胃黏膜树突状细胞与幽门螺杆菌相关性胃炎的关系

目的:研究胃黏膜树突状细胞在幽门螺杆菌(Hp)相关性胃炎发生中的作用。方法:内镜下收集正常/慢性胃炎胃黏膜标本,快速尿素酶试验、C14呼气试验和Warthin-Star-ry银染色检测Hp,Ficoll-Hypaque密度梯度离心法分离胃黏膜标本中的单个核细胞,进一步采用磁珠分选技术分离HLA-DR+DCs,分析DCs数量与Hp分布密度和胃黏膜炎症程度的关系。结果:Hp阴性正常胃黏膜中巨噬细胞平均含HLA-DR+DCs4.93%,Hp阳性正常胃黏膜中HLA-DR+DCs含量为17.93%,明显高于Hp阴性组(P<0.01);胃黏膜DCs数量与Hp分布密度成正相关(P<0.05);胃黏膜炎症程度为中度和重度的标本中HLA-DR+DCs含量明显高于轻度(P<0.05),中度和重度相比差异无统计学意义。结论:成功分离了胃黏膜DCs,并证实DCs与Hp相关性胃炎发生的早期阶段密切相关。     

The role of apoptosis and proliferation of epitheliocytes in morphogenesis of Helicobacter pylori-associated gastritis

77 patients with chronic Helicobacter gastritis verified endoscopically and exacerbation of duodenal ulcer were examined. H. pylori infection was identified by the rapid ureasa test (CLO-test) and Giemza staining. The patients received 7-day three-component therapy for eradication of H. pylori. Apoptosis and proliferation were studied in 16 patients in serial sections with the use of monoclonal antibodies. Eradication of H. pylori resulted in relief of inflammation and transformation of active gastritis in inactive one. H. pylori-associated gastritis is associated with activation of apoptosis of gastric mucosa epithelial cells and epitheliocytes proliferation. H. pylori eradication alters correlation between apoptosis of epitheliocytes and their proliferation: successful eradication of the infection decreases apoptosis, high proliferative activity of epitheliocytes persists reflecting enhancement of regeneration in gastric mucosa.     

IgE-containing cells in gastric mucosa with and without Helicobacter pylori infection

Gastric mucosa responds with inflammation to Helicobacter pylori (H. pylori) infection. While numerous reports have shown that the immune system produces specific IgG, IgA, and IgM isotype anti H. pylori antibodies, IgE-mediated pathways of H. pylori-associated gastritis are mostly unknown. Our aim was to evaluate whether an increased presence of IgE in the antral gastric mucosa is responsible for the severity of the H. pylori-associated gastritis. The number of IgE-containing cells was estimated in formalin-fixed, paraffin-embedded antral gastric biopsy specimens using immunohistochemistry in three groups of patients: (i) 20 H. pylori-positive cases with moderate inflammation, (ii) 19 H. pylori-negative cases with moderate inflammation, and (iii) 19 H. pylori-negative cases with normal mucosa. In chronic gastritis, the number of IgE-positive cells increased significantly as compared to normal mucosa. In gastritic patients, H. pylori positivity was accompanied by a significant accumulation of IgE-positive cells, mainly plasma cells. These data suggest that IgE-mediated immune response probably plays an important role in the development of H. pylori-associated gastritis.     

Association of Helicobacter pylori with HLA-DR antigen expression in gastritis.

AIMS: To assess the association between Helicobacter pylori-associated gastritis and HLA-DR antigen (class II antigen) expression. METHODS: Fifty endoscopic gastric biopsy specimens were studied for the presence of H pylori, degree and type of inflammation, and for HLA-DR antigen expression in the epithelium. The cases were chosen to represent different categories: inflamed gastric mucosa with (n = 13) and without (n = 20) H pylori, and non-inflamed mucosa (n = 17). RESULTS: The antigen was aberrantly expressed in the antral mucosal epithelium in 11 of 12 cases (92%) with acute-on-chronic gastritis when H pylori was also present. It was present in the antrum in only seven of 18 H pylori negative cases (39%) with acute-on-chronic/chronic gastritis. One of three cases of acute gastritis and three of seven cases of chronic gastric erosions (non-inflamed category) showed positive staining. Generally, there was more staining in the antral than body mucosa and in the surface/foveolar epithelium than in the glands. No aberrant HLA-DR antigen expression was found in the 10 cases of normal gastric mucosa examined. CONCLUSIONS: These findings suggest that H pylori may have a role in the induction of class II HLA antigen expression in chronic gastritis and lend support to the view that these organisms may be responsible for part of the inflammatory response.     

Involvement of mast cells in gastritis caused by Helicobacter pylori: a potential role in epithelial cell apoptosis

BACKGROUND: The role(s) of mast cells (MC) in gastric mucosal inflammation caused by Helicobacterpylori is (are) still debated. AIM: To determine whether there is an association between MC density and epithelial cell apoptosis in antral gastric mucosa infected by H pylori. Patients and methods: Biopsy specimens from 122 H pylori-positive subjects with chronic active gastritis, 84 patients with non-steroidal anti-inflammatory drug-induced gastritis and 48 volunteers were included. H pylori genotypes were determined by PCR amplification of bacterial cultures. Immunohistochemical analysis was performed on tissue microarrays with anti-CD117, anti-chymase, anti-tryptase, anti-myeloperoxidase, anti-Bcl-2, anti-Bcl-x, anti-Bax and anti-caspase 3 antibodies. RESULTS: Of the 122 patients infected with H pylori, 76 (62.3%) harboured cagA positive strains. H pylori isolates belonged to the vacAs1/m1 genotype in 82 (67%) cases, to the vacAs2/m2 genotype in 23 (18.8%) cases and to the vacAs1/m2 genotype in 17 (13.9%) cases. 61 (50%) H pylori isolates were babA2+. In patients infected with H pylori, the density of MC, and in particular the number of MC-associated epithelial cells, was correlated with a high number of apoptotic epithelial cells. Moreover, the density of MC was correlated with the number of neutrophils infiltrating the antral gastric mucosa, and was strongly increased in patients infected with cagA, vacAs1/m1 and babA2 positive strains. CONCLUSIONS: Taken together, these data show that the density of MC can be considered as a histopathological criterion of gastritis activity in patients infected with H pylori.     

Gastrin (G) cells and somatostatin (D) cells in patients with dyspeptic symptoms: Helicobacter pylori associated and non-associated gastritis

BACKGROUND: Gastrin G cells and somatostatin D cells are important regulators of gastric acid secretion and alterations in their relative numbers may play a key role in gastroduodenal disease. AIM: To investigate the effect of Helicobacter pylori infection on the density of immunoreactive G and D cells in gastric antral and corpus biopsies from patients with dyspeptic complaints. METHODS: One hundred and twenty two patients with dyspeptic complaints had two antrum and two corpus biopsies taken during upper endoscopy. The severity of inflammation and the density of H pylori were evaluated semiquantitatively. In addition, the density and distribution of neuroendocrine cells, especially G and D cells, were examined using immunohistochemistry. Patients were divided into three groups, those with H pylori positive gastritis, H pylori negative gastritis, and histologically normal gastric mucosa. RESULTS: The number of immunoreactive G cells was significantly higher and the number of immunoreactive D cells lower in patients with H pylori positive gastritis compared with H pylori negative gastritis or histological normal gastric mucosa. The percentage of G cells as a percentage of mucosal endocrine cells was also raised and that of D cells was decreased. CONCLUSIONS: Helicobacter pylori infection produces alterations in the number of endocrine cells responsible for regulating acid secretion in relation to intragastric pH and feeding. The alterations correlate best with the severity of inflammation and not with H pylori density.     

Helicobacter pylori und antigastrale Autoimmunität

Recent studies report a significant association between Helicobacter pylori gastritis and autoimmune reaction. Antigastric autoantibodies are detectable in about 30% of H. pylori infected patients. Two major in situ binding sites have been found: first, at the luminal membrane of the foveolar epithelium in antrum and corpus mucosa and, second, at canalicular membranes within parietal cells in the corpus mucosa. The presence of latter type of autoantibodies is correlated with histological and clinical parameters of corpus mucosa atrophy. The gastric H+/K(+)-ATPase, which is already known as an autoantigen in classic autoimmune gastritis, also represents a major target in atrophic H. pylori gastritis. According to recent data molecular mimicry between H. pylori and the host does not play a pathogenic role in the formation these autoantibodies. In conclusion, antigastric autoimmunity represents a relevant host factor which contributes to the final outcome of H. pylori gastritis.     

Acute inflammation of the proliferative zone of gastric mucosa in Helicobacter pylori gastritis.

The neutrophilic infiltration has been regarded to represent the activity of Helicobacter pylori gastritis. It may involve the epithelium and/or lamina propria. The incidence and degree of the two types of infiltration do not correlate with each other frequently. We correlated the two types of neutrophilic infiltration with H. pylori infection and other pathologic parameters respectively in 300 randomly selected gastric biopsies as well as serial biopsies from a separate group of 95 patients who were treated for H. pylori infection. The "random biopsies" had chronic gastritis of various degrees, and the organisms were identified in 239 cases (79.7%); in the "treated group," the organisms disappeared completely in 62 cases (65.3%). Characteristically, the intraepithelial neutrophilic infiltration was predominantly localized to the proliferative zone of the gastric mucosa (zone 2) where the density of H. pylori was considerably lower than the surface epithelium. In the "random biopsies," both acute epithelial and interstitial neutrophilic infiltration correlated significantly (p < 0.01) with the H. pylori infection. In the "treated group," however, only acute epithelial inflammation correlated significantly (p < 0.01) with the eradication of infection while acute interstitial inflammation did not. Acute epithelial inflammation was no less frequently present in advanced chronic gastritis than in early chronic gastritis. Acute epithelial inflammation of the proliferative zone is a characteristic pathologic finding of H. pylori gastritis, and appears to be directly associated with the pathogenesis of H. pylori gastritis and its progression.     

Expression and subcellular distribution of toll-like receptors TLR4, TLR5 and TLR9 on the gastric epithelium in Helicobacter pylori infection

Toll-like receptors (TLRs) expressed by mucosal epithelium play an essential role in the defense against microbes by recognizing conserved bacterial molecules. For the first time TLR4, TLR5 and TLR9 have been microanatomically localized in patients with noninflamed gastric mucosa and Helicobacter pylori gastritis by immunohistochemistry. Because polarized expression of TLRs in apical and basolateral epithelial compartments is thought to modulate mucosal immunity, subcellular TLR distribution by gastric epithelium was investigated using confocal microscopy. TLR4, TLR5 and TLR9 were expressed by gastric epithelium in antrum and corpus of all patients with H. pylori gastritis (n = 14) and with noninflamed gastric mucosa (n = 5). TLR4 was expressed at the apical and the basolateral pole of the gastric epithelium as well in noninflamed gastric mucosa as in H. pylori gastritis. TLR5 and TLR9 expression in the noninflamed gastric mucosa was identical to that of TLR4 with localization at the apical and the basolateral epithelial pole. However, in H. pylori gastritis TLR5 and TLR9 expression on the gastric epithelium changed to an exclusive basolateral localization without detectable expression at the apical pole. In the human stomach, the gastric epithelium expressed TLR4, TLR5 and TLR9, which gives it the possibility to interact with H. pylori. Furthermore, gastric epithelial TLR4 expression is highly polarized in an apical and a basolateral compartment, whereas TLR5 and TLR9 polarization seems to be a process dynamically influenced by H. pylori infection. This polarized and dynamically regulated gastric epithelial expression of TLRs supports a sentinel role for these receptors in the mucosal immunity to H. pylori.     

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.     

Alterations in the proliferating compartment of gastric mucosa during Helicobacter pylori infection: the putative role of epithelial cells expressing p27(kip1).

The proliferating zone contains stem cells that give rise to all epithelial cells of the gastric mucosa. In the present study, we investigated the turnover of gastric epithelial cells in the proliferating zone of Helicobacter pylori-infected mucosa, with or without intestinal metaplasia, before and after eradication of the microorganism. In addition, we studied the topographical distribution of the cyclin dependent kinase inhibitor p27(Kip1), which plays a critical role in cell cycle progression and differentiation programs. Twenty-eight patients (22 male), aged 32-78 years and with dyspeptic symptoms, were endoscoped, and gastric biopsies were obtained from antrum and corpus for histopathological examination and the Campylobacter-like organisms test; eradication therapy was given to infected patients, and all patients were re-endoscoped after 105 +/- 33 days (mean +/- SD). The kinetics of gastric epithelial cells and p27(Kip1) status was assessed by means of immunohistochemistry and TUNEL (Tdt-mediated dUTP-biotin nick end labeling) assay. Twenty-one (21) of 28 patients were H. pylori positive, and 7 were found H. pylori negative and served as controls. In antrum, intestinal metaplasia was detected in 7/21 (33.3%). In H. pylori gastritis, Ki67 expression was found increased in the proliferating zone, compared with normal (P =.03); analogous results were obtained with the other proliferation markers, namely retinoblastoma protein and topoisomerase IIalpha. An inverse relationship between proliferation index and atrophy was disclosed (P =.02). A reduction in the proliferation index was observed after eradication, albeit not significant. Apoptotic epithelial cells were found significantly increased (P <.01) in H. pylori gastritis, and a significant reduction was observed after eradication (P <.01). In addition, apoptotic index was found to correlate with H. pylori density. The topographical study of p27(Kip1) revealed a p27(kip1)-positive epithelial cell population that resided deep in the proliferating zone; these cells were considered to be stem cells and were found significantly increased in areas with intestinal metaplasia (P <.05); in H. pylori gastritis, there was also an increase that did not reach statistical significance. H. pylori infection induces apoptosis and increases proliferation in the proliferating zone. The increased cellular turnover, together with the increased number of putative p27(Kip1)-positive stem cells in the context of intestinal metaplasia, provides further evidence for the role of H. pylori infection in gastric carcinogenesis.     

Clinical, endoscopic and histologic aspects of chronic Helicobacter pylori gastritis in Côte d'Ivoire: study of 102 patients

BACKGROUND: Helicobacter pylori (H. pylori) is the most frequent aetiological factor of chronic gastritis (CG). The relationship between H. pylori gastritis, gastro-duodenal ulcer and some gastric cancers (adenocarcinoma, gastric MALT lymphoma) has now been proven. AIM: Describe clinical, endoscopical and histological aspects of H. pylori gastritis in C?te d'Ivoire. METHODS: Retrospective analysis of 1960 gastroscopy reports carry out between January 1994 and December 1995. Analysis of clinical and gastric histological results in 137 patients. FINDINGS: Among 137 patients with gastric biopsy, 102 had H. pylori gastritis (68 men, 38 women, mean age: 39.3 years) and 35 had chemical gastritis. Epigastric pain was the most frequent symptom. The mucosa was frequently erythematous or exsudative at endoscopy. Histological anomalies were located in the antrum, the fundus or generalised, respectively in 33.3%, 25.5% and 41.2% of cases. Mild atrophic CG was more frequent in various locations. Gastritis activity was present in 81.4%, intestinal metaplasia in 18.6% and follicular lymphoid hyperplasia in 36.3% of cases. CONCLUSION: Clinical and endoscopical aspects of H. pylori gastritis did not present any particularities. Fundic gastritis without antral localisation was not unusual. This situation could be the result of antibiotic and gastric acid secretion inhibitor treatments.     

Campylobacter-like organisms and heterotopic gastric mucosa in Meckel''s diverticula.

To assess the possibility that Campylobacter pylori might colonise heterotopic gastric mucosa a detailed histological review of 69 cases of Meckel's diverticula resected over 17 years was undertaken. Twenty three were resected incidentally while 46 were excised as the suspected cause of symptoms. Gastric mucosa was found in 13 diverticula (19%), 10 from the symptomatic group and three from the incidental cases, of which eight showed active gastritis affecting the heterotopic mucosa. Specific staining showed spiral bacteria with the typical morphology of C pylori adherent to gastric mucosa in four of the diverticula showing active gastritis. Campylobacter-like organisms were not seen on normal heterotopic gastric mucosa or on adjacent intestinal epithelium. The findings show that Campylobacter-like organisms, identical in appearance, staining, and distribution with C pylori, colonise and possibly inflame heterotopic gastric mucosa in Meckel's diverticulum.     

重组幽门螺杆菌疫苗免疫保护作用与免疫后胃炎

目的：研究以减毒鼠伤寒沙门菌为载体构建的幽门螺杆菌(Helicobacter pylori，Hp)疫苗的免疫保护机制。方法：将表达不同Hp抗原的减毒鼠伤寒沙门菌(Salmonella typhimurium)分别免疫小鼠，免疫4周后以Hp攻击；在攻击前及攻击后5周分批处死小鼠，比较各组小鼠Hp定植密度及各项免疫指标的变化。结果：(1)和NS(Normal salin，NS)对照组相比各免疫组的Hp定植密度显著下降。(2)和NS组相比攻击前后各免疫组血清IgG2a和胃黏膜Th1型细胞因子表达显著升高。(3)和NS组相比攻击后免疫组鼠胃黏膜出现明显的炎症反应。结论：以减毒鼠伤寒沙门菌为载体构建的重组幽门螺杆菌疫苗在小鼠体内诱导出以Th1反应为主并伴随免疫后胃炎的保护性免疫应答。     

Features of gastritis predisposing to gastric adenoma and early gastric cancer

BACKGROUND/AIMS: Helicobacter pylori gastritis is a risk factor for the development of gastric cancer. The results of several studies indicate that gastric adenomas, which are considered premalignant lesions, may also be associated with H pylori gastritis. However, it is not clear whether there are different patterns of gastritis in these patients compared with patients with gastric cancer or patients with H pylori gastritis alone. Therefore, this study was designed to investigate the patterns of gastritis in these three groups of patients. METHODS: The histological features of gastric mucosa at a distance from the tumour were analysed prospectively in 118 patients with gastric adenoma (mean age, 71.8; female to male ratio, 6 : 4). In addition, for every patient with H pylori associated gastric adenoma an age and sex matched control patient with either H pylori associated early gastric cancer of the intestinal type or H pylori gastritis only was investigated. RESULTS: Only 60 patients (50.9%) with gastric adenoma were infected with H pylori. In the remaining patients, complete atrophic gastritis predominated. In those patients with adenoma and H pylori infection, the gastritis was similar to that seen in patients with early gastric cancer (median score, 2 for activity and degree of gastritis in the antrum and corpus); intestinal metaplasia was common to both groups. These two groups differed significantly from patients with H pylori gastritis only (median grade and activity of gastritis, 1 in antrum and corpus), in whom intestinal metaplasia was rare. CONCLUSIONS: It appears that gastric adenomas and gastric intestinal cancer arise by analogous mechanisms. However, owing to severe atrophic gastritis and a lower incidence of H pylori, adenomas do not appear to be definite precursor lesions for gastric cancer.     

Malgun (clear) cell change in Helicobacter pylori gastritis reflects epithelial genomic damage and repair

Cancers may develop in the background of genomic instability with accumulated mutations. Helicobacter pylori gastritis is characterized by acute foveolitis of the proliferative zone, which is found in any stage of the gastritis as long as the infection persists. Because acute foveolitis targets specifically the proliferative zone of pits, the proliferating epithelial cells are under severe and persistent mutagenic pressure. In H. pylori gastritis, a characteristic morphological change of epithelial cells, the malgun (clear) cell change is frequently present in association with acute foveolitis. Malgun cells have enlarged euchromatic nuclei and abundant cytoplasm. The expression of proliferating cell nuclear antigen and cytokeratin 8 are typically up-regulated in them indicating that they are mitotically and metabolically active. Here, we report evidence for DNA damage and repair in malgun cells. Significant double-strand DNA breaks were shown by the consistent terminal dUTP nick-end labeling in the nuclei of malgun cells. Proteins related to DNA damage and repair, such as Ku, poly(ADP-ribosyl) polymerase, OGG1, and MSH2 were selectively up-regulated in malgun cells. Inducible nitric oxide synthase was also up-regulated. There were occasional bcl2- and p53-expressing cells suggesting that further steps of carcinogenesis took place at the single cell level. Our results suggest that the malgun cell change represents a characteristic morphological sign of cellular genomic damage and repair, and may be implicated in an early stage of carcinogenesis. It is suggested that acute foveolitis of the proliferative zone is a major pathogenetic step of gastric carcinogenesis in H. pylori gastritis.     

Increase in proliferation and apoptosis of gastric epithelial cells early in the natural history of Helicobacter pylori infection.

Childhood acquisition of Helicobacter pylori is a critical risk factor for gastric cancer. Since tumorigenesis involves deregulation of proliferation and apoptosis, we examined gastric epithelial cell proliferation and apoptosis in H. pylori-infected children. Apoptosis and proliferation of gastric antral epithelial cells in biopsy specimens from patients with H. pylori-induced gastritis, secondary gastritis, and noninflamed controls were compared. p53 protein expression was examined immunohistochemically. Apoptotic cells were identified in the surface epithelium in each group. The apoptotic index was higher in specimens from patients with H. pylori gastritis (120 +/- 10) than secondary gastritis (50 +/- 10) and noninflamed controls (40 +/- 10, analysis of variance P < 0.005). Apoptosis decreased following H. pylori eradication and resolution of gastritis (P < 0.02). An expanded proliferative compartment was identified in H. pylori-induced gastritis (32.4 +/- 3.5; proliferative labeling index +/- SE) compared with secondary gastritis (18.9 +/- 2.8) and noninflamed controls (13.7 +/- 3.1, analysis of variance P < 0.01). The accelerated cell turnover was associated with p53 overexpression (analysis of variance P < 0.005). Accumulation of p53 was not associated with expression of the cyclin-dependent kinase inhibitor p21. The occurrence of altered cell turnover early in the natural history of chronic infection provides an explanation for the increased risk of gastric cancer development associated with childhood acquisition of infection.     

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.     

Prevalence of lymphoid follicles and aggregates in Helicobacter pylori gastritis in antral and body mucosa.

AIMS--To evaluate the prevalence of lymphoid follicles and aggregates in the antral and body mucosa in Helicobacter pylori gastritis and to assess if there were correlations with ulcers in the duodenum, pylorus, or stomach, and with chronic antral erosions. METHODS--Patients (n = 2692) with histologically confirmed H pylori antral gastritis were investigated. These comprised five groups: those with duodenal ulcers; those with pyloric ulcers; those with gastric ulcers; those with chronic erosions; and those with no associated lesions. In 1446 cases at least two additional biopsy specimens from the oxyntic mucosa were available. RESULTS--Lymphoid follicles and aggregates were found in 53.8% of cases in the antral mucosa compared with 14.8% in the oxyntic mucosa (p < 0.001). The various diseases showed significant differences in terms of the prevalence of follicles and aggregates: The highest numbers in the antral mucosa as well as the lowest in the oxyntic mucosa were found in patients with duodenal ulcers (60.5% and 9.2%, respectively). The highest numbers of follicles and aggregates in the oxyntic mucosa occurred in patients with gastric ulcers. CONCLUSIONS--The detection of lymphoid follicles and aggregates in oxyntic mucosa and the higher prevalence in antral mucosa fits well with the distribution of primary gastric lymphomas. This adds further weight to the notion that the development of follicles and aggregates, triggered by H pylori, might be an early precursor to gastric lymphoma. The differences between the groups investigated might be due to different strains of H pylori or differences in the respective sizes of antral and oxyntic mucosa.