Gastritis In Children Research Articles

Autoimmune gastritis in children with autoimmune diseases

The results of inspection of 70 children for autoimmune gastritis are represented. Children with blood serum antibodies to stomach parietal cells were selected for more profound investigation. It was shown, that autoimmune gastritis in the childhood is one of the components of multiorgan autoimmune pathology in 0-33 % of patients and is characterized by minimum clinical, morphological and endoscopic data, combination with Helicobacter pylori.

Клініко-імунологічні аспекти пробіотичної терапії хронічних НР-асоційованих гастритів у дітей

У статті наведені результати дослідження продукції НВD2 у слизовій оболонці шлунка при хронічних НP-асоційованих гастритах у дітей до та після антихелікобактерної терапії з включенням пробіотичного штаму E.coli Nissle 1917.

Su1859 Eosinophilic Gastritis in Children: Clinicopathological Correlation, Disease Course, and Response to Therapy

Su1859 Eosinophilic Gastritis in Children: Clinicopathological Correlation, Disease Course, and Response to Therapy

The Clinical Significance of Focally Enhanced Gastritis in Children

Focally enhanced gastritis (FEG) was initially described in patients with inflammatory bowel disease (IBD), but subsequent reports found this to be a nonspecific finding in adults. Initial reports suggest that FEG may be more predictive of IBD in pediatric patients, but this has yet to be confirmed. The aim of our study was to characterize and determine clinical correlates of FEG in pediatric patients. Gastric biopsies from pediatric patients who were diagnosed with FEG at a single tertiary care center over a 5-year period were reviewed (5-y cohort study). In a subsequent study, all gastric biopsies from pediatric patients in the single center over a 1-year period were reviewed. Biopsies were reviewed in a blinded manner by 2 pathologists, and histologic data of interest were recorded. Clinical data and follow-up data were recorded from review of the electronic medical records. Of the 25 patients with FEG in the 5-year cohort study, IBD was present in 19 (76%) patients. Crohn disease (CD) was more common than ulcerative colitis (UC) among these patients (68% vs. 16%). In the 1-year review study with 262 gastric biopsies, FEG was present in 31 (11%) cases. Patients with FEG were significantly more likely to have IBD than non-FEG patients (61.3% vs. 11.6%, P≤0.001). Of the 19 patients with FEG and IBD, 9 patients had CD, 9 patients had UC, and 1 had indeterminate colitis. The presence of FEG is highly associated with IBD in pediatric patients. The presence of FEG does not reliably distinguish between patients with CD and those with UC.

Імуноморфологічні особливості змін локального імунного гомеостазу слизової оболонки шлунка при хронічних НР-асоційованих гастритах у дітей після ерадикаційної терапії

У статті наведені результати стандартного морфологічного, імуногістохімічного дослідження біоптатів слизової оболонки шлунка та визначення бета-дефензину-2 у дітей, хворих на хронічний НР-асоційований гастрит, з урахуванням CagA-статусу, до та після антихелікобактерної терапії, модифікованої холекальциферолом. Продемонстровано підвищення ефективності комплексного лікування завдяки протизапальному, імуномодулюючому, антипроліферативному ефектам холекальциферолу.

Бета-дефензини у локальному антихелікобактерному захисті слизової оболонки шлунка в дітей

У статті наведені дані дослідження продукції місцевих факторів уродженого мукозального захисту — бета-дефензинів при хронічних НР-асоційованих гастритах у дітей.

The Significance of Small Intestinal Epithelium in Gastric Antral Biopsies in Children

Intestinal metaplasia of the gastric antrum is common in adults with chronic gastritis and occurs in Helicobacter -associated gastritis in children. This study examined the frequency and clinical correlates of intestinal epithelium in 1690 consecutive antral biopsies obtained from children over a 2-year period in a tertiary pediatric care facility. Intestinal epithelium in gastric glands not associated with overlying villi was present in 22 (1.3%) biopsies. These came from 20 patients, 2-17 years of age, none of whom had clinical or histologic evidence of Helicobacter infection or significant chronic gastritis. Eight (40%) had an antral pancreatic rest, 8 had some other localized antral abnormality, and 4 were endoscopically normal. Four additional patients with a pancreatic rest had no intestinal epithelium. Six surgically resected rests and 2 rests found at autopsy were also reviewed. Heterotopic intestinal epithelium was present in 1 of the 2 postmortem specimens but was absent from all 6 surgically resected lesions. No intestinal epithelium was present in 67 antral biopsies with Helicobacter gastritis observed during this same period. Although the intestinal epithelium in these patients could be metaplastic, it more likely represents inadvertent sampling of the gastroduodenal junction induced by a lesion in the distal antrum or a focus of heterotopic epithelium and might best be addressed in the surgical pathology report by a comment to this effect. The distinction from metaplasia is more than semantic, because a diagnosis of intestinal metaplasia can have adverse clinical implications and should be made with caution in a child.

Relationship between Helicobacter pylori detection and an increased risk of infection in childhood

The risk of developing gastric cancer is believed to be related to differences among Helicobacter pylori strains and the inflammatory responses mediated by host genetic factors. H. pylori infection is acquired at an early age and in the absence of appropriate antibiotic therapy, it generally persists for life. Tp53 gene regulates the transcription of several cytokines and chemokines involved in innate immunity and its action may be influenced by the presence of different H. pylori strains. The present study aimed to detect H. pylori in pediatric patients, to access Tp53 polymorphism at codon 72 and to correlate such findings with age and histopathological results. Three hundred and forty-two patients were analyzed. DNA from their gastric biopsies was extracted and the detection of H. pylori was performed through polymerase chain reaction assays, urease test and histopathologic examination. Allelic discrimination of SNP rs1042522 (Tp53) was performed by real-time polymerase chain reaction. Our results suggest a possible relationship between the presence of H. pylori and chronic gastritis in children and young patients, and showed a significant association between ageing and positivity for H. pylori. It was verified that patients aged < 10 years were 1.3 times more likely to have infection by H. pylori when compared with those aged > 10 years. Finally, no association was found between Tp53 polymorphisms and the presence of H. pylori.

A regulatory instead of an IL-17 T response predominates in Helicobacter pylori-associated gastritis in children

Th17 cells seem to have an important role in the efficacy of vaccines against Helicobacter pylori. Because children are a target group for human vaccination and Th17/Treg cells have intrinsically linked and antagonic commitments, we compared the gastric levels of Th17- and Treg-associated cytokines of children and adults. IL-6, IL-10 and TGF-β1 levels and Foxp3+ cell numbers were higher, but IL-1β, IL-17A and IL-23 were lower in infected children than in infected adults. In conclusion Treg instead of Th17 cell response to H. pylori-infection predominates in children.

Gastric phenotype in children with Helicobacter pylori infection undergoing upper endoscopy

Introduction. Helicobacter pylori is a definite risk factor for the development of gastric cancer, especially in the context of corpus-predominant gastritis. The infection is usually acquired in early childhood, implying lifelong exposure to this carcinogen if untreated. Our objective was to analyze the prevalence of H. pylori induced corpus-predominant gastritis in children. Material and methods. We analyzed the results of 265 esophagogastroduodenoscopies (EGD) in children performed between February 2006 and August 2008; 34 endoscopies were excluded (24 with follow-up investigations, 5 with incomplete data, 5 adults). H. pylori gastritis was defined by the presence of H. pylori in histology or by a positive rapid urease test. Grade of inflammation was rated according to the updated Sydney Scoring System. Gastritis was classified as corpus-predominant when the degree of chronic inflammation was higher in the corpus than in the antrum and vice versa for antrum-predominant gastritis. Results. Two hundred thirty-one patients (128 female; mean age ± SEM: 10.5 ± 3.5 years) were analyzed. Eighty-four (36%) were H. pylori positive, 147 (64%) patients were negative for H. pylori. In H. pylori positive patients, 39 (46%) patients had pangastritis (one patient with mucosal atrophy, which is regarded as precancerous lesion), 42 (50%) had antrum-predominant gastritis and 3 (4%) had corpus-predominant gastritis. One female patient (15.6 years old) with severe (grade 3) pangastritis had focal mucosal atrophy in both antrum and corpus, but no patient had intestinal metaplasia. Conclusions. Corpus-predominant gastritis develops in H. pylori infected children, while mucosal atrophy and intestinal metaplasia develop later in the course of the infection.

Analysis of Gene Expression in Helicobacter pylori-associated Nodular Gastritis in Children Using Microarray

Purpose: Nodular gastritis is a characteristic finding of Helicobacter pylori infection in children. The aim of this study was to evaluate the difference in gene expression in the gastric mucosa of H. pylori-infected and non-infected children, and to analyze the difference in gene expression using cDNA microarray analysis of nodular gastritis caused by H. pylori infection. Methods: Twelve children (6 boys and 6 girls; mean age 9.8 years) who underwent upper gastrointestinal endoscopy and biopsy at Seoul National University Bundang Hospital were included in the study. The subjects were divided into three groups according to the presence of H. pylori infection and nodular gastritis on endoscopic examination. Gastric mucosa tissue was kept at −70 o C and RNA was extracted to perform cDNA microarray analysis in each patient. Results: cDNA microarray analysis in children revealed a clear distinction between H. pylori-infected and non-infected gastric mucosa. Specifically, 182 over-expressed genes and 29 under-expressed genes were identified in H. pylori-infected gastric mucosa compared to non-infected mucosa. H. pylori-infected nodular gastritis revealed different gene expression patterns from H. pylori-infected normal gastric mucosa; five genes were over-expressed and five genes were under-expressed. Conclusion: In the presence of H. pylori infection, gastric mucosa shows distinct differences in gene expression, and nodular gastritis with H. pylori infection in children may be associated with over- or under-expression of some genes. Further studies are required to clarify the host response and the pathogenesis of nodular gastritis in children. (Korean J Pediatr Gastroenterol Nutr 2010; 13: 7∼22)

Helicobacter pylori Promotes the Production of Thymic Stromal Lymphopoietin by Gastric Epithelial Cells and Induces Dendritic Cell-Mediated Inflammatory Th2 Responses

Helicobacter pylori colonizes the stomach and induces strong, specific local and systemic humoral and cell-mediated immunity, resulting in the development of chronic gastritis in humans. Although H. pylori-induced chronic atrophic gastritis is characterized by marked infiltration of T helper type 1 (Th1) cytokine-producing CD4(+) T cells, almost all of the inflamed gastric mucosae also contain focal lymphoid aggregates with germinal centers. In addition, typical H. pylori-induced chronic gastritis in children, called follicular gastritis, is characterized by B-cell follicle formation in the gastric mucosa. The aim of this study was to examine whether thymic stromal lymphopoietin (TSLP), an epithelial-cell-derived cytokine inducing a dendritic cell (DC)-mediated inflammatory Th2 response, is involved in Th2 responses triggering B-cell activation in H. pylori-induced gastritis. Here, we show that H. pylori triggered human gastric epithelial cells to produce TSLP, together with the DC-attracting chemokine MIP-3alpha and the B-cell-activating factor BAFF. After DCs were incubated with supernatants from H. pylori-infected epithelial cells, the conditioned cells expressed high levels of costimulatory molecules, such as CD80, and triggered naïve CD4(+) T cells to produce high levels of the Th2 cytokines interleukin-4 and interleukin-13 and of the inflammatory cytokines tumor necrosis factor alpha and gamma interferon. In contrast, after incubation of the supernatants with the neutralizing antibodies to TSLP, the conditioned DCs did not prime T cells to produce high levels of Th2 cytokines. These results, together with the finding that TSLP was expressed by the epithelial cells of human follicular gastritis, suggest that H. pylori can directly trigger epithelial cells to produce TSLP. It also suggests that TSLP-mediated DC activation may be involved in Th2 responses triggering B-cell activation in H. pylori-induced gastritis.

Helicobacter pylori increases expression of proapoptotic markers Fas and FasL on CD4 lymphocytes in children.

The pathomechanism of Helicobacter pylori action upon gastric mucosa and its role in the pathogenesis of gastritis have not been fully elucidated. The aim of this study was to evaluate the most prevalent lymphocyte subpopulations of the gastric mucosa in gastritis in children, as well as to evaluate the expression of Fas and Fas ligand receptors (FasL), periapoptotic markers of gastric mucosa lymphocytes before and after H. pylori eradication. Forty nine patients aged 6 to 17 years, investigated due to chronic abdominal pain, were studied. The obtained tissue samples were analysed by immunohistochemistry. Different lymphocyte subsets were quantified on the basis of surface antigen expression (CD3, CD4, CD8, CD20), secreted cytokines (IL-4, IL-6, IFNgamma) and Fas and FasL proteins in the gastric mucosa. B and T helper lymphocytes were found to play a major role in the inflammatory infiltration in the gastric mucosa in children during H. pylori infection. Their expression was found to decrease after eradication. The enhanced expression of Fas receptor on lymphocytes before treatment and a decrease of this expression after eradication of H. pylori were shown. It was demonstrated that there is a correlation between CD4 and Fas receptor expression that may induce apoptosis of the helper lymphocytes in infected children.

High-Grade Bacterial Colonization and Severe Helicobacter pylori-Associated Gastritis in Children with EHPVO

6.2% (104/1669) of all children without prior TB. During the first 100 days of ART, the risk of unmasking TB-IRIS increased 2.7 fold compared to pre-ART (95% CI = 2.1 to 3.5; P < .001) with probable immune protection thereafter (RR = 0.41; 95% CI = 0.30 to 0.54; P = .002) through a median ART follow up of 439 days (IQR = 332 to 503). Only two paradoxical IRIS reactions occurred in children previously on anti-TB therapy. In time-to-event analysis, children with CD4 counts <200 cells/ L had a 41% longer time to TB unmasking (P = 0.04), implying a longer time was needed for restoration of antigen specific immunity. Conclusion: Unmasking of TB during immune reconstitution with ART is common among Ugandan children. This TB may represent: undiagnosed active TB at time of ART, latent or occult TB reactivating with ART, or incident TB cases via nosocomial spread in the clinic. More research is needed to enrich scientific output in this area.

M1063 Immunohistochemical Confirmation of the Causitive Role of Helicobacter pylori in Severe Gastritis in Children

M1063 Immunohistochemical Confirmation of the Causitive Role of Helicobacter pylori in Severe Gastritis in Children

Diagnostic Utility of Nodular Gastritis in Children with Chronic Abdominal Pain Undergoing Endoscopy

This study was aimed to describe the endoscopic picture and laboratory findings in children with chronic abdominal pain and to determine the utility of nodular gastritis in diagnosing HPI in these patients. This prospective study was done between November, 2004 and May, 2007. A total of 70 patients (36 male and 34 female) aged 3-14 years, underwent upper endoscopy. H-pylori infection was diagnosed when both urease test and histology were positive for the infection. Seventy percent (n = 49) of them were diagnosed to have endoscopic nodular gastritis. HPI was confirmed in 33 (47.1%) of 70 patients. The endoscopic antral nodularity had a sensitivity of 100%, specificity of 56.8%, positive predictive value of 67.3%, negative predictive value of 100% and a positive LR of 2.32 for diagnosis of HPI. It may be recommended that if nodular gastritis observed in a pediatric patient with chronic abdominal pain he/she should be investigated to exclude HPI otherwise no further work up is necessary to confirm HPI.

Helicobacter pylori Gastritis in Children Is Associated With a Regulatory T-Cell Response

Helicobacter pylori infection in children infrequently causes gastroduodenal mucosal ulceration. Because H pylori induces T-cell dependent gastric inflammation in adults and T regulatory (Treg) cells suppress T-cell-dependent pathology, we evaluated gastric histopathology and Treg cell responses in H pylori-infected children and adults. Gastric tissue from 36 children and 79 adults with abdominal symptoms in Santiago, Chile, was evaluated prospectively for H pylori bacteria and histopathology using the Sydney classification and Treg responses using immunoassay, immunohistochemistry, and real-time polymerase chain reaction. Eighteen (50%) of the children and 51 (65%) of the adults were infected with H pylori. Children and adults were colonized with similar levels of H pylori. However, the level of gastritis in the children was reduced substantially compared with that of the adults (P < .05). Coincident with reduced gastric inflammation, the number of Treg cells and levels of Treg cytokines (transforming growth factor [TGF]-beta1 and interleukin-10) were increased markedly in the gastric mucosa of H pylori-infected children compared with that of infected adults (P < .03 and < .05, respectively). Also, H pylori infection in the children was associated with markedly increased levels of gastric TGF-beta1 and interleukin-10 messenger RNA. Importantly, gastric TGF-beta1 in H pylori-infected children localized predominantly to mucosal CD25(+) and Foxp3(+) cells, indicating a Treg source for the TGF-beta1. Gastric pathology is reduced and local Treg cell responses are increased in H pylori-infected children compared with infected adults, suggesting that gastric Treg cell responses down-regulate the inflammation and ulceration induced by H pylori in children.

A Report of Two Children withHelicobacter HeilmanniiGastritis and Review of the Literature

An 11-year-old boy with epigastric abdominal pain and a 2 year-old girl with failure to thrive underwent esophagogastroduodenoscopy. Endoscopic biopsies from the gastric antrum of both children revealed corkscrew-like spiral bacteria, consistent with the diagnosis of Helicobacter heilmannii infection. H. heilmannii is a rare finding in children and is thought to be present in approximately 0.3% of patients undergoing upper endoscopy. Clinical presentation, gross and histologic appearance, and treatment regimens are discussed. The clinical and histologic features of previously reported cases of H. heilmannii gastritis in children living in the United States are reviewed in table form.

Gastropathy and Gastritis in Children With Portal Hypertension

The aim of this study was to determine the frequency of portal hypertensive gastropathy (PHG) and gastritis in children with portal hypertension and related factors. The study included 24 children with portal hypertension secondary to liver disease or extrahepatic venous obstruction. PHG was seen in 14 of 24 patients. PHG was significantly associated with the presence of esophageal varices and a history of hematemesis. Histologically, gastritis was identified in 14 of 24 patients and was significantly associated with cirrhosis. PHG is frequently found in children with portal hypertension, and it develops regardless of the cause of the portal hypertension.

Long‐term aspects of nodular gastritis in children

Close association of nodular gastritis and Helicobacter pylori infection has been initially proved by various studies. There have been some studies reporting microscopic and histologic recovery in a short time after eradication therapy. But there is not enough data about the long-term course of this condition. The aim of this study is to document current clinical conditions, presence of H. pylori and results of endoscopic and histologic examination, after a long-term period, in children with endoscopically diagnosed antral nodularity. A total of 35 patients diagnosed as nodular antral gastritis by upper gastrointestinal endoscopy during a 2 year period, were invited for re-evaluation and re-endoscopy after 3 years. Histopathologically, H. pylori detected ones had been treated with standard triple eradication therapy. In total, 27 patients were accepted for enrollment in the study. Repeated endoscopy could be performed in all 27 patients. The persistence of antral nodularity was detected in 18 of 27 patients. Decrease in symptoms, absence of symptoms and presence of H. pylori infection were detected in 6, 8 and 16 (89%) of them, respectively. There was no statistical significance between the first and last endoscopic biopsies when activity, atrophy, intestinal metaplasia and presence of follicles were regarded. Malt lymphoma could not be detected in any of the patients. There is a strong association between nodular gastritis and H. pylori. Presence of antral nodularity in the long-term period may be related to H. pylori re-infection. New therapeutic approaches are required for treatment and management of the patients diagnosed as nodular gastritis and living in areas endemic for H. pylori infection.