The prevalence of lymphoid follicles in Helicobacter pylori associated gastritis in patients with ulcers and non-ulcer dyspepsia.

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.     

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 peptic ulcer

To study the role of Campylobacter pyloridis (CP) in the etiology of peptic ulcer and chronic gastritis, biopsies were obtained from gastric and duodenal mucosa of 54 ulcer patients and 8 healthy controls. In normal histological appearance and moderate gastritis without signs of exacerbation CP were not registered contrary to atrophic antral gastritis demonstrating CP irrespective of ulcer location. CP resided on the epithelium under the mucous layer between epitheliocytes. Contamination proved mild in 13%, moderate in 50% and profound in 80% of cases. CP were associated with peptic ulcer in 78% of relevant patients, with duodenal ulcer in 80% of those. The duodenal presentation was observed only in the regions of gastric metaplasia. CP did not occur in fundal mucosa, ulcer boundaries and intestinal metaplasia. There was no significant difference in CP amount at various ulcer sites. It is suggested that CP may play a role in the etiology and pathogenesis of peptic ulcer.     

Antral histopathological changes in acid peptic disease associated with Helicobacter pylori

The histopathology of the antral mucosa of patients with acid peptic disease was studied in relation to Helicobacter pylori infection. Three hundred and fifty-five patients underwent gastroscopy and biopsy on 443 occasions. During each gastroscopy, two antral samples were taken for Rapid Urease Test (RUT) for H. pylori and two antral samples for histopathology. Haematoxylin and Eosin and modified Giemsa stained sections were studied. Histopathological changes in the antrum and the density of H. pylori were graded according to the Sydney System criteria. There was a significant association between the RUT and histology results for detection of H. pylori. The overall prevalence of H. pylori was 61.4% with a maximum incidence in the third and fourth decades of life, and an equal sex distribution. H. pylori colonisation was seen in 90.7% of patients with duodenal ulcer, 66.7% with gastric ulcer and 44.3% with non-ulcer dyspepsia. H. pylori colonisation was associated with more severe antral chronic active gastritis, lymphoid follicles, intestinal metaplasia and dysplasia. Elimination of H. pylori by treatment with anti-H. pylori regimens resulted in regression of the changes.     

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.     

Clinical and histological associations of cagA and vacA genotypes in Helicobacter pylori gastritis.

AIMS: To determine the relation among the cytotoxin associated gene (cagA) and vacuolating cytotoxin gene (vacA) status of Helicobacter pylori isolates, the associated clinical diseases, and the severity and pattern of chronic gastritis. METHODS: Helicobacter pylori was cultured from gastric biopsies obtained from dyspeptic patients. DNA was extracted from the isolates and the cagA and vacA status determined by the polymerase chain reaction (PCR). The prevalence of the different cagA and vacA genotypes in three clinical groups, duodenal ulcer, gastric ulcer, and non-ulcer dyspepsia was compared. The histological features in sections from two antral and two corpus biopsies were graded by one blinded observer. The grades were compared with age and sex matched groups with different cagA and vacA genotypes, and with duodenal ulcers, or non-ulcer dyspepsia. RESULTS: Isolates from 161 patients were included. One hundred and nine (68%) harboured a cagA+ strain and 143 (89%) harboured a vacA s1 strain. The prevalence of cagA+ strains in duodenal ulcer patients (94%) was highly significantly greater than in those with non-ulcer dyspepsia (56%). However, of the patients infected with a cagA+ strain, almost equal numbers had non-ulcer dyspepsia or peptic ulceration. Chronic inflammation, polymorph activity, surface epithelial degeneration, atrophy, and intestinal metaplasia were all significantly more severe in the cagA+ than in the cagA- group, whereas only corpus epithelial degeneration was significantly more severe in the vacA s1 group compared with the vacA s2 group. Patients infected with cagA+ strains were almost four times more likely to have antral intestinal metaplasia than cagA- patients. An antral predominant gastritis was present in duodenal ulcer patients compared with matched non-ulcer dyspepsia patients, but this was not attributable to cagA or vacA status. CONCLUSIONS: Helicobacter pylori strains showing cagA positively and the vacA s1 genotype are associated with more severe gastritis but these virulence factors do not appear to determine the overall pattern. The pattern is closely linked to clinical disease. Therefore, it is likely that the nature of the disease complicating chronic infection is determined by host and environmental factors, while bacterial factors determine the magnitude of the risk of developing such disease.     

Co-expression in Helicobacter pylori of cagA and non-opsonic neutrophil activation enhances the association with peptic ulcer disease

AIMS: To investigate the association of cagA positivity and non-opsonic neutrophil activation capacity in wild-type Helicobacter pylori strains with peptic ulcer disease or chronic gastritis only. METHODS: Helicobacter pylori were isolated from antral biopsies of 53 consecutive patients with chronic antral gastritis, of whom 24 had peptic ulcer disease endoscopically. The presence of cagA, a marker for the cag pathogenicity island, was determined by polymerase chain reaction with specific oligonucleotide primers, and non-opsonic neutrophil activation capacity by luminol enhanced chemiluminescence. RESULTS: The cagA gene was present in 39 of 53 (73.6%) strains, 20 of which (83.3%) were from the 24 patients with peptic ulcer disease and 19 (65.5%) from the 29 patients with chronic gastritis only. Non-opsonic neutrophil activation was found in 29 (54.7%) strains, 16 of which (66.7%) were from patients with peptic ulcer disease, and 13 (44.8%) from those with chronic gastritis. Non-opsonic neutrophil activation was found more frequently in cagA+ than cagA- strains (59% v 42.9%). Whereas four of the 14 cagA- strains and eight of the 24 non-opsonic neutrophil activation negative strains were from patients with peptic ulcer disease, only two of 24 (8.3%) peptic ulcer disease strains expressed neither cagA nor non-opsonic neutrophil activation. The cagA gene and non-opsonic neutrophil activation capacity were co-expressed in 14 of 24 (58.3%) strains from patients with peptic ulcer disease, and in nine of 29 (31%) strains from individuals with chronic gastritis. CONCLUSIONS: Positivity for cagA and non-opsonic neutrophil activation occur independently in wild-type H pylori strains. However, co-expression of the two markers enhanced the prediction of peptic ulcer disease.     

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.     

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.     

Gastric mucosa in patients with portal hypertension: prevalence of capillary dilatation and Campylobacter pylori.

To determine whether the "congestive" gastropathy associated with portal hypertension showed distinctive histological features independent of inflammatory gastritis, endoscopic biopsy specimens of gastric mucosa from 23 patients with portal hypertension and 25 patients with non-ulcer dyspepsia were examined. Active chronic gastritis associated with Campylobacter pylori was found in three patients with portal hypertension compared with 13 patients with non-ulcer dyspepsia. The changes of reflux gastritis were seen in nine patients with portal hypertension compared with three patients with non-ulcer dyspepsia. Mucosal capillary dilatation, assessed on sections stained for factor VIII related antigen, a specific marker for endothelial cells, was significantly greater in biopsy specimens from patients with portal hypertension but this difference was not apparent on sections stained conventionally. The degree of capillary dilatation was unrelated to the presence of histological gastritis. These observations support the view that portal hypertension is associated with a distinctive gastropathy characterised by prominence and dilatation of mucosal capillaries.     

Association of Campylobacter pylori on the gastric mucosa with antral gastritis in children

We investigated the presence of Campylobacter pylori colonization of the gastric mucosa and of histologic evidence of gastritis in a prospective study of 71 consecutive children undergoing upper gastrointestinal tract endoscopy and gastric biopsies because of gastrointestinal symptoms. Two tissue samples from the gastric antrum were obtained from 67 of the 71 children (mean age [+/- SD], 11.4 +/- 3.8 years). One sample was evaluated for evidence of gastritis and stained with silver to detect organisms morphologically resembling campylobacter. The second sample was cultured for C. pylori, and a portion was used to perform a urease-screening test for the presence of C. pylori. Antral gastritis was diagnosed histologically in 18 of 67 patients. C. pylori was identified by both culture and silver staining on the antral mucosa in 7 of 10 patients with unexplained gastritis (primary gastritis) but in none of 8 patients with gastritis associated with an identifiable underlying cause (secondary gastritis). C. pylori was not identified in any of the 49 cases with normal histologic features. The urease-screening test was positive in only three of six patients with a positive culture for C. pylori. Duodenal ulcers were diagnosed by endoscopy in five patients. Each of the five had C. pylori on the antral mucosa, but organisms were not identified on the duodenal mucosa. We conclude that the presence of C. pylori on the antral mucosa is specifically associated with primary antral gastritis and may also be associated with primary duodenal ulceration.     

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）。     

Bacteria of the gastric antrum and their relation to chronic gastritis

Biopsy samples from the gastric antrum were taken from 61 patients. On bacteriological culture, Campylobacter pylori was isolated in 27 subjects. Thirty-four patients had chronic gastritis, as seen in routine-stained histological sections. By means of the May-Grünwald-Giemsa (MGG) staining technique, bacteria were demonstrated in sections from 26 subjects. Of these, 22 had gastritis histologically. In 13 subjects, structures similar to Campylobacter pylori were found in MGG-stained sections, 11 of these having chronic active gastritis histologically. Scanning electron microscopy demonstrated bacteria with the typical appearance of Campylobacter pylori, but other types of bacteria were also found, both on electron microscopy and on bacteriological culture. The study confirms that there is an increased frequency of histological gastritis when Campylobacter pylori is present in the samples (p = 0.009). However, a causative role of the bacteria could not be demonstrated in this study, and bacterial penetration into the epithelium was not observed.     

Immunocytochemical identification of Campylobacter pylori in gastritis and correlation with culture

Endoscopic biopsy specimens of antral mucosa from 25 patients presenting with gastric complaints were obtained for culture and histologic and immunocytochemical studies. The histopathologic study revealed chronic gastritis in 22 patients and borderline chronic gastritis in three patients. The unlabeled-antibody peroxidase-antiperoxidase (PAP) method was applied for the detection of Campylobacter pylori, and its results were compared with those obtained with the culture technique. Strongly positive immunoperoxidase staining was localized in spiral, curved bacteria that were present in the mucus layer adjacent to the gastric epithelial cell surface. The microorganisms were frequently congregated in clumps and were sectioned in several directions. The PAP stains were positive in 19 specimens (76%), and the cultures were positive in 20 (80%). All results negative by culture were also negative by PAP method. Compared with the cultures, the sensitivity and positive predictive value of the PAP method for identification of C pylori in antral mucosa obtained from endoscopic biopsy specimens were 95% and 100%, respectively.     

Helicobacter pylori and associated gastroduodenal diseases. Review article

Helicobacter pylori is a microaerophilic, Gram-negative, spiral rod, the role of which in different gastric diseases has been investigated worldwide since the beginning of the 1980s. H. pylori has been shown to be the causative agent in active chronic gastritis, and it is regularly found in patients endoscopied for duodenal ulcer. The bacterium is also frequently isolated from persons with gastric ulcer, gastric carcinoma and non-ulcer dyspepsia. Apart from cultivation of the bacterium, other diagnostic procedures include various staining methods and urease tests of gastric biopsy samples. The application of non-invasive diagnostic methods, serology and urea breath tests, is rapidly increasing. H. pylori is susceptible to several antimicrobials in vitro, but eradication of the bacterium from the gastric mucosa is not always achieved. The best results until now have been obtained with the combined use of bismuth salts and two antibiotics. In active chronic gastritis and duodenal ulcer patients, eradication of the bacteria has resulted in healing of the disease with permanent decrease of circulating antibodies and negative urease tests. H. pylori has been found worldwide and the infection shows an age-dependent increase. Man, apparently, is the reservoir of the bacterium, but the exact mechanisms of interhuman transmission are still not defined.     

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 (aka Campylobacter) pylori as the major causal factor in chronic hypochlorhydria.

Helicobacter (formerly known as Campylobacter) pylori, a recently discovered gastrointestinal bacterial pathogen, has been shown to be etiologic for Type B or antral gastritis, and usually has chronic active pathological changes associated with its presence. Acute Helicobacter infection in most cases induces reduced stomach acid secretion which usually returns to normal levels of secretion after a few months. Yet Helicobacter gastritis has never been known to spontaneously remit after it has been established, and there is evidence suggesting that it often progresses to cause atrophic changes in the gastric mucosa. Since chronic gastritis has been shown in past studies to lead to chronic persistent hypochlorhydria from atrophic damage to secretory tissue, and Helicobacter has been shown to cause most chronic gastritis, the reasonable conclusion is that Helicobacter infection is etiologic for most chronic persistent hypochlorhydria. The apparent exception of the hyperchlorhydria in duodenal ulcer disease associated with Helicobacter infection is explained. The possible clinical relevance of hypochlorhydria will be the subject of a subsequent paper.     

Helicobacter pylori and gastro-duodenal pathology

Helicobacter Pylori (HP) were found in 878 (73%) of 1205 patients undergoing upper G-I endoscopy with multiple biopsies for gastroduodenal diseases. HP were present in similar percentages among patients with active (89%) or healed (81%) peptic ulcer as well as in non ulcerous dyspeptics affected with gastritis (85%). 96% of active chronic gastritis were infected by HP as compared with 55% of quiescent gastritis. Antral gastritis was more frequently active in patients with ulcer diseases (76%) than in dyspeptic and asyntomatic patients (50%). Healed gastric and duodenal ulcers showed decreased incidence of active antral gastritis (69) as compared with active ulcers. Conversely body gastritis was more frequently active in healed (37%) than in overt (18%) duodenal ulcers. 95 histologically normal stomachs as well as 9 cases exhibiting type A gastritis were devoid of HP. High rates of infection were found in 610 cases of chronic gastritis without atrophy as well as in 151 atrophic antral (type B) gastritis. Cytoplasmic vacuolization and swelling of foveolar-superficial cells with adhering bacteria, micropapillae and microerosions were commonly found in HP-infected mucosa. In 16 of 19 children with type B chronic gastritis antibacterial therapy eradicated HP. This was followed by resolution or striking improvement of gastritis and disappearance of epithelial lesions.     

Pathology of the gastric antrum and body associated with Helicobacter pylori infection in non-ulcerous patients: is the bacterium a promoter of intestinal metaplasia?

A series of 115 consecutive, non-ulcerous, dyspeptic patients were examined for Helicobacter pylori (H. pylori) colonization in the gastric antral and/or body mucosa using Giemsa staining. Findings were correlated with the presence and degree of activity of superficial gastritis, deep gastritis, atrophic gastritis and with the presence of intestinal metaplasia. The prevalence of H. pylori positivity was 61.7%. In 59 of the 71 positive patients (83%), H. pylori was detected in the antrum or in both the antral and oxyntic mucosa. In the remaining 12 positive patients, H. pylori was detected only in the oxyntic mucosa and in all these cases, the antrum showed intestinal metaplasia associated with atrophic gastritis (25%). In both antral and oxyntic mucosa, the activity of the gastritis was significantly correlated with H. pylori colonization. Linear logistic regression analysis showed that in patients with intestinal metaplasia the presence of H. pylori infection was significant in predicting the presence of more extensive intestinal metaplasia after adjusting for age. The prevalence of intestinal metaplasia types II and III was 65.5% in the H. pylori positive and 25% in the H. pylori negative patients. The antral mucosa is thought to be the elective site for H. pylori related histological lesions. At a later stage, H. pylori can be detected only in the oxyntic area while the antral mucosa shows extensive metaplastic or atrophic lesions. We would suggest that H. pylori plays a promotional role in the morphogenesis of intestinal metaplasia.     

Spectrotypic analysis of antibodies to Helicobacter pylori in patients with antral gastritis and duodenal ulcer.

AIMS--To investigate the anti Helicobacter pylori (H pylori) spectrotype associated with (a) antral gastritis and duodenal ulcer; (b) the H pylori eradicating treatment. METHODS--Spectrotypic analysis was performed by isoelectric focusing and reverse blotting (IEFRB) in a cross sectional study on sera from 70 patients with antral gastritis and duodenal ulcer. In addition, a longitudinal study was performed on 40 of these patients (20 with antral gastritis and 20 with duodenal ulcer) who underwent eradicating treatment. RESULTS--The cross sectional study showed that the oligoclonal spectrotype was present in 74% of antral gastritis patients and in 85% of duodenal ulcer patients. In only a minority of subjects (23% with antral gastritis and 3% with duodenal ulcer) was a polyclonal spectrotype observed. The longitudinal study showed a reduction in the intensity of the spectrotypic bands in 5/10 antral gastritis patients with eradicated H pylori as opposed to only 2/10 patients without eradication. A reduction was also observed in 6/11 eradicated v 0/9 non-eradicated patients with duodenal ulcer. Collectively, a reduction in the spectrotype was observed in 11/21 patients (52%) who--independently of the disease--underwent H pylori eradication, as opposed to 2/19 of the non-responder patients (10.5%). The polyclonal spectrotype was found exclusively in four patients with antral gastritis, all belonging to the group without eradication of H pylori after eradicating treatment. CONCLUSIONS--The anti H pylori oligoclonal spectrotype is the most common pattern observed in patients with antral gastritis and duodenal ulcer. After H pylori eradicating treatment the spectrotype does not change qualitatively, but the polyclonal pattern seems to be predictive of a poor response to eradication.