Gastritis In Children Research Articles

Nodular Gastritis and Pathologic Findings in Children and Young Adults with Helicobacter pylori Infection

PurposeThe aim of this study was to investigate the pathologic characteristics of nodular gastritis in children and young adults infected with Helicobacter pylori (H. pylori).Materials and MethodsA total of 328 patients were enrolled in this study, and the diagnosis of H. pylori infection was done with gastroduodenal endoscopy concomitant with a CLO™ test and pathologic analysis of the biopsy specimens. Diagnoses of normal, superficial gastritis, nodular gastritis, and peptic ulcer disease were made from the gastroduodenal endoscopic findings. The density of H. pylori organisms in the gastric mucosa was rated as normal, mild, moderate, or marked. The pathologic findings of nodular gastritis were based on the histopathologic findings of inflammation, immune activity, glandular atrophy and intestinal metaplasia. Each of these findings was scored as either normal (0), mild (1), moderate (2), or marked (3) according to the updated Sydney system and using visual analog scales. The gastritis score was the sum of the four histopathologic scores.ResultsIn this study, nodular gastritis (50.6%) was most common, and mild density (51.5%) H. pylori infection was also common upon microscopic examination. Intestinal metaplasia occurred in 9 patients (2.7%).ConclusionLogistic regression revealed a significant increase in the incidence of nodular gastritis with gastritis score (p = 0.008), but not an association with sex, age, or H. pylori density. Gastritis score was the only significant factor influencing the occurrence of nodular gastritis. Intestinal metaplasia, which was originally thought to be a pre-malignant lesion, occurred in 2.7% of the patients with H. pylori infection.

Improvement of the eradication rate of Helicobacter pylori gastritis in children is by adjunction of omeprazole to a dual antibiotherapy

The possible improvement of efficacy and tolerability of a 7-day dual antibiotherapy amoxicillin-clarithromycin (AC) on the eradication of Helicobacter pylori (H. pylori) gastritis in children by the adjunction of omeprazole (OAC) was studied. Forty-six children presenting with H. pylori gastritis, assessed at inclusion by endoscopy, H. pylori urease test, histology and/or culture were randomised to a twice-daily regimen of AC or OAC. A (13)C-urease breath test was performed 4-6 weeks after the end of the treatment period to evaluate H. pylori eradication. A larger proportion of patients was H. pylori negative (69%) in the OAC regimen treatment 4-6 weeks after eradication treatment compared with those who received dual AC therapy (15%). A total of seven patients (three in the OAC and four in the AC group) reported adverse events (AEs). Only vomiting was reported in more than one patient (one in each treatment regimen) and only one AE was severe (urticaria: in the OAC group, but considered not related to treatment). A larger eradication rate of H. pylori was obtained in the triple OAC group than in the dual AC group. Both therapy regimens can be safely administered to children for 7 days.

The Low Prevalence of Helicobacter pylori Gastritis in Children with Newly Diagnosed IBD Cannot Be Implicated in Previous Medical Treatment

The Low Prevalence of <i>Helicobacter pylori</i> Gastritis in Children with Newly Diagnosed IBD Cannot Be Implicated in Previous Medical Treatment

Is GastroPanel serum assay useful in the diagnosis of Helicobacter pylori infection and associated gastritis in children?

GastroPanel (Biohit, Helsinki, Finland) is a serum test kit that measures Helicobacter pylori antibodies (HPABs) and pepsinogens I and II and gastrin 17, which reflect the degree of atrophic gastritis. We assessed whether GastroPanel can replace endoscopic biopsies in the diagnostics of H. pylori in children and whether the H. pylori-infected children show markers for atrophic gastritis. Eighty children (median age, 6.8 years; range, 0.6–18.7 years) underwent gastroscopy for H. pylori-related abdominal complaints ( n = 40), surveillance after surgery for gastrointestinal tract malformations ( n = 20), gastroesophageal reflux (GER) ( n = 10), and miscellaneous diseases ( n = 10). Gastric biopsies and a serum sample were obtained from all 80 children. HPAB levels of 38 and 15 IU were tested as cutoff values for H. pylori gastritis. The biopsies showed H. pylori-positive gastritis in 30 children, 9 had gastritis not associated with H. pylori, and 41 had normal biopsies. Atrophic gastritis was not found. The sensitivity and specificity of HPAB for H. pylori were 47% and 98% (cutoff, 38 IU), and 73% and 85% (cutoff, 15 IU), respectively. The assays of pepsinogens and gastrin did not improve sensitivity. None of the markers of pepsinogen (PG) I, PGII, and gastrin 17 (G17) indicated atrophic gastritis. GastroPanel is too insensitive for H. pylori screening and does not replace endoscopy. Markers indicative of atrophic gastritis were negative in all children with H. pylori gastritis.

Myocarditis Presenting as Gastritis in Children

Vomiting and abdominal pain are common pediatric complaints encountered by emergency physicians. The differential diagnosis of abdominal pain is extensive. Herein, we report 2 cases with fatal myocarditis who initially presented with abdominal pain and vomiting. Both cases were presented with abdominal pain, vomiting, and loose stools. On arrival at our emergency department, hypotension, tachycardia, and cyanotic extremities were found. Their serum troponin-I levels were elevated. The echocardiogram demonstrated poor left ventricular performance and a decreased ejection fraction. In both cases, an arrhythmia and a coma developed within hours and were shortly followed by death. The clinical presentations of acute myocarditis are variable, ranging from an initial mild discomfort to acute progressive heart failure, and at times, even death. Abdominal pain may be a manifestation of systemic disease, an extra-abdominal lesion, or myocarditis. Although myocarditis associated with abdominal pain or vomiting remains a diagnostic challenge to physicians, it should be considered in the differential diagnosis of children with gastritis and hypotension or who are refractory to rehydration therapy.

Furazolidone-based triple therapy forH pylorigastritis in children

To evaluate the furazolidone-based triple therapy in children with symptomatic H pylori gastritis. A prospective and consecutive open trial was carried out. The study included 38 patients with upper digestive symptoms sufficiently severe to warrant endoscopic investigation. H pylori status was defined based both on histology and on positive (13)C-urea breath test. Drug regimen was a seven-day course of omeprazole, clarithromycin and furazolidone (100 mg, 200 mg if over 30 kg) twice daily. Eradication of H pylori was assessed two months after treatment by histology and (13)C -urea breath test. Further clinical evaluation was performed 7 d, 2 and 6 mo after the treatment. Thirty-eight patients (24 females, 14 males) were included. Their age ranged from 4 to 17.8 (mean 10.9 +/- 3.7) years. On intent-to-treat analysis (n = 38), the eradication rate of H pylori was 73.7% (95% CI, 65.2%-82%) whereas in per-protocol analysis (n = 33) it was 84.8% (95% CI, 78.5%-91%). All the patients with duodenal ulcer (n = 7) were successfully treated (100% vs 56.2% with antral nodularity). Side effects were reported in 26 patients (68.4%), mainly vomiting (14/26) and abdominal pain (n = 13). Successfully treated dyspeptic patients showed improvement in 78.9% of H pylori-negative patients after six months and in 50% of H pylori-positive patients after six months of treatment. Triple therapy with furazolidone achieves moderate efficacy in H pylori treatment. The eradication rate seems to be higher in patients with duodenal ulcer.

Immunohistochemical Evaluation of p53 Expression and Proliferative Activity in Children with Helicobacter pylori Associated Gastritis

The aim of this study was to evaluate the significance of p53 expression and proliferative activity of glandular epithelium and intestinal metaplasia in Helicobacter pylori associated gastritis of pediatric patients. The study included endoscopic gastric biopsies of 54 children with dyspeptic complaints. Immunohistochemistry was performed for evaluation of p53 expression and Ki-67 labeling index, an indicator of proliferative activity. Grading of H. pylori density, intestinal metaplasia and inflammatory cell infiltration were performed in histologic tissue sections stained with hematoxylin-eosin, Giemsa and Alcian-blue. Of 54 children, 35 (64%) were infected by H. pylori. Positive immunostaining for p53 was observed in 11 of 54 cases (20.4%). H. pylori infection was found in 10 (91%) of the p53-positive patients. There was a positive correlation between H. pylori density and Ki-67 labeling index in H. pylori infected children. H. pylori density, Ki-67 labeling index and inflammatory cell infiltration in the p53-positive group were significantly higher than in the p53-negative group. Although intestinal metaplasia was more common in H. pylori infected children (n = 11; 31.4%), there was no difference in the rate of intestinal metaplasia between the p53-positive and p53-negative groups. The present study shows that p53 mutations and higher proliferative activity of glandular epithelium may be related to H. pylori associated gastritis in children. Because p53 mutation does not appear to be associated with intestinal metaplasia, a precursor for gastric cancer in adults, we think that H.pylori associated p53 alterations do not initiate and promote gastric cancer that may occur in adulthood.

Endoscopic nodular gastritis: an endoscopic indicator of high-grade bacterial colonization and severe gastritis in children with Helicobacter pylori.

To investigate the significance of endoscopic nodular gastritis associated with Helicobacter pylori infection. This prospective study included 185 children (50.8% boys) aged 1 to 12 years (mean, 6.9 +/- 3.0 years) who underwent upper intestinal endoscopy during evaluation of chronic abdominal pain. The authors assessed the endoscopic appearance of the stomach, noting those patients with endoscopic nodular gastritis. Urease activity of gastric mucosal biopsies was measured. With histologic examination, the presence and density of H. pylori organisms, the presence of follicular gastritis, the nature of inflammation, and the gastritis activity grade and overall gastritis score were assessed. H. pylori infection was identified in 50 children (27%). Endoscopic nodular gastritis was significantly associated with active chronic gastritis and follicular gastritis. Nodularity in the stomach showed a high specificity (98.5%) and positive predictive value (91.7%) for the diagnosis of H. pylori infection and was observed in 22 of 50 (44%) H. pylori-positive patients and in 2 of 135 (1.5%) H. pylori-negative patients. A significant association was observed between older age and the prevalence of this finding (P< 0.001). There was a significant increase in endoscopic nodular gastritis with increased H. pylori density and a positive correlation (Pearson coefficient = 0.97) with increased gastritis score on histologic examination. Increase in gastritis score was dependent on increased H. pylori density in patients with gastric nodularity; this finding was independent of age. Endoscopic findings of antral nodularity in children suggest the presence of H. pylori infection and follicular gastritis and may identify cases of severe gastritis and marked bacterial colonization.

Refractory iron-deficiency anaemia due to silent Helicobacter pylori gastritis in children

We describe the cases of three children with chronic active Helicobacter pylori gastritis and iron-deficiency anaemia without evidence of oesophagogastrointestinal bleeding. In all cases, long-standing iron supplementation became effective only after eradication of Helicobacter pylori. Iron-deficiency anaemia may be due to clinically inapparent H. pylori gastritis.

Histopathological Parameters of Helicobacter pylori -associated Gastritis in Children and Adolescents: Comparison with Findings in Adults

Background: The pathohistological features of Helicobacter pylori -associated gastritis in children and adolescents are less well understood than they are in adults. The aim of the study was to compare histological parameters of H. pylori -infected children with those of adults. Methods: The retrospective study compared histological features of 111 children (mean age 10.8 ± 3.8). Three paediatric age groups were analysed and the findings were compared with those of 111 adults (mean age 64.2 ± 12.1). Degree of chronicity and activity of inflammation, mucus depletion and regeneration of foveolar epithelium by regenerating epithelium and H. pylori colonization were scored in antral biopsies. Results: The histological parameters in children, i.e. degree of chronicity, activity of gastritis and the summed gastritis score, were not significantly different compared to those in adults. Replacement of foveolar epithelium by regenerating epithelium was significantly larger in adults compared to that of paediatric patients. The rate of low-grade mucus depletion and of the strongest degree of H. pylori colonization was higher in children than in adults. Children with antral nodularity had significantly higher histological score values. Conclusion: The histological differences between paediatric patients and adults are focused on signs of chronic inflammation and regeneration. Our results imply that antral nodularity is an important sign of highest-grade gastritis, especially in young children.

Cag pathogenicity island of Helicobacter pylori in Korean children.

cag pathogenicity island is reported to be a major virulence factor of Helicobacter pylori. The aim of this study was to investigate the status of cag pathogenicity island genes and gastric histology in Korean children with H. pylori gastritis. Helicobacter pylori DNA was extracted from antral biopsy specimens from 25 children with H. pylori gastritis. Specific polymerase chain reaction assays were used for four genes of cag pathogenicity island. The features of gastritis were scored in accordance with the updated Sydney System. cagA was present in 23 (92%) of 25 children, and cagE in 24 (96%). Twenty-two (88%) children were cagT positive and 19 (76%) virD4 positive. All of the selected genes of the cag pathogenicity island were present in 17 (68%) children and completely deleted in one child. There were no differences in neutrophil activity and chronic inflammation between children infected with intact cag pathogenicity island strains and those with partially or totally deleted-cag pathogenicity island strains. cag pathogenicity island is not a uniform, conserved entity in Korea. Completeness of cag pathogenicity island may not be the major factor to determine the severity of H. pylori gastritis in children.

Focally enhanced gastritis in children with Crohn's disease and ulcerative colitis.

Focally enhanced gastritis (FEG) has been suggested as a specific diagnostic marker for patients with Crohn's disease. However, the utility of FEG for distinguishing Crohn's disease from ulcerative colitis is uncertain in adults, and the occurrence of this lesion in children has not been defined. The aim of this study was to evaluate the occurrence of FEG and other gastric histological abnormalities in children with inflammatory bowel disease (IBD) and to examine the utility of FEG in discriminating between ulcerative colitis and Crohn's disease. This is a retrospective, case-controlled study of upper GI histopathological findings in children with IBD. Gastric histopathology was defined and graded according to the Updated Sydney System. FEG was present in 28 of 43 (65.1%) children with Crohn's disease and five of 24 (20.8%) children with ulcerative colitis, compared to three of 132 (2.3%) children without IBD or one of 39 (2.6%) children with Helicobacter pylori infection. There were no differences between those with and without FEG with regard to upper GI symptoms or previous anti-inflammatory drug ingestion (5-aminosalicylic acid compounds or steroids). All patients with H. pylori infection had chronic antral gastritis, but only one child with H. pylori had FEG. In addition, mild to moderate chronic gastritis was present in 15 of 43 (34.9%) children with Crohn's disease and in 12 of 24 (50%) patients with ulcerative colitis. The presence of FEG suggests underlying IBD. Although FEG is particularly common in children with Crohn's disease, it does not reliably differentiate between Crohn's disease and ulcerative colitis.

Focally enhanced gastritis in children with Crohn’s disease and ulcerative colitis

OBJECTIVES: Focally enhanced gastritis (FEG) has been suggested as a specific diagnostic marker for patients with Crohn’s disease. However, the utility of FEG for distinguishing Crohn’s disease from ulcerative colitis is uncertain in adults, and the occurrence of this lesion in children has not been defined. The aim of this study was to evaluate the occurrence of FEG and other gastric histological abnormalities in children with inflammatory bowel disease (IBD) and to examine the utility of FEG in discriminating between ulcerative colitis and Crohn’s disease. METHODS: This is a retrospective, case-controlled study of upper GI histopathological findings in children with IBD. Gastric histopathology was defined and graded according to the Updated Sydney System. RESULTS: FEG was present in 28 of 43 (65.1%) children with Crohn’s disease and five of 24 (20.8%) children with ulcerative colitis, compared to three of 132 (2.3%) children without IBD or one of 39 (2.6%) children with Helicobacter pylori infection. There were no differences between those with and without FEG with regard to upper GI symptoms or previous anti-inflammatory drug ingestion (5-aminosalicylic acid compounds or steroids). All patients with H. pylori infection had chronic antral gastritis, but only one child with H. pylori had FEG. In addition, mild to moderate chronic gastritis was present in 15 of 43 (34.9%) children with Crohn’s disease and in 12 of 24 (50%) patients with ulcerative colitis. CONCLUSIONS: The presence of FEG suggests underlying IBD. Although FEG is particularly common in children with Crohn’s disease, it does not reliably differentiate between Crohn’s disease and ulcerative colitis.

Approaching Helicobacter pylori infection in children: Level I evidence at last and a word of caution

Approaching Helicobacter pylori infection in children: Level I evidence at last and a word of caution

Omeprazole combined with amoxicillin and clarithromycin in the eradication of Helicobacter pylori in children with gastritis: A prospective randomized double-blind trial

Objectives: The aim of this multicenter prospective, randomized, double-blind study was to assess the efficacy of the combination of omeprazole, amoxicillin, and clarithromycin (OAC) for the treatment of Helicobacter pylori gastritis in children. Study design: Seventy-three children with dyspeptic symptoms were included in the trial (mean age 10.8 years; range, 3.3 to 15.4). Patients were randomized to receive OAC or amoxicillin and clarithromycin (AC) for 7 days. H pylori status was assessed before and 4 weeks after eradication treatment, by use of the carbon 13–labeled urea breath test. Results: In intent-to-treat analysis (n = 63), eradication rates were 74.2% (95% CI, 58.7 to 89.6) in the OAC group and 9.4% (95% CI, 0 to 19.5) in the AC group. In per-protocol analysis (n = 53), the eradication rate increased to 80% (95% CI, 64.3 to 95.7), remaining significantly higher than in AC group (10.7%; 95% CI, 0 to 22.2). Resistance of strains to clarithromycin was rare (3/39 = 7.7%) and was not associated with failure of treatment. Adverse events were reported in 24.6% of patients and remained mild. Conclusion: This study shows that 1-week OAC triple therapy results in successful eradication of H pylori in 75% of children with gastritis. (J Pediatr 2001;139:664–8)

Gastritis

A wide variety of infectious, inflammatory, and other disorders affect the gastric mucosa in pediatric patients. The most common cause of gastritis in children is Helicobacter pylori infection, which is also responsible for the majority of duodenal ulcers. Acute erosive gastritis is most commonly the result of metabolic stress or drug or corrosive injury. Other major causes of gastritis include celiac disease, allergic disorders, and Crohn’s disease. The distinctive clinical, endoscopic, and histologic features of these disorders are discussed.

Histopathology of Helicobacter pylori associated gastritis in children from high-and low-gastric cancer risk populations

Histopathology of Helicobacter pylori associated gastritis in children from high-and low-gastric cancer risk populations

Histopathology of Helicobacter pylori associated gastritis in children from high-and low-gastric cancer risk populations

Histopathology of Helicobacter pylori associated gastritis in children from high-and low-gastric cancer risk populations

Prominent area gastricae is associated with Helicobacter pylori gastritis in children

Prominent area gastricae is associated with Helicobacter pylori gastritis in children

Helicobacter pylori gastritis in children and adults: Comparative histopathologic study

The inflammatory response to Helicobacter pylori in adults has been well characterized. In children, studies of H. pylori gastritis have been based on small numbers of patients and have used loose definitions of the inflammatory components. Comparative study of the inflammatory response to H. pylori in children and adults can help our understanding of the natural history of this infection. Using the Updated Sydney Classification, we performed a retrospective, blinded pathology review of gastric biopsy specimens from 42 children and 40 adults with H. pylori infection, and we quantified each inflammatory cell separately (neutrophils, lymphocytes, plasma cells, and eosinophils). Differences in inflammatory cell components of children and adults were assessed by logistic regression analysis. More children had marked amounts of H. pylori (P = .05) and mild degree of neutrophils (P = .02), plasma cells (P = .005), and eosinophils (P = .0001) compared with adults. No differences existed when quantifying mononuclear cells or atrophy. Ulcers and intestinal metaplasia were present only in adults. We found that the numbers of inflammatory cells present in H. pylori-infected biopsy specimens is different in children and adults. We hypothesize that these differences demonstrate how H. pylori infection evolves from an acute childhood infection to an adult chronic disease.