Intestinal Metaplasia In Antrum Research Articles

Relationship between endoscopic gastric atrophy according to Kimura - Takemoto classification and histopathological characteristics in H. Pylori infected patients

Background: Endoscopic gastric atrophy according to Kimura-Takemoto classification has been shown to be closely related to histopathological atrophy. Gastric atrophy and intestinal metaplasia are considered precancerous gastric lesions that need to be assessed and monitored for early detection of dysplasia and cancer, especially in H. pylori infected patients. The aim of this study was to evaluate the associations between these endoscopic atrophy according to Kimura - Takemoto classification and pathologic characteristics. Methods: A cross-sectional study was conducted in 72 dyspepsia patients at Hue University of Medicine and Pharmacy Hospital, assigned endoscopic assessment and testing H. pylori positive. Assessing endoscopic gastric atrophy according to Kimura-Takemoto classification and compared with histopathological precancerous lesions (atrophy, intestinal metaplasia, dysplasia) according to the modified Sydney system. Results: The mean age was 55.6 ± 13.13, male/female ratio was 1.4/1.0. The rate of endoscopic gastric atrophy at stage C1 was 37.5%, C2: 40.3%, C3: 9.7%, O1: 11.1% and O3: 1.4%. On histo-pathology, the rate of gastric atrophy in antrum was 81.9%, in both antrum and body: 16.7%. The rate of intestinal metaplasia in antrum, body, both antrum and body was 36.1%, 2.5% and 11.1%, respectively. The rate of low-grade dysplasia 12.5% (9/72), high-grade dysplasia 6.9% (5/72) and 2 cases of early gastric cancer. Endoscopic gastric atrophy stages C2 and C3 had a higher rate of atrophy on histopathology than stage C1 (91.7% vs 63%) and stages O had a higher rate of intestinal metaplasia than stages C (77.8% vs 30.2%) with p < 0.05. Conclusion: The degree of endoscopic gastric atrophy was related to the degree of histopathologic atrophy and intestinal metaplasia, the more severe the stage of endoscopic gastric atrophy, the higher the frequency of atrophy and metaplasia on histopathology. Evaluation of endoscopic gastric atrophy according to Kimura-Takemoto classification is a relatively simple strategy for monitoring for each patient with H. pylori chronic gastritis to detect dysplasia and early cancer. Key words: Atrophic gastritis, H. pylori, Kimura-Takemoto classification

The Difference of Endoscopic and Histologic Improvements of Atrophic Gastritis and Intestinal Metaplasia After Helicobacter pylori Eradication.

Helicobacter pylori (H. pylori) is an important risk factor of atrophic gastritis (AG), intestinal metaplasia (IM), and gastric cancer (GC). However, no report to date has described the endoscopic improvement of AG and IM after H. pylori eradication. Thus, the aim of this study was to evaluate the improvement of AG and IM after H. pylori eradication using endoscopic and histologic analyses. A total of 380 subjects were prospectively enrolled for up to 12years and grouped by their H. pylori infection status: negative, non-eradicated, and eradicated. Endoscopic and histologic analyses of AG and IM were performed in the antrum and the corpus, by annual follow-up endoscopy. Endoscopic AG and IM in the antrum and corpus in the eradicated group improved compared to that in the non-eradicated group (AG, P = 0.002 and P = 0.005; IM, P = 0.038 and P = 0.048, respectively). Histologic AG and IM in the antrum and corpus in the eradicated group also improved compared to that in the non-eradicated group (all P < 0.001). Time taken to the endoscopic improvement of AG and IM after H. pylori eradication was significantly longer than time taken to the histologic improvement in the antrum and corpus (AG in antrum: 3.47 ± 2.60 vs. 2.34 ± 1.71years, P = 0.004; AG in corpus: 3.19 ± 2.30 vs. 1.87 ± 1.48years, P = 0.002; IM in antrum: 4.40 ± 2.38 vs. 3.62 ± 2.35years, P = 0.043; and IM in corpus: 4.82 ± 1.08 vs. 3.61 ± 2.22years, P = 0.007, respectively). Both endoscopic and histologic improvements of AG and IM were observed after H. pylori eradication, while endoscopic improvement took significantly longer time than histologic improvement.

Rebamipide for the Improvement of Gastric Atrophy and Intestinal Metaplasia: A Prospective, Randomized, Pilot Study.

The presence of atrophic gastritis (AG) and intestinal metaplasia (IM) is associated with an increased risk of gastric cancer (GC). Thus, the development of new strategies to improve AG/IM is essential for reducing the incidence of GC. We aimed to evaluate the efficacy of rebamipide for improving AG/IM. This was a prospective, randomized, pilot study from a single tertiary referral center. Fifty-three (rebamipide, n = 34 vs. placebo, n = 19) patients, who underwent endoscopic resection for gastric dysplasia or early GC, were analyzed. We obtained tissue samples from the antrum and corpus of the stomach, at the time of screening and 1-year later. The histologic grading of inflammation was performed by histopathologists RESULTS: The AG grade in the antrum improved significantly after rebamipide treatment (pre-administration, 1.870 ± 0.932 vs. post-administration, 1.430 ± 0.986; P = 0.013). Additionally, the severity of IM in the antrum was significantly improved (pre-administration, 1.750 ± 0.963 vs. post-administration, 1.370 ± 1.032; P = 0.038). The rebamipide subgroup analysis revealed that patients with no Helicobacter pylori (HP) infection showed significant improvements in AG in the antrum (pre-administration, 1.880 ± 1.040 vs. post-administration, 1.250 ± 0.894; P = 0.028) and IM in antrum (pre-administration, 1.840 ± 1.012 vs. post-administration, 1.180 ± 0.912; P = 0.020). This study demonstrated that the administration of rebamipide improves AG and IM in the antrum, especially in patients with HP non-infection (KCT0001915).

Reversibility of atrophic gastritis and intestinal metaplasia after Helicobacter pylori eradication - a prospective study for up to 10 years.

Atrophic gastritis and intestinal metaplasia are premalignant conditions for gastric cancer. Their reversibility by Helicobacter pylori eradication remains controversial. To evaluate the reversibility of atrophic gastritis and intestinal metaplasia by H. pylori eradication with long-term follow-up. 598 subjects were prospectively enrolled and followed for up to 10 years. They were categorised as H. pylori-negative (n = 65), H. pylori non-eradicated (n = 91), and H. pylori-eradicated (n = 442). Histological assessment was performed for antrum and corpus by Sydney classification. Histological follow-up was performed regularly at 1, 2, 3-4 and ≥5 years, with mean follow-up of 1.07 ± 0.21, 2.29 ± 0.83, 3.93 ± 1.02, and 6.45 ± 1.28 years, respectively. Atrophic gastritis in antrum and corpus gradually and significantly (both P < .05 for all timepoints) improved only in the H. pylori-eradicated group compared to that at baseline. Significant difference in atrophic gastritis between H. pylori-eradicated and H. pylori-negative groups disappeared from 1-year follow-up. Similarly, intestinal metaplasia in antrum and corpus improved significantly (both P < .05 for all timepoints) only in the H. pylori-eradicated group in comparison with that at baseline. Significant difference in intestinal metaplasia between H. pylori-eradicated and H. pylori-negative groups disappeared from ≥5 years of follow-up in the antrum and from 3 years of follow-up in the corpus. H. pylori eradication may be a preventative strategy for intestinal-type gastric cancer by regression of atrophic gastritis and intestinal metaplasia.

Detection Rate of Helicobacter pylori Against a Background of Atrophic Gastritis and/or Intestinal Metaplasia

To evaluate the detection rate of the CLOtest, Giemsa stain, and culture for the diagnosis of Helicobacter pylori organisms in patients with or without atrophic gastritis (AG) and/or intestinal metaplasia (IM). We used either the CLOtest, Giemsa staining, or culture to determine the presence of H. pylori in 430 participants who were documented to be infected with H. pylori from September 2003 to June 2006. The detection rates of the methods were evaluated according to the presence of AG and IM in antrum and body, which were classified using the updated Sydney system classification. Positivity by the CLOtest markedly reduced depending on the degree of AG and IM in both antrum and body (P<0.05), and the positivity of Giemsa staining was markedly reduced as the degree of IM increased (P<0.01), but was not affected by the degree of AG (P=0.08) in antrum or body. When the results of these tests were evaluated in terms of combinations of AG and IM, the positivity of CLOtest was found to be lower in AG with IM than in AG without IM, (50.0% vs. 80.0% in antrum, 47.5% vs. 78.0% in body, respectively, P<0.01). In addition, the positivity of Giemsa stain was less frequent in AG with IM than in AG without IM in antrum (65.1% vs. 100%, respectively, P<0.01). However, the positivity of Giemsa stain in the body showed no statistical difference between AG without IM and AG with IM (97.6% vs. 91.7%, respectively). Invasive H. pylori tests, especially the CLOtest, had a lower detection rate for H. pylori in the presence of mucosal atrophy and IM, and this became more prominent in the presence of higher levels of IM and AG.

Precancerous gastric conditions in high Helicobacter pylori prevalence areas: comparison between Eastern European (Lithuanian, Latvian) and Asian (Taiwanese) patients

The aim of the study was to compare the prevalence and severity of precancerous condition--gastric atrophy and intestinal metaplasia (IM) between Eastern European (Lithuania and Latvia) and Asian (Taiwan) countries in population older than 55 years. Patients aged 55 years and older, referred for upper endoscopy due to dyspeptic symptoms, were included in the study. Gastric biopsies were histological investigated according modified Sydney classification. Helicobacter pylori (H. pylori) was detected if any two of three methods (urease test, histology, and serology) were positive. Overall 322 patients included: 52 from Taiwan (TW), 171 from Latvia (LV) and 99 from Lithuania (LT). There were 227 (70%) females and 95 (30%) males. The mean age of TW patients was significantly lower (61.0+/-5.8 years), than of LV (68.1+/-7.3 years) and LT (66.5+/-7.5 years) patients. H. pylori was established in 224 (69.6%) patients. H. pylori positivity was established in 43 (82.7%) TW patients, in 112 (65.5%) LV patients, and in 69 (69.7%) LT patients (P>0.05). In H. pylori-infected patients, any atrophy either in the corpus or in the antrum of the stomach was detected in 26 (60.5%) TW patients, in 40 (35.7%) LV patients, and in 36 (52.2%) LT patients (between TW and LV patients P<0.005). Severe atrophy (grade 2 or 3) detected in 8 (18.6%) TW patients, in 17 (15.2%) LV patients, and in 18 (26.1%) LT patients (P>0.05). Intestinal metaplasia was detected in 22 (51.2%) TW patients, in 37 (33.0%) LV patients and in 31 (44.9%) LT patients among countries (P>0.05). There were no significant differences in proportions of different degrees of both atrophy and intestinal metaplasia among countries. Intestinal metaplasia was found in 79 (77.5%) of 102 patients with any degree of atrophy and in 11 (9.0%) of 122 patients without atrophy (P<0.0001). We found strong statistically significant correlations between atrophy and intestinal metaplasia in antrum (r=0.89), P<0.01, and corpus (r= 0.73), P<0.01. The prevalence of H. pylori in the elderly population is still high in LT, LV, and TW. There are no significant differences in prevalence of gastric atrophy and intestinal metaplasia among TW, LT, and LV. There is a strong correlation between gastric atrophy and intestinal metaplasia.

Frequent and Rapid Progression of Atrophy and Intestinal Metaplasia in Gastric Mucosa of Patients with MALT Lymphoma

Association of gastric mucosa-associated lymphoid tissue (MALT) low-grade lymphoma and adenocarcinoma has repeatedly been reported. The aim of this study was to evaluate the frequency and the spreading of atrophy and intestinal metaplasia in gastric mucosa of patients with gastric MALT lymphoma followed after conservative treatment. Forty-five patients (mean age 45 +/- 2.1 yr) with gastric MALT lymphoma, treated by Helicobacter pylori eradication, chemotherapy with per os single alkylating agents, or both treatments have been followed by gastroscopy with biopsies in antrum and corpus at least once a year. Univariate and multivariate analysis evaluated the association between the appearance of atrophy and intestinal metaplasia in antrum or corpus and different factors related to patients, H. pylori status, lymphoma features, and treatment. In addition, histological aspects of gastric biopsies at the diagnosis period and at the end of follow-up were compared with those of two control groups of age-matched patients with H. pylori gastritis. At the diagnosis time, only intestinal metaplasia in corpus was more frequent in patients with gastric MALT lymphoma than in patients with nonulcer dyspepsia. Within median follow-up of 54.4 months (range 9-196), the percentage of patients with gastric atrophy and intestinal metaplasia increased significantly and became significantly higher than in age-matched nonulcer dyspepsia patients. Multivariate analysis showed significant association between corpus intestinal metaplasia and corpus atrophy, intestinal metaplasia in antrum, and duration of the follow-up. Conservative management of gastric MALT lymphoma including H. pylori eradication is associated with progression of gastric atrophy and intestinal metaplasia with frequent involvement of the corpus which is known to be a precancerous condition. These findings show that long-term endoscopic monitoring should be recommended in such patients.

Comparative Classification and Grading of Helicobacter pylori Gastritis in Patients with Gastric Cancer and Patients with Functional Dyspepsia

Background: It has previously been shown that corpus-dominant grade and activity of Helicobacter pylori gastritis in combination with intestinal metaplasia in the antrum or corpus are risk markers for the development of stomach cancer. If one point is scored for each of these three parameters, a gastric cancer risk index is obtained that permits prediction of the risk of gastric cancer developing on the soil of H. pylori gastritis. The aim of the present study was to evaluate the accuracy of the gastric cancer risk index based on a large number of patients compared with dyspeptic controls. Methods: In 415 biopsied patients with gastric carcinoma, biopsy specimens taken from the antrum and corpus were investigated retrospectively. From this group of patients, 244 patients positive for H. pylori were compared with 244 sex- and age-matched H. pylori -infected patients with functional dyspepsia. Results: H. pylori gastritis was detected in 395 carcinoma patients (95.2%). The 244 sex- and age-matched patients significantly more frequently had corpus-dominant H. pylori gastritis (compared with NUD controls). The incidence of intestinal metaplasia was also significantly increased. For a gastric cancer risk index score of 3 points (i.e. corpus pronounced grade and activity of gastritis, and intestinal metaplasia in antrum or corpus), a sensitivity of 93% and a specificity of 85% for the presence of gastric carcinoma can be calculated. Conclusion: Using the proposed risk index, the topographic grading of H. pylori gastritis in the antrum and corpus enables the diagnosis of a 'risk gastritis' to be made.

Close correlation of intestinal metaplasia and corpus gastritis in patients infected with Helicobacter pylori.

The role of intestinal metaplasia as a precancerous condition for Helicobacter pylori associated gastric carcinoma has been the subject of numerous investigations. The aim of the present study was to investigate whether other diffuse gastritis markers such as H. pylori gastritis in the corpus correlate with the presence of intestinal metaplasia and gastric carcinoma. The histological records of 2,000 patients with H. pylori gastritis were retrospectively investigated for grade/activity of gastritis, and presence of intestinal metaplasia. There was a strong correlation between the degree and activity of H. pylori gastritis in the corpus and the presence of intestinal metaplasia in antrum or corpus (all P < 0.001). Intestinal metaplasia and pronounced corpus gastritis were found predominately in H. pylori infected persons with gastric cancer or benign gastric ulcers. On the basis of its close correlation with intestinal metaplasia, pronounced corpus gastritis may be considered as a marker of gastric cancer. In comparison with intestinal metaplasia, this marker of gastric cancer risk has the advantage of being associated with less interobserver variation, and - due to its diffuse presentation - a lower risk of sampling bias.

Cyclooxygenase-2 and Bcl-2 expression in the stomach mucosa of Wistar rats exposed to Helicobacter pylori, N'-methyl- N'-nitro- N-nitrosoguanidine and bile.

Cyclooxygenase-2 (COX-2) and Bcl-2 have been implicated in upper gastrointestinal tract carcinomas, but the underlying mechanisms are not known. In the present study we assessed the correlation of COX-2 and Bcl-2 to known cell kinetics in the glandular stomach mucosa of 104 Wistar rats given combinations of Helicobacter pylori, MNNG ( N'-methyl- N'-nitro- N-nitrosoguanidine) and bile. COX-2 expression, Bcl-2 and cell proliferation (Ki-67) in antral and corpus mucosa were determined immunohistochemically. Apoptotic cells were detected using terminal uridine deoxynucleotidyl nick end labelling technique. Expression of COX-2 was found in the lower portion of glandular corpus epithelium, and Bcl-2 positivity was mainly seen in the proliferative zone of both antrum and corpus mucosa. COX-2 expression in histologically normal-appearing corpus mucosa was associated with cell proliferation, atrophy and intestinal metaplasia in antrum and with Bcl-2 expression in corpus mucosa. No correlation was found between apoptosis and Bcl-2 expression. MNNG but not H. pylori significantly increased COX-2 in corpus mucosa. H. pylori, however, promoted the COX-2 expression in corpus when bile was added and Bcl-2 expression in antrum. Abnormal expression of both COX-2 and Bcl-2 seem to be involved in H. pylori-induced gastric carcinogenesis by altering the gastric cell kinetics.

Gastric carcinoma risk index in patients infected with Helicobacter pylori.

Epidemiological data show an association between Helicobacter pylori gastritis and gastric carcinoma. However, most people infected with H. pylori do not develop gastric cancer. We have therefore evaluated histological criteria indicating an increased risk for gastric cancer. H. pylori gastritis was investigated in 117 patients with small (O<2 cm) early gastric carcinomas and in 117 age-matched duodenal ulcer patients infected with H. pylori, who are known to have a low risk for developing gastric carcinoma. The results showed that infiltration with lymphocytes/plasma cells and infiltration with neutrophils predominating in the corpus, and intestinal metaplasia in antrum and corpus were associated with both types of gastric carcinoma (intestinal and diffuse, P<0.0001). If an index is computed by giving one point to each of these features, the predictive value for the presence of gastric carcinoma was 0.79 with a score of 2, and 0.94 with a score of 3 (all points on the index used). Application of this index might be a simple method of identifying patients infected with H. pylori and carrying a higher risk for gastric carcinoma.