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PubMed2004

Phenotypic differences between esophageal and gastric intestinal metaplasia.

Intestinal metaplasia is a cancer precursor in the esophagus and the stomach. Marked differences exist between the carcinogenic processes in the two locations in terms of natural history and clinical significance. We investigated biopsies from 52 patients with Barrett's esophagus and from 50 patients with gastric intestinal metaplasia in an attempt to throw light on their pathogenic processes. Morphologic characteristics, presence of Helicobacter pylori (H. pylori), and markers of differentiation, inflammation, and proliferation were evaluated by histochemical and immunohistochemical techniques. The area covered by incomplete type of intestinal metaplasia and the proportion of sulfomucins were significantly higher in the esophagus than in the stomach. Immunoreactivity with MUC1, MUC2, MUC5AC, Das-1, cytokeratins 7 and 20, inducible nitric oxide synthase and cyclooxygenase-2 antibodies was also significantly greater in Barrett's esophagus than in gastric intestinal metaplasia. In gastric intestinal metaplasia, the presence of MUC1, MUC5AC, Das-1 and cytokeratin 7 was restricted to areas with the incomplete type of metaplasia. Cell proliferation (Ki-67) was significantly higher in Barrett's esophagus than in gastric intestinal metaplasia. H. pylori was absent in all of the patients with Barrett's esophagus, while it was present in 70% of the patients with gastric intestinal metaplasia. Our observations made clear that Barrett's esophagus shares some phenotypic characteristics with gastric intestinal metaplasia, leading us to suggest that both could arise in response to injuries with eventual carcinogenic potential. However, the progression to more advanced lesions could be modulated by the nature of the carcinogenic insult.

Aged↗
PubMed2001

Effect of Helicobacter pylori eradication on expression of cyclin D2 and p27 in gastric intestinal metaplasia.

BACKGROUND AND AIMS: Cyclins and cyclin-dependent kinase inhibitors play a crucial role in the control of cell cycle transitions. Enhanced expression of cyclin D2 and reduced expression of p27kip1 (p27) have been implicated in the pathogenesis of cancer. Because intestinal metaplasia has been regarded as a pre-malignant lesion, we investigated the expression of cyclin D2 and p27 in Helicobacter pylori-associated chronic gastritis with and without intestinal metaplasia, and followed the changes after H. pylori eradication. METHODS: Expression of cyclin D2 and p27 was studied by immunohistochemistry in 59 patients (including 35 patients with intestinal metaplasia) and in 10 gastric cancer patients. Among them, 29 H. pylori-infected patients had serial gastric biopsies taken before and at 1-year after eradication of H. pylori. RESULTS: Expression of cyclin D2 was significantly higher in gastric cancers when compared to their adjacent non-tumour tissues (median score 3 vs. 1, P=0.015). Over-expression of cyclin D2 was detected in H. pylori-associated chronic gastritis and intestinal metaplasia, which was reduced after eradication of the organism (median score 2 vs. 1, P=0.037 in chronic gastritis; median score 2 vs. 0, P=0.008 in intestinal metaplasia). While the normal gastric mucosa showed strong p27 expression, five of the 10 gastric cancer tissues exhibited reduced p27 expression (P=0.039). Diminished p27 expression was also seen in intestinal metaplasia, which was restored 1-year after H. pylori eradication (eight out of 16 vs. one out of 16, P=0.018). Reduced expression of p27 was frequently associated with increased cyclin D2 expression in H. pylori-associated intestinal metaplasia (P=0.02). CONCLUSION: Over-expression of cyclin D2 and reduced expression of p27 are closely linked to H. pylori-associated intestinal metaplasia. Eradication of H. pylori infection reverses the aberrant expression of cyclin D2 and p27 in intestinal metaplasia.

Cyclin D2↗
PubMed2001

Apoptosis and proliferation in Helicobacter pylori-associated gastric intestinal metaplasia.

BACKGROUND: Imbalance between apoptosis and proliferation may be one of the mechanisms underlying H. pylori associated gastric carcinogenesis. AIM: To examine the cell kinetics of gastric intestinal metaplasia and the effect of H. pylori eradication. METHODS: Endoscopic gastric biopsies were obtained from 100 H. pylori-infected patients. Apoptosis was determined by triphosphate nick-end labelling (TUNEL) and apoptotic nuclei counting, whereas proliferation was assessed by Ki67 immunostaining. Gastric biopsies were repeated in a sub-group of intestinal metaplasia patients after H. pylori eradication. RESULTS: Antral apoptotic index was significantly lower in intestinal metaplasia than in non-intestinal metaplasia (0.19% vs. 0.51%; P < 0.0001) whereas the level of proliferation was comparable (28% vs. 22%, P=0.15). Serial antral biopsies taken from 14 intestinal metaplasia patients before and 1 year after H. pylori eradication showed a significant drop in proliferation in both intestinal metaplasia (50% vs. 12%, P < 0.001) and non-intestinal metaplasia area (47% vs. 9%, P < 0.001). A similar fall in apoptosis was detected in non-metaplastic region (0.58% vs. 0.38%, P < 0.001) but not in intestinal metaplasia (0.24% vs. 0.27%, P=0.56), resulting in a significant increase in the apoptosis/proliferation ratio (0.005-0.021; P=0.03). CONCLUSIONS: Dysregulation in apoptosis control of gastric intestinal metaplasia may contribute to gastric carcinogenesis, which may be retarded by clearance of H. pylori.

Adult↗
PubMed2002

Immunohistochemical staining with MIB1, bcl2 and p16 assists in the distinction of cervical glandular intraepithelial neoplasia from tubo-endometrial metaplasia, endometriosis and microglandular hyperplasia.

AIMS: Preinvasive endocervical glandular lesions, termed cervical glandular intraepithelial neoplasia, are increasing in incidence. The distinction of cervical glandular intraepithelial neoplasia from benign mimics, especially tubo-endometrial metaplasia, endometriosis and microglandular hyperplasia, can be difficult. This study investigates the value of immunohistochemical staining with MIB1, bcl2 and p16 in the distinction of cervical glandular intraepithelial neoplasia from these benign mimics. METHODS AND RESULTS: Immunohistochemical staining using the monoclonal antibodies MIB1, bcl2 and p16 was performed on cases of cervical glandular intraepithelial neoplasia (n = 21), tubo-endometrial metaplasia (n = 13), endometriosis (n = 7) and microglandular hyperplasia (n = 14). With tubo-endometrial metaplasia and microglandular hyperplasia staining with MIB1 was either negative or involved <10% of cells, while with cervical glandular intraepithelial neoplasia the majority of cases (86%) exhibited >10% positive cells. Two cases of endometriosis exhibited a MIB1 index of 10-30% while in the other cases <10% cells stained. With bcl2 the cells of microglandular hyperplasia were negative although there was staining of associated reserve cells in 43% of cases. All cases of tubo-endometrial metaplasia except one and all cases of endometriosis stained diffusely positive with bcl2. Cases of cervical glandular intraepithelial neoplasia were negative or exhibited focal staining. With p16 all cases of cervical glandular intraepithelial neoplasia exhibited diffuse strong positivity, generally involving 100% of cells, while all cases of microglandular hyperplasia were negative. Sixty-two percent of cases of tubo-endometrial metaplasia showed focal positivity, the remainder being negative. Cases of tubo-endometrial metaplasia were never diffusely positive with p16. In three cases of endometriosis there was staining of >50% of cells while the other cases were either focally positive or negative. CONCLUSIONS: A panel of antibodies, comprising MIB1, bcl2 and p16, is a useful adjunct to histology in distinguishing cervical glandular intraepithelial neoplasia from tubo-endometrial metaplasia, endometriosis and microglandular hyperplasia. Cases of cervical glandular intraepithelial neoplasia are diffusely positive for p16 and generally exhibit a high proliferation index with MIB1, while bcl2 is negative or, at most, focally positive. Tubo-endometrial metaplasia and endometriosis are characterized by strong diffuse positivity with bcl2 and a low proliferation index with MIB1 (although occasional cases of endometriosis show moderate proliferative activity). p16 is negative or exhibits focal positivity in tubo-endometrial metaplasia but in endometriosis there may be quite widespread positivity. Microglandular hyperplasia shows a low proliferation index with MIB1 and is negative for bcl2 and p16.

Antibodies, Monoclonal↗
PubMed2003

Mucin core peptide expression can help differentiate Barrett's esophagus from intestinal metaplasia of the stomach.

It is important to distinguish Barrett's esophagus (BE) from intestinal metaplasia related to carditis because these conditions have a different natural history, risk of malignancy, and treatment. However, the distinction between these entities is difficult both clinically and pathologically. The aim of this study was to evaluate and compare the immunostaining pattern of five mucin core polypeptides in BE to cases of carditis or antritis with intestinal metaplasia. Routinely processed mucosal biopsies from 22 patients with intestinal-type BE, 24 patients with cardia intestinal metaplasia (10 Helicobacter pylori positive), 17 patients with antral intestinal metaplasia (all H. pylori positive), 20 control patients with a normal antrum, and 22 control patients with a normal cardia were immunostained with monoclonal antibodies against MUC1, MUC2, MUC3, MUC5AC, and MUC6 mucin core polypeptides. Staining was evaluated separately for goblet cells and non-goblet columnar cells and compared between all groups. A significantly higher number of BE cases (P < 0.05) showed goblet cell staining for MUC1 (55%) or MUC6 (32%) compared with patients with carditis with intestinal metaplasia (MUC1 14%, MUC6 7%) or antritis with intestinal metaplasia (MUC1 6%, MUC6 0%). BE also showed a higher frequency of MUC1 and MUC6 positivity in non-goblet columnar cells compared with carditis and antritis cases with intestinal metaplasia. Only cases of BE showed combined MUC1 and MUC6 staining (sensitivity 23%, specificity 100%). The sensitivity and specificity of MUC1 staining for BE are 55% and 96%, respectively, and for MUC6 staining 30% and 96%, respectively. Interestingly, normal gastric cardia mucosa also showed a significantly higher prevalence of MUC2 and MUC3 expression in glandular epithelium (29% and 38%, respectively) compared with the antrum (0% for both markers) (P < 0.05). In conclusion, MUC1 and MUC6 expression in BE is distinct from that of the cardia and antrum with intestinal metaplasia; thus, immunophenotyping for these markers may have some value in a subset of patients in helping to separate BE from patients with intestinal metaplasia of the cardia. Columnar epithelium in the "normal" gastric cardia has a partially intestinalized phenotype and, as a result, may represent an early form of metaplastic epithelium.

Antibodies, Monoclonal↗
PubMed1999

Oncocytic metaplasia and carcinoma of the endometrium: an immunohistochemical and ultrastructural study.

Endometrial oncocytic carcinoma is an unusual neoplasm, with few cases reported. Endometrial curettage specimens coded as prominent oxyphilic metaplasia (N = 5) and oxyphilic or oncocytic carcinoma (N = 4) were reviewed, and hysterectomy slides from the four carcinomas were also examined. Immunohistochemical and ultrastructural analyses were performed in three of five metaplasias and in all four carcinomas. Most patients (89%) with oncocytic metaplasia and carcinoma had vaginal bleeding. Oncocytic metaplasia was characterized by a single layer of cells with abundant eosinophilic, granular cytoplasm, minimal pleomorphism, and rare mitotic activity. Carcinoma was diagnosed on the basis of an altered stroma (n = 2) and/or a confluent growth pattern (n = 4) and had a papillary (n = 4), glandular (n = 2), or solid (n = 1) morphology. Carcinomas showed a similar population of oncocytic cells as metaplasias, but with occasional nuclear stratification and greater pleomorphism and mitotic activity. Tumors were International Federation of Gynecology and Obstetrics (FIGO) grade 1 (n = 2) or 2 (n = 2) and FIGO stage Ib, Ic, IIb, and IIIc. Omental metastases developed in the patient with the stage III tumor at 13 months; the two patients with stage I tumors were alive with no evidence of disease at a mean of 29 months. All carcinomas expressed p53 and 75% and 100% were estrogen receptor (ER)- and progesterone receptor (PR)-negative, respectively, whereas all metaplasias were p53 negative- and ER- and PR-positive. Ki-67 labeling index was 1 to 3% in metaplasias and 14 to 33% in carcinomas. Oncocytic metaplasias and carcinomas contained abundant mitochondria and free ribosomes, accounting for the oncocytic appearance. Because oncocytic carcinomas frequently show deep myometrial invasion and require surgical staging, it is important to distinguish oncocytic metaplasia from carcinoma on biopsy material. Ki-67, p53, and ER and PR immunostains may assist in this potentially difficult differential.

Adenocarcinoma↗
PubMed2000

Gastric metaplasia: a frequently overlooked feature of duodenal biopsy specimens in untreated celiac disease.

BACKGROUND: Duodenal gastric metaplasia is rarely reported in untreated celiac disease, although it is seen in 60% to 100% of duodenal biopsy specimens in nonceliac patients with histologic duodenitis. The low incidence could represent underreporting, a decreased incidence in pediatric patients generally, or the more distal sampling site that is customary for most biopsy specimens that are obtained to diagnose celiac disease. It could also be a unique feature of the inflammatory reaction that characterizes this disease. The purpose of this study was to examine the incidence of gastric metaplasia in duodenal specimens from children with untreated celiac disease with special reference to patient age and biopsy site. METHOD: Formalin-fixed paraffin-embedded specimens of duodenal mucosa were selected from the pathology department's archival material. Sections were either stained histochemically or by immunochemical methods, according to an antigen-retrieval protocol. Forty-four duodenal specimens from untreated patients with celiac disease (n = 22) and control subjects of similar age with normal histology (n = 22) were examined. Ten of each were obtained during upper endoscopy from the proximal duodenum (proximal site) and 12 of each by Crosby capsule near the ligament of Treitz (distal site). RESULTS: All specimens from patients with celiac disease exhibited marked villous atrophy. None had been noted to have gastric metaplasia during routine examination of sections stained by hematoxylin and eosin. Fifteen (68%) of 22 of the celiac specimens and 2 of 22 (9%) control specimens contained gastric metaplasia, identified as patches of gastric-type cells containing MUC5AC (gastric mucin), pS2 (gastric trefoil factor) and neutral (periodic acid-Schiff-positive) mucin. Five of the seven celiac specimens that had no metaplasia showed increased numbers of goblet cells expressing gastric markers. The incidence of gastric metaplasia was not different for endoscopic (70%) or capsule (67%) specimens. Sixty-eight percent (7/11) of patients aged less than 3 years had gastric metaplasia. CONCLUSION: The presence of gastric metaplasia has been previously underreported in celiac disease specimens. Detection would be improved by the routine use of period acid-Schiff/ alcian blue staining. The incidence of gastric metaplasia in celiac disease is not significantly influenced by biopsy site or age at time of the biopsy.

Age Factors↗
PubMed2006

Does CDX2 expression predict Barrett's metaplasia in oesophageal columnar epithelium without goblet cells?

BACKGROUND: Intestinal metaplasia (Barrett's oesophagus), but not cardiac-type mucosa in columnar-lined oesophagus, is regarded as premalignant. As intestinal metaplasia and cardiac-type mucosa are endoscopically indiscernible, it is difficult to take targeted samples from columnar-lined oesophagus with consequently a risk of having undetected intestinal metaplasia. AIM: To investigate whether the intestinal markers CDX2, MUC2 and villin can predict the presence of undetected intestinal metaplasia in columnar-lined oesophagus. Methods Presence of intestinal metaplasia or cardiac-type mucosa was identified in 122 biopsy sets of columnar-lined oesophagus from 61 patients, collected at two subsequent follow-up upper endoscopies. CDX2, MUC2 and villin expression were determined by immunohistochemistry. RESULTS: All intestinal metaplasia samples (55) were positive for CDX2 and MUC2 and 32 of 55 for villin. CDX2 expression was detected in 23 of 67 (34%) samples with only cardiac-type mucosa. Detection of CDX2 in cardiac-type mucosa increased the likelihood of finding intestinal metaplasia in another biopsy set of columnar-lined oesophagus (odds ratio 3.5, 95% CI = 1.2-10, P = 0.02). MUC2 was positive in 13 of 23 (57%) of CDX2-positive cardiac-type mucosa samples, whereas villin was detected in seven of 23 (30%). CONCLUSIONS: CDX2 expression in cardiac-type mucosa might be able to predict the presence of undetected intestinal metaplasia in columnar-lined oesophagus, and thus may be a putative marker for the presence of intestinal metaplasia in the absence of goblet cells.

Adult↗
PubMed2001

Cytokeratin subsets for distinguishing Barrett's esophagus from intestinal metaplasia in the cardia using endoscopic biopsy specimens.

OBJECTIVES: It has been suggested that Barrett's epithelium and intestinal metaplasia in the gastric cardia have different cyotokeratin (CK) staining patterns and that Barrett's epithelium can be distinguished by CK staining pattern. The aim of this study was to test the utility of CK staining for distinguishing Barrett's esophagus from gastric intestinal metaplasia. METHODS: Topographically mapped gastric biopsy specimens were obtained from patients without Barrett's esophagus, and esophageal biopsies were obtained from patients with long-segment Barrett's esophagus (>3 cm). Serial sections were stained with Genta or El-Zimaity triple stain, and biopsies with intestinal metaplasia were stained with antibodies against CK 4, 13, 7, and 20. RESULTS: Sections from 33 biopsies with Barrett's esophagus, 23 with intestinal metaplasia of the gastric cardia, 27 with intestinal metaplasia of the gastric body, and 33 with intestinal metaplasia of the antrum were examined. CK 4 and CK 13 stained squamous epithelium only. The proposed "diagnostic" CK Barrett's 7/20 pattern was found in only 39% of long-segment Barrett's compared to 35%, 4%, and 24% in intestinal metaplasia from the gastric cardia, body, and antrum, respectively. The criteria proposed had a sensitivity of 45% and a specificity of 65%. CONCLUSIONS: These results do not support keratin phenotyping as a tool for differentiating intestinal metaplasia originating in the cardia from intestinal metaplasia of Barrett's.

Barrett Esophagus↗
PubMed1990

Variants of intestinal metaplasia in the evolution of chronic atrophic gastritis and gastric ulcer. A follow up study.

A follow up study with biopsy was initiated in 1982 to define the relations between variants of intestinal metaplasia and the evolution of chronic atrophic gastritis and gastric ulcer. All patients (58 with chronic atrophic gastritis and 66 with gastric ulcer) had intestinal metaplasia at the start of the study. In the six year period to 1988 a total of 241 biopsies were performed on the patients with chronic atrophic gastritis and 243 on the patients with gastric ulcer. Initially, 81% of the patients with chronic atrophic gastritis presented with type I intestinal metaplasia and 14% with type III intestinal metaplasia. During follow up type I was predominant, often associated with grades 2 and 3 active disease (81%) and 45% of these patients reverted to a non-intestinal metaplasia status by the third year of follow up. In contrast, type III metaplasia was more common in the absence of appreciable inflammation (78% of biopsy specimens), being persistent in five of seven patients in the third year of follow up, and was found to be associated with dysplasia in three of these patients. Similarly, the initial biopsy specimen showed type I metaplasia in most patients with gastric ulcer (82%) and type III in only 4%. Type I metaplasia was also predominant in these patients (80%), particularly in active disease (68%), gradually regressing with healing. In contrast, type III was associated with delayed ulcer healing and reactivation (75%; six of eight patients). We conclude that (a) type I is a short term reactive process which regresses with healing; (b) type III is related to prolonged injury and chronicity and may regress or progress to dysplasia; (c) persistent and more immature forms of metaplasia may carry an increased risk of malignancy.

Adult↗
PubMed1995

Effect of Helicobacter pylori eradication on gastric metaplasia of the duodenum.

Helicobacter pylori associated duodenal ulcers occur in patches of gastric metaplasia. The pathogenesis of gastric metaplasia is unclear, but it has been produced in experimental animals by acute injury and has been shown to be present to a greater extent of H pylori positive subjects. This study aimed to discover if gastric metaplasia regressed with eradication of H pylori or healing of duodenal ulcers, or both. Thirty two duodenal ulcer patients with H pylori infection confirmed by biopsy urease test and by antral histological examination were studied. Patients were treated with triple therapy (deNol 240 mg twice daily, amoxycillin 500 mg three times daily, and metronidazole 400 mg three times daily) for two weeks after the first endoscopy and were subsequently re-endoscoped. Three duodenal bulb biopsy specimens were obtained per patient at each endoscopy. Biopsy sections were stained with haematoxylin and eosin to determine the severity of duodenitis, and with diastase periodic acid-Schiff/alcian blue to assess the extent of gastric metaplasia. Slides were assessed by two histopathologists unaware of treatment status. H pylori was eradicated in 63% of subjects and all ulcers were healed at follow up. The median extent of gastric metaplasia at the start of treatment and 6-18 months (median 10) after treatment was compared in the two groups. Gastric metaplasia declined in eradicators from 16% to 8% (p < 0.05) while in non-eradicators there was no significant change (25% initially and at follow up). A positive relation between extent of gastric metaplasia and duodenal inflammation score was present before treatment (r(s) = 0.74, p < 0.001) and was unchanged after treatment in the non-eradicator group (r(s) = 0.89, p < 0.001). In the eradicator group, however, the inflammation score had significantly declined (p < 0.02) and the close relation with gastric metaplasia was no longer present. These results suggest that H pylori itself is at least in part responsible for producing gastric metaplasia of the duodenum.

Adult↗
PubMed1996

Circadian gastric acidity in Helicobacter pylori positive ulcer patients with and without gastric metaplasia in the duodenum.

BACKGROUND: The presence of gastric metaplasia allows helicobacter pylori to colonise the duodenum and this condition is thought to be acquired as a response to acid hypersecretion. This functional disorder, however, is present only in a subgroup of duodenal ulcer patients and, in addition, surface gastric metaplasia has been frequently found in the proximal duodenum of normal subjects and patients with non-ulcer dyspepsia, who cannot be certainly considered as acid hypersecretors. AIMS: To clarify the role of acid in inducing gastric type epithelium in the duodenum. This study aimed at assessing whether the pattern of circadian gastric acidity differs between H pylori positive duodenal ulcer patients with and without duodenal gastric metaplasia. PATIENTS: Seventy one patients with duodenal ulcer confirmed by endoscopy and who were found to be positive for H pylori infection by histology on antrum biopsy specimens were enrolled into this study. METHODS: Gastric type epithelium in the duodenum was found in 49 of 71 ulcer patients (69%). Continuous 24 hour gastric pH metry was performed in 50 healthy subjects and in the two subgroups of duodenal ulcer patients with and without gastric metaplasia in the duodenum. Gastric acidity was calculated for 24 hours (1700-1659), night (2000-0759) and day-time (0800-1959). RESULTS: Ulcer patients without gastric metaplasia showed a significantly higher gastric acidity (p < 0.001) than controls for every time interval considered, while the ulcer subgroup with gastric metaplasia was more acid than healthy subjects (p < 0.001) during the whole 24 hour period and the daytime. There was no difference between the two subgroups of duodenal ulcer patients with and without gastric metaplasia during the various time segments analysed. CONCLUSION: The findings confirm that the circadian gastric acidity of duodenal ulcer patients is higher than that of controls. As there is no difference in gastric pH between duodenal ulcer patients with and without gastric metaplasia, gastric hyperacidity is not specific to patients with duodenal gastric metaplasia. It is probable that this histological change is a non-specific response to mucosal injury resulting from various factors and not exclusively to acid.

Adult↗
PubMed1995

Genetic determination of cartilaginous metaplasia in mouse aorta.

Calcification frequently occurs in atherosclerotic plaques in humans, but the cellular and genetic factors contributing to this pathological trait are unknown. We previously reported that the arterial calcification among inbred strains is genetically determined, and we now report that cartilaginous metaplasia, associated with the presence of arterial chondrocytes that express type II collagen, may underlie this calcification. Both uncalcified and calcified cartilaginous metaplasia were often colocalized with aortic atheromatous lesions and calcification, and clear genetic differences were observed in the occurrence of aortic cartilaginous metaplasia among inbred strains. Analysis of a genetic cross between strains C57BL/6J (exhibiting aortic cartilaginous metaplasia) and C3H/HeJ (no aortic cartilaginous metaplasia) revealed a recessive inheritance pattern; thus, F1 mice were entirely devoid of cartilaginous metaplasia, in common with the C3H/HeJ parental strain. Analyses of an F2 cross and a set of recombinant inbred strains derived from parental strains C57BL/6J and C3H/HeJ were consistent with a major gene effect exhibiting incomplete penetrance. The occurrence of aortic calcification was correlated with the occurrence of cartilaginous metaplasia in these genetic crosses, suggesting a link between the traits. Finally, we observed widespread calcified cartilaginous metaplasia within spontaneous atherosclerotic lesions in mice targeted for a null mutation in the apoE gene, suggesting that cartilaginous metaplasia is a potential pathway for artery wall calcification associated with the atherosclerotic plaque.

Animals↗
PubMedDate not supplied

[Intestinal metaplasia in the esophageal-gastric junction, frequency and correlations].

UNLABELLED: The incidence of adenocarcinoma around the esophagogastric junction is increasing. The significance of intestinal metaplasia found in biopsy taken from normal appearing squamocolumnar junction is not clear. The aim of this study was to define the frequency of intestinal metaplasia at normal-appearing esophagogastric junction and clinical, endoscopic and histological associations. METHODS: 239 patients referred for gastroscopy participated in the study. Of 192 patients, two groups were compared. Group I included 40 patients with metaplasia intestinal at the esophagogastric junction and group II included 152 patients with no metaplasia intestinal at the same location. Biopsy specimens were taken from above and below the squamocolumnar junction, and gastric antrum The biopsy specimens were stained with haematoxylin-eosin. RESULTS: Intestinal metaplasia at the squamocolumnar junction was found in 40 patients (21%). Metaplasia was associated with increasing age (p=0.002) and antral intestinal metaplasia (p<0.001)(OR 14.6). There was no association with gastro-oesophageal reflux disease. CONCLUSION: Intestinal metaplasia at the esophagogastric junction occurs frequently in Peruvian patients. It is associated with increasing age and antral intestinal metaplasia but not gastro-esophageal reflux disease.

Esophagogastric Junction↗
PubMed2003

Long-term follow-up of gastric metaplasia after eradication of Helicobacter pylori.

BACKGROUNDS AND AIMS: There is no commonly accepted view concerning changes in gastric metaplasia after the eradication of Helicobacter pylori. The aim of this study was to evaluate the long-term course of gastric metaplasia after the eradication of this bacterium. METHODS: The subjects were 59 patients with duodenal ulcer who were positive for Helicobacter pylori. Forty patients were classified as the eradication group. Gastric metaplasia was endoscopically and histologically evaluated before and after eradication of this bacterium. The follow-up period was 2-7.1 years. In the other 19 patients in the non-eradication group, gastric metaplasia was evaluated before and after treatment of the ulcer. Gastric metaplasia was evaluated in terms of its extent and type in all patients. RESULTS: Gastric metaplasia showed the incomplete type before eradication but changed to the complete type after eradication, which persisted for a long period. The extent of gastric metaplasia increased after eradication. In the non-eradication group, gastric metaplasia infrequently changed to the complete type during the scarring period of ulcer. CONCLUSION: Gastric metaplasia changed to the complete type after the eradication of Helicobacter pylori, which persisted for a long period.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed2003

Intestinal metaplasia: evolution after Helicobacter pylori eradication and influence in the success of eradicating therapy.

INTRODUCTION: intestinal metaplasia associated with Helicobacter pylori infection is a stage of the temporal sequence of histological lesions gradually induced by this microorganism. It is considered a preneoplastic lesion and its regression after eradication is controversial. AIM: to assess the evolution of intestinal metaplasia after eradication and to investigate whether metaplasia is a factor that contributes to successful treatment. MATERIAL AND METHODS: four hundred Helicobacter pylori positive patients were studied. Eradicating therapy was administered and endoscopic biopsies of gastric antrum and body were taken before and after eradication. Among other histological data, the presence of intestinal metaplasia was assessed. RESULTS: of all patients successfully treated, biopsies were taken before and after eradication in 268 of them: 71 (26,5%) had metaplasia before and 50 (18,7%) after eradication. A significant difference was observed in the outcome (p = 0,036) of the first eradicating treatment between the group without initial metaplasia (72,7%) and the group with initial metaplasia (61.2%). DISCUSSION: Helicobacter pylori eradication can revert intestinal metaplasia in some patients. On the other hand, the first treatment could be less successful in patients with intestinal metaplasia.

Adult↗
PubMed2000

Intestinal metaplasia is the probable common precursor of adenocarcinoma in barrett esophagus and adenocarcinoma of the gastric cardia.

BACKGROUND: Intestinal metaplasia in the tubular esophagus is the recognized precancerous lesion of adenocarcinoma in Barrett esophagus. However, it is not yet clear whether adenocarcinoma of the gastric cardia arises from the same premalignant lesion, i.e., intestinal metaplasia of the gastric cardia. The purpose of this study was to compare adenocarcinomas in Barrett esophagus and adenocarcinomas of the gastric cardia at an early stage, when it was more likely that intestinal metaplasia had not been completely overgrown by the tumor. METHODS: The authors compared the epidemiologic, clinical, and pathologic features of early stage adenocarcinoma in Barrett esophagus and adenocarcinoma of the gastric cardia from 42 patients who underwent resection surgery. The presence of intestinal metaplasia was assessed in the resected specimens by using Alcian blue (pH 2.5) staining. RESULTS: Intestinal metaplasia was detected in the mucosa adjacent to neoplasia in 25 of 26 patients with adenocarcinoma in Barrett esophagus and in 11 of 16 (69%) patients with adenocarcinoma of the gastric cardia. Patient and tumor characteristics and survival were comparable in both groups. CONCLUSIONS: Intestinal metaplasia is a very common finding in the mucosa adjacent to early stage adenocarcinoma of the gastric cardia. Adenocarcinoma in Barrett esophagus and adenocarcinoma of the gastric cardia may represent the same disease; the former arises from longer segments of intestinal metaplasia and the latter from intestinal metaplasia of the cardia.

Adenocarcinoma↗
PubMed2002

Expression of homeobox gene CDX2 precedes that of CDX1 during the progression of intestinal metaplasia.

BACKGROUND: The CDX1 and CDX2 genes are intestinal transcription factors that may be involved in the regulation of proliferation and differentiation of intestinal epithelial cells. There have been no detailed reports directly comparing the expression of CDX1 with that of CDX2 in chronic gastritis and intestinal metaplasia. Accordingly, we examined the expression of CDX1/2 and its association with the expression of other intestinal metaplasia-associated genes during the development of intestinal metaplasia. METHODS: The expression of CDX1/2 genes was analyzed, using the reverse transcriptase-polymerase chain reaction, in 44 human gastric tissue samples obtained endoscopically. The expressions of mucin markers (MUC2, MUC5AC), intestine-specific genes (sucrase-isomaltase, human defensin-5, alkaline phosphatase), a gene marker for fundic gland area (H+/K+ATPase beta subunit), and a gene for entire gastric glands (pepsinogen C) were also comparatively analyzed. RESULTS: There was no expression of CDX1/2 in gastric mucosa not infected by Helicobacter pylori. The prevalence of CDX1 mRNA expression was significantly higher in mucosa with intestinal metaplasia than in mucosa without intestinal metaplasia. It is noteworthy that CDX2 was expressed in the antral and fundic mucosa in the absence of the expression of CDX1 and gene markers for intestinal metaplasia. CONCLUSIONS: The expression of CDX2 precedes those of CDX1, sucrase-isomaltase, other intestine-specific genes (human defensin-5, alkaline phosphatase), and MUC2 during the progression of intestinal metaplasia. These findings imply that the expression of CDX2 may trigger the initiation and development of intestinal metaplasia.

Adult↗