Prevalence of Helicobacter pylori infection and gastric mucosal abnormalities in chronic pancreatitis

OBJECTIVE: Chronic pancreatitis is often associated with abnormal gastric acid secretion. However, previous studies have taken into consideration neither the potential role of Helicobacter pylori (H. pylori) infection nor histological features of the gastric mucosa in this context. The aim of this study was to analyze the prevalence of H. pylori infection as well as the pattern of gastritis in patients with chronic pancreatitis. METHODS: Forty patients with chronic alcoholic pancreatitis were included in the study: 40 patients with alcoholic liver cirrhosis and normal exocrine pancreatic function and 40 asymptomatic nonalcoholic subjects matched for age and sex used as control subjects. Endoscopy was performed in all patients, and five biopsy specimens from the antrum (three from the gastric body and two from the cardia) were taken for histological grading of gastritis and H. pylori assessment. RESULTS: Prevalence of H. pylori infection was similar in subjects with chronic pancreatitis (38%), asymptomatic subjects (28%) and liver cirrhosis (30%). Topography and expression of H. pylori-associated chronic gastritis was also not different among the three groups of subjects. In H. pylori-negative subjects, the presence of moderate to severe chronic antral gastritis was significantly more common in patients with chronic pancreatitis (40%) than in subjects with liver cirrhosis (18%) and in asymptomatic subjects (14%) (p < 0.05). No difference was found among the three groups of patients with regard to gastritis activity, atrophy, and intestinal metaplasia in the various gastric regions. The chronicity grade of gastritis did not correlate with the severity of pancreatic insufficiency. CONCLUSION: Prevalence of H. pylori infection is not different in patients with chronic pancreatitis as compared with subjects alcoholic liver cirrhosis and asymptomatic subjects. A severe H. pylori-negative chronic gastritis is more common in patients with chronic pancreatitis. This chronic inflammation of the gastric mucosa could contribute to determining the changes in gastric physiology described in patients with chronic pancreatitis.     

Prevalence and pattern of Helicobacter pylori gastritis in the gastric cardia

OBJECTIVES: Helicobacter pylori has a predilection for antral colonization. Local acid production is the major determinant of colonization. Because production is low in the antrum and cardia, H. pylori should also colonize the cardia. We therefore investigated the histologic pattern of gastritis and the prevalence of H. pylori in the cardia compared with the antrum and corpus. METHODS: From 135 H. pylori-infected patients with gastritis, ulcer disease, or reflux esophagitis, biopsies were obtained from the antrum, corpus, and cardia. The prevalence, topography, and histologic parameters of gastritis were examined. RESULTS: All 135 patients had active antral H. pylori gastritis: in the cardia, 132 of these patients (97.7%) showed active gastritis, and 124 patients (91.9%) had H. pylori visible on staining. Gastritis of the cardia in most patients resembled antral gastritis, but the density of bacteria and the inflammatory responses were less marked. The most striking finding in the cardia of patients with gastroesophageal reflux was a lower density of bacteria compared with antrum and corpus. Intestinal metaplasia was found in 32 patients in antral mucosa (23.7%) versus 28 patients in the cardia (20.7%), versus 11 patients in the corpus (8.1%), and was multifocal in 17 patients (12.6%). CONCLUSIONS: H. pylori gastritis commonly involves the cardia. The histologic density of the bacteria and inflammatory responses are lower than in the antrum. Intestinal metaplasia in the cardia is a common finding in H. pylori gastritis. The cause of the lower bacterial density in the cardia of patients with reflux esophagitis needs further investigation.     

Superoxide dismutase activity in Helicobacter pylori-positive antral gastritis in children

Reactive oxygen metabolites have been implicated in gastric mucosal injuries. Superoxide dismutase, a scavenger of superoxide radical, is a key enzyme in gastric mucosal protection against several damaging factors. This study was aimed at investigating the relationship of superoxide dismutase activity to Helicobacter pylori-induced antral gastritis in children. Two groups of 11 children each, one positive and the other negative for Helicobacter pylori, were studied. Biopsies from the antrum and corpus were obtained for evaluation of Helicobacter pylori by CLOtest and histology as well as for superoxide dismutase activity (cytochrome c method). Erythrocytic and serum superoxide dismutase levels were determined as well. Superoxide dismutase activity was significantly higher only in the antrum of children with Helicobacter pylori-induced antral gastritis. There was no significant difference in superoxide dismutase activity in the corpus, erythrocytes, or serum of both groups. These findings may suggest a pathogenic relationship between the presence of Helicobacter pylori and oxygen radicals in inducing antral mucosal injury.     

Diagnosis of otitis media with effusion by acoustic reflectometry

Colonization of human gastric mucosa with Helicobacter pylori leads to chronic active gastritis and induces the occurrence of an acquired mucosa-associated lymphoid tissue (MALT) in the stomach. This remodelling of the gastric mucosa together with chronic antigen persistence may induce autoimmune reactions. The aim of this study was to investigate humoral autoimmune reactions to human gastric mucosa in H. pylori gastritis and their clinical relevance. Sera from patients with dyspeptic symptoms were tested for presence of IgG immunoglobulins against H. pylori. Gastric infection with H. pylori and alterations of gastric mucosa were demonstrated by histological examination of gastric biopsy specimens. All sera were tested for reactivity against human gastric mucosa by immunohistochemistry. Two different in-situ binding sites of antigastric autoantibodies were observed. Binding to canalicular structures within parietal cells was significantly correlated with antibodies to H. pylori, elevated basal gastrin levels and atrophy of gastric corpus glands. Our data indicate that autoimmune reactions to antigens in the human gastric mucosa occur in H. pylori gastritis and that they may play a role in the pathogenesis of the disease.     

Helicobacter pylori and gastroduodenal lesions in 547 symptomatic young adults

OBJECTIVES: Helicobacter pylori (H. pylori) is involved in the pathogenesis of gastric inflammatory disorders. Both antral chronic gastritis and H. pylori infection prevalence increase with age. The aim of the study was to assess the prevalence of H. pylori infection in young adults and to study the relationship between endoscopical and histological features and H. pylori infection. METHODS: The study concerned 547 young patients (age: 18-25 years), undergoing endoscopy for upper gastrointestinal symptoms. The severity and the activity of chronic gastritis was graded by histological examination of antral biopsies. The diagnosis of H. pylori infection was based on histology and culture or urease test. RESULTS: Fifty-three percent of the patients had a normal endoscopy; 44 ulcers were found: 34 duodenal ulcers and 10 gastric ulcers. H. pylori infection was detected in 34% of cases. The prevalence of H. pylori infection was 29.8% in non-ulcer patients, 50% in gastric ulcers and 91% in duodenal ulcers (P < 0.01). Duodenal ulcer, aspect of antral mosaic mucosa and nodular gastritis, were closely related to the presence of H. pylori. There was a significant relationship between H. pylori infection and both the severity (P < 0.01) and the activity (P < 0.01) of the antral chronic gastritis. The prevalence of follicular gastritis was 22% : it was present in 60% of H. pylori positive patients and 2.4% of H. pylori negative patients. H. pylori infection was more frequent in patients from Africa than in Europeans (P < 0.01). There was no significant association between H. pylori infection and different types of diets, settlements (rural vs urban) or symptoms. CONCLUSION: These results show that in the young population studied, duodenal ulcer, nodular gastritis, antral mosaic mucosa, active chronic gastric and follicular gastritis are closely related to H. pylori infection. They suggest that in the subgroup of non ulcer symptomatic patients, H. pylori prevalence is higher than in the general population.     

Management of febrile infants under 3 years old

BACKGROUND: Rapid ureas tests (RUTs) provide a simple, sensitive method of detecting Helicobacter pylori infection. OBJECTIVES: Our aim, therefore, was to determine whether the yield of detecting H. pylori infection by RUT varied depending on the site of gastric biopsy. MATERIALS AND METHODS: Gastric biopsies were obtained from 50 patients for RUT by use of hpfast (GI Supply, Camp Hill, PA). Biopsies were taken from the prepyloric greater curve antrum, from the gastric angle, and from the greater curve in mid-corpus. One biopsy specimen was placed in the RUT gel, and the biopsy from the adjacent mucosa was placed in formalin for subsequent histological evaluation by using the Genta stain. RUTs were examined and scored at intervals of 5, 10, 15, 30, and 45 minutes and after 1, 2, 4, and 24 hours. RESULTS: Fifty patients were entered in the rest (150 RUTs), 32 having H. pylori infection. There were no false-positive RUTs (specificity, 100%). The gastric angle site was positive in 100%. The prepyloric site was positive in 87%, and the corpus site was positive in 84.4% (p < .052 for angle or prepyloric antrum versus corpus). The most common pattern was for all to be positive (74%). The median time to positivity was similar with angle and prepyloric sites (37.5 and 60 minutes, respectively, p = not significant) and shorter than the corpus biopsy (180 minutes); (p < .05 for angle or prepyloric antrum versus corpus). CONCLUSION: The maximum probability for detecting H. pylori infection using a RUT is to obtain a biopsy from the gastric angle. To prevent missing a positive result when intestinal metaplasia is present, we recommend that (at a minimum) biopsies be taken from both the angle and the corpus.     

Adaptation and radiographic evaluation of four adhesive systems

Specific pathogen-free Mongolian gerbils were infected orally with Helicobacter pylori to establish a new small animal model of severe gastritis H. pylori was recovered by culture from both antrum and body over a 16-week period after a single inoculation. The number of H. pylori colonising the antrum was about 100-fold higher than in the body, and this was consistent throughout the experiment. Histological examination showed that all animals developed severe inflammation with infiltration of polymorphonuclear leucocytes and mononuclear cells into the lamina propria and submucosa of the antrum from 4 weeks after infection. From 8 weeks after infection, multifocal lymphoid follicles appeared in the lamina propria and submucosa, and micro-erosions were also observed in the epithelial layer. At 16 weeks after infection, ulceration with disruption of the lamina muscularis mucosae was observed in the antral mucosa. To determine whether H. pylori caused gastritis or not, infected gerbils were treated with amoxycillin. After the treatment, gastritis could not be seen in the gastric mucosa. Therefore, the Mongolian gerbil is a useful small animal model to study the pathogenesis of H. pylori in gastric ulceration and severe gastritis and to assess anti-H. pylori treatment.     

Beta1B subunit of voltage-dependent Ca2+ channels is predominant isoform expressed in human neuroblastoma cell line IMR32

BACKGROUND: In adults, Helicobacter pylori infection is always associated with gastritis or ulcer. However, very active gastritis and ulcers are rarely seen in children. The aim of the present work was to study the relationships between H. pylori and gastric mucosa in children. METHODS: Eighty infected children and adolescents including 48 (60%) neurologically impaired institutionalized patients, aged 2 months-22 years (mean 11.7 +/- 5.2 years) were studied retrospectively. All the patients underwent gastroscopy, and three antral and two fundic biopsy specimens were taken for histology and bacteriology. RESULTS: A normal gastric mucosa was found in 22 of 80 patients (27.5%), whereas the others had gastritis (n = 58, 72.5%). There were no statistical differences between patients with normal histology and those presenting with gastritis for age, sex, ethnic background, symptoms, and the degree of bacterial colonization. The macroscopic aspect of gastritis was less frequently found in children with a normal histology compared with those with histological gastritis (p < 0.001). CONCLUSIONS: These data show that H. pylori infection can be associated with a normal gastric histology in children.     

Identification of Helicobacter in gastric biopsies by PCR based on 16S rDNA sequences: a matter of little significance for the prediction of H. pylori-associated gastritis?

The aim of the present study was to correlate molecular evidence of the presence of Helicobacter pylori in gastric biopsy samples, based on analysis of 16S rDNA, vacuolating toxin (vacA), urease A (ureA) and cagA genes, with the clinical, histological and serological findings in patients with H. pylori-associated gastritis. Fresh biopsy samples were collected from the gastric antrum and corpus of 22 asymptomatic volunteers with or without H. pylori-associated gastritis. Total DNA was extracted from the biopsy material and subjected to 16S rDNA PCR amplification, Southern blotting and 16S rDNA sequence analysis of the PCR products. The vacA, ureA and cagA genes were characterised by PCR amplification and Southern blot analysis. Based on partial 16S rDNA sequence analysis, DNA belonging to the genus Helicobacter was detected in gastric biopsy samples from 20 of 22 subjects, including seven of nine histologically and serologically normal controls. Six of 20 partial 16S rDNA sequences revealed variations within variable regions V3 and V4 that deviated from those of the H. pylori type strain ATCC 4350T and, therefore, possibly represented other species of Helicobacter. VacA genes identical with those of the type strain were found predominantly in the subjects with H. pylori gastritis, and all the patients except one were found to be cagA-positive. There was no evidence of false positive PCR reactions. In conclusion, the PCR-based molecular typing methods used here were apparently too sensitive when applied to the detection of H. pylori in human gastric tissues. The lack of quantitative analysis makes them inappropriate as clinical tools for the diagnosis of H. pylori-associated gastritis, despite the fact that they provide a qualitative and sensitive tool for the detection and characterisation of H. pylori in the gastrointestinal tract.     

Transplantation of hepatocytes for prevention of intracranial hypertension in pigs with ischemic liver failure

BACKGROUND: How Helicobacter pylori infection affects gastric acid secretion is still unclear. METHODS: Gastric juice pH, ammonia concentration in gastric juice, serum gastrin level, and grade of gastritis in accordance with the Sydney System were determined for patients with gastric ulcer (GU) and duodenal ulcer (DU) before and after treatment with lansoprazole and amoxicillin, and results were compared with those of H. pylori-negative controls. RESULTS: Scores for H. pylori density, atrophy, metaplasia, and activity of gastritis in the corpus were higher in patients with GU, especially those with proximally located GU, than in those with DU. Gastric juice pH was significantly higher in GU patients than in DU patients and controls. After H. pylori eradication, gastric juice pH and serum gastrin levels in both GU and DU patients were significantly decreased to control levels. In patients without eradication, no significant changes in these factors were observed. CONCLUSIONS: These findings suggest that H. pylori infection and gastritis in the corpus suppress acid secretion and increase gastric juice pH, resulting in hypergastrinemia, and that eradication of H. pylori normalizes acid secretion and serum gastrin levels.     

Development of Helicobacter pylori-induced gastric carcinoma in Mongolian gerbils

Helicobacter pylori is classified by IARC/WHO as a definite human gastric carcinogen, despite "inadequate experimental evidence." To obtain direct evidence concerning this relationship, we investigated the histopathological findings of gastric mucosa using a model of H. pylori infection in Mongolian gerbils. The animals were challenged p.o. with H. pylori ATCC-43504 and sacrificed at 6, 12, and 18 months after inoculation for histological examination. All inoculated animals were infected with H. pylori. Severe infiltration of the lamina propria by polymorphonuclear and mononuclear cells appeared in the lesser curvature of the antrum, with an increase in epithelial cell proliferation, and the infiltration extended to the body. Atrophic gastritis and focal intestinal metaplasia also appeared in the lesser curvature of the antral mucosa at 6 months after inoculation. Intestinal metaplasia became severe, with dysplasia, after that. At 18 months after H. pylori inoculation, two of five infected animals showed three well-differentiated gastric cancers. The uninfected control animals showed no abnormal findings throughout the entire observation period. Here, it was confirmed that H. pylori infection alone causes gastric cancer in an animal model.     

Significant improvement of atrophy after eradication therapy in atrophic body gastritis

Chronic atrophic body gastritis may be induced by H. pylori. Results on the effect of H. pylori eradication therapy have been conflicting. Here, we report on the effect of eradication therapy on both body atrophy and inflammation in 7 patients. They presented with severe or moderate atrophy of the oxyntic mucosa and positive H. pylori histology (Warthin-Starry) and/or serology. Eradication was performed with a standard double or triple therapy regimen. At least 6 weeks after successful eradication therapy, patients underwent rebiopsy and histopathological evaluation of the gastric body. In all 7 patients, the grade of body gastritis improved significantly. Among the patients with severe atrophy before H. pylori eradication, 2 had normal mucosa, 3 low-grade atrophy, and one moderate atrophy after treatment. The one case with moderate atrophy before treatment had normal mucosa after H. pylori eradication. In addition, inflammatory infiltration of the mucosa cleared up in 6 cases and improved from severe to mild in one case after treatment. From these results, we conclude that in patients with histologically demonstrated H. pylori and/or positive H. pylori serology atrophic body mucosa can recover after successful eradication therapy.     

Antibody-secreting cells in the stomachs of symptomatic and asymptomatic Helicobacter pylori-infected subjects

In this study we analyzed whether infection with Helicobacter pylori gives rise to specific B-cell responses against a number of putative virulence factors of H. pylori, e.g., urease, flagellin, and different bacterial surface antigens, locally in the gastric mucosa. This was studied in antrum and corpus biopsies collected from 11 H. pylori-infected patients with duodenal ulcers, 11 asymptomatic H. pylori carriers, and 13 noninfected, healthy controls. Mononuclear cells were isolated from the biopsies and assayed for frequencies of total and H. pylori-specific antibody-secreting cells (ASCs) by means of the enzyme-linked immunospot technique. The H. pylori-infected subjects had remarkably higher frequencies of total immunoglobulin A (IgA)- and IgM-secreting cells than the noninfected subjects, while the frequencies of IgG-secreting cells were virtually the same in the different groups. In addition, most of the infected subjects had IgA ASCs reacting with H. pylori membrane proteins, flagellin, and urease, while none of the noninfected subjects had any detectable H. pylori-reactive ASCs. Furthermore, half of the infected subjects also had ASCs reacting with a Helicobacter-specific 26-kDa protein, while only a few of them had ASCs reacting with neutrophil-activating protein, the neuraminyllactose-binding hemagglutinin HpaA, or lipopolysaccharides purified from different H. pylori strains. The frequencies of H. pylori-specific ASCs in the antrum and corpus were almost identical, and no differences in either antigen specificity or magnitude of the B-cell response in the stomach could be detected between the ulcer patients and the asymptomatic H. pylori carriers. This study demonstrates that H. pylori infection induces strong antibody responses in the human gastric mucosa, both in asymptomatic carriers and in duodenal ulcer patients. However, the outcome of infection could not be explained by differences in the local B-cell response to any of the antigens used in this study.     

Bilateral osteonecrosis of the head of the femur complicating acute promyelocytic leukemia: a sequel to treatment of retinoic acid syndrome with dexamethasone

BACKGROUND: Isolating Helicobacter pylori on culture media and performing antibiotic susceptibility testing is potentially the most useful tool for guiding antibiotic therapy, especially when antimicrobial resistance is suspected. The aim of this study was to determine whether the yield of H. pylori culture was related to the site from which the gastric specimen was obtained either before or after therapy. METHODS: Gastric mucosal biopsies from the antrum and the corpus of the stomach were cultured. H. pylori status was determined by histological assessment using the Genta stain. RESULTS: Fifty-two patients with documented H. pylori infection were studied: Twenty-three were tested before antibiotic therapy and 29 after therapy had failed. In 47 patients (90%), both antral and corpus culture specimens were positive. In 5 patients (10%), only one site was positive, with three false-negative antral and two false negative corpus cultures. The overall sensitivity of culture in detecting H. pylori infection was 95% (95% confidence interval = 89-98%) and was not significantly different for the antrum or corpus, either before or after therapy. CONCLUSION: Culture of gastric biopsies from either the antrum or the corpus has an excellent diagnostic yield even in patients who failed antimicrobial therapy.     

Once-daily gentamicin therapy for experimental Escherichia coli meningitis

BACKGROUND: Eradication of Helicobacter pylori by antibiotics in combination with gastric acid inhibition can result in overgrowth of non-H. pylori bacterial flora. This may confound the histological detection of H. pylori at eradication control if non-specific staining methods are used. OBJECTIVE AND METHODS: In 18 patients treated with amoxycillin (2 weeks) and omeprazole (6 weeks), endoscopically obtained gastric juice was cultured and two biopsies of corpus, antrum and duodenum were taken before and after eradication therapy (with gastric acid inhibition still going on) for culture and for histology to assess the intragastric bacterial flora. By histology, modified Giemsa (MG) and an H. pylori-specific immunohistochemical stain (IMM) were evaluated. RESULTS: Median pH of gastric juice was 1.5 (n = 18) before and 7 (n = 17) after eradication therapy, when patients were still on omeprazole. After therapy, culture showed a significant decrease (P < 0.05) in mean amount of H. pylori in corpus, antral and duodenal biopsies and a significant increase of non-H. pylori flora (P < 0.05) in gastric juice, corpus, antral and duodenal mucosa. With culture as a standard, 16 and 4 biopsy specimens were scored falsely positive for H. pylori by MG and IMM, respectively, and H. pylori was not detected in 23 and 13 biopsy specimens when culture was H. pylori-positive. CONCLUSION: Because of the possible presence of non-H. pylori flora after eradication therapy, the use of IMM is recommended in this situation for the histological detection of H. pylori, especially in those patients with ongoing gastric acid inhibitory therapy.     

Free and total bupivacaine plasma concentrations after continuous epidural anaesthesia in infants and children

OBJECTIVES: The aim of this study was to elucidate the prevalence of Helicobacter pylori and its distribution in order to clarify the frequency of H. pylori infection and the most appropriate site of endoscopic biopsy for studies of H. pylori infection associated with different gastric diseases. DESIGNS AND METHODS: Swiss role mucosal strips from 275 resected stomachs, which included the greater curvature, anterior wall and lesser curvature of the antrum, incisura and corpus, were stained with haematoxylin-eosin and H. pylori antibody. RESULTS: The prevalence of H. pylori infection was 97% in duodenal ulcers, 98% in gastric ulcers, 98% in intestinal-type carcinomas and 99% in diffuse-type carcinomas. H. pylori was present at a rate of 100% in any site in cases of duodenal ulcer, but was diffusely distributed in the antrum and patchily distributed in the corpus. The detection rate of H. pylori was 50-100% in gastric ulcers, 30-100% in intestinal-type adenocarcinomas and 63-100% in diffuse-type adenocarcinomas depending on the site of the stomach examined. CONCLUSIONS: The prevalence of H. pylori infection was very high in peptic ulcers of the duodenum and stomach and gastric carcinomas of Japanese patients. Biopsy specimens for evaluation of H. pylori infection should be taken routinely from both the greater curvature of the antrum and corpus. Immunohistochemical staining should be used to assay for H. pylori when few organisms are present or eradication therapy has been used.     

Oral health status of an industrial population in Romania

BACKGROUND: We investigated whether addition of bismuth subcitrate (BSC, 4 x 120 mg) to a two week therapy scheme of omeprazole (OME, 2 x 40 mg)/amoxicillin (AMO, 4 x 500 mg) increases Helicobacter pylori eradication. MATERIALS AND METHODS: Patients with dyspepsia underwent upper endoscopy. H. pylori positive patients were randomized to treatment A (OME/AMO, 83 patients) or treatment B (OME/AMO/BSC, 84 patients). RESULTS: In 65 patients of group A (78%) H. pylori was eradicated as determined from the histological assessment (Sydney classification) of antrum and corpus biopsies. In comparison, in 68 patients of group B (81%) H. pylori was eradicated (p = NS between groups). H. pylori eradication in both groups was associated similarly with a decrease of inflammation and activity whereas atrophy and intestinal metaplasia were not affected. A positive association was revealed between the decrease of H. pylori score and the decrease of both inflammation and activity scores for antrum as well as corpus biopsies. CONCLUSIONS: Addition of BSC to OME/AMO does not increase H. pylori eradication in patients with dyspepsia. Eradication of H. pylori is associated with disappearance of epithelial damage (inflammation and activity) in antral and corpus mucosa.     

Hazards from surgical gloves

We describe the case of a child with Sch?nlein-Henoch purpura (SHP), bleeding duodenal ulcer and Helicobacter pylori (H. pylori) associated gastritis. 5-year-old girl was hospitalized with typical symptoms of SHP. On the third day, the child has several episodes of hematemesis with bright red blood, accompanied by increased pain of the epigastric region. Gastroduodenal endoscopy revealed signs of atrophic gastritis in the antrum, duodenitis with diffuse petechiae, small erosions and bleeding ulcer. The gastric biopsy showed a moderately severe chronic gastritis with activity and H. pylori was detected. The therapy with ranitidine, metronidazole and amoxycillin was introduced for a period of 30 days. At follow-up 2 months later, clinical examination and routine laboratory tests were normal. A repeated endoscopy revealed no evidence of lesions and H. pylori negative gastric biopsy. In our case, the associated chronic antral gastritis and H. pylori infection may well have aggravated the gastrointestinal symptoms of SHP. We feel it would be useful to check for H. pylori in patients with gastrointestinal manifestations of SHP, such as bleeding and important epigastric pain.     

Consistent improvement in sphincterotome orientation with manual grooming

AIMS: To determine the prevalence of lymphoid follicles in Helicobacter pylori positive and negative gastritis in antral and body type gastric mucosa in patients with non-ulcer dyspepsia (NUD), duodenal ulcer, or gastric ulcer; to correlate follicle presence with patient age; to evaluate the correlation between the prevalence of lymphoid follicles and active and inactive gastritis and its severity; and to assess the positive predictive value of lymphoid follicle prevalence with respect to H pylori infection. METHODS: Gastric biopsy specimens, graded according to the Sydney system, from 337 patients were studied. RESULTS: Lymphoid follicles occurred more often in antral mucosa (78%) than in body type mucosa (41%) and were observed in 85% of patients with H pylori positive gastritis. There was no significant difference between NUD and gastric and duodenal ulcer disease with regard to the presence of lymphoid follicles. The positive predictive value of the presence of lymphoid follicles in H pylori infection was 96%. Lymphoid follicles were more commonly observed in patients aged between 10 and 29 years. Lymphoid follicles were more frequently found in pangastritis of all subtypes than in antral gastritis and also in active gastritis than in inactive gastritis. The presence of lymphoid follicles correlated strongly with the degree and severity of gastritis. CONCLUSION: Lymphoid follicles are a constant morphological feature of H pylori associated gastritis.     

Pathology of Helicobacter infection

The colonization of gastric mucosa by Helicobacter pylori (H.p.) is a special form of chronic bacterial infection characterized by long term persistence of microbes because cause of an inefficiency of local immune responses. The resulting chronic gastritis causes decisive transformations of gastric mucosa. They comprise the acquisition of an active mucosa-associated lymphoid tissue as well as the development of glandular atrophy and intestinal metaplasia in the stomach. Both transformations change normal gastric functions, and create abnormal microenvironments with an increased risk for gastric cancer and lymphoma. Own recent investigations indicate, that the distribution and severity of chronic gastritis might be decisively influenced by a rise of antigastric autoimmune reactivity during the H.p. infection. The histologic examination of gastric biopsy samples is essential for an exact diagnosis of the complex pathogenic processes in chronic gastritis. In the future special emphasis of histologic analyses has to be put on the subtypes of gastritis, which are prone for complications and on the evaluation of gastritis remission after H.p. eradication.