Histological analysis of gastritis and Helicobacter pylori infection in patients with early gastric cancer: a case-control study

BACKGROUND AND AIMS: Infection with Helicobacter pylori is associated with an increased risk of gastric adenocarcinoma. However, most patients with H. pylori infection will not develop gastric cancer. The aims of the present study were to examine which histological features, including H. pylori infection, would increase the risk of gastric cancer using a case-control study. METHODS: Three gastric biopsy specimens were taken from 72 patients with early gastric cancer and 72 age- and sex-matched control subjects. The grade of gastritis was examined according to the updated Sydney System. The presence of H. pylori infection was determined by serology and histology. Odds ratio (OR) of developing gastric cancer was calculated for H. pylori positivity and histological features using conditional logistic regression. For patients with H. pylori infection, histological features in cancer patients and control subjects were compared. RESULTS: The OR of the presence of mononuclear cell infiltration in the corpus and intestinal metaplasia in the angulus were significantly elevated. The grade of mononuclear cell infiltration in the corpus and antrum was significantly higher in both types of cancer patients than controls. Glandular atrophy and intestinal metaplasia were increased in patients with intestinal-type cancer in the angulus and antrum. Bacterial density in the corpus and polymorphonuclear cell infiltration in the antrum were increased in patients with diffuse-type cancer. CONCLUSIONS: Severe chronic gastritis induced by H. pylori infection seems to be associated with diffuse-type gastric cancer. Glandular atrophy and intestinal metaplasia, which occur in gastric mucosa with chronic inflammation, are significantly associated with intestinal-type cancer.     

Helicobacter pylori Infection and Gastric Neoplasia: Correlations With Histological Gastritis and Tumor Histology

Objective: Several authors have reported an association between Helicobacter pylori ( H. pylori ) and gastric carcinoma, but the data are conflicting. Atrophic gastritis and intestinal metaplasia (IM) have also been linked to gastric carcinoma, especially the intestinal tumor type. We investigated the relationship between H. pylori infection, gastric neoplasms, and histological gastritis.
Methods: A total of 105 patients with gastric carcinoma, 36 patients with gastric adenoma, and 105 age- and sex-matched control subjects were examined for H. pylori infection and histological gastritis. H. pylori status was evaluated by Giemsa staining and IgG serology. Mucosal inflammation, atrophy, and IM were evaluated in biopsy specimens from antrum and corpus.
Results: H. pylori seroprevalence was higher in patients with gastric carcinoma (98 of 105, 93%) and adenoma (34 of 36, 94%) than in control subjects (82 of 105, 71%,   p < 0.05  ). H. pylori was more prevalent in patients with noncardia (OR, 5.67; 95% CI, 2.25–14.44) than cardia (OR, 5.20; 95% CI, 0.65–41.68) tumors. Histologic types and tumor stage (early; OR, 6.60; 95% CI, 2.23–19.69, advanced; OR, 4.27; 95% CI, 1.21–15.03) showed no difference in H. pylori prevalence. Atrophy and IM scores were higher in patients with the intestinal- but not diffuse-type of carcinoma and adenoma than in H. pylori -positive control subjects. Smoking was associated with gastric carcinoma (OR, 3.05; 95% CI, 1.58–5.93) but not alcohol or coffee use, blood group A, or a family history of gastric cancer.
Conclusions: Our results confirm a strong association between H. pylori and gastric carcinoma and adenoma. The intestinal-type gastric carcinoma is associated with atrophic gastritis and IM.     

The gastric mucosa in gastric cancer patients in a low-incidence area

BACKGROUND AND AIMS: Atrophic gastritis, intestinal metaplasia, and pyloric metaplasia are frequent precursors of noncardial intestinal-type gastric adenocarcinoma in populations in which both gastric cancer and Helicobacter pylori infection are common. We hypothesized that such lesions would be less prevalent in European gastric cancer patients. METHODS: Slides from patients who underwent gastrectomy for adenocarcinoma between 1997 and 2004 were reviewed. Tumors were categorized as intestinal or diffuse; non-neoplastic mucosa was evaluated for gastritis, atrophy, intestinal metaplasia and pyloric metaplasia. RESULTS: We studied 81 patients: 48 Swiss (mean age 68.5 years); 17 Italians (mean age 67.8 years); and 16 Iberians (mean age 54.8 years; P<0.001). Twelve tumors were proximal (all intestinal type), 12 in the corpus (six intestinal-type), and 57 antral (30 intestinal type). Patients with diffuse cancers were younger than those with intestinal type (P<0.05). Nineteen patients (23.4%) had a normal stomach; 30% of T1 tumors and 90% of T4s arose in a normal stomach (P<0.02). H. pylori gastritis was found in 47 patients (58%); they did not differ in age, sex, national origin, cancer location or type from those without gastritis. Intestinal metaplasia correlated with H. pylori gastritis (P=0.002). Pyloric metaplasia was infrequent and limited to rare microfoci. CONCLUSIONS: A quarter of the patients had a normal stomach, and pyloric metaplasia was distinctly uncommon. Approaches to prevention and early detection of gastric cancer based on bioptic or serological demonstration of atrophy and metaplasia could overlook at least 25% of the people at risk in certain populations and may need to be adapted to local conditions.     

Density of Helicobacter pylori infection evaluated semiquantitatively in gastric cancer

Helicobacter pylori infection may play a role in the development of gastric cancer; however, a quantitative evaluation of the density of H. pylori infection has not been reported previously in relation to the histologic stage and type of cancer. This study was designed to compare the density of H. pylori infection to the histologic stage and type of gastric cancer. Between March 1996 and March 1998, surgical resection of primary lesion was performed in 50 patients with gastric cancer (39 men and 11 women with a mean age of 67 years) at our institution. Using immunohistochemical stains, the density of H. pylori infection was evaluated semiquantitatively at cancer site as well as noncancerous mucosa adjacent to cancer. This density was compared with the histologic stage and the type of gastric cancer. The severity of the mucosal atrophy was evaluated using the updated Sydney System. The prevalences and density of H. pylori infection decreased in proportion to advances in the cancer stage and the mucosal atrophy. In early cancer of the intestinal- and diffuse-type, the prevalence of H. pylori in adjacent sites was almost 90% and was significantly higher (p < 0.01) than that seen in the advanced cancer lesions. In the intestinal-type early cancer, the prevalence and density of infection was higher (p < 0.05) in the adjacent mucosa than in the cancer site, whereas in the diffuse-type early cancer, H. pylori was found in all cases at the cancer site and the adjacent site. In advanced cancer, the prevalence of H. pylori was about 40% in the adjacent site and about 10% in the cancer site in both histologic types. These figures were significantly lower (p < 0.01) than in the early cancers. The prevalence and density of infection did not differ in the intestinal- and diffuse-type gastric cancers, but did decrease with more advanced cancer stages. The changes in local environment of the advanced cancer may not be conducive to the survival of H. pylori. Thus, the prevalence of H. pylori may be affected by the histologic stage rather than the histologic type of gastric cancer, and the organism may play a similar role, but through different pathways, in the pathogenesis of both types of cancer.     

Most gastric cancer occurs on the distal side of the endoscopic atrophic border

BACKGROUND: The endoscopic atrophic border indicates the extent of atrophic gastritis. The aims of this study were to examine the relation of intestinal and diffuse types of gastric cancer to the atrophic border and to study the pathologic condition of the atrophic border. METHODS: In 83 patients with gastric cancer the extent of atrophic gastritis was assessed macroscopically. In 46 patients gastric biopsy specimens were also taken, to compare the histologic features of gastritis proximal and distal to the atrophic border. RESULTS: Eighty-five per cent of gastric cancers (including 93% of intestinal type) occurred on the distal side of the atrophic border. Early diffuse gastric cancer arose closer to the atrophic border than intestinal-type cancer and was more likely to be sited proximal to it. Histologically, the grade of polymorphonuclear cell infiltration (inflammatory activity) and Helicobacter pylori density were significantly greater on the proximal side (P < 0.05), whereas the grades of glandular atrophy and intestinal metaplasia were significantly greater distally (P < 0.001). CONCLUSIONS: The atrophic border delineates the area of atrophic gastritis and intestinal metaplasia, and it is within the distal part of the stomach that gastric cancer occurs most frequently. Endoscopists should observe the distal side particularly carefully to identify early gastric cancer. The relationship of the two histologic types of cancer to areas of intestinal metaplasia and 'active' inflammation may have implications for the pathogenesis of cancer and, if so, for the potential protective effect of H. pylori eradication.     

Multifocal atrophic gastritis and gastric carcinoma

Gastric carcinoma remains a major cause of morbidity and mortality worldwide despite its significant decline in recent years. H. pylori infection begins with nonatrophic gastritis, and most individuals continue to have nonatrophic H. pylori gastritis throughout their lifetime. A minority of those with severe antral inflammation will develop a duodenal ulcer, and a few, for unknown reasons, may develop gastric MALT lymphoma. Others, who acquired the H. pylori infection in early childhood, develop progressive multifocal atrophic gastritis with loss of gastric glands. A small proportion of these individuals develop extensive, incomplete (type III) intestinal metaplasia, and an even smaller proportion will progress to dysplasia and intestinal-type gastric carcinoma. H. pylori-associated gastritis is also a risk factor for diffuse-type gastric carcinoma, which is not preceded by atrophy, intestinal metaplasia, or dysplasia. Appropriate screening and preventive measures should be considered in high-risk groups. It is also crucial to identify cofactors such as genetic susceptibility and environmental factors that might interact with H. pylori infection to increase gastric cancer risk. To make an impact on gastric cancer incidence and mortality, serious consideration should be given to early H. pylori eradication in high-risk groups and endoscopic surveillance according to the updated Sydney system in some patients with high-risk preneoplastic lesions, whereas dysplastic lesions should be removed without delay. Studies currently in progress may tell us whether H. pylori eradication can prevent later development of gastric carcinoma and thus eliminate a major cause of mortality worldwide.     

Helicobacter pylori infection is a major risk factor for gastric carcinoma in young patients

BACKGROUND: Helicobacter pylori has been established as a risk factor for gastric carcinoma (GCa). Since before the discovery of H. pylori, atrophic gastritis and intestinal metaplasia have been linked to GCa, especially the intestinal-type tumor. The prevalence of H. pylori infection and atrophic gastritis increase with age. Thus, analysis of H. pylori infection in young patients with GCa could help clarify the role of this bacterium in the development of GCa. Accordingly, we investigated the relationship between H. pylori infection, GCa, and histologic gastritis in patients less than 30 years old. METHODS: Fifty GCa patients less than 30 years (mean, 26.4 years) and 100 sex- and age-matched controls (mean, 26.8 years) were examined for the presence of H. pylori infection and histologic gastritis. RESULTS: The prevalence of H. pylori infection was significantly higher in GCa patients than in controls (94% versus 40%, P < 0.01). Its prevalence was not associated with tumor location, tumor stage, or histologic type. Gastritis, atrophy, and intestinal metaplasia significantly increased the risk of GCa. By means of multiple logistic regression analysis, the odds ratio for the risk of GCa in H. pylori-positive subjects was found to be 23.5 (95% confidence interval, 6.84-80.7). CONCLUSIONS: We confirmed a strong association between H. pylori infection and GCa in young patients. Along with H. pylori infection, histologic gastritis might play an important role in the pathogenesis of GCa in these patients.     

Helicobacter pylori Infection Is a Major Risk Factor for Gastric Carcinoma in Young Patients

Background: Helicobacter pylori has been established as a risk factor for gastric carcinoma (GCa). Since before the discovery of H. pylori, atrophic gastritis and intestinal metaplasia have been linked to GCa, especially the intestinal-type tumor. The prevalence of H. pylori infection and atrophic gastritis increase with age. Thus, analysis of H. pylori infection in young patients with GCa could help clarify the role of this bacterium in the development of GCa. Accordingly, we investigated the relationship between H. pylori infection, GCa, and histologic gastritis in patients less than 30 years old. Methods: Fifty GCa patients less than 30 years (mean, 26.4 years) and 100 sex- and age-matched controls (mean, 26.8 years) were examined for the presence of H. pylori infection and histologic gastritis. Results: The prevalence of H. pylori infection was significantly higher in GCa patients than in controls (94% versus 40%, P &lt; 0.01). Its prevalence was not associated with tumor location, tumor stage, or histologic type. Gastritis, atrophy, and intestinal metaplasia significantly increased the risk of GCa. By means of multiple logistic regression analysis, the odds ratio for the risk of GCa in H. pylori-positive subjects was found to be 23.5 (95% confidence interval, 6.84-80.7). Conclusions: We confirmed a strong association between H. pylori infection and GCa in young patients. Along with H. pylori infection, histologic gastritis might play an important role in the pathogenesis of GCa in these patients.     

Helicobacter pylori infection, glandular atrophy and intestinal metaplasia in superficial gastritis, gastric erosion, erosive gastritis, gastric ulcer and early gastric cancer

AIM: To evaluate the histological features of gastric mucosa, including Helicobacter pylori infection in patients with early gastric cancer and endoscopically found superficial gastritis, gastric erosion, erosive gastritis, gastric ulcer. METHODS: The biopsy specimens were taken from the antrum, corpus and upper angulus of all the patients. Giemsa staining, improved toluidine-blue staining, and Hpylori-specific antibody immune staining were performed as appropriate for the histological diagnosis of H pylori infection. Hematoxylin-eosin staining was used for the histological diagnosis of gastric mucosa inflammation, gastric glandular atrophy and intestinal metaplasia and scored into four grades according to the Updated Sydney System. RESULTS: The overall prevalence of H pylori infection in superficial gastritis was 28.7%, in erosive gastritis 57.7%, in gastric erosion 63.3%, in gastric ulcer 80.8%, in early gastric cancer 52.4%. There was significant difference (P<0.05), except for the difference between early gastric cancer and erosive gastritis. H pylori infection rate in antrum, corpus, angulus of patients with superficial gastritis was 25.9%, 26.2%, 25.2%, respectively; in patients with erosive gastritis 46.9%, 53.5%, 49.0%, respectively; in patients with gastric erosion 52.4%, 61.5%, 52.4%, respectively; in patients with gastric ulcer 52.4%, 61.5%, 52.4%, respectively; in patients with early gastric cancer 35.0%, 50.7%, 34.6%, respectively. No significant difference was found among the different site biopsies in superficial gastritis, but in the other diseases the detected rates were higher in corpus biopsy (P<0.05). The grades of mononuclear cell infiltration and polymorphonuclear cell infiltration, in early gastric cancer patients, were significantly higher than that in superficial gastritis patients, lower than that in gastric erosion and gastric ulcer patients (P<0.01); however, there was no significant difference compared with erosive gastritis. The grades of mucosa glandular atrophy and intestinal metaplasia were significantly highest in early gastric cancer, lower in gastric ulcer, the next were erosive gastritis, gastric erosion, the lowest in superficial gastritis (P<0.01). Furthermore, 53.3% and 51.4% showed glandular atrophy and intestinal metaplasia in angular biopsy specimens, respectively; but only 40.3% and 39.9% were identified in antral biopsy, and 14.1% and 13.6% in corpus biopsy; therefore, the angulus was more reliable for the diagnosis of glandular atrophy and intestinal metaplasia compared with antrum and corpus (P<0.01). The positivity rate of glandular atrophy and intestinal metaplasia of superficial gastritis with H pyloripositivity was 50.7%, 34.1%; of erosive gastritis 76.1%, 63.0%; of gastric erosion 84.8%, 87.8%; of gastric ulcer 80.6%, 90.9%; and of early gastric cancer 85.5%, 85.3%, respectively. The positivity rate of glandular atrophy and intestinal metaplasia of superficial gastritis with H pylorinegativity was 9.9%, 6.9%; of erosive gastritis 42.5%, 42.1%; of gastric erosion 51.1%, 61.9%; of gastric ulcer 29.8%, 25.5%; and of early gastric cancer 84.0%, 86.0%, respectively. The positivity rate of glandular atrophy and intestinal metaplasia of superficial gastritis, erosive gastritis, gastric erosion, and gastric ulcer patients with H pylon positivity was significantly higher than those with H pylori negativity (P<0.01); however, there was no significant difference in patients with early gastric cancer with or without H pylori infection. CONCLUSION: The progression of the gastric pre-cancerous lesions, glandular atrophy and intestinal metaplasia in superficial gastritis, gastric erosion, erosive gastritis and gastric ulcer was strongly related to H pylori infection. In depth studies are needed to evaluate whether eradication of H pylori infection will really diminish the risk of gastric cancer.     

Helicobacter pylori-associated gastritis and gastric cancer in Nigeria.

BACKGROUND: The etiology of gastric cancer has not been clearly delineated. There is some evidence of an association of gastric cancer with Helicobacter pylori-induced chronic gastritis, atrophic gastritis and intestinal metaplasia. Previous studies report a high rate of H. pylori infection and chronic gastritis among Nigerians. METHODS: We retrospectively reviewed 84 tissue specimens with gastric cancer seen in our department over an 18-year period for for the presence of H. pylori infection, chronic gastritis, atrophic gastritis, and intestinal metaplasia in the adjacent non-cancerous gastric mucosa. RESULTS: H. pylori infection was detected in 15 (17.9%) of 84 specimens. Moderate to severe gastritis was found in non-cancerous areas in 77 (91.7%) specimens, and was equally frequent in patients with 'intestinal' and 'diffuse' types of cancer. Atrophic gastritis and intestinal metaplasia were observed in 22 (26.2%) and 35 (41.7%) specimens, respectively, and were more common in 'intestinal' type of gastric cancer. CONCLUSION: Chronic gastritis was seen in the adjacent non-cancerous mucosa in most specimens with gastric cancer. However, its severity did not correlate with the histological subtype of gastric cancer.     

Coordinate increase of telomerase activity and c-Myc expression in Helicobacter pylori-associated gastric diseases

AIM: To detect the telomerase activity and c-Myc expression in gastric diseases and to examine the relation between these values and Helicobacter pylori (H pylori) as a risk factor for gastric cancer. METHODS: One hundred and seventy-one gastric samples were studied to detect telomerase activity using a telomerase polymerase chain reaction enzyme linked immunosorbent assay (PCR-ELISA), and c-Myc expression using immunohistochemistry. RESULTS: The telomerase activity and c-Myc expression were higher in cancers (87.69% and 61.54%) than in noncancerous tissues. They were higher in chronic atrophic gastritis with severe intestinal metaplasia (52.38% and 47.62%) than in chronic atrophic gastritis with mild intestinal metaplasia (13.33% and 16.67%). In chronic atrophic gastritis with severe intestinal metaplasia, the telomerase activity and c-Myc expression were higher in cases with H pylori infection (67.86% and 67.86%) than in those without infection (21.43% and 7.14%). c-Myc expression was higher in gastric cancer with H pylori infection (77.27%) than in that without infection (28.57%). The telomerase activity and c-Myc expression were coordinately up-regulated in H pylori infected gastric cancer and chronic atrophic gastritis with severe intestinal metaplasia. CONCLUSION: H pylori infection may influence both telomerase activity and c-Myc expression in gastric diseases, especially in chronic atrophic gastritis.     

Association between infections with CagA-positive or -negative strains of Helicobacter pylori and risk for gastric cancer in young adults. Research Group on Prevention of Gastric Carcinoma Among Young Adults

OBJECTIVE: We assessed the association between infection with CagA-positive and -negative Helicobacter pylori and the risk of gastric cancer in young adults. METHODS: CagA IgG antibodies were measured in sera of subjects participating in a case-control study in Japan. The study subjects were 103 gastric cancer patients <40 yr of age, 100 inpatients with benign diseases, and 101 screenees younger than age 43 yr. RESULTS: Compared with the H. pylori-negative/CagA-negative (H. pylori-/CagA-) group, both the H. pylori-positive/CagA-negative (H. pylori+/CagA-) group and the H. pylori-positive/CagA-positive (H. pylori+/CagA+) groups showed elevated odds ratios for intestinal-type, diffuse-type, early, advanced, proximal, and distal gastric cancers. All the relationships were significant except for the H. pylori+/CagA- group in relation to proximal cancer. The overall odds ratios (95% confidence intervals) for gastric cancer in the H. pylori+/CagA- and the H. pylori+/CagA+ groups were 15.0 (6.4, 35.2) and 14.6 (6.7, 31.9), respectively. Between these two groups, no significant difference was observed in risks for intestinal-type, diffuse-type, early, advanced, proximal, or distal gastric cancer. CONCLUSIONS: In those <40 yr of age, it is concluded that both CagA-positive and CagA-negative H. pylori infections are related to risks of intestinal-type, diffuse-type, early, advanced, and distal gastric cancers.     

Prevalence of Helicobacter pylori infection and gastric cancer precursor lesions in patients with dyspepsia

BACKGROUND: Helicobacter pylori infection has been considered to play significant role in gastric carcinogenesis, but only a minority of people who harbor this organism will develop gastric cancer. H. pylori infection first causes chronic non atrophic gastritis. Chronic non atrophic gastritis may evolve to atrophic gastritis and intestinal metaplasia and finally to dysplasia and adenocarcinoma. AIMS: To estimate the prevalence of H. pylori infection and the precancerous gastric lesions and their relationship, in patients with dyspeptic symptoms who underwent upper gastrointestinal endoscopy at a reference center in the central region of Rio Grande do Sul state, Brazil. METHODS: We analyzed gastric biopsies taken from corpus and antrum of patients who underwent upper gastrointestinal endoscopy for H. pylori detection, between 1994 and 2003. According to Sydney system, chronic non atrophic gastritis, atrophic gastritis and intestinal metaplasia were diagnosed by histological examination (H-E stain). The histological diagnoses were related to H. pylori infection status. RESULTS: Biopsies from 2,019 patients were included in the study. Patients mean age was 52 (+/-15) and 59% were female. Seventy six percent had H. pylori infection. Normal mucosa, chronic non atrophic gastritis, atrophic gastritis and intestinal metaplasia were diagnosed in 5%, 77%, 3% and 15%, respectively. The OR for any degree of gastric mucosa lesion in infected patients was 10 (CI95% 6.50 - 17%). The OR for infected patients had chronic non atrophic gastritis was 3 (CI95% 2,2 - 3,4). The OR for infected patients had atrophic gastritis or intestinal metaplasia was less than 1. CONCLUSIONS: The prevalence of H. pylori infection in this population was high (76%) and infected individuals had the probability 10 folds greater than non infected individuals to have any lesion of gastric mucosa. The prevalence of precancerous lesions was 77% for non atrophic chronic gastritis, 3% for atrophic gastritis and 15% for intestinal metaplasia. Infected patients had risk 3 folds greater than non-infected for the occurrence of non atrophic chronic gastritis. H. pylori infection did not show risk for occurrence of atrophic gastritis and intestinal metaplasia, suggesting that other risk factors should be involved in the carcinogenesis process.     

Helicobacter pylori and early gastric cancer.

The relation between Helicobacter pylori, intestinal metaplasia, and early gastric cancer was studied by examining gastrectomy specimens from 31 intestinal type and 22 diffuse type carcinomas. A total of 298 patients with antral gastritis were used as controls. Atrophic changes and intestinal metaplasia were significantly more common in intestinal type early gastric cancer compared with diffuse type early gastric cancer (p < 0.05 and p < 0.001, respectively). H pylori was found in 61.3% of intestinal type early gastric cancer and in 54.5% of diffuse type early gastric cancer (NS). The age adjusted prevalence of intestinal metaplasia in the patients with antral gastritis was higher in H pylori positive patients in all age groups studied. Comparing gastritis patients with patients with intestinal type early gastric cancer showed the age adjusted prevalence of intestinal metaplasia to be significantly higher in the patients with early gastric cancer in all age groups studied. In conclusion, H pylori is associated with both types of early gastric carcinoma. Intestinal metaplasia formation seems to be a multifactorial process in which H pylori may play a part. These findings suggest that gastric cancer may be included in the spectrum of H pylori associated diseases, although many questions about causality remain to be answered.     

Effect of Helicobacter pylori infection and its eradication on cell proliferation, DNA status, and oncogene expression in patients with chronic gastritis.

BACKGROUND: Helicobacter pylori, the main cause of chronic gastritis, is a class I gastric carcinogen. Chronic gastritis progresses to cancer through atrophy, metaplasia, and dysplasia. Precancerous phenotypic expression is generally associated with acquired genomic instability. AIM: To evaluate the effect of H pylori infection and its eradication on gastric histology, cell proliferation, DNA status, and oncogene expression. METHODS/SUBJECTS: Morphometric and immunohistochemical techniques were used to examine gastric mucosal biopsy specimens from eight controls, 10 patients with H pylori negative chronic gastritis, 53 with H pylori positive chronic gastritis, and 11 with gastric cancer. RESULTS: All patients with chronic gastritis were in a hyperproliferative state related to mucosal inflammation, regardless of H pylori infection. Atrophy was present in three of 10 patients with H pylori negative chronic gastritis and in 26 of 53 with H pylori positive chronic gastritis, associated in 18 with intestinal metaplasia. DNA content was abnormal in only 11 patients with atrophy and H pylori infection; eight of these also had c-Myc expression, associated in six cases with p53 expression. Fifty three patients with H pylori positive chronic gastritis were monitored for 12 months after antibiotic treatment: three dropped out; infection was eradicated in 45, in whom cell proliferation decreased in parallel with the reduction in gastritis activity; atrophy previously detected in 21/45 disappeared in five, regressed from moderate to mild in nine, and remained unchanged in seven; complete metaplasia disappeared in 4/14, and markers of genomic instability disappeared where previously present. In the five patients in whom H pylori persisted, atrophy, metaplasia, dysplasia, and markers of genomic instability remained unchanged. CONCLUSIONS: Chronic H pylori infection seems to be responsible for genomic instability in a subset of cases of H pylori positive chronic atrophic gastritis; eradication of H pylori infection can reverse inflammation and the related atrophy, metaplasia, and genomic instability.     

早期胃癌和进展期胃癌患者幽门螺杆菌感染与胃黏膜组织学特点的关系

背景幽门螺杆菌(H.pylori)感染已被确认为慢性胃炎的主要病因,由慢性非萎缩性胃炎、慢性萎缩性胃炎至肠化生,经过数十年最终可能导致胃癌发生。目的评价H.pylori感染与胃镜检查正常者、慢性胃炎、早期胃癌和进展期胃癌患者胃黏膜组织学特点的关系。方法在受检者胃窦大弯侧、胃体大弯侧和胃角处各取一块黏膜活检标本,以Giemsa染色和免疫组化染色检测H.pylori感染情况;以HE染色评价胃黏膜炎症、活动性、萎缩和肠化生情况。结果慢性胃炎、早期胃癌和进展期胃癌患者的总体H.pylori感染率均显著高于胃镜检查正常者(52.4%、52.4%和81.2%对44.9%,P<0.05),慢性胃炎与早期胃癌患者的感染率无显著差异,但均显著低于进展期胃癌患者(P<0.05)。胃镜检查正常和慢性胃炎组H.pylori感染者的胃黏膜炎症、活动性、萎缩和肠化生检出率均显著高于无感染者(P<0.05);早期胃癌和进展期胃癌组H.pylori感染者的炎症活动性检出率显著高于无感染者(P<0.05),而炎症、萎缩和肠化生检出率与无感染者无显著差异。结论由H.pylori感染引起的胃黏膜慢性炎症、萎缩和肠化生可能在胃癌的发生、发展过程中起直接或间接作用。     

Comparison of Helicobacter pylori infection and gastric mucosal histological features of gastric ulcer patients with chronic gastritis patients

AIM: To compare Helicobacter pylori infection and gastric mucosal histological features of gastric ulcer patients with chronic gastritis patients in different age groups and from different biopsy sites. METHODS: The biopsy specimens were taken from the antrum, corpus and upper angulus of gastric ulcer and chronic gastritis patients. Giemsa staining, improved Toluidine-blue staining and H pylori-specific antibody immune staining were performed as appropriate for the histological diagnosis of H pylori infection. Hematoxylin-eosin staining was used for the histological diagnosis of activity of H pylori infection, mucosal inflammation, glandular atrophy and intestinal metaplasia and scored into four grades according to the Updated Sydney System. RESULTS: Total rate of H pylori infection, mucosal inflammation, activity of H pylori infection, glandular atrophy and intestinal metaplasia in 3 839 gastric ulcer patients (78.5%, 97.4%, 82.1%, 61.1% and 64.2%, respectively) were significantly higher than those in 4 102 chronic gastritis patients (55.0%, 90.3%, 56.2%, 36.8%, and 37.0%, respectively, P<0.05). The rate of H pylori colonization of chronic gastritis in <30 years, 31-40 years, 41-50 years, 51-60 years, 61-70 years and >70 years age groups in antrum was 33.3%, 41.7%, 53.6%, 57.3%, 50.7%, 43.5%, respectively; in corpus, it was 32.6%, 41.9%, 53.8%, 60.2%, 58.0%, 54.8%, respectively; in angulus, it was 32.4%, 42.1%, 51.6%, 54.5%, 49.7%, 43.5%, respectively. The rate of H pylori colonization of gastric ulcer in <30 years, 31-40 years, 41-50 years, 51-60 years, 61-70 years and >70 years age groups in antrum was 60.5%, 79.9%, 80.9%, 66.8%, 59.6%, 45.6%, respectively; in corpus, it was 59.7%, 79.6%, 83.6%, 80.1%, 70.6%, 59.1%, respectively; in angulus, it was 61.3%, 77.8%, 75.3%, 68.8%, 59.7%, 45.8%, respectively. The rate of H pylori colonization at antrum was similar to corpus and angulus in patients, below 50 years, with chronic gastritis and in patients, below 40 years, with gastric ulcer. In the other age- groups, the rate of H pylori colonization was highest in corpus, lower in antrum and lowest in angulus (all P<0.05). The rates of glandular atrophy and intestinal metaplasia were higher and earlier in H pylori-positive patients than those without H pylori infection (both P<0.01). In comparison of gastric ulcer patients with chronic gastritis patients, the rate of glandular atrophy and intestinal metaplasia was higher in H pylori-positive patients with gastric ulcer than in H pylori-positive patients with chronic gastritis (both P<0.01); the rate of glandular atrophy and intestinal metaplasia were also higher in H pylori-negative patients with gastric ulcer than in H pylori-negative patients with chronic gastritis (both P<0.01). Both glandular atrophy and intestinal metaplasia were much more commonly identified in the angulus than in the antrum, lowest in corpus (all P<0.01). CONCLUSION: Rate of H pylori infection, glandular atrophy and intestinal metaplasia in gastric ulcer were higher than in chronic gastritis in all-different age -groups. Distribution of H pylori colonization is pangastric in the younger patients. It is highest in corpus, lower in antrum and lowest in angulus in the older age groups. Progression of glandular atrophy and intestinal metaplasia seem to have a key role in the distribution of H pylori colonization. H pylori appears to be the most important risk factor for the development of glandular atrophy and intestinal metaplasia, but it is not the only risk.     

Comparison of He/icobacter py/ori infection and gastric mucosal histological features of gastric ulcer patients with chronic gastritis patients

AIM: To compare Helicobacter pylori infection and gastric mucosal histological features of gastric ulcer patients with chronic gastritis patients in different age groups and from different biopsy sites. METHODS: The biopsy specimens were taken from the antrum, corpus and upper angulus of gastric ulcer and chronic gastritis patients. Giemsa staining, improved Toluidine-blue staining and H pylori-specific antibody immune staining were performed as appropriate for the histological diagnosis of H pylori infection. Hematoxylineosin staining was used for the histological diagnosis of activity of H pylori infection, mucosal inflammation, glandular atrophy and intestinal metaplasia and scored into four grades according to the Updated Sydney System. RESULTS: Total rate of H pylori infection, mucosal inflammation, activity of H pylori infection, glandular atrophy and intestinal metaplasia in 3 839 gastric ulcer patients (78.5%, 97.4%, 82.1%, 61.1% and 64.2%, respectively) were significantly higher than those in 4 102 chronic gastritis patients (55.0%, 90.3%, 56.2%, 36.8%, and 37.0%, respectively, P<0.05). The rate of H pylori colonization of chronic gastritis in <30 years, 31-40 years, 41-50 years, 51-60 years, 61-70 years and >70 years age groups in antrum was 33.3%, 41.7%, 53.6%, 57.3%, 50.7%, 43.5%, respectively; in corpus, it was 32.6%, 41.9%, 53.8%, 60.2%, 58.0%, 54.8%, respectively; in angulus, it was 32.4%, 42.1%, 51.6%, 54.5%, 49.7%, 43.5%, respectively. The rate of H pylori colonization of gastric ulcer in <30 years, 31-40 years, 41-50 years, 51-60 years, 61-70 years and >70 years age groups in antrum was 60.5%, 79.9%, 80.9%, 66.8%, 59.6%, 45.6%, respectively; in corpus, it was 59.7%, 79.6%, 83.6%, 80.1%, 70.6%, 59.1%, respectively; in angulus, it was 61.3%, 77.8%, 75.3%, 68.8%, 59.7%, 45.8%, respectively. The rate of H pylori colonization at antrum was similar to corpus and angulus in patients, below 50 years, with chronic gastritis and in patients, below 40 years, with gastric ulcer. In the other age- groups, the rate of H pylori colonization was highest in corpus, lower in antrum and lowest in angulus (all P<0.05). The rates of glandular atrophy and intestinal metaplasia were higher and earlier in H pylori-positive patients than those without H pylori infection (both P<0.01). In comparison of gastric ulcer patients with chronic gastritis patients, the rate of glandular atrophy and intestinal metaplasia was higher in H pylori-positive patients with gastric ulcer than in H pylori-positive patients with chronic gastritis (both P<0.01); the rate of glandular atrophy and intestinal metaplasia were also higher in H pylori-negative patients with gastric ulcer than in H pylori-negative patients with chronic gastritis (both P<0.01). Both glandular atrophy and intestinal metaplasia were much more commonly identified in the angulus than in the antrum, lowest in corpus (all P<0.01). CONCLUSION: Rate of H pylori infection, glandular atrophy and intestinal metaplasia in gastric ulcer were higher than in chronic gastritis in all-different age -groups. Distribution of H pylori colonization is pangastric in the younger patients. It is highest in corpus, lower in antrum and lowest in angulus in the older age groups. Progression of glandular atrophy and intestinal metaplasia seem to have a key role in the distribution of H pylori colonization. H pylori appears to be the most important risk factor for the development of glandular atrophy and intestinal metaplasia, but it is not the only risk.     

Mucosal changes in the gastric remnant: long-term effects of bile reflux diversion and Helicobacter pylori infection

OBJECTIVE: Bile reflux is thought to be responsible for reflux gastritis and stump carcinoma occurring after partial gastrectomy for peptic ulcer. Gastritis and gastric carcinoma are also correlated with Helicobacter pylori. The aim of this study was to investigate whether diversion of enteric reflux and the presence of H. pylori infection alter long-term histological developments in the gastric remnant. METHODS: Twenty-nine patients partially gastrectomized for peptic ulcer were reoperated on with re-resection and a Roux-en-Y reconstruction because of reflux gastritis (12 patients) or severe dysplasia/early gastric cancer (17 patients). The resected specimens and subsequent biopsies from the new anastomotic region taken at endoscopies 5-17 years after reoperation were evaluated regarding the presence of H. pylori, the grade of active and non-active chronic gastritis, and the premalignant changes--atrophy, intestinal metaplasia and dysplasia. RESULTS: A progression of active chronic gastritis, atrophy, intestinal metaplasia and dysplasia was seen after re-resection and Roux-en-Y reconstruction. Non-active chronic gastritis remained unchanged. The development was, in general, independent of H. pylori infection. CONCLUSIONS: Enteric reflux may perhaps induce a histological transformation of the gastric mucosa that cannot be reversed, even if the reflux is diverted. In our study, H. pylori infection had no impact on the histological development. Factors other than enteric reflux and H. pylori infection might also be of importance.     

Pathogenic implications of interleukin-8 activity and bacterial phenotype in antral gastritis associated with Helicobacter pylori.

OBJECTIVE: Helicobacter pylori (Hp) infection is characterized by an intense inflammatory infiltrate in the gastric mucosa, which is chemoattracted by different cytokines. Interleukin-8 (IL-8) seems to play an important role in the recruitment of circulating neutrophils, and modulation of IL-8 secretion seems to be a strain marker. This study was designed to examine IL-8 concentrations in the gastric mucosa and their relationship with H. pylori phenotype and histologic findings. METHODS: Gastric biopsies were obtained from the antrum and corpus in 106 patients (69 Hp-positive and 37 Hp-negative). IL-8 levels in the gastric mucosa were analyzed by ELISA and Hp phenotype was determined with a western blot test. RESULTS: 75% of H. pylori strains were CagA+ and 54.2% were VacA+. The Houston classification was used for histologic findings. No association between gastric atrophy or intestinal metaplasia and Hp phenotype was found. The highest IL-8 levels were found in CagA+ infected gastric mucosa, but the difference with respect to infection by a VacA+ strain was not statistically significant. IL-8 levels were highest when neutrophils were the predominant cell in the gastric inflammatory infiltrate (p < 0.05). IL-8 levels were higher in patients with atrophic gastritis than in patients with nonatrophic gastritis (p < 0.05). CONCLUSIONS: In patients with H. pylori infection, IL-8 levels are higher than in Hp-negative patients regardless of Hp phenotype. There is an association between IL-8 and a neutrophilic infiltrate. Perpetuation of a chronic infiltrate could lead to more severe lesions such as atrophic gastritis or intestinal metaplasia, as deduced from the IL-8 levels found in these types of lesion.