Association of Helicobacter pylori with gastritis and peptic ulcer diseases

The occurrence of Helicobacter pylori(H.pylori) and its relationship with gastric mucosa were studied by light and electron microscopy and culture of biopsy specimens from gastric mucosa of 160 patients with upper gastrointestinal symptoms. H. pylori were present in 96.6% of patients with active chronic gastritis, 100% of patients with duodenal ulcer and 76.9% of patients with gastric ulcer, while present in only 6.3% of individuals with histologically normal gastric mucosa. The bacteria colonized the antral mucosa more frequently than the body or than the duodenal cap mucosa. The bacteria were rarely seen in the intestinalized epithelium per se, but there was no significant difference in prevalence of H. pylori between gastritis with intestinal metaplasia and gastritis without intestinal metaplasia. H. pylori could be seen in close association with the surface of gastric epithelial cells below the mucus layer without evidence of intracellular parasitism, All of the strains tested were susceptible to penicillin, erythromycin, and most of them susceptible to tinidazole and bismuth salts. It is concluded that H. pylori are highly associated with gastritis and peptic ulcer diseases and its prevalence rates in patients with those diseases is higher than in developed countries. This strong association of H. pylori infection with gastritis and peptic ulcer diseases suggest a possible etiologic role for the bacterium in those diseases.     

Campylobacter pyloridis in duodenal ulcer

A morphologic study of antral gastric and duodenal mucosa was carried out in patients with duodenal ulcers. Peptic ulcers were in the phase of exacerbation in 55 patients, and that of remission, in 10. Campylobacter pyloridis (CP) were detected in 83% of the cases by histologic investigation of gastric and duodenal mucosa biopsy specimens obtained from patients with duodenal ulcers. CP were more common and numerous during exacerbation rather than remission of peptic ulcers. Bacterial dissemination in gastric and duodenal mucosa was greater in patients with a long history of ulcers, which might possibly indicate pathogenetic involvement of CP in ulcerogenesis. CP are recovered more commonly in individuals with normal or reduced gastric juice acidity as compared to those showing hypersecretion. Although conventional antiulcer treatment reduces CP dissemination, the bacteria are not eliminated in most cases, which might be a cause of peptic ulcer relapses.     

Gastritis, intestinal metaplasia and dysplasia versus benign ulcer in stomach and duodenum and gastric carcinoma -- a histotopographical study.

In histological examination of gastrectomy specimens from patients with duodenal ulcer, gastric ulcer, and early and advanced cancer, both chronic atrophic gastritis and intestinal metaplasia were identified in 54% of the cases with duodenal ulcer. At 90 to 100%, respectively, these mucosal changes were approximately twice as frequent with gastric ulcer and early and advanced gastric cancer. Mild dysplasia occurred in 54% of the cases with duodenal ulcer; occurred somewhat more frequently with gastric ulcer, in 75% of the cases; and in almost all cases with early and advanced gastric cancer, at 90% and 100%, respectively. Whereas 27% of the cases with duodenal ulcer, 62% with gastric ulcer, and 90% and 95% of the respective cases with early and advanced gastric cancer showed moderate dysplasia, only severe dysplasia in early gastric cancer (40%) and advanced gastric (81%) was clearly more frequent in comparison to duodenal ulcer (9%) and gastric ulcer (12%). In the cases with duodenal ulcer chronic atrophic gastritis and intestinal metaplasia were limited mostly to the antrum; with gastric ulcer and cancerous stomach disorders, they also occurred in other stomach sections. Mild and moderate dysplasia conformed to the same distribution pattern. Severe dysplasia, which was only detected in two ulcer cases, was not only substantially more frequent in cases with early and advanced gastric cancer, but also showed a clear topographic relationship to cancer localization in the stomach.     

Duodenal ulcer with gastrin cell hyperplasia--a special form of peptic ulcer

Pap test was used to study gastric and duodenal G and D cells, blood gastrin levels, basal and stimulated acid production, clinical manifestations, and morphological characteristics of the mucosa in 39 patients with duodenal ulcer and 13 controls. The findings enable the authors to outline a special form of peptic ulcer that is characterized by gastrin cellular hyperplasia concurrent with relative pyloric D cell deficit, gastric metaplasia in the duodenum and gastric hypersecretion. Such patients have more frequently multiple ulcers, predominantly 0(I) blood group, complication-aggravated course of the disease, and ulcer history in close relatives. Moreover, it has been demonstrated that incidence of gastric metaplasia is due to gastric hypersecretion; hyperplasia of duodenal gastrin cells is associated with incidence of gastric metaplasia in patients with peptic ulcer.     

Clinicopathological features of duodenal bulb biopsies and their relationship with upper gastrointestinal diseases

AimTo assess the prevalence of the lesions in duodenal bulb mucosa and the relationship between duodenal lesions and upper gastrointestinal diseases, including helicobacter pylori infection.MethodsClinical, endoscopic and pathological data of the cases with duodenal bulb and gastric mucosal biopsy from January 2005 to May 2017 were analyzed retrospectively.ResultsA total of 3540 patients were enrolled. The biopsy from protuberant lesions with endoscopic morphology are mostly duodenal gastric heterotopia or adenoma. The biopsy from duodenal ulcers are often observed in inflammatory changes and gastric metaplasia.Patients with gastric heterotopia had a significantly lower prevalence of chronic atrophic gastritis, intestinal metaplasia, and gastric ulcer; and much higher prevalence of gastroesophageal reflux disease and gastric fundic polyps.Patients with gastric metaplasia had been positively associated with gastroesophageal reflux disease, and negatively associated with gastric fundic polyps.There were positive correlation between helicobacter pylori infection and duodenal active inflammation, Brunner gland hyperplasia, gastric metaplasia and duodenal ulcer. However, Patients with gastric heterotopia in bulb had been negatively associated with helicobacter pylori infection.ConclusionsThe mucosa lesions in duodenal bulb were associated with concurrent gastric fundic gland polyps, gastroesophageal reflux disease, duodenal ulcer, and helicobacter pylori infection.     

Topography of changes in the mucosa of the gastro-duodenal region in chronic gastritis and peptic ulcer]

Topographic studies of 789 gastro- and duodenobiopsies obtained from 493 patients with chronic gastritis and peptic ulcer and from 37 individuals without gastro-duodenal pathology obtained various regions of the stomach and the duodenum were carried out. It was found out that investigation of only one piece of the tissue not in all cases reflected a histological state of the mucosa of the certain regions of the gastro-duodenal area. An isolated gastritis in the body of the stomach in patients with chronic gastritis was found to occur 3 times as seldom as in its distal region. The mucosa of the duodenum was affected almost equally often both in peptic ulcer of this organ and in chronic gastritis. In a number of patients the clinical picture diagnosed as chronic gastritis in reality turned out to be caused by morphological changes in the mucosa of the duodenum, but not of the stomach. At the same time, in a duodenal localization of ulcer not infrequently there were observed histological changes in the gastric mucosa aggravating the course of the main pathological process.     

Detection of Campylobacter pyloridis in patients with antrum gastritis and peptic ulcers by culture, complement fixation test, and immunoblot.

The association of Campylobacter pyloridis with antrum gastritis and peptic ulcers was described. We investigated antral biopsies from 180 patients who underwent gastroscopy. By culture or Gram stain or both, we found overall 98 (54%) of them to be positive for C. pyloridis. In the various groups the following percentages were found to be positive: normal antral mucosa 3% (n = 30); moderate superficial antrum gastritis, 49% (n = 83); severe superficial antrum gastritis, 86% (n = 44); duodenal ulcer, 83% (n = 54); and gastric ulcer, 72% (n = 18). A serological screening that used a complement fixation test yielded the following results: highest rates of positive complement fixation titers were seen in patients with severe gastritis and those with duodenal ulcers, both with 79%; the lowest incidence was in a group of 20 blood donors, with 5%. Positive complement fixation titers in gastritis patients also correlated well with characteristic patterns on immunoglobulin G and A immunoblots, while there was no specific reactivity observed on immunoglobulin M immunoblots.     

Campylobacter pyloridis and acid induced gastric metaplasia in the pathogenesis of duodenitis.

Biopsy specimens of gastric and duodenal mucosa from 290 patients were examined histologically for metaplasia and Campylobacter pyloridis. Estimates of pH on samples of fasting gastric juice from 55 of the patients were performed, and mucosal biopsy specimens from 33 patients were also cultured for C pyloridis. Active duodenitis was seen in 34 duodenal biopsy specimens. Thirty (88%) of the patients with active duodenitis had both greater than 5% gastric metaplasia in the duodenal specimen and C pyloridis associated gastritis. These two factors coexisted in only 0.43% of patients with no duodenal inflammation. When C pyloridis were seen histologically in duodenal biopsy specimens they were confined to areas of gastric metaplasia and never occurred in the absence of a polymorph infiltrate. Of the 55 patients with measurements of gastric juice pH, gastric metaplasia was present in the duodenum in 20 of 42 with a pH of less than 2.5, and in 0 of 13 with a pH of greater than 2.5. These results suggest that acid induced gastric metaplasia in the duodenum and C pyloridis associated gastritis may be synergistic in the pathogenesis of duodenitis; the metaplastic gastric epithelium allows C pyloridis to colonise the duodenal mucosa, where it produces an acute inflammatory response.     

Implications for a role of interleukin‐23 in the pathogenesis of chronic gastritis and of peptic ulcer disease

The present study aimed to investigate the role of gastric mucosa for the secretion of interleukin (IL)‐23 in chronic gastritis. One hundred and one patients were enrolled; 47 with duodenal ulcer, 33 with gastric ulcer and 31 with chronic gastritis. Biopsies were incubated in the absence/presence of endotoxins. Supernatants were collected and IL‐23 and IL‐1β were measured by enzyme‐linked immunosorbent assay. Scoring of gastritis was performed according to the updated Sydney score. Patients with duodenal and gastric ulcer and those with chronic gastritis had similar scores of gastritis. IL‐23 was higher in supernatants of tissue samples of Helicobacter pylori‐positive than of H. pylori‐negative patients. No differences were recorded in concentrations of IL‐23 and IL‐1β between patients with duodenal ulcer, gastric ulcer and chronic gastritis. Positive correlations were found between IL‐23 of patients with both duodenal and gastric ulcer and chronic gastritis and the degree of infiltration of neutrophils and monocytes. Similar correlations were observed between IL‐23 and IL‐1β. IL‐23 secreted by the gastric mucosa could be implicated in the pathogenesis of chronic gastritis. IL‐23 was released in the presence of H. pylori from the inflamed gastric mucosa and followed the kinetics of IL‐1β.     

Impact of Helicobacter pylori eradication on morphological changes in gastric mucosa

The purpose of the study was to examine gastric mucosal morphological changes in patients with gastroduodenal pathology after eradication therapy for Helicobacter pylori (H. pylori). A hundred and thirty-eight patients (40 females and 98 males) were examined. Of them, there were 122 patients with duodenal peptic ulcer, 8 with gastric peptic ulcer, 5 with erosive gastritis, 2 with chronic atrophic antral gastritis, and 1 with non-atrophic gastritis. Two months and a year after therapy, manifestations of gastric mucosal atrophy, the degree of inflammation, and its activity significantly diminished in patients with complete H. pylori eradication. Positive changes were observed mainly in the antral portion of the stomach. In patients with partial eradication, chronic inflammation and its activity became less. Two months and a year following therapy, positive changes in the gastric mucosa were absent in patients without H. pylori eradication.     

The comparison of histologic gastritis in patients with duodenal ulcer, chronic gastritis, gastric ulcer and gastric cancer

This study was designed to investigate the differences of histologic gastritis according to the endoscopic diagnosis, and between H. pylori positive and negative gastritis, using the Sydney system. A total of 122 patients (42 duodenal ulcer, 31 chronic gastritis, 35 gastric ulcer and 14 gastric cancer) underwent endoscopy with biopsies from the antrum and body. Among the 122 patients, 104 (85%) were H. pylori positive. H. pylori density of the antrum was significantly higher in duodenal ulcer than in chronic gastritis, gastric ulcer, and gastric cancer. The positivity of intestinal metaplasia was lowest in duodenal ulcer and highest in gastric cancer. H. pylori density as well as grade of activity, inflammation and atrophy were significantly higher in the antrum than in the body in duodenal ulcer, while in chronic gastritis, gastric ulcer and gastric cancer there was no difference of H. pylori density, activity, inflammation and atrophy between the antrum and body. The grade of activity and chronic inflammation were significantly higher in H. pylori positive patients than in H. pylori negative patients in both the antrum and body. In conclusion, the gastritis of duodenal ulcer was mainly localized to the antrum, while the gastritis of chronic gastritis, gastric ulcer or gastric cancer was rather uniform in the antrum and body. H. pylori seemed to be related to the development of chronic inflammation and activity.     

The gastro-duodenal epithelium in peptic ulceration

Mucosa-related bacteria, intra-epithelial lymphocytes and intra-epithelial polymorphonuclear leucocytes have been studied in 35 patients with duodenal ulceration, 27 patients with gastric ulceration and eight control subjects with normal gastro-duodenal mucosa. Mucosa-related bacteria were found in approximately 80 per cent of peptic ulcer patients and rarely in controls. The bacteria were most numerous at the sites of active chronic gastritis. There was a positive correlation between the number of bacteria and the number of intra-epithelial polymorphonuclear leucocytes. There was no correlation between the peripheral blood white cell count and the number of intra-epithelial polymorphonuclear leucocytes. The number of intra-epithelial lymphocytes was increased in peptic ulceration.     

Helicobacter-associated duodenitis and gastric metaplasia in duodenal ulcer patients.

Biopsy specimens were taken from the duodenal bulb and the distal duodenum in 45 duodenal ulcer patients before and after treatment with histamine-2 antagonists, prostaglandin analogues or antacids. After four weeks of treatment, the ulcer had healed in 31 patients. The treatment did not lead to a reduced frequency of helicobacter-associated duodenitis or gastric metaplasia of the duodenal epithelium. We found gastric metaplasia in 52.3% of all biopsy specimens from the duodenal bulb, chronic active duodenitis in 71.9% and helicobacter-like structures in 15.9%. The helicobacter organisms were found only in areas of gastric metaplasia, and an accompanying chronic active duodenitis was found in 94.1%. In the distal duodenum, we observed chronic active duodenitis in 15.0% of the specimens. Here the inflammation was not associated with gastric metaplasia or helicobacter-like structures. These observations support the hypothesis that Helicobacter pylori colonizes the duodenal mucosa only in areas of gastric metaplasia, and that such colonization may lead to an active duodenitis.     

不同胃黏膜病变患者的血清胃蛋白酶原变化

目的：探讨胃溃疡、十二指肠球部溃疡、非萎缩性胃炎、萎缩性胃炎、胃癌患者胃蛋白酶原(pepsinogen,PG)Ⅰ、PGⅡ水平和PGⅠ/PGⅡ比值变化。方法：选择2015年1月至2015年10月因消化道症状行胃镜检查的门诊及住院患者共133例,根据胃镜检查及组织病理学结果,将受检者分为5组。非萎缩性胃炎组42例、萎缩性胃炎组33例、胃溃疡组20例、十二指肠球部溃疡组23例、胃癌组15例、比较各组血清PGⅠ、PGⅡ水平。结果：与非萎缩性胃炎组相比,胃溃疡、十二指肠球部溃疡患者PGI明显升高(P<0.05),胃溃疡PGII明显升高(P<0.05),萎缩性胃炎组、胃癌组血清PGⅠ及PGⅠ/PGⅡ水平降低(P<0.05)。结论：血清PGⅠ、PGⅡ水平以及PGⅠ/PGⅡ比值对提高消化性溃疡、胃癌前病变及胃癌的诊断有重要的临床价值。     

Histological study of chronic gastritis from the United Arab Emirates using the Sydney system of classification.

AIMS--To determine the prevalence of Helicobacter pylori in five main nationality groups with gastric ulcer, duodenal ulcer, and non-ulcer dyspepsia; and to determine the histopathological types of gastritis and assess the graded variables of Helicobacter associated gastritis. METHODS--Gastric antral and corpus biopsy specimens from 437 patients were examined for the prevalence of H pylori, 337 of which were classified and graded histologically according to the Sydney system. RESULTS--The overall colonisation rate of H pylori was 90%, and there was no significant difference between groups of different ethnic origins. The colonisation rates were 99%, 89%, and 78% in patients with duodenal ulcer, non-ulcer dyspepsia, and gastric ulcer, respectively. Helicobacter associated gastritis was the most common form of chronic gastritis (87%). H pylori density was greater in the antrum than the body. Gastric atrophy in helicobacter associated gastritis was seen in 54% of the cases (43% grade I, 10% grade II, 1% grade III) and increased the older the patients. Atrophy of the corpus alone was very rare (1%). Atrophy and intestinal metaplasia were more prevalent in patients with gastric ulcer than duodenal ulcer. CONCLUSION--The colonisation rate of H pylori was similar in the five groups studied and was almost invariably present in gastric biopsy specimens in patients with duodenal ulcer. H pylori associated gastritis was the most common form of gastritis. Atrophy was mainly of low grade and increased the older the patient.     

Helicobacter (Campylobacter) pylori in the etiology and pathogenesis of gastritis and peptic ulcer

Current information on the role of Helicobacter pylori (HP) in the stomach and duodenum pathology is presented. HP is always found in active chronic gastritis and duodenal ulcer. HP damage to gastric superficial epithelium may result in the accelerated proliferation and incomplete differentiation of epithelium, this being a basis of chronic gastritis morphogenesis. Factors of aggression such as HCl hypersecretion provoke a stomach metaplasia of the duodenal mucosa. HP damage to such areas combined with the factors of aggression result in the transition of a preulcer state into ulcer.     

Nodular gastritis and pathologic findings in children and young adults with Helicobacter pylori infection

PURPOSE: The 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 METHODS: A 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(TM) 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. RESULTS: In 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%). CONCLUSION: Logistic 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.     

不同胃病患者血清、胃液、胃粘膜锌含量的测定

本文对消化性溃疡及慢性胃炎患者进行了血清、胃液、胃粘膜组织微量元素（Ｚｎ）含量测定及幽门螺杆菌检测。结果表明：消化性溃疡及慢性胃炎患者血清、胃液、组织Ｚｎ含量均比正常人明显降低（Ｐ＜０．００１）。胃内幽门螺杆菌感染者比非感染者胃液、组织微量元素Ｚｎ下降更为显者（Ｐ＜０．０５）。     

Role ofHelicobacter pylori in gastritis and duodenitis in man

AlthoughHelicobacter pylori is now accepted as the major aetiological factor in chronic gastritis in man, many of the factors which determine its pathogenicity are unknown. The organism has adapted to survive in the low-pH environment of the stomach, partly through its ability to buffer hydrogen ion by the hydrolysis of urea and by the presence of lectins on its surface, which bind to gastric mucosa and epithelial cells. After attachment, harmful toxins and enzymes have access to the gastric cells and cellular damage and an immune response ensues. In patients with duodenal ulceration,Helicobacter pylori-related gastritis predominantly affects the gastric antrum and has a high prevalence. Excessive gastrin production has been suggested as a potential aetiological factor linking infection with duodenal ulcer development. Perhaps more important is the association between gastric metaplasia of the duodenal epithelium, which is correlated with acid load and is more extreme inH. pylori positive patients with duodenitis. Organisms may subsequently spread from the gastric antrum into areas of gastric metaplasia in the duodenal bulb, leading to areas of chronic duodenitis and ultimately frank ulceration. It should not be overlooked, however, that other factors such as genetic predisposition, blood group, stress, drugs and smoking all have a role to play in the outcome, given the comparatively small number of patients in the general population infected withH. pylori who develop ulcer disease.