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.     

Antral-type mucosa in the gastric incisura, body, and fundus (antralization): a link between Helicobacter pylori infection and intestinal metaplasia?

OBJECTIVES: Helicobacter pylori is a carcinogen; gastric carcinoma involves a multistep process from chronic gastritis to atrophy, intestinal metaplasia, and dysplasia. The aims of this study were to determine the types of mucosa at different gastric sites in H. pylori-infected and uninfected patients, and whether the presence of antral-type mucosa in the incisura, body, and fundus is associated with gastric atrophy and intestinal metaplasia. METHODS: Two hundred and sixty-eight patients with dyspepsia were enrolled. Eight biopsies (i.e., antrum x3, body x2, fundus x2, and incisura x1) were obtained. One antral biopsy was used for the CLO-test. Three (each from the antrum, body, and fundus) were cultured. The remaining biopsies were examined histologically according to the updated Sydney System after staining with hematoxylin and eosin and Giemsa. A validated serological test was also applied. RESULTS: Overall, 113 (42%) patients were infected with H. pylori. At the incisura, antral-type mucosa was more prevalent in infected than in uninfected patients (84% vs. 18%; odds ratio [OR] = 23.9, 95% confidence interval [CI] 12.5-45.8; p<0.001). Atrophic gastritis and intestinal metaplasia at the incisura was present in 19.5% and 13.3%, respectively, of infected, and 4.5% and 3.2%, respectively, of uninfected patients (both p<0.01). Moreover, atrophic gastritis at the incisura was associated with the presence of antral-type mucosa at the site (termed antralization); the prevalence of atrophic gastritis was 19.5% (24/123) in the presence of antralization, whereas the rate was 2.1% (3/145) without antralization (OR = 11.4, 95% CI 3.4-39.2; p<0.001). Similarly, at the incisura, 16.3% (20/123) of "antralized" cases and 1.4% (2/145) of "unantralized" cases had intestinal metaplasia (OR = 13.8, 95% CI, 3.2-60.7; p<0.001). The association between antralization at gastric body and fundus also appeared to be associated with atrophic gastritis and intestinal metaplasia at these sites. CONCLUSIONS: Atrophic gastritis and intestinal metaplasia occurs predominantly at the gastric antrum and incisura with H. pylori infection. Antralization of the gastric incisura is a common event in H. pylori-infected patients, and appears to be associated with an increased risk of atrophic gastritis and intestinal metaplasia.     

Complete and incomplete intestinal metaplasia at the oesophagogastric junction: prevalences and associations with endoscopic erosive oesophagitis and gastritis

BACKGROUND/AIMS: Intestinal metaplasia (IM) is a common finding at the oesophagogastric junction, but the aetiopathogenesis of the different IM subtypes-that is, incomplete IM (specialised columnar epithelium, SCE) and complete IM- and their associations with gastro-oesophageal reflux disease and Helicobacter pylori gastritis are unclear. METHODS: 1058 consecutive dyspeptic patients undergoing gastroscopy were enrolled. The gastric, oesophagogastric junctional, and oesophageal biopsy specimens obtained were stained with haematoxylin and eosin, alcian blue (pH 2.5)-periodic acid Schiff, and modified Giemsa. RESULTS: Complete junctional IM was detected in 196 (19%) of the 1058 subjects, and in 134 (13%) was the sole IM subtype. Incomplete junctional IM (SCE) was detected in 101 (10%) subjects, of whom 62 (61%) also had the complete IM subtype. Of patients with normal gastric histology (n = 426), 6% had complete IM and 7% junctional SCE. The prevalence of both types of IM increased with age in patients with either normal gastric histology or chronic gastritis (n = 611). Epithelial dysplasia was not detected in any patients with junctional IM. In multivariate analysis, independent risk factors for incomplete junctional IM were age (odds ratio (OR) 1.3 per decade, 95% confidence interval (CI) 1.2 to 1.6), endoscopic erosive oesophagitis (OR 1.9, 95% CI 1.1 to 3.2), and chronic cardia inflammation (OR 2.9, 95% CI 1.3 to 6.2), but not gastric H pylori infection (OR 1.0, 95% CI 0.6 to 1.7). In univariate analysis, junctional incomplete IM was not associated with cardia H pylori infection. Independent risk factors for "pure" complete junctional IM (n = 134) were age (OR 1.2 per decade, 95% CI 1.0 to 1.4), antral predominant non-atrophic gastritis (OR 2.6, 95% CI 1.3 to 5.2), antral predominant atrophic gastritis (OR 2.1, 95% CI 1.1 to 5.2), and multifocal atrophic gastritis (OR 7.1, 95% CI 2.5 to 19.8). In univariate analysis, junctional complete IM was strongly associated with chronic cardia inflammation and cardia H pylori infection (p<0. 001). CONCLUSIONS: Both complete and incomplete junctional IM are independent acquired lesions that increase in prevalence with age. Although IM subtypes often occur simultaneously, they show remarkable differences in their associations with gastritis and erosive oesophagitis: junctional complete IM is a manifestation of multifocal atrophic gastritis, while the incomplete form (SCE) may result from carditis and gastro-oesophageal reflux disease. The frequency of dysplasia in intestinal metaplasia at the oesophagogastric junction appears to be low.     

Specialized columnar epithelium of the esophagogastric junction: prevalence and associations. The Central Finland Endoscopy Study Group

OBJECTIVES: In Barrett's esophagus (BE) normal squamous esophageal epithelium is replaced by specialized columnar epithelium (SCE). BE is related to gastroesophageal reflux disease (GERD) and is a risk factor for esophageal adenocarcinoma. SCE is detected also at normal-appearing esophagogastric junction without BE (junctional SCE). The relationships between junctional SCE, GERD, and cardia adenocarcinoma are obscure and controversial. The aims of the present study were to investigate the prevalence and demographics of junctional SCE and to compare these figures with those reported for BE, and esophageal and cardia adenocarcinoma. A further aim was to examine the association between junctional SCE and GERD, Helicobacter pylori infection, and gastritis. METHODS: One thousand one hundred-nineteen consecutive dyspeptic patients underwent gastroscopy and were enrolled into the study. RESULTS: Junctional SCE was detected in 110 patients (10%). The age-specific prevalence of junctional SCE increased with age. The male:female ratio was 1:1.1. In multivariate analysis, junctional SCE was independently and positively related to endoscopic erosive esophagitis (odds ratio [OR], 1.8; 95% confidence interval [CI], 1.1-3.1), cardia inflammation (carditis) (OR, 3.1; 95% CI, 1.4-6.8), and age (OR, 1.4 per decade; 95% CI, 1.2-1.6), but not to corpus H. pylori infection (OR, 1.4; 95% CI, 0.7-2.8), antral (OR, 1.0; 95% CI, 0.5-2.1) or corpus (OR, 0.8; 95% CI, 0.4-1.8) gastritis, or intestinal metaplasia of the antral mucosa in stomach (OR, 1.2; 95% CI, 0.7-2.1). In univariate analysis, junctional SCE was, however, significantly more common in patients with antral-predominant atrophic gastritis (20%), compared with those with normal gastric histology (8%, p < 0.001). CONCLUSIONS: Junctional SCE is age related and may therefore be an acquired lesion. It is associated with cardia inflammation and endoscopic erosive esophagitis, but not with H. pylori infection or gastric intestinal metaplasia. Unlike BE and cardia cancer, junctional SCE occurs with similar frequency in men and women.     

Chronic inflammation at the gastroesophageal junction (carditis) appears to be a specific finding related to Helicobacter pylori infection and gastroesophageal reflux disease. The Central Finland Endoscopy Study Group

OBJECTIVE: The clinical significance of chronic inflammation at the gastroesophageal junction (carditis) is unknown: it may be associated with Helicobacter pylori (H. pylori) gastritis or with gastroesophageal reflux disease (GERD). We aimed to examine the association between carditis and H. pylori gastritis and endoscopic erosive esophagitis. METHODS: One thousand and fifty-three patients undergoing gastroscopy were enrolled in the study. Biopsy specimens were obtained from gastric antrum and corpus, immediately distal to normal-appearing squamocolumnar junction and distal esophagus. RESULTS: Chronic inflammation at the gastroesophageal junctional mucosa (carditis) was detected in 790 (75%) of 1053 patients. The male:female ratio of the carditis group was 1:1.5 and of the noncarditis group 1:1.6 (p = 0.6). The mean age of the carditis group was 58.7 yr (95% confidence interval [CI], 57.6-59.9) and of the noncarditis group, 52.6 yr (95% CI, 50.7-54.6, p < 0.001). Of the carditis group (N = 790), 549 (69%) had chronic gastritis (70% H. pylori positive) and 241 (31%) had normal gastric histology. In multivariate analyses, the only risk factor for carditis in subjects with chronic gastritis was H. pylori infection (odds ratio [OR], 2.9; 95% CI, 1.6-5.0), whereas the independent risk factor for carditis in subjects with histologically normal stomach was endoscopic erosive esophagitis (OR, 1.8; 95% CI, 1.1-3.1). The prevalence of complete intestinal metaplasia (IM) in the gastric cardia mucosa was 7% in the noncarditis group, 19% (p < 0.001) in the carditis group with chronic gastritis, and 10% (p = 0.3) in the carditis group with normal stomach. The respective prevalences of incomplete IM were 3%, 12% (p < 0.001), and 12% (p < 0.001). Among carditis patients with normal stomach histologically (N = 241), those with complete and/or incomplete IM (N = 49) were older than those with carditis only (63.6 yr [95% CI, 59.9-67.2] vs 51.4 yr [95% CI, 48.9-53.9]; p < 0.001). CONCLUSIONS: Two dissimilar types of chronic inflammation of the gastric cardia mucosa seem to occur, one existing in conjunction with chronic H. pylori gastritis and the other with normal stomach and erosive GERD. Most cases of chronic gastric cardia inflammation and intestinal metaplasia are detected in patients with chronic H. pylori gastritis.     

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 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 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.     

Helicobacter pylori-induced inflammation masks the underlying presence of low-grade dysplasia on gastric lesions

BACKGROUND Helicobacter pylori(H. pylori) infection has been associated with a long-term risk of precancerous gastric conditions(PGC) even after H. pylori eradication.AIM To investigate the efficacy of High-Resolution White-Light Endoscopy with Narrow-Band Imaging in detecting PGC, before/after H. pylori eradication.METHODS We studied 85 consecutive patients with H. pylori-related gastritis with/without PGC before and 6 mo after proven H. pylori eradication. Kimura-Takemoto modified and endoscopic grading of gastric intestinal metaplasia classifications, were applied to assess the endoscopic extension of atrophy and intestinal metaplasia. The histological result was considered to be the gold standard. The Sydney System, the Operative-Link on Gastritis-Assessment, and the OperativeLink on Gastric-Intestinal Metaplasia were used for defining histological gastritis, atrophy and intestinal metaplasia, whereas dysplasia was graded according to World Health Organization classification. Serum anti-parietal cell antibody and anti-intrinsic factor were measured when autoimmune atrophic gastritis was suspected.RESULTS After H. pylori eradication histological signs of mononuclear/polymorphonuclear cell infiltration and Mucosal Associated Lymphoid Tissue-hyperplasia, disappeared or decreased in 100% and 96.5% of patients respectively, whereas the Operative-Link on Gastritis-Assessment and Operative-Link on Gastric-Intestinal Metaplasia stages did not change. Low-Grade Dysplasia prevalence was similar on random biopsies before and after H. pylori eradication(17.6% vs 10.6%, P = 0.19), but increased in patients with visible lesions(0% vs 22.4%, P 0.0001). At a multivariate analysis, the probability for detecting dysplasia after resolution of H. pylori-related active inflammation was higher in patients with regression or reduction of Mucosal Associated Lymphoid Tissue hyperplasia, greater alcohol consumption, and anti-parietal cell antibody and/or anti-intrinsic factor positivity [odds ratio(OR) = 3.88, 95% confidence interval(CI): 1.31-11.49, P = 0.01; OR = 3.10, 95%CI: 1.05-9.12, P = 0.04 and OR = 5.47, 95%CI: 1.33-22.39, P 0.04, respectively].CONCLUSION High-Resolution White-Light Endoscopy with Narrow-Band Imaging allows an accurate diagnosis of Low-Grade Dysplasia on visible lesions after regression of H. pylori-induced chronic gastritis. Patients with an overlap between autoimmune/H. pylori-induced gastritis may require more extensive gastric mapping.     

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.     

Aging increases, and duodenal ulcer reduces the risk for intestinal metaplasia of the gastric corpus in Japanese patients with dyspepsia

BACKGROUND AND AIMS: The classification of gastritis by using the revised Sydney system suggests that there are two types of Helicobacter pylori-related gastritis. The aim of the present study was to examine the risk factors that might be involved in the presence of either atrophic gastritis or intestinal metaplasia of the gastric corpus of Japanese patients. METHODS: Biopsy samples were obtained from the gastric corpus in 154 patients with dyspepsia, and the degree of atrophy or intestinal metaplasia was determined histologically. The correlation between several variables and presence of atrophy or intestinal metaplasia was evaluated by using multivariate analysis. RESULTS: Among the 11 variables, which included age, peptic ulcer diseases and H. pylori infection, H. pylori infection was the major risk factor associated with the presence of atrophic gastritis or intestinal metaplasia of the gastric corpus. In contrast, duodenal ulcer (DU) disease reduced the risk of contracting both conditions. Age was an independent risk factor only for intestinal metaplasia of the gastric corpus. When 128 H. pylori-positive subjects were analyzed, DU and age were similarly associated with the presence of both conditions. CONCLUSIONS: These results suggest that DU reduces the risk for contracting atrophic gastritis and intestinal metaplasia, and age is an independent risk factor for intestinal metaplasia of the gastric corpus in dyspeptic Japanese patients.     

Two distinct aetiologies of cardia cancer; evidence from premorbid serological markers of gastric atrophy and Helicobacter pylori status

BACKGROUND: Non-cardia gastric adenocarcinoma is positively associated with Helicobacter pylori infection and atrophic gastritis. The role of H pylori infection and atrophic gastritis in cardia cancer is unclear. AIM: To compare cardia versus non-cardia cancer with respect to the premorbid state of the stomach. METHODS: Nested case-control study. To each of 129 non-cardia and 44 cardia cancers, three controls were matched. Serum collected a median of 11.9 years before the diagnosis of cancer was tested for anti-H pylori antibodies, pepsinogen I:II and gastrin. RESULTS: Non-cardia cancer was positively associated with H pylori (OR 4.75, 95% CI 2.56 to 8.81) and gastric atrophy (pepsinogen I:II <2.5; OR 4.47, 95% CI 2.71 to 7.37). The diffuse and intestinal histological subtypes of non-cardia cancer were of similar proportions and both showed a positive association with H pylori and atrophy. Cardia cancer was negatively associated with H pylori (OR 0.27, 95% CI 0.12 to 0.59), but H pylori-positive cardia cancer showed an association with gastric atrophy (OR 3.33, 95% CI 1.06 to 10.5). The predominant histological subtype of cardia cancer was intestinal and was not associated with gastric atrophy compared with the diffuse subtype ((OR 0.72, 95% CI 0.19 to 2.79) vs (OR 3.46, 95% CI 0.32 to 37.5)). Cardia cancer in patients with atrophy had an intestinal: diffuse ratio (1:1) similar to non-cardia cancer (1.9:1), whereas cardia cancers in patients without atrophy were predominantly intestinal (7:1). CONCLUSION: These findings indicate two aetiologies of cardia cancer, one associated with H pylori atrophic gastritis, resembling non-cardia cancer, and the other associated with non-atrophic gastric mucosa, resembling oesophageal adenocarcinoma. Serological markers of gastric atrophy may provide the key to determining gastric versus oesophageal origin of cardia cancer.     

Classical Barrett esophagus contrasted with Barrett-type epithelium at normal-appearing esophagogastric junction. Central Finland Endoscopy Study Group

BACKGROUND: Incomplete intestinal metaplasia or specialized columnar epithelium (SCE) is the histologic hallmark of Barrett esophagus (BE), but it may also occur at a normal-appearing gastroesophageal junction without BE. We studied whether differences occur between BE patients and those with SCE at the squamocolumnar junction but without BE (abbreviated JSCE), in terms of endoscopic and histologic signs of gastroesophageal reflux disease (GERD) and Helicobacter pylori gastritis. METHODS: A total of 1059 consecutive patients referred for endoscopy in one hospital district in Finland were enrolled in the study. Biopsy specimens (at least two from each site) were obtained from the gastric antrum and the corpus of the stomach and from the esophagogastric junction and distal esophagus. RESULTS: Classical BE was detected in 25 (2%) and JSCE in 99 (9%) patients. Dysplasia in the metaplastic mucosa was observed in six BE patients but in none of the JSCE patients (P < 0.001). In multivariate analysis the independent risk factors for BE were endoscopic erosive esophagitis (odds ratio (OR), 6.08; 95% confidence interval (CI), 2.50-14.82), male sex (OR, 3.02; 95% CI, 1.20-7.65), and age (OR, 1.02 per year; 95% CI, 1.00-1.06). The independent risk factors for JSCE were endoscopic erosive esophagitis (OR, 1.88; 95% CI, 1.08-3.29) and age (OR, 1.03; 95% CI, 1.02-1.05) but not H. pylori infection (OR, 1.57; 95% CI, 0.83-2.97) or chronic gastritis (OR, 0.88; 95% CI, 0.44-1.75). In univariate analysis, however, JSCE was associated with antral-predominant atrophic gastritis (77% H. pylori-positive). Unlike in JSCE patients, male sex strongly predominated among BE patients (P = 0.01). The mean ages of BE and JSCE patients did not differ. CONCLUSIONS: Both BE and JSCE without BE increase in prevalence with age, and both associate with endoscopic erosive esophagitis but not with H. pylori gastritis. However, because of the marked sex disparity, JSCE cannot be a direct precursor of BE, and some factors other than GERD alone also play a role in the pathogenesis of BE. Compared with BE, dysplasia is a rare finding in JSCE, and endoscopic surveillance with biopsy specimens from JSCE patients without dysplasia is not recommended.     

Helicobacter pylori gastritis in Africa

* Helicobacter pylori gastritis progresses to gland loss and intestinal metaplasia in a considerable proportion of colonized subjects. * The progression to atrophic gastritis is a slow process, occurring with an incidence of 1-2% per year. * The progression of chronic H. pylori gastritis is the same in Africa as in Europe and South America. * This supports the concept of H. pylori as a causative factor of pre-neoplastic conditions of the gastric mucosa; other factors must play a modulating role in the progression to cancer. H. pylori gastritis may progress to atrophic gastritis and lead to the development of intestinal metaplasia, dysplasia and eventually gastric cancer in a minority of subjects. The available data on the kinetics of H. pylori gastritis are limited, but nevertheless very consistent. They suggest that the progression to gland loss or atrophic gastritis among H. pylori-positive subjects occurs at a rate of 1-2% per year. As H. pylori gastritis usually persists for life, a considerable proportion of H. pylori-positive subjects thus eventually show signs of gastric gland loss. The majority of these subjects progress to intestinal metaplasia. Despite these consistent findings in different areas of the world, the incidence of gastric cancer is only moderately related to the prevalence of H. pylori. An example is the so-called African enigma, referring to a low incidence of gastric cancer in certain countries of Africa, despite a high prevalence of H. pylori in all age groups. This is not due to differences in progression to atrophic gastritis; other yet unidentified factors therefore must play a role.     

Gastric metaplasia and chronic inflammation at the duodenal bulb mucosa

BACKGROUND: Chronic inflammation and gastric metaplasia are often observed in biopsy specimens from the duodenal bulb of Heliobacter pylori positive patients with duodenal ulcer disease (DU). AIMS: We set out to investigate the prevalence of these lesions and their associations with other gastric and duodenal histopathological lesions. PATIENTS: A total of 1255 consecutive patients who underwent upper gastrointestinal endoscopy were recruited into the present study. METHODS: Two biopsy specimens were obtained from each of the following sites: duodenal bulb, gastric antrum, gastric body, and distal to the superior duodenal angle. These specimens were stained with hematoxylin-eosin, alcian blue periodic acid Schiff (pH 2.5) and modified Giemsa (Heliobacter pylori infection was determined only by histology). RESULTS: The mean age of the study population was 57 years, and male:female ratio 1:1.6. Overall, 235 (19%) had gastric metaplasia and/or chronic inflammation in the duodenal bulb mucosa, and H. pylori organisms could be found in 17 (1%). In univariate analyses, gastric metaplasia and/or chronic duodenal bulb inflammation positively associated with male sex (p = 0.046), Heliobacter pylori-positive chronic gastritis (p = 0.033), villous atrophy of distal duodenal mucosa, i.e., coeliac disease (p < 0.001), duodenal ulcer (p < 0.001), and duodenal bulb deformity and scarring in endoscopy (p < 0.001), but not with age (p = 0.7) nor use of nonsteroidal anti-inflammatory drugs (p = 0.055). Multivariate analysis revealed that independent risk factors for gastric metaplasia and chronic inflammation in duodenal bulb were duodenal Heliobacter pylori infection (odds ratio 1.6, 95% confidence interval CI 1.1-2.1), and villous atrophy of the distal duodenal mucosa (odds ratio 12.7, 95% CI 4.4-36.5), while chronic atrophic gastritis was protective against them (odds ratio 0.5, 95% CI 0.3-0.8). CONCLUSIONS: In addition to Heliobacter pylori infection, duodenal bulb gastric metaplasia and chronic inflammation may result from predisposition to toxic dietary components in gluten-sensitive subjects.     

Diagnosis of Helicobacter pylori infection in patients with atrophic gastritis: comparison of histology, 13C-urea breath test, and serology

BACKGROUND: Atrophic gastritis, a risk factor for gastric cancer, is a late consequence of Helicobacter pylori infection in approximately one-third of the infected patients. It has been suggested that gastric cancer would develop less frequently if H. pylori were eradicated. However, the prevalence of H. pylori infection may be underestimated in patients with atrophic gastritis and intestinal metaplasia if only biopsy-based diagnostic methods are used. METHODS: We compared histology, 13C-urea breath test (13C-UBT), and serology in H. pylori diagnostics in 50 male patients with atrophic corpus gastritis. RESULTS: H. pylori was detected in 15 (30%) patients by histology and in 14 (28%) by 13C-UBT, whereas increased serum antibody levels indicating H. pylori infection were found in 41 (82%) patients (P < 0.0001 between serology and both histology and 13C-UBT). H. pylori infection was associated with atrophic corpus gastritis in 84% of the present patients (in one patient with normal antibody titres H. pylori was defined histologically). CONCLUSIONS: H. pylori infection would have been missed in most patients with atrophic gastritis without the analysis of H. pylori antibodies. Therefore, in patients with atrophic gastritis, the use of serology is encouraged in diagnosing H. pylori infection.     

Classical Barrett Esophagus Contrasted with Barrett-Type Epithelium at Normal-Appearing Esophagogastric Junction: Comparison of Demographic,Endoscopic, and Histologic Features

Background: Incomplete intestinal metaplasia or specialized columnar epithelium (SCE) is the histologic hallmark of Barrett esophagus (BE), but it may also occur at a normal-appearing gastroesophageal junction without BE. We studied whether differences occur between BE patients and those with SCE at the squamocolumnar junction but without BE (abbreviated JSCE), in terms of endoscopic and histologic signs of gastroesophageal reflux disease (GERD) and Helicobacter pylori gastritis. Methods: A total of 1059 consecutive patients referred for endoscopy in one hospital district in Finland were enrolled in the study. Biopsy specimens (at least two from each site) were obtained from the gastric antrum and the corpus of the stomach and from the esophagogastric junction and distal esophagus. Results: Classical BE was detected in 25 (2%) and JSCE in 99 (9%) patients. Dysplasia in the metaplastic mucosa was observed in six BE patients but in none of the JSCE patients (P &lt; 0.001). In multivariate analysis the independent risk factors for BE were endoscopic erosive esophagitis (odds ratio (OR), 6.08; 95% confidence interval (CI), 2.50-14.82), male sex (OR, 3.02; 95% CI, 1.20-7.65), and age (OR, 1.02 per year; 95% CI, 1.00-1.06). The independent risk factors for JSCE were endoscopic erosive esophagitis (OR, 1.88; 95% CI, 1.08-3.29) and age (OR, 1.03; 95% CI, 1.02-1.05) but not H. pylori infection (OR, 1.57; 95% CI, 0.83-2.97) or chronic gastritis (OR, 0.88; 95% CI, 0.44-1.75). In univariate analysis, however, JSCE was associated with antral-predominant atrophic gastritis (77% H. pylori-positive). Unlike in JSCE patients, male sex strongly predominated among BE patients (P = 0.01). The mean ages of BE and JSCE patients did not differ. Conclusions: Both BE and JSCE without BE increase in prevalence with age, and both associate with endoscopic erosive esophagitis but not with H. pylori gastritis. However, because of the marked sex disparity, JSCE cannot be a direct precursor of BE, and some factors other than GERD alone also play a role in the pathogenesis of BE. Compared with BE, dysplasia is a rare finding in JSCE, and endoscopic surveillance with biopsy specimens from JSCE patients without dysplasia is not recommended.     

Helicobacter pylori infection and early gastric cancer

BACKGROUND: Helicobacter pylori has recently been associated with an increased risk of gastric cancer. This study aimed to examine the association between H. pylori, histologic chronic gastritis, and intestinal metaplasia in early gastric cancers of different histologic types. STUDY: Seventy-four patients who were surgically diagnosed as having early gastric cancer were included in this study. All tissue specimens were obtained from patients by endoscopic biopsy and were classified histopathologically as intestinal-type early gastric cancer in 55 patients and diffuse-type early gastric cancer in 19 patients. RESULTS: H. pylori infection was found in 67 patients (90.5%) but not found in seven (9.5%). And the prevalence of H. pylori infection with nongastric cancer patients was also high (68.5%). There was no significant difference between the intestinal-type and the diffuse-type early gastric cancer in chronic active gastritis and atrophic chronic gastritis. Intestinal metaplasia was observed more frequently in patients with the intestinal-type than with the diffuse-type early gastric cancer (P = 0.0102). CONCLUSIONS: Infection with H. pylori has an important relationship to both histopathologic types of early gastric cancer.     

Prevention by bovine milk against Helicobacter pylori-associated atrophic gastritis through its adherence inhibition

BACKGROUND/AIMS: The effects of Helicobacter pylori infection on the development of atrophic gastritis and intestinal metaplasia in relation to lifestyle and diet and the effect of the bovine milk on H. pylori adherence to gastric antral mucosa were investigated. METHODOLOGY: H. pylori infection was investigated in 63 patients without endoscopic evidence of gastroduodenal disease. Presence of H. pylori infection was assessed by culture and histologic examination of antral and corpus biopsy samples. Grades of atrophic gastritis and intestinal metaplasia were judged with chromoendoscopy (Congo red-methylene blue test). Adherence of H. pylori was evaluated with scanning electron microscopic examination of antral mucosa in Mongolian gerbils. RESULTS: Cross-sectional analysis of lifestyle and diet showed that a high intake of bovine milk was significantly related to prevention of H. pylori infection and the developments of atrophic gastritis and intestinal metaplasia. H. pylori adherence to the gastric mucosa was inhibited by bovine milk in a dose-dependent manner. CONCLUSIONS: Bovine milk prevents the development of atrophic gastritis and intestinal metaplasia through its defense mechanisms against the attachment of H. pylori to the gastric mucosa.     

Helicobacter pylori and gastric premalignant conditions.

A hypothetical sequence occurs in the stomach from H. pylori infection to premalignant conditions. This sequence is characterized by several well documented steps. First, the H. pylori infection seems to be the main course of chronic gastritis, and is seen to be associated with gastritis at least in 80% of the cases. Second, chronic gastritis tends to slowly progress to atrophy and intestinal metaplasia of the underlying mucosa in a great proportion of affected subjects, this progression of chronic gastritis to atrophy being, however, multifactorial in nature, and being obviously affected also by factors other than the H. pylori. Third, there occurs an increased risk of gastric cancer in atrophic stomach (atrophic gastritis) with intestinal metaplasia, this risk being dependent upon the extend and grade of atrophic and metaplastic alterations in the stomach. Thus, it can be suggested that the H. pylori infection may trigger a sequence which will finally result in a development of conditions that favour the cancer formation. Recent epidemiological observations support this view: gastric cancer tends to be common in populations in which the H. pylori infection and the gastritis are common and in which the people will be commonly infected already in childhood, or in young age.