Expression of melanoma differentiation associated gene 5 is increased in human gastric mucosa infected with Helicobacter pylori

Helicobacter pylori infection is associated with gastroduodenal diseases. Melanoma differentiation associated gene 5 (MDA5) plays a role in antiviral host defense. We investigated the effect of H pylori infection on MDA5 expression in human gastric mucosa. Biopsy samples from the antrum and corpus were obtained from 33 patients. MDA5 mRNA and protein were examined by real-time PCR and immunohistochemical staining. Histological gastritis was graded according to updated Sydney System. MDA5 mRNA was significantly increased in the antrum infected with H pylori. MDA5 protein positively stained in infiltrating mononuclear cells. MDA5 mRNA expression was significantly correlated with the grade of glandular atrophy (rs = 0.767) and intestinal metaplasia (rs = 0.748) in the corpus with H pylori infection. These results indicate that MDA5 may be involved in innate immune reactions against H pylori and associate with glandular atrophy and intestinal metaplasia in patients with H pylori infection.     

Atrophic gastritis in young children and adolescents

BACKGROUND: Helicobacter pylori associated gastric cancer arises via a multistage process, with atrophic gastritis being the precursor lesion. Helicobacter pylori is typically acquired in childhood, yet little is known of the prevalence of atrophic gastritis in childhood. AIM: To study atrophic gastritis among children from countries with high gastric cancer incidence. METHODS: Sections from topographically mapped gastric biopsy specimens from children undergoing clinically indicated endoscopy in Korea and Colombia were evaluated using visual analogue scales. Atrophy was defined as loss of normal glandular components, including replacement with fibrosis, intestinal metaplasia (IM), and/or pseudopyloric metaplasia of the corpus (identified by the presence of pepsinogen I in mucosa that was topographically corpus but phenotypically antrum). RESULTS: One hundred and seventy three children, 58 from Korea (median age, 14 years) and 115 from Colombia (median age, 13 years), were studied. Helicobacter pylori was present in 85% of Colombian children versus 17% of Korean children (p<0.01). Atrophic mucosa near the antrum-corpus border was present in 16% of children, primarily as pseudopyloric metaplasia (31%, IM; 63%, pseudopyloric metaplasia; 6%, both). The median age of children with corpus atrophy was 15 (range, 7-17) years. CONCLUSION: Gastric atrophy occurs in H pylori infected children living in countries with high gastric cancer incidence. Identification and characterisation of the natural history of H pylori gastritis requires targeted biopsies to include the lesser and greater curve of the corpus, starting just proximal to the anatomical antrum-corpus junction, in addition to biopsies targeting the antrum and cardia.     

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

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

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.     

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.     

In patients with Helicobacter pylori gastritis and functional dyspepsia, a biopsy from the incisura angularis provides useful diagnostic information

The aim of this study was to assess whether the taking of an additional biopsy from the incisura angularis increases the chance of detecting maximal degrees of atrophy and intestinal metaplasia (IM) in patients with Helicobacter pylori gastritis and functional dyspepsia. At entry into a randomised trial, biopsies were taken from 328 patients (mean age 48 years), two from both the gastric antrum and corpus, and one from the incisura angularis, and comparative grading of gastritis variables was carried out. Biopsy material from the gastric antrum, corpus, and the incisura angularis revealed no notable differences in atrophy or an incidence of IM and mucosa-associated lymphatic tissue. However, when the incisura biopsies were classified histologically, 58% contained antral mucosa (AM), 18% corpus mucosa (CM), and 24% intermediate zone mucosa. AM at the incisura was associated with considerably more severe gastritis in both the incisura and antrum (14% atrophy, 20% IM) than in CM of incisura (2% atrophy, 6% IM). Corpus atrophy and IM were rare in the AM group and absent from the CM group. Incisura angularis biopsy in patients with H. pylori gastritis and functional dyspepsia does give additional information regarding the severity of gastritis expected in the corpus and antrum. Antral-type mucosa in the incisura angularis region seems to indicate an increased risk for the development of atrophy and/or IM.     

Immune response to Helicobacter pylori and its association with the dynamics of chronic gastritis in the antrum and corpus

The aim of the study was to establish possible factors which play a role in progression of gastritis to atrophic gastritis in long-term follow-up among the Estonian population, to assess the association between the host immune response and different Helicobacter pylori antigens and autoantigens in relation to the histological parameters of gastritis in the antrum and corpus. ELISA and immunoblot were used for detection of IgG to H. pylori acid glycine-extracted cell surface proteins, CagA protein, and H. pylori HSP60. Anticanalicular autoantibodies (ACAB) in the serum were evaluated according to Faller et al. (1996). Apoptosis was evaluated using the TUNEL method. Study subjects were 1958 persons from an unselected Estonian population, and 70 persons from a sample from Saaremaa Island, who had been investigated over a period of 18 years. Seropositivity for CagA was a sign of gastritis activity [OR=14.8 (4.5-50.3)] and atrophy [OR=7.0 (2.1-23.1)] and might predict development of atrophy, particularly in the corpus [OR=7.1 (1.8-27.7)]. The prevalence of ACAB increased significantly with duration of H. pylori gastritis from 22% in 1985 to 46% in 1997 (p=0.004). Immune response to H. pylori HSP60 indicates chronic inflammation in the antrum (p=0.003). Apoptosis of gastric epithelial cells is largely dependent on grade of activity of gastritis, and, particularly in the antrum, on grade of H. pylori colonization (p=0.01; p=0.02), but is not associated with development of atrophy. Seropositivity for different H. pylori antigens (CagA, HSP 60) serves as a marker of different histological manifestations in the antrum and corpus mucosa.     

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

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

Cell proliferation in the post-surgical stomach, dietary salt, and the effect of H pylori eradication

AIMS: To study the epithelial kinetics of the post-surgical stomach with reference to dietary salt intake and H pylori. METHODS: Endoscopic biopsies of the antrum/anastomosis and corpus were taken for histology and MIB-1 immunostaining. The labelling index (LI%) was determined in the three zones of the gastric glands (zone 1 = surface + gastric pit; zone 2 = isthmus; zone 3 = gland base) in patients with vagotomy and pyloroplasty (n = 12), gastroenterostomy + vagotomy (n = 4), partial gastrectomy (n = 3), and Billroth I operation (n = 3). Dietary salt was determined by urinary sodium/creatinine ratio. Twelve patients were H pylori positive (10 vagotomy and pyloroplasty; 2 partial gastrectomy) and had a repeat biopsy three months after antihelicobacter treatment (10 were H pylori negative after treatment). RESULTS: There was no correlation between salt intake and antrum/anastomosis (r = -0.34; p = 0.2) or corpus (r = -0.16; p = 0.2) labelling indices. Gastric mucosal proliferation is increased in the antrum/ anastomosis compared to the corpus in H pylori positive (p = 0.014) but not H pylori negative subjects (p = 0.084). This may reflect the different types of post-surgical stomach in each group. Gastric mucosal proliferation is reduced in antrum/anastomosis (p = 0.002) and corpus (p = 0.016) following H pylori eradication. CONCLUSIONS: Dietary salt does not influence gastric mucosal proliferation in the post-surgical stomach but H pylori may have a role in gastric stump carcinogenesis.     

Histologic changes of the gastric mucosa associated with primary gastric lymphoma in endoscopic biopsy specimens

CONTEXT: Recently, we have observed intestinal metaplasia, atrophy, and dysplasia in the mucosa adjacent to primary gastric lymphoma (PGL) in gastrectomy specimens. OBJECTIVE: To determine the frequency and type of epithelial disorders at the histopathologic level in the mucosa adjacent to PGL in endoscopic specimens. DESIGN: We studied 54 endoscopic biopsies from patients harboring PGL. We searched for the following morphologic changes in the gastric mucosa: intestinal metaplasia; atrophy; dysplasia; epithelial erosion; and atypical regeneration of the glandular epithelium. Other nonepithelial findings such as lymphoid follicles, Helicobacter pylori, and lymphoma grade, were also recorded. For comparative purposes, 50 endoscopic biopsies with gastric adenocarcinoma and 50 biopsies with chronic gastritis associated with H pylori infection were also studied. RESULTS: The 54 biopsies included 28 (52%) low-grade and 26 (48%) high-grade PGLs. We found intestinal metaplasia in 32 biopsies (59%), atrophy in 20 biopsies (37%), dysplasia in 2 biopsies (4%), erosion of the epithelium in 33 biopsies (61%), and atypical regenerative changes of the glandular epithelium in 10 biopsies (19%). Lymphoid follicles were found in 21 biopsies (39%), and H pylori was demonstrated in 31 biopsies (57%). When groups were compared, the frequency of epithelial changes in biopsies from patients with PGL and adenocarcinoma was similar. Intestinal metaplasia or atrophy were present in only 10% of biopsies from patients with gastritis, and dysplastic glands were not identified. CONCLUSIONS: Biopsies from patients with PGL showed chronic damage of the gastric mucosa at diagnosis, including precancerous conditions. Intestinal metaplasia and atrophy were among the most frequent disorders, but dysplasia was also occasionally present. Endoscopists and pathologists must be acquainted with such changes and look for them in the initial biopsy, as well in subsequent samples. This practice is particularly important when reviewing biopsies from patients with low-grade mucosa-associated lymphoid tissue (MALT)-lymphomas who are eligible for eradication treatment for H pylori.     

Improvement of gastric inflammation and resolution of epithelial damage one year after eradication of Helicobacter pylori.

AIMS--To investigate the effect of eradication of Helicobacter pylori infection on gastric epithelial damage and gastritis, scored according to the Sydney system. METHODS--Gastritis scores and epithelial damage were assessed in gastric biopsy specimens before, and five weeks and one year after anti-H pylori therapy in 66 patients with H pylori related gastritis. RESULTS--The mean initial levels of activity, inflammation, atrophy, intestinal metaplasia, and H pylori scores were higher in the antrum than in the corpus or fundus. Eradication of H pylori resulted in an improvement in the mean inflammatory score in antral biopsy specimens from 2.23 before treatment to 1.32 and 1.06, respectively, five weeks and one year after treatment. Corresponding values for fundic biopsy specimens were 1.30, 0.36 and 0.35. Activity scores improved from 1.41 before treatment to 0.13 and zero, respectively, five weeks and one year after treatment in antral biopsy specimens and from 0.60 before treatment to zero in fundic biopsy specimens. Before treatment, epithelial damage was present in 51% of biopsy specimens taken from the antrum and 23% of those from the corpus. Five weeks after eradication of H pylori none of the biopsy specimens revealed evidence of epithelial damage. CONCLUSION--Eradication of H pylori is followed by a rapid, significant improvement in the gastritis score and resolution of epithelial damage in antral and fundic mucosa.     

Spontaneous disappearance of Helicobacter pylori antibodies in patients with advanced atrophic corpus gastritis

Background. Only a few reported studies focus on the natural history and course of advanced and severe chronic atrophic gastritis. Methods. In this study we followed 47 men (mean age 62 years) with advanced (moderate or severe) Helicobacter pylori-positive atrophic corpus gastritis. Duration of endoscopic follow-up was 6 years and follow-up based on serum levels of pepsinogen I and antibodies to H. pylori covered a period of 10 years. None of the patients was treated for H. pylori infection prior to end of follow-up. Results. The median H. pylori antibody titre declined (IgG from 4000 to 1300; IgA from 200 to 50) in the study population, and 11 men (23%) converted to seronegative (p=0.0005, Fisher's exact test). There was a small but significant (p=0.0004, Page's test) declining trend in mean atrophy score of the corpus during follow-up (from 2.5 to 2.2). However, no significant changes were observed in grade of atrophy or intestinal metaplasia of the antral mucosa or in grade of intestinal metaplasia in the corpus. The mean SPGI level remained at the initial low level during the entire follow-up. Conclusions. H. pylori antibodies disappear spontaneously within 10 years in almost one fourth of patients with advanced atrophic corpus gastritis. The disappearance of H. pylori antibodies is accompanied by no or more than a mild improvement of the gastric mucosa.     

Response of IgG1 and IgG2 subclasses to Helicobacter pylori in subjects with chronic inflammation of the gastric mucosa, atrophy and gastric cancer in a country with high Helicobacter pylori infection prevalence

Polarized immune response to Helicobacter pylori and induction of chronic inflammation may increase the risk of gastric atrophy and adenocarcinoma. We studied the association of the response of IgG1 and IgG2 antibodies to H. pylori with grade of gastric chronic inflammation and atrophy in a population with a high prevalence of H. pylori, and compared these data with the data obtained from the study of gastric cancer patients, as well as with the data for CagA positivity. Altogether, 114 persons from two adult population samples from Estonia and 45 consecutive gastric cancer patients were studied. All patients were positive for the H. pylori antibody determined by ELISA. Adenocarcinoma was classified histologically according to the Laurén's system. The response of the IgG subclasses to H. pylori (acid glycine-extracted whole cell proteins) was determined by ELISA and the results were compared with the ELISA results for the recombinant fragment of the CagA protein. Helicobacter pylori IgG level was lower in atrophic gastritis compared with nonatrophic gastritis (chronic inflammation) (p=0.001). In the group of cancer patients, the response of IgG and IgG1 was lower compared with both gastritis groups (p=0.01 and p=0.0002 for IgG, and p=0.001 and p=0.0005 for IgG1). IgG2 was lower for gastric cancer localized in the corpus (p=0.03). In conclusion, atrophic gastritis and gastric cancer were associated with a significant decline in IgG and IgG1 response to H. pylori compared with nonatrophic gastritis. Higher value of CagA antibodies was seen in gastric cancer and in gastric atrophy compared with nonatrophic gastritis; in gastric cancer patients, IgG1 response to H. pylori was correlated with CagA status.     

Chronic gastritis with intestinal metaplasia: clinico-statistical, histological and immunohistochemical study

Chronic gastritis has a high incidence in adults, causing progressive destruction of glandular structures, favoring the development of gastric atrophy. The association of chronic gastritis with intestinal type metaplasia of gastric mucosa has a poor outcome as intestinal metaplasia is regarded as a precancerous lesion. Metaplasia is common in patients with Helicobacter pylori infection and also heavy smokers. The aim of our study was to evaluate the relationship between chronic gastritis and intestinal metaplasia. The study was conducted on a total of 1218 patients, aged between 5 and 90 years, who presented for dyspeptic disorders in the period 2007-2010 and were examined clinically and endoscopically. During the gastroscopic examination, fragments of gastric mucosa were collected for the histopathological study and for highlighting the H. pylori infection. For the histopathological study, the Hematoxylin-Eosin and PAS-Alcian Blue stains were performed, while for the immunohistochemical study the anti-TAG72 and anti-PCNA antibodies were used. A diagnosis of gastritis was established in 615 patients, representing approximately 50.5% of all cases. Most cases with gastritis were found in people of middle age. Gastritis was present in almost all age groups, from teenagers to the elders. Of the 615 cases of gastritis, urease test was positive in 353 patients, representing approximately 57.40% of all patients with gastritis. Histopathological examination identified the presence of intestinal metaplasia in 61.60% of patients with chronic gastritis, mostly complete metaplasia. PCNA immunohistochemistry revealed that cell proliferation processes are intensified in intestinal metaplasia. This study highlights the importance of chronic gastritis, intestinal metaplasia, and H. pylori infection in the etiopathogeny of gastric cancer.     

Ausmaß, Topographie und Erscheinungsmuster der Helicobacter-pylori-Gastritis Phänotypisierung zur zielgerichteten Diagnose und Therapie?

Helicobacter pylori gastritis, a very common condition, may lead to serious sequelae such as peptic ulcer, gastric carcinoma, and mucosa-associated lymphoid tissue lymphoma. Histological grading of the various gastritis parameters can help to identify the risk of these sequelae and thus improve the indication for prophylactic treatment of the H. pylori infection. This applies in particular to two types of "risk gastritis": gastritis of the duodenal ulcer phenotype and gastritis of the carcinoma phenotype. In the former the antrum shows pronounced inflammatory changes while only low-grade gastritis is seen in the corpus. In the latter, by contrast, the gastritis in the corpus is at least equally as severe as that in the antrum; in addition, intestinal metaplasia and focal atrophy is also frequently found in this phenotype. By establishing topographic grading of the gastritis in antrum and corpus the pathologist can therefore play the role of a "litmus test" for prophylactic H. pylori eradication treatment.     

Helicobacter pylori infection and chronic gastritis in gastric cancer.

AIMS: To investigate the prevalence of Helicobacter pylori associated chronic gastritis in patients with gastric cancer. METHODS: Serum IgG antibodies for H pylori were determined in 54 consecutive patients with gastric carcinoma. The prevalence of H pylori in gastric mucosa was also examined histologically (modified Giemsa) in 32 patients from whom adequate biopsy specimens of the antrum and corpus were available. Thirty five patients with gastrointestinal tumours outside the stomach and 48 with non-gastrointestinal malignancies served as controls. RESULTS: Of the 54 patients, 38 (70%) had H pylori antibodies (IgG) in their serum (three additional patients had H pylori antibodies IgA, class specific but not IgG specific). This prevalence was significantly higher (p less than 0.05) than that (49%) in the 35 controls. No differences in prevalence of H pylori antibodies were found between gastric cancer cases of intestinal (IGCA) or diffuse (DGCA) type, both these types showing H pylori antibodies (IgG) in 71% of the patients. In the subgroup of 32 subjects, five patients had normal gastric mucosa and four showed corpus limited atrophy ("pernicious anaemia type" atrophy of type A). All of these nine patients had no evidence of current or previous H pylori infection in serum (no IgG antibodies) or in tissue sections (negative Giemsa staining). The remaining 23 patients had antral or pangastritis, and all had evidence of current or previous H pylori infection. CONCLUSIONS: H pylori associated chronic gastritis was the associated disease in 75% of the patients with gastric cancer occurring equally often in both IGCA and DGCA groups. About 25% of cases seem to have a normal stomach or severe corpus limited atrophy, neither of which showed evidence of concomitant H pylori infection.     

B-Cell monoclonality in Helicobacter pylori-associated chronic atrophic gastritis

B-cell monoclonality has been reported not only in gastric lymphoma, but also in 1.3-21% of Helicobacter pylori-associated chronic gastritis (Hp-CG) cases. The aim of this study was to determine the significance of B-cell monoclonality in Hp-CG. We examined 134 gastric biopsy specimens from 99 patients with Hp-CG. The density of Hp, polymorphonuclear neutrophil activity, chronic inflammation, glandular atrophy, and intestinal metaplasia (IM) were scored according to the updated Sydney System. B-cell monoclonality was analyzed for immunoglobulin heavy chain gene rearrangement using polymerase chain reaction amplification. B-cell monoclonality was detected in 6% of informative samples. B-cell monoclonality was found in 18% of the samples from Hp-CG patients with marked glandular atrophy but in none of the samples from Hp-CG patients with none to moderate glandular atrophy. Monoclonality was also detected in 20% of the samples from Hp-CG patients with marked IM, in 11% of the samples from Hp-CG patients with moderate IM, and in none of the samples from Hp-CG patients without IM. Therefore, B-cell monoclonality was significantly more frequent in Hp-CG patients with marked glandular atrophy than in Hp-CG patients with none to moderate atrophy. It was also more significantly frequent in Hp-CG patients with moderate or marked IM than in Hp-CG patients without IM (P < 0.05). Of 35 Hp-CG patients, 26 (74%) had identical B-cell populations in the antrum and the corpus, and all were polyclonal. The remaining nine (26%) Hp-CG patients had B-cell populations that differed in the antrum and the corpus. Four of the nine (44%) showed monoclonal B-cell populations in at least one gastric biopsy specimen. There were no patients with monoclonal B-cell populations in both the antrum and the corpus. These data suggest that glandular atrophy and IM in gastric biopsy specimens may be markers for gastric mucosa-associated lymphoid tissue (MALT) lymphoma-genesis and that multiple gastric biopsy specimens from both the antrum and the corpus may be needed to assess the risk of gastric MALT lymphoma.     

Interobserver agreement in the assessment of gastritis reversibility after Helicobacter pylori eradication

AIM: Our aim was to determine interobserver agreement in the application of the Sydney system to assess reversibility of gastritis after Helicobacter pylori eradication. METHODS AND RESULTS: Forty-three patients with a Helicobacter pylori-positive duodenal ulcer disease were included in the study. All patients included had successful H. pylori eradication after different antimicrobial drug combinations. Biopsy samples were collected from antrum and body, according to the Sydney recommendations, before antimicrobial therapy, 2 months after and at yearly intervals during 2-4 years of follow up. Three pathologists, who were blind to clinical data, evaluated histological changes in 221 antral and 219 body specimens stained with haematoxylin and eosin and with Warthin Starry. The percentage of pairwise agreement, kappa and weighted kappa statistic were used. Agreement in recognizing the presence of H. pylori colonization of the gastric mucosa, activity of inflammation and intestinal metaplasia was over 90%. Agreement in recognizing chronic inflammation in the body and atrophy in the antrum was between 78 and 89% respectively. The kappa values were excellent (more than 0.75) for the grade of H. pylori in the body, good (between 0.50 and 0.75) for the grade of H. pylori in the antrum, grade of inflammatory activity and intestinal metaplasia in the antrum and moderate to good (0.38-0.53) for the grade of chronic inflammation. Kappa values were poor to good (from 0.17 to 0.57) only in evaluation of the grade of atrophy. CONCLUSION: Interobserver agreement in the application of the Sydney system to reversibility of gastritis after H. pylori was good. More strict criteria should be used for atrophy and to differentiate normal and mild chronic inflammation.     

Prevalence of gastric precancerous lesions in Ardabil, a high incidence province for gastric adenocarcinoma in the northwest of Iran

BACKGROUND/AIMS: Ardabil Province, in northwestern Iran, has the highest rate of gastric (predominantly cardia) adenocarcinoma in Iran. This study aimed to investigate the feasibility of endoscopic screening and to look for associated Helicobacter pylori infection and gastric precancerous lesions. METHODS: One thousand one hundred and five adult volunteers, residents of Ardabil and Meshkinshahr, districts, 40 years old and above were selected and invited by a simple random household canvass in rural and urban locations. Informed consents were obtained and upper gastrointestinal video endoscopy was performed to biopsy all visible lesions and standard sites in the antrum, corpus, and cardia. RESULTS: One thousand and eleven of the invited individuals agreed to participate, including 494 men and 517 women, with a mean (SD) age of 53.32 (10.39) years. Endoscopy was well tolerated by all subjects; 96.7% of antral and 80.7% of cardia mucosal biopsies were satisfactory. The urease test or histology for H pylori was positive in at least 89.2% of subjects. Histological evidence of mucosal atrophy was seen in 39.3% of antral and 21.9% of cardia samples. Chronic gastritis with or without activity, reactive atypia of glandular epithelium, intestinal metaplasia, dysplasia, and cancer were found in 95.1%, 38.0%, 8.7%, 0.2%, and 0.3% of antral and 85.3%, 22.9%, 3.8%, 0.3%, and 0.1% of cardiac biopsies, respectively. CONCLUSION: Endoscopic screening for upper gastrointestinal diseases was feasible and well tolerated in Ardabil, Iran. Most subjects showed H pylori infection. Atrophic gastritis, reactive atypia, and intestinal metaplasia were common in antrum, corpus, and cardia subsites.