Numerous Metabolites in Both the Corpus and Antrum.

Helicobacter pylori is a chronic bacterial pathogen that thrives in several regions of the stomach, causing inflammation that can vary by site and result in distinct disease outcomes. Whether the regions differ in terms of host-derived metabolites is not known. We thus characterized the regional variation of the metabolomes of mouse gastric corpus and antrum organoids and tissue. The uninfected secreted organoid metabolites differed between the corpus and antrum in only seven metabolites as follows: lactic acid, malic acid, phosphoethanolamine, alanine, uridine, glycerol, and isoleucine. Several of the secreted chemicals were depleted upon H. pylori infection in both regions, including urea, cholesterol, glutamine, fumaric acid, lactic acid, citric acid, malic acid, and multiple nonessential amino acids. These results suggest a model in which H. pylori preferentially uses carboxylic acids and amino acids in complex environments, and these are found in both the corpus and antrum. When organoid metabolites were compared to mouse tissue, there was little overlap. The tissue corpus and antrum metabolomes were distinct, including antrum-elevated 5-methoxytryptamine, lactic acid, and caprylic acid, and corpus-elevated phospholipid products. The corpus and antrum remained distinct over an 8-month infection time course. The antrum displayed no significant changes between the time points in contrast to the corpus, which exhibited metabolite changes that were consistent with stress, tissue damage, and depletion of key nutrients, such as glutamine and fructose-6-phosphate. Overall, our results suggest that the corpus and antrum have largely but not completely overlapping metabolomes that change moderately upon H. pylori infection.

Disease Course and Treatment Response of Eosinophilic Gastrointestinal Diseases in Children With Liver Transplantation: Long-Term Follow-Up.

INTRODUCTION: To describe the clinical and laboratory profile, natural course, treatment outcome, and risk factors of posttransplant esophageal and nonesophageal eosinophilic gastrointestinal disorders (EGIDs). METHODS: All children (aged <18 years) who underwent liver transplantation, between 2011 and 2019, in a single transplant center with a follow-up period of 1 year or more posttransplant and with a history of posttransplant endoscopic evaluation were included in this study. RESULTS: During the study period, 89 children met the inclusion criteria. Patients were followed for a median of 8.0 years. A total of 39 (44%) patients were diagnosed with EGID after transplantation. Of these, 29 (33%) had eosinophilic esophagitis (EoE), and 10 (11%) had eosinophilic gastritis, gastroenteritis or enterocolitis. In comparison with the non-EGID group, patients with EGID were younger at transplant (P ≤ 0.0001), transplanted more frequently due to biliary atresia (P ≤ 0.0001), and had higher rates of pretransplant allergy (P = 0.019). In the posttransplant period, they had higher rates of mammalian Target of Rapamycin inhibitor use (P = 0.006), Epstein-Barr virus viremia (P = 0.03), post-transplant lymphoproliferative disease (P = 0.005), and allergen sensitization (P ≤ 0.0001). In regression analysis, young age at transplant, age at diagnosis, pretransplant atopic dermatitis, and post-transplant lymphoproliferative disease were associated with an increased risk of EGID or EoE. Laboratory abnormalities such as anemia (P = 0.007), thrombocytosis (P = 0.012), and hypoalbuminemia (P = 0.031) were more commonly observed in the eosinophilic gastritis, gastroenteritis or enterocolitis group than in the EoE group. Following treatment, most patients had symptomatic resolution at 3 months and histologic resolution at 6 months postdiagnosis. Among the patients who had 5 years of follow-up, none recurred. DISCUSSION: EGID is a common posttransplant diagnosis, which seems to affect patients who are transplanted earlier and who have pretransplant atopy. Posttransplant EGID is responsive to treatment, but as histologic remission occurs after symptomatic resolution, the decision to perform control endoscopy should be delayed.

Role of Th22 cells in Helicobacter pylori-related gastritis and peptic ulcer diseases.

Helicobacter pylori (H. pylori) has been shown to be one of the leading causes of peptic ulcer diseases (PUDs) and gastritis. T helper-22 (Th22) cells and its most important cytokine, interleukin-22 (IL-22) are importantly active in inflammation and inflammatory tissues. Since inflammation is one of the main attributes of infection caused by H. pylori and resulting complications (gastritis and gastrointestinal ulcer), this study was designed to evaluate the Th22 cells count and the IL-22 protein expression in people suffering from PUD and gastritis. The present study was conducted on 55 patients with gastritis, 47 patients with PUD and 48 uninfected subjects. After preparation of section and extraction of protein from antral biopsies, immunohistochemistry and western blot methods were used to evaluate the Th22 cells and IL-22 protein expression level, respectively. According to findings, the Th22 cells count and the IL-22 protein expression level in the infected subjects were siginficantly more than in the uninfected subjects. It should be noted that the Th22 cells count and the IL-22 protein expression level in the infected subjects with PUD were significantly greater than those in the infected subjects with gastritis. In addition, the Th22 cells count had positive correlation with the density of H. pylori, chronic inflammation score and acute inflammatory score in the infected subjects with PUD. The Th22 cells count had positive correlation with the Th17 cells count and inverse correlation with the Treg cells count in the infected subjects with PUD and gastritis. Our data demonstrated that abnormal hyper-activation of Th22 cells as well as its correlation with the Th17 cells during infection caused by H. pylori might damage tissues through immunopathological responses.

Abnormalities in acute salivary biochemical characteristic responses to gustatory stimulation with citric acid in chronic non-atrophic gastritis.

BACKGROUND AND AIM: Salivary characteristics are altered in gastrointestinal diseases and related to oral taste disorder. However, specific salivary biochemical characteristics and their relationships with oral taste disturbances in chronic non-atrophy gastritis (CNAG) remain uncertain. METHODS: Seventy patients with CNAG and 70 subjects in healthy control group (HCG) were enrolled in our study. The levels of salivary flow rate (SFR), pH, salivary α-amylase (sAA) activity, total protein density (TPD), chloride concentration, and calcium concentration were determined before and after citric acid stimulation and compared between CNAG with and without oral taste disturbances. RESULTS: Average body mass index (BMI) of CNAG (17.75 ± 2.08) was lower than that of HCG (21.96 ± 1.72, P < 0.01). Compared with HCG, CNAG showed increased TPD and calcium concentration but decreased SFR both before and after acid stimulation (P < 0.01), as well as reduced sAA and salivary chloride responses to acid stimulation (P < 0.01). Compared with CNAG with normal BMI (24.29%, 17/70), sAA activity response to acid stimulation was reduced in those with low BMI (75.71%, 53/70, P < 0.05). Under resting condition, CNAG with dry mouth (55.71%, 39/70) showed increased SFR and decreased TPD (P < 0.05), as compared with CNAG without dry mouth (44.29%, 31/70). Compared with CNAG without bitter taste (57.14%, 40/70), pH was decreased in those with bitter taste (42.86%, 30/70) under both resting and stimulated conditions (P < 0.05). CONCLUSION: Decreased sAA activity may reflect malnutrition state and be one potential marker of poor digestion, decreased salivary pH may contribute to bitter taste perception, and reduced TPD might be a cause of dry mouth in CNAG.

Eosinophilic Gastrointestinal Disease.

This JAMA Insights Clinical Update discusses the symptoms, diagnosis, and management of eosinophilic gastrointestinal diseases.

Endoscopic and Histological Findings among Israeli Populations Infected with Helicobacter pylori: Does Ethnicity Matter?

BACKGROUND: The prevalence of Helicobacter pylori varies geographically by age, race, and socioeconomic status (SES). However, the impact of ethnicity on endoscopic outcomes in infected individuals is not well known. OBJECTIVES: To assess the impact of ethnicity among Israelis with biopsy-proven H. pylori infection. METHODS: A retrospective study, including patients who underwent gastroscopy and were diagnosed histologically with H. pylori infection, was conducted. Information on demographics, SES, medications, and co-morbidities were extracted from medical records. Univariate (Student's t-test, chi-square test) and multivariate (multinomial and logistic) regression analysis were conducted to examine the predictors of the clinical outcome. RESULTS: The study included 100 Israeli Jews and 100 Israeli Arabs diagnosed with biopsy-proven H. pylori infection. At univariate analysis, the number of households was higher among Arabs (P < 0.001), whose family income and parental education were lower than among Jews (P < 0.001 for both variables). The response to amoxicillin and clarithromycin differed between the two groups, being higher among Jews (P < 0.001).In clinical outcomes (gastritis severity, gastric and duodenal ulcer, intestinal metaplasia, atrophic gastritis, and MALT), no statistically significant differences could be detected between Jews and Arabs. Concerning intestinal metaplasia, lack of consumption of nonsteroidal anti-inflammatory drugs resulted a statistically significant protective factor (odds ratio 0.128, 95% confidence interval 0.024-0.685, P = 0.016). CONCLUSIONS: Although in the literature ethnicity seems to be a risk factor for H. pylori colonization, no statistical significance was detected in various endoscopic and histological findings related to H. Pylori infection between Israeli Arabs and Jews.

The Reduction in Gastric Atrophy after Helicobacter pylori Eradication Is Reduced by Treatment with Inhibitors of Gastric Acid Secretion.

BACKGROUND: Helicobacter pylori (H. pylori) eradication therapy may improve gastric atrophy and intestinal metaplasia, but the results of previous studies have not always been consistent. The aim of this study was to compare the histological changes of intestinal metaplasia and gastric atrophy among the use of acid-suppressing drugs after H. pylori eradication. METHODS: A cohort of 242 patients who underwent successful eradication therapy for H. pylori gastritis and surveillance endoscopy examination from 1996 to 2015 was analyzed. Changes in the histological scores of intestinal metaplasia and atrophy according to drug use (proton-pump inhibitors (PPIs), H2 receptor antagonists (H2RAs), and non-acid suppressant use) were evaluated in biopsies of the antrum and corpus using a generalized linear mixed model in all patients. RESULTS: The mean follow-up period and number of biopsies were 5.48 ± 4.69 years and 2.62 ± 1.67 times, respectively. Improvement in the atrophy scores of both the antrum (p = 0.042) and corpus (p = 0.020) were significantly superior in patients with non-acid suppressant drug use compared with those of PPI and H2RA use. Metaplasia scores in both the antrum and corpus did not improve in all groups, and no significant differences were observed among groups in the antrum (p = 0.271) and corpus (p = 0.077). CONCLUSIONS: Prolonged acid suppression by PPIs or H2RAs may limit the recovery of gastric atrophy following H. pylori eradication.

Is there a possible relationship between gastric intestinal metaplasia and systemic arterial stiffness?

BACKGROUND AND AIM: Helicobacter pylori (H. pylori) is closely associated with pre-neoplastic lesions such as atrophic gastritis (AG) and gastric intestinal metaplasia (GIM). The relationshionship between inflammation, hyperhomocysteinemia and arterial stiffness is of pathophysiological relevance for the development of cardiovascular disease. This study aimed to investigate the relationship between vitamin B12, folic acid, homocysteine (Hcy) and pulse wave velocity (PWV) levels in patients with GIM, AG and non-atrophic non-metaplastic chronic gastritis. PATIENTS AND METHODS: ninety-seven patients with GIM, 67 patients with AG and 69 patients with chronic gastritis were included in the study. Glucose, creatinine, total cholesterol, triglyceride, low-density lipoprotein, cholesterol, high-density lipoprotein cholesterol, vitamin B12, folic acid and Hcy levels were measured by biochemical methods. PWV and other vascular parameters were measured using the Phsyio-port AS device. MAIN RESULTS: PWV was higher in patients with GIM and AG than in controls (p < 0.05 and p < 0.05, respectively). Vitamin B12 levels were significantly lower in patients with GIM and AG than in controls (p < 0.01 and p < 0.01, respectively). Folic acid levels were significantly lower in patients with GIM than in controls (p < 0.05). Hcy levels were significantly higher in patients with GIM and AG than in controls (p < 0.001 and p < 0.05, respectively). A logistic regression analysis showed that GIM, AG and vitamin B12 deficiency were predictors for arterial stiffness. CONCLUSIONS: PWV values increased in patients with GIM and AG compared to non-atrophic non-metaplastic chronic gastritis, without different conventional cardiovascular risk factors.

Can mean platelet volume IndIcate HelIcobacter posItIvIty and severIty of gastrIc InflammatIon? An orIgInal study and revIew of the lIterature.

Helicobacter pylori (H. pylori) is a common problem and a significant cause of chronic gastric inflammation. H. pylori, ongoing gastric inflammation and its severity are the most critical component of precursors of gastric cancer. Hypothetically, every chronic tissue injury activates platelets, and the mean platelet volume (MPV) reflects this action well. The potential relationship between H. pylori and platelet count has been shown before. However, there are few and conflicting papers about the relationship between MPV and H. pylori related chronic gastric inflammation and its severity. The study aimed to assess any potential relationship between MPV and presence of H. pylori, as well as the severity of chronic gastric inflammation. A total of 6890 endoscopic reports were initially evaluated, and a total of 218 dyspeptic patients having undergone upper endoscopy were included. Of these, 118 (54.2%) were H. pylori positive and 100 (45.8%) were H. pylori negative. At least four gastric biopsies were obtained and evaluated according to Sydney classification. Age, gender, hemoglobin, mean corpuscular volume, ferritin, serum iron and C-reactive protein, as well as endoscopic findings were also recorded. A p<0.05 was accepted as significant. The MPV and platelet count did not differ between H. pylori positive and H. pylori negative groups of patients (p>0.05). There were no differences and correlation between MPV and gastric inflammation severity according to Sydney classification (p>0.05). When stratifying MPV as <9.15 fL and >9.15 fL, there was no difference between H. pylori positive and H. pylori negative groups either (p>0.05). In this study, we found no relationship between MPV and presence of H. pylori or severity of gastric inflammation. Although there are still conflicting publications on this issue, in our opinion and according to the results of this study, MPV is not a suitable marker for evaluation of gastric inflammation severity, being H. pylori either positive or negative.

Nonesophageal Eosinophilic Gastrointestinal Disorders: Clinical Care and Future Directions.

Eosinophilic gastrointestinal disorders are a set of conditions with a wide range of clinical manifestations and treatment modalities. The disorders are suspected to result from an abnormal inflammatory response to allergen (s), and individuals may develop a relapsing or chronic disease, if the allergen is not eliminated. Mechanisms of disease pathogenesis, including the humoral immune response, need to be fully elucidated. A variety of therapies are used, although there is a lack of well-defined randomized, prospective studies. Other therapeutic options are needed as the current treatments have potential concerns; elimination diets may impair a child's quality of life, and corticosteroids have adverse risks with long-term use. We review what is known about nonesophageal eosinophilic gastrointestinal disorders, and discuss research investigations which need to be conducted to facilitate diagnosis and enhance treatment methods.

Pediatric Collagenous Gastritis and Colitis: A Case Series and Review of the Literature.

INTRODUCTION: Collagenous gastritis is a rare disease characterized by the subepithelial deposition of collagen bands. Two phenotypes of the disease have been described: a pediatric-onset and an adult-onset type. The adult-onset form is associated with collagenous colitis and autoimmune disorders. No effective treatment has been identified to date. OBJECTIVE: We aim to describe the clinical features and outcomes of patients in our cohort and provide a summary of published pediatric cases with collagenous gastritis and colitis reported to date to gather information that will contribute to improved knowledge of this rare condition. METHODS: A retrospective chart review of all patients with collagenous gastritis and/or colitis who were treated at the Royal Children's Hospital, Melbourne, was performed. A literature review was also conducted. RESULTS: A total of 12 cases of collagenous gastritis were reviewed. Three of 12 (25%) patients had associated collagenous colitis. The most common clinical presentation was iron deficiency anemia. Nine (75%) patients were followed up, and repeat endoscopies were performed in 8 (67%). Iron deficiency anemia resolved in all patients on oral iron supplementation. Histologic improvement was only identified in one patient with the adult phenotype who had been treated with oral corticosteroids and azathioprine. CONCLUSIONS: Collagenous gastritis is a rare condition in children. A small proportion of children develop features of the "'adult" phenotype at a very young age. Patients with collagenous gastritis require long-term follow-up and monitoring of their disease. Further randomized clinical trials are needed to establish an effective therapeutic strategy.

Impact on Health-Related Quality of Life in Adults with Eosinophilic Gastritis and Gastroenteritis: A Qualitative Assessment.

BACKGROUND: Eosinophilic gastritis (EG) and eosinophilic gastroenteritis (EGE) are chronic immune-mediated conditions of the digestive tract, which affect the stomach only, or the stomach and small intestines, respectively. Though these disorders are uncommon, they are being increasingly recognized and diagnosed. While health-related quality of life (HRQOL) has been evaluated in other eosinophilic gastrointestinal diseases, this study is the first to describe HRQOL impacts unique to EG/EGE. AIMS: This study aims to qualitatively describe experiences of adults diagnosed with EG and EGE. We aim to identify impacts on HRQOL in this population in order to inform clinical care and assessment. METHODS: Seven patients diagnosed with EG or EGE participated in semi-structured interviews assessing common domains of HRQOL. RESULTS: Four distinct themes emerged from qualitative analyses, which represent impacts to HRQOL: the psychological impact of the diagnosis, impact on social relationships, financial impact, and impact on the body. These generally improved over time and with effective treatment. CONCLUSIONS: This study demonstrated that patients with EG/EGE experience impacts to HRQOL, some of which differ from HRQOL of other eosinophilic gastrointestinal diseases. These results support the development of a disease-specific measure, or adaptation of an existing measure, to assess HRQOL in EG/EGE.

Eosinophilic Gastrointestinal Diseases in Childhood.

Eosinophilic gastrointestinal diseases (EGIDs) comprise a group of chronic, inflammatory diseases of the gastrointestinal (GI) tract, that are characterized, clinically, by symptoms related to the dysfunction of the involved segment(s) of the GI tract, and histologically, by dense eosinophilic inflammation, in the absence of an identifiable secondary cause. The group of EGIDs comprises eosinophilic esophagitis (EoE), eosinophilic gastritis (EG), eosinophilic gastroenteritis (EGE), and eosinophilic colitis (EC). EoE is the most common and the best described EGID compared to EG, EGE, and EC. The clinical presentation of the EGIDs differs depending on the location and the extent of the eosinophilic infiltration in the GI tract, as well as its depth through the bowel wall. In the absence of biological markers, the diagnosis is based on the combination of clinical symptoms with the histological features of EGIDs, after the exclusion of secondary causes of eosinophilic inflammation of the GI tract. Treatment is individualized and includes elimination diets (mainly empiric or elemental) and/or drugs, according to the involved GI segment: proton pump inhibitors or local steroids in EoE; local or oral systemic steroids in EG/EGE limited to the duodenum; oral systemic steroids in EGE with lower small intestine and/or colon involvement. In patients with EoE, maintenance treatment with lower doses may be considered following histological remission with the means of drugs. In patients treated with elimination diets, disease food triggers identified during food reintroduction need to be further eliminated. Esophageal stenosis despite medical treatment requires endoscopic dilation, while the use of thiopurines or anti-TNF drugs may be considered in refractory or steroid-dependent EGID (other than EoE). The aim of this review is to provide the available evidence on each of the above disorders, to aid clinicians to interpret the clinical manifestations and the laboratory findings and choose the best available treatment option.

Interleukin-17C in Human Helicobacter pylori Gastritis.

The interleukin-17 (IL-17) family of cytokines (IL-17A to IL-17F) is involved in many inflammatory diseases. Although IL-17A is recognized as being involved in the pathophysiology of Helicobacter pylori-associated diseases, the role of other IL-17 cytokine family members remains unclear. Microarray analysis of IL-17 family cytokines was performed in H. pylori-infected and uninfected gastric biopsy specimens. IL-17C mRNA was upregulated approximately 4.5-fold in H. pylori-infected gastric biopsy specimens. This was confirmed by quantitative reverse transcriptase PCR in infected and uninfected gastric mucosa obtained from Bhutan and from the Dominican Republic. Immunohistochemical analysis showed that IL-17C expression in H. pylori-infected gastric biopsy specimens was predominantly localized to epithelial and chromogranin A-positive endocrine cells. IL-17C mRNA levels were also significantly greater among cagA-positive than cagA-negative H. pylori infections (P = 0.012). In vitro studies confirmed an increase in IL-17C mRNA and protein levels in cells infected with cagA-positive infections compared to cells infected with either cagA-negative or cag pathogenicity island (PAI) mutant. Chemical inhibition of IκB kinase (IKK), mitogen-activated protein extracellular signal-regulated kinase (MEK), and Jun N-terminal kinase (JNK) inhibited induction of IL-17C proteins in infected cells, whereas p38 inhibition had no effect on IL-17C protein secretion. In conclusion, H. pylori infection was associated with a significant increase in IL-17C expression in human gastric mucosa. The role of IL-17C in the pathogenesis of H. pylori-induced diseases remains to be determined.

The importance of TH22 and TC22 cells in the pathogenesis of Helicobacter pylori-associated gastric diseases.

BACKGROUND: An association exists between Helicobacter pylori (H. pylori), peptic ulcers, gastritis, and sometimes gastric carcinomas. Th22 cells have protective and inflammatory roles in defense against microbes. AIM: We investigated the frequencies of Th22, Tc22, Th22/17, and Tc22/17 cells in addition to the changes in levels of cytokines IL-22, IL-6, IL-23, TNF-α, IL-1ß, and TGF-ß in sera from patients with H. pylori-associated gastritis, and peptic ulcer, and in uninfected patients. METHODS: A total of 76 patients with H. pylori-associated disorders formed the studied group. Frequencies of T-cell subsets were determined by flow cytometry. Levels of cytokines IL-22, IL-6, IL-23, TNF-α, IL-1ß, and TGF-ß in the sera and supernatants of patients were measured by ELISA and flow cytometry. RESULTS: The study participants included 32 males and 44 females with a mean age of 38.5±15.3 years. We divided the infected group into peptic ulcer and gastritis (mild, moderate, active chronic, and chronic). The frequencies of Th22, Tc22, and Tc22/17 increased significantly in the peptic ulcer, moderate, active chronic, and chronic gastritis groups compared to the uninfected group. Th22/17 only increased significantly in the chronic gastritis group. We observed significant increases in IL-22 in the moderate and active chronic gastritis, IL-23 in the active chronic and chronic gastritis, and TNF-α in the peptic ulcer and moderate gastritis groups. Following in vitro antigenic stimulation, we observed significantly higher levels of IL-1ß, IL-23, and IL-6 in the active chronic gastritis group, as well as IL-6 and IL-1ß in the chronic gastritis group compared to the uninfected group. CONCLUSION: Increased Th22, Tc22, and Tc22/17 cells and IL-22 levels appear to be influential in progression and severity of H. pylori infection. Th22/17 can be an interesting therapeutic target for chronic H. pylori infections where eradication is more difficult.

No evidence of a role for mitochondrial complex I in Helicobacter pylori pathogenesis.

BACKGROUND: Complex I is the first enzyme complex in the mitochondrial respiratory chain, responsible for generating a large fraction of energy during oxidative phosphorylation. Recently, it has been identified that complex I deficiency can result in increased inflammation due to the generation of reactive oxygen species by innate immune cells. As a reduction in complex I activity has been demonstrated in human stomachs with atrophic gastritis, we investigated whether complex I deficiency could influence Helicobacter pylori pathogenesis. MATERIALS AND METHODS: Ndufs6gt/gt mice have a partial complex I deficiency. Complex I activity was quantified in the stomachs and immune cells of Ndufs6gt/gt mice by spectrophotometric assays. Ndufs6gt/gt mice were infected with H. pylori and bacterial colonization assessed by colony-forming assay, gastritis assessed histologically, and H. pylori -specific humoral response quantified by ELISA. RESULTS: The immune cells and stomachs of Ndufs6gt/gt mice were found to have significantly decreased complex I activity, validating the model for assessing the effects of complex I deficiency in H. pylori infection. However, there was no observable effect of complex I deficiency on either H. pylori colonization, the resulting gastritis, or the humoral response. CONCLUSIONS: Although complex I activity is described to suppress innate immune responses and is decreased during atrophic gastritis in humans, our data suggest it does not affect H. pylori pathogenesis.

Impaired Interoception in a Preclinical Model of Functional Dyspepsia.

INTRODUCTION: The etiologies of functional dyspepsia symptoms, including postprandial distress syndrome, remain unknown. We tested the hypothesis that neonatal colon inflammation induces postprandial distress syndrome-like symptoms in adult life that associate with increased activation of vagal afferent pathways and forebrain limbic regions. RESULTS: These rats showed a significant decrease in nutrient meal consumption to satiety after an overnight fast, decrease in gastric emptying, decrease in total distance traveled, and decrease in percent distance traveled in midfield versus control rats in open field test, indicating postprandial anxiety- and depression-like behaviors. Adult naïve rats treated with oral iodoacetamide to induce H. pylori-like mild gastritis demonstrated similar postprandial effects as the above rats. CONCLUSIONS: We concluded that neonatal colon inflammation is a risk factor for the development of postprandial distress syndrome-like symptoms. While mild gastritis can induce symptoms similar to those of neonatal colon inflammation, gastritis in these rats does not worsen the symptoms.

[Chronic gastritis: Instructions for use of medications]. / Khronicheskii gastrit: instruktsii po primeneniiu lekarstvennykh preparatov.

The paper highlights the features of drug use in the legal aspect. It analyzes instructions for medical use of proton pump inhibitors (PPIs) and gastric protective agents. Taking into account the characteristics of indications registered in the instruction, the authors discuss the possibility of using various PPIs. The instruction for medical application is an official document approved by the Ministry of Health, the basis of which is the data of trials carried out by a manufacturer, and it should be a key or fundamental source for a physician in choosing a medication. The use of a drug with no indications given in the manual (the so-called 'off-label' use in foreign practice), is a clinical trial of a sort conducted by a physician individually, by taking upon himself/herself a legal liability. If arguments break out over the correct choice of this or that drug in treating the specific patient, the instruction containing the indications for use of specific medications to treat a specific disease is one of the proofs that the physician has correctly chosen the drug or a criterion for skilled medical care. The inclusion of chronic gastritis as a primary and only diagnosis into the primary documentation substantially limits the possibilities of using PPIs. When a PPI is indicated for therapy of erosive gastritis, a formal rationale is contained only in the instruction for use of Controloc. There are no registered indications for PPI use to treat chronic non-erosive gastritis; the gastric protective agent Rebagit is indicated.

Relationships between autonomic nerve function and gastric emptying in patients with autoimmune gastritis.

PURPOSE: Autonomic nervous system dysfunction exists in autoimmune diseases. Symptoms of autoimmune gastritis are not specific, and some patients may present symptoms suggestive of delayed gastric emptying. This study aims to investigate whether any autonomic dysfunction exists in autoimmune gastritis patients, and if so, to clarify the relationship between the autonomic nervous dysfunction, delayed gastric emptying, and gastrointestinal symptoms. METHODS: 75 patients (50 women, mean age 56.73 ± 11.77) diagnosed with autoimmune gastritis were investigated by means of autonomic nervous system and gastric emptying tests. All patients underwent a standardized scintigraphic gastric emptying study and five tests evaluating autonomic nervous system. Patients with autonomic nervous system dysfunction were then analyzed and compared by means of existence of delayed gastric emptying and gastrointestinal symptoms. RESULTS: 62 patients had autonomic nervous system dysfunction (14 mild, 40 moderate, and 8 severe autonomic dysfunction). The mean total score of autonomic tests was 3.85 ± 2.35. Total autonomic score of patients (n = 60) with delayed gastric emptying was significantly higher than patients (n = 15) with normal gastric emptying (4.68 ± 1.7 vs. 1.53 ± 0.58, p < 0.001). Mean gastroparesis cardinal symptom index was significantly higher in patients (n = 60) with delayed gastric emptying half-time compared to patients (n = 15) with normal gastric emptying half-time (1.89 ± 1.16 vs 0.4 ± 0.3, p < 0.001). CONCLUSIONS: Most of patients with autoimmune gastritis also have autonomic nerve dysfunction. There is a close relationship between autonomic nervous system dysfunction and delayed gastric emptying. Gastroparesis cardinal symptom index has a high sensitivity and specificity in predicting both autonomic nerve function and delay in gastric emptying.