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PubMed1998

Methylene blue staining for intestinal metaplasia of the gastric cardia with follow-up for dysplasia.

BACKGROUND: Previous studies by our group have identified a 23% prevalence of intestinal metaplasia involving the gastric cardia in patients undergoing elective esophagogastroduodenoscopy (EGD). The current study evaluates the potential clinical utility of vital staining with methylene blue for detecting intestinal metaplasia of the cardia. In addition, the prevalence of Helicobacter pylori infection and incidence of dysplasia in cardia intestinal metaplasia was assessed. METHODS: Twenty-four of 104 patients undergoing elective EGD were previously identified with cardia intestinal metaplasia. Twenty-one of these 24 returned for follow-up EGD with methylene blue staining and cardia biopsies. During EGD four random biopsies were taken in the cardia. After staining with methylene blue, four targeted biopsy specimens were taken from any stained areas. H. pylori infection was assessed by rapid urease testing and serologic evaluation. RESULTS: Staining with methylene blue was positive in 16, equivocal in 4, and negative in 1. Overall, cardia intestinal metaplasia was identified in 17 of 21 patients (81%) by at least one of the 8 biopsies. The sensitivity of detecting intestinal metaplasia by targeted biopsies to stained areas was 67% as opposed to 38% for random biopsies (odds ratio 3.0: 95% CI [0.88,10.24]). The prevalence of H. pylori infection in patients with cardia intestinal metaplasia was 76%. One patient developed low-grade dysplasia, whereas the others remained negative. CONCLUSIONS: Intestinal metaplasia of the gastric cardia is associated with a high prevalence of H. pylori infection and is a reproducible finding in the majority of patients. Methylene blue staining and an increasing number of biopsies improve the sensitivity of detecting this potentially neoplastic lesion.

Aged↗
PubMed2004

Expression of the intestinal marker Cdx2 in the columnar-lined esophagus with and without intestinal (Barrett's) metaplasia.

Barrett's esophagus is diagnosed when goblet cells are found in the lower esophageal mucosa. However, the distribution of these cells is patchy and they may not represent the earliest marker of intestinal metaplasia. Cdx2 is a transcription factor whose expression in normal tissues is restricted to intestinal-type epithelium. Its distribution in the columnar-lined esophagus with and without intestinal metaplasia has been seldom studied. We evaluated Cdx2 expression in lower esophageal biopsies from 90 patients with endoscopic diagnosis of short segment Barrett's esophagus, including 45 consecutive cases showing intestinal metaplasia (goblet cells present in hematoxylin eosin and/or Alcian blue stains) and 45 consecutive cases without goblet cells. 25 samples of cardiac-type mucosa without intestinal metaplasia biopsied from the stomach served as controls. All cases with intestinal metaplasia revealed Cdx2 reactivity in goblet cells and adjacent nongoblet columnar cells. Dysplastic foci, seen in five cases from this group, were Cdx2 positive. In the group without goblet cells, Cdx2 was focally expressed by columnar cells in 17 (38%) cases. All control cases were Cdx2 negative. Strips of Alcian blue-positive nongoblet columnar cells ('columnar blues') were observed in 11 (24%) of the cases without intestinal metaplasia. All these foci were Cdx2 negative. In conclusion, Cdx2 is a highly sensitive marker for Barrett's esophagus. It is also expressed in a significant minority of cases of columnar-lined esophagus without goblet cells, suggesting that it may detect intestinal phenotypic modifications in the absence of goblet cells. Accordingly, Cdx2 immunostaining could help identify patients with Barrett's metaplasia in cases where no goblet cells are visible in biopsies from the columnar-lined esophagus. Finally, lack of Cdx2 expression in the 'columnar blues' suggests that these cells are not diagnostic of intestinal metaplasia.

Adult↗
PubMed2002

Review article: intestinal metaplasia and gastric carcinogenesis.

Gastric intestinal metaplasia, an intermediate step in Correa's cascade of gastric carcinogenesis, is generally regarded as a pre-malignant lesion. Epidemiological studies suggest that patients with intestinal metaplasia have more than a 10-fold increased risk of developing gastric cancer. Within the subclassification of intestinal metaplasia, incomplete or type III intestinal metaplasia appears to be associated with even higher malignant potential. The topographical distribution of intestinal metaplasia may also have prognostic implications. Certain genetic and epigenetic alterations have been demonstrated in gastric intestinal metaplasia which straddle into gastric cancer. These findings suggest that genetic changes occur early in the multistep gastric carcinogenesis process. Unlike Barrett's oesophagus and colonic polyp, which have well-defined surveillance guidelines, there is no widely accepted surveillance programme for gastric intestinal metaplasia. An annual surveillance programme may allow early detection of gastric cancer, which theoretically may improve survival. It remains elusive whether the treatment of Helicobacter pylori infection may reverse gastric intestinal metaplasia or reduce the subsequent risk of cancer development. Further controlled studies with longer follow-up are needed to resolve this controversy. The role of chemo-prophylactic agents, e.g. cyclo-oxygenase-2 inhibitor, should be investigated.

Disease Progression↗
PubMed2001

Atrophy-metaplasia-dysplasia-carcinoma sequence in the stomach: a reality or merely an hypothesis?

The results of recent investigations have suggested that the old hypothesis of an atrophy-metaplasia-dysplasia-carcinoma sequence in the stomach needs to be qualified. The most common cause of intestinal metaplasia is Helicobacter pylori gastritis. The consequence of this intestinal metaplasia is focal atrophy. Helicobacter pylori infection may also trigger an autoimmune gastritis of the corpus mucosa, with atrophy and intestinal metaplasia. Most intestinal metaplasias are only 'paracancerous' but not 'precancerous' lesions. Diffuse gastric carcinomas, such as the signet ring cell carcinoma, arise independently of intestinal metaplasia. Histogenetically, numerous carcinomas of the stomach are primarily of the gastric type, and may secondarily change into the intestinal type.High-grade intra-epithelial neoplasias (dysplasias) detected during the biopsy-based diagnostic work-up appear to be a marker for carcinoma and must, therefore, be removed endoscopically. The detection of intestinal metaplasia in routinely obtained biopsy material is subject to sampling error and is, therefore, not a suitable marker for an increased risk of a gastric carcinoma developing. As an alternative, the concept of gastritis of the carcinoma phenotype, which is more frequently found in early gastric carcinomas and in the relatives of gastric carcinoma patients, has been developed. In this concept, the diffuse parameters of grade and activity of the gastritis in the antrum and corpus, which are independent of sampling error, are subjected to a comparative analysis. A risk gastritis of the carcinoma phenotype is diagnosed when the grade and activity of the gastritis in the corpus are at least equally as pronounced as in the antrum. Currently, this concept is being tested in a prospective ongoing study. Future studies must show whether, and if so which, immunohistochemical or molecular-genetically detectable changes can be applied as risk markers in the diagnostic work-up. Helicobacter pylori eradication probably does not lead to complete regression of the intestinal metaplasia and ensuing focal atrophy. However, eradication of H. pylori does lead to the normalization of changes that can lead to mutations of the stem cells of the gastric mucosa (free radicals, nitric oxide, cell proliferation and vitamin C secretion).

Gastric Mucosa↗
PubMed2002

Cdx2 ectopic expression induces gastric intestinal metaplasia in transgenic mice.

BACKGROUND & AIMS: Intestinal-type gastric cancer is often preceded by intestinal metaplasia in humans. The genetic events responsible for the transdifferentiation that occurs in intestinal metaplasia are not well understood. Cdx2, a transcription factor whose expression is normally limited to the intestine, has been detected in gastric intestinal metaplasia. Cdx2 induces differentiation of intestinal epithelial cells in vitro; therefore, we sought to establish whether a causal relationship exists between Cdx2 activation and intestinal metaplasia. METHODS: Cdx2 expression was directed to the gastric mucosa in transgenic mice using cis-regulatory elements of Foxa3 (Hnf3gamma). Transgenic mice were analyzed for histologic and gene expression changes. RESULTS: Histologic examination of the gastric mucosa of the Foxa3/Cdx2 mice revealed the presence of alcian blue-positive intestinal-type goblet cells, a hallmark of intestinal metaplasia. In addition, Cdx2 induced the expression of intestine-specific genes. CONCLUSIONS: Gastric expression of Cdx2 alone was sufficient to induce intestinal metaplasia in mice. These mice represent a powerful tool to investigate the molecular mechanisms that promote intestinal metaplasia. Moreover, as gastric cancer in humans is often preceded by intestinal metaplasia, the phenotype described here strongly suggests involvement of Cdx2 in the initiation of the process leading to intestinal neoplasia of the gastric mucosa.

Animals↗
PubMed2003

A randomized, prospective cross-over trial comparing methylene blue-directed biopsy and conventional random biopsy for detecting intestinal metaplasia and dysplasia in Barrett's esophagus.

BACKGROUND AND STUDY AIMS: The value of methylene blue-directed biopsies (MBDB) in detecting specialized intestinal metaplasia and dysplasia in Barrett's esophagus remains unclear. The aim of this study was to compare the accuracy of MBDB with random biopsy in detecting intestinal metaplasia and dysplasia in patients with Barrett's esophagus. PATIENTS AND METHODS: A prospective, randomized, cross-over trial was undertaken to compare MBDB with random biopsy in patients with Barrett's esophagus segments 3 cm or more in length without macroscopic evidence of dysplasia or cancer. Dysplasia was graded as: indefinite for dysplasia, low-grade dysplasia, high-grade dysplasia, or carcinoma, and was reported in a blinded fashion. RESULTS: Fifty-seven patients were recruited, 44 of whom were male. A total of 1,269 biopsies were taken (MBDB-651, random biopsie-618). Analysis of the results by per-biopsy protocol showed that the MBDB technique diagnosed significantly more specialized intestinal metaplasia (75 %) compared to the random biopsy technique (68 %; P = 0.032). The sensitivity and specificity rates of MBDB for diagnosing specialized intestinal metaplasia were 91 % (95 % CI, 88 - 93 %) and 43 % (95 % CI, 36 - 51 %), respectively. The sensitivity and specificity rates of MBDB for diagnosing dysplasia or carcinoma were 49 % (95 % CI, 38 - 61 %) and 85 % (95 % CI, 82 - 88 %), respectively. There were no significant differences in the diagnosis of dysplasia and carcinoma - MBDB 12 %, random biopsy 10 %. The methylene blue staining pattern appeared to have an influence on the detection of specialized intestinal metaplasia and dysplasia/carcinoma. Dark blue staining was associated with increased detection of specialized intestinal metaplasia (P < 0.0001), and heterogeneous staining (P = 0.137) or no staining (P = 0.005) were associated with dysplasia and/or carcinoma detection. The MBDB technique prolonged the endoscopy examination by an average of 6 min. CONCLUSION: The diagnostic accuracy of the MBDB technique was superior to that of the random biopsy technique for identifying specialized intestinal metaplasia, but not dysplasia or carcinoma. The intensity of methylene blue staining has an influence on the detection of specialized intestinal metaplasia and dysplasia or carcinoma, which may help in targeting the biopsies. Although MBDB prolongs the endoscopy procedure slightly, it is a safe and well-tolerated procedure. Further clinical studies on the MBDB technique exclusively in endoscopically normal dysplastic Barrett's esophagus are needed.

Adult↗
PubMed2000

The esophageal Z-line appearance correlates to the prevalence of intestinal metaplasia.

BACKGROUND: Intestinal metaplasia at the gastroesophageal junction is associated with Barrett esophagus, gastric cardiac cancer, and gastritis. The aim of this study was to determine the prevalence of intestinal metaplasia among patients with symptoms suggestive of gastroesophageal reflux disease (GERD) and to study clinical, endoscopic, and histologic associations with intestinal metaplasia at the squamocolumnar junction. METHODS: One hundred and eighty-six patients with symptoms indicating gastroesophageal reflux were included in the study. A new classification of the Z-line appearance was used. RESULTS: The Z-line appearance was found to correlate with the prevalence of intestinal metaplasia at the squamocolumnar junction (P = 0.0001). Intestinal metaplasia at the squamocolumnar junction was found in 15.0% of the patients. There was a statistically significant association between intestinal metaplasia at the squamocolumnar junction and tongues of columnar epithelium at the Z-line (P = 0.020), intestinal metaplasia in the cardia (P = 0.020), positive CLO test (P = 0.026), smoking (P = 0.041), and age (P = 0.050). There was no association with endoscopic or histologic signs of esophagitis or with the severity or duration of GERD symptoms. CONCLUSION: Intestinal metaplasia at the squamocolumnar junction correlates with the Z-line appearance, which would justify a new classification.

Adult↗
PubMed1991

Carcinomas with metaplasia and sarcomas of the breast.

The clinicopathologic, immunohistochemical, and flow cytometric characteristics of 34 cases of mammary carcinoma with metaplasia were compared with those of 20 cases of pure sarcoma of the breast. All 20 of the latter tumors showed the pattern of malignant fibrous histiocytoma. There were 20 cases of carcinoma with mesenchymal metaplasia, 7 cases of carcinoma with mixed epithelial (squamous) and mesenchymal metaplasia, and 7 cases of carcinoma with epithelial metaplasia (four mixed ductal/squamous and three pure squamous cell carcinomas). No patient with pure sarcoma had lymph node metastases develop; all nodal metastases were found in patients who had carcinoma with metaplasia, although in one case the carcinomatous component was seen only within a lymph node metastasis. Epithelial antigens were found not only within the epithelial elements of all cases of carcinoma, but also within the apparent mesenchymal elements of 44% of the carcinomas showing divergent differentiation. Flow cytometric analysis of eight cases of carcinoma with mesenchymal metaplasia showed aneuploidy/tetraploidy in six neoplasms. For patient management purposes, the distinction of pure sarcoma from carcinoma with metaplasia is important, but additional subclassification of carcinoma with metaplasia is of greater biologic than clinical interest.

Adult↗
PubMed1990

Tubal metaplasia of the uterine cervix.

Eleven cases of tubal metaplasia of the uterine cervix are presented. These are characterized histologically by architecturally normal endocervical glands containing ciliated or clear cells, nonciliated cells, and intercalary or peg cells, resembling normal tubal mucosa. Transitions from normal to ciliated epithelium within a single gland are frequently seen. Eight of these cases involved endocervical glands near the squamocolumnar junction, and six showed tubal metaplasia along the overlying surface epithelium. Superficial and (in one case) deep endocervical glands were involved. No correlation was found between the presence of tubal metaplasia and the degree of inflammation of the cervix or the presence or extent of squamous metaplasia. Immunohistochemically, the epithelium of tubal metaplasia was negative for carcinoembryonic antigen in five cases studied. In situ squamous carcinoma and a variety of benign glandular lesions, such as microglandular hyperplasia, mesonephric remnants, and endometriosis, were concurrently identified. Two cases also accompanied tubal metaplasia in proliferative and hyperplastic endometria, and tubal metaplasia was seen in the lower uterine segment in five cases. We emphasize that, as with other types of metaplasia, the main significance of recognizing this lesion in the cervix is in not confusing it with early endocervical glandular neoplasia.

Adult↗
PubMed2003

CD44v6: a potential marker of malignant transformation in intestinal metaplasia of the stomach? An immunohistochemical study using tissue microarrays.

OBJECTIVE: Intestinal metaplasia is a well-established risk factor in the development of stomach cancer. However, since the specificity is low it would be of great practical value to find a marker to separate cases of intestinal metaplasia into low and high risk for progression to dysplasia/carcinoma. So far this has not been achieved. CD44 is a cell surface molecule involved in cell-cell and cell-matrix interactions, and the spliced variant 6 has been shown to play a role in the progression of gastric carcinoma. The aim of this study was therefore to evaluate CD44v6 as a marker of increased cancer risk in intestinal metaplasia. METHODS: The current study investigated immunohistochemical CD44v6 expression in biopsies of normal gastric mucosa (n = 154) and gastric mucosa with intestinal metaplasia (n = 127). A third group consisted of cancer gastrectomies (n = 117) in which both tumour and uninvolved mucosa was studied. Proximal (cardia) and distal (corpus/antrum) locations were noted in all cases. RESULTS: There was a significant sequential increase in CD44v6 expression from normal mucosa and mucosa showing intestinal metaplasia to uninvolved mucosa adjacent to cancers without and with intestinal metaplasia to tumour. The most striking increase was from 'normal' to intestinal metaplastic mucosa adjacent to cancers. There were no differences between proximal and distal cases in any group. CONCLUSION: These findings strongly suggest that CD44v6 expression is a late phenomenon in the transformation of intestinal metaplasia to dysplasia/cancer. It may therefore be a useful marker of cancer risk in patients with intestinal metaplasia.

Adult↗
PubMed1998

Intestinal metaplasia subtypes and Helicobacter pylori infection: a comparison of ethnic groups in New Zealand.

Gastric cancer is two to four-fold more common in Maori and Pacific Island ethnic groups compared with Europeans. This study aimed to determine if intestinal metaplasia was more common in these ethnic groups. Patients attending for endoscopy for dyspepsia had six biopsies to determine the presence of Helicobacter pylori by at least two of the following tests: rapid urease test, 13C urea breath test, culture of histology and the presence, extent and subtypes of intestinal metaplasia. Biopsies were taken from 158 patients: Europeans (42%), Maori (23%), Pacific Islanders (35%). Helicobacter pylori and intestinal metaplasia were detected in 88 and 60% of Maori/Pacific Island patients, respectively, and 47 and 29% of Europeans, respectively. Type I intestinal metaplasia was detected in 43% of all patients, type II (26%) and type III (7.0%). The mean age of Maori/Pacific Island patients with intestinal metaplasia and type III intestinal metaplasia was 53 and 51 years respectively, compared with Europeans aged 65 and 72 years. Univariate analysis showed that intestinal metaplasia was associated with ethnicity and H. pylori (P < 0.001) but not age, smoking, endoscopic diagnosis or gender. Intestinal metaplasia is more common and occurs at an earlier age in Maori and Pacific Island patients.

Adult↗
PubMed2005

Gastric and intestinal differentiation in Barrett's metaplasia and associated adenocarcinoma.

Intestinal metaplasia is a prerequisite criterion for the diagnosis of Barrett's metaplasia and the sole columnar esophageal lining associated with malignancy. It is recognized by the presence of goblet cells, but columnar non-goblet elements, producing gastric or intestinal proteins, are the prevalent cell population. The cellular heterogeneity of Barrett's metaplasia is well documented but the relationship between the distinct cell subtypes and neoplasia is unclear. Our aim was to clarify the relationship between the different metaplastic populations and malignancy in order to investigate putative markers for risk stratification of Barrett's patients. We studied 46 columnar-lined esophageal segments, 15 with associated adenocarcinoma. The presence of the gastric, MUC5AC and MUC6, and the intestinal, MUC2, proteins was evaluated in metaplastic (columnar and goblet) and neoplastic cells. In neoplasia MUC5AC and MUC6 were detected in 100% and 86.6% of the cases, respectively. In metaplasia there were no differences in MUC5AC and MUC6 immunoreactivity, between cases with and without associated neoplasia, except for goblet elements producing MUC6 that were exclusive of metaplasia adjacent to adenocarcinoma (P < 0.05). MUC2 was present in 86.6% of the neoplasia. In metaplasia it was restricted to Barrett's cases and was more frequent in areas with intestinal metaplasia. Columnar-lined esophagus without intestinal metaplasia did not express MUC2. Our study suggests a relationship between the metaplastic population with gastric phenotype and malignancy, and points to the involvement of columnar as well as goblet elements in tumorigenesis. The association between goblet cells aberrantly producing MUC6 and the presence of neoplasia suggests they may be useful for risk stratification.

Adenocarcinoma↗
PubMed1987

Nephroid metaplasia of the urinary tract. A survey of the literature, with the contribution of 5 new immunohistochemically studied cases, including one case examined by electron microscopy.

Nephroid metaplasia is an unusual lesion confined to the lamina propria of the lower urinary tract. It is defined by a characteristic histologic picture of tubular structures, formed by a single layer of cuboidal cells, surrounded by a thick basement membrane. Two main theories concerning the histogenesis of the condition have been proposed: embryonic origin, or metaplasia. Five cases of nephroid metaplasia were studied light-microscopically and by immunohistochemistry for the content of Tamm Horsfall's uromucoprotein. In addition, one case was examined by electron microscopy. The results were compared to current knowledge of the lesion obtained from a survey of the literature, with special reference to histogenesis. Morphologically, one case of nephroid metaplasia was associated with mesonephroid adenocarcinoma. It is concluded that nephroid metaplasia arises as a metaplastic lesion, nearly always in previously traumatized urothelial mucosa. The natural history of the typical nephroid metaplasia is benign, but a possible relationship to mesonephroid adenocarcinoma, representing the malignant counterpart of the lesion, is discussed in relation to the histological findings, suggesting a rare but possible malignant potential of nephroid metaplasia. The diverse nomenclature used for this histologic entity needs re-evaluation and should be changed to: nephroid metaplasia.

Adenocarcinoma↗
PubMed1977

Gastric gland metaplasia in the small and large intestine.

Fifty-six surgical specimens with various ulcerative intestinal disorders were microscopically investigated for evidence of gastric gland metaplasia. Thiry-one specimens (55-4%) showed pyloric gland metaplasia. Among the 31 patients with pyloric gland metaplasia, five showed true gastric metaplasia, consisting of parietal cells, chief cells, and mucous neck cells. The percentage of true gastric metaplasia among pyloric gland metaplasia was as high as 16%, an overall frequency of 9% among various ulcerative intestinal disorders. The mechanism of pyloric gland metaplasia and true gastric metaplasia is not understood, but may occur secondary to submucosal response to ulcer healing and subsequent alteration of the intraluminal condition in the intestine.

Adolescent↗
PubMed1985

Incomplete sulphomucin-secreting intestinal metaplasia for gastric cancer. Preliminary data from a prospective study from three centres.

A joint prospective long term study of gastric biopsies has been undertaken to survey intestinal metaplasia Types I, II, and III in terms of their incidence, distribution and value in the selection of high risk cancer patients. This study is based on protocols agreed between three centres for endoscopy, histological interpretation, and mucin histochemistry. The results on the first 1350 gastric biopsies examined during 1981-1982 are presented. Intestinal metaplasia was found in 267 biopsies (20%), being common in association with carcinoma (71%), less so in benign conditions such as gastric ulcer (39%), and chronic gastritis (24%), but rare in 'normal' (3%). Type I intestinal metaplasia was predominant (73%) in all the biopsies with intestinal metaplasia and was most common in benign conditions, 70% in gastric ulcer and 76% in chronic gastritis. Type III intestinal metaplasia (incomplete sulphomucin-secreting intestinal metaplasia) was recorded in only 9.8% of all the biopsies with intestinal metaplasia and had a higher incidence in carcinoma (35%), than in benign conditions (7%) (p less than 0.0001). These results suggest that intestinal metaplasia types may have different malignant potential and their identification may be useful in screening patients for early detection of cancer.

Adult↗
PubMed1996

Gastric metaplasia and duodenal ulcer disease in children infected by Helicobacter pylori.

BACKGROUND: Helicobacter pylori infection of the gastric mucosa is vital in the pathogenesis of duodenal ulcer disease. H pylori will only colonise gastric epithelium and its association with duodenal disease is therefore not easily explained. AIMS: To determine if gastric metaplasia in the duodenum increases the risk of duodenal ulcer disease in children infected with H pylori. PATIENTS: All children undergoing upper endoscopy over a 20 month period in a children's hospital in Ireland. METHODS: Two biopsy specimens were obtained from the antral mucosa and two from the first part of the duodenum. One antral biopsy specimen was used in a rapid urease test (Clo Test). Biopsy sections were stained with haematoxylin and eosin and also with cresyl violet for identification of H pylori. Periodic acid Schiff (PAS) stain was performed to identify areas of gastric metaplasia. RESULTS: Gastric and duodenal biopsy specimens were obtained from 148 patients (M:F 1:2:1). Twenty five children (17%) had H pylori positive gastritis. Thirty four children (23%) had gastric metaplasia in the duodenum. Nine per cent of children under the age of 8 years had gastric metaplasia compared with 38% in those 12 years of age or over (p < 0.005). Seven children had duodenal ulcer disease. Gastric metaplasia was present in six of seven (86%) children with duodenal ulcer disease compared with 28 of 141 (20%) without ulceration (p < 0.001). While both H pylori and gastric metaplasia were each significant risk factors for duodenal ulcer disease, the combined presence of both factors was associated with a pronounced increase in duodenal ulcer disease. Duodenal ulcer disease occurred in over 50% of children with both H pylori infection and gastric metaplasia. In contrast duodenal disease did not occur in children (0 of 100) when both were absent. CONCLUSION: The presence of gastric metaplasia in the duodenum is the major risk factor for duodenal ulcer disease in patients colonised by H pylori.

Adolescent↗
PubMed1996

Relation between gastric acid output, Helicobacter pylori, and gastric metaplasia in the duodenal bulb.

BACKGROUND: Factors that determine gastric metaplasia in the duodenal bulb are ill defined. It is more common and extensive in the presence of high acid output and possibly in the presence of Helicobacter pylori. However, no quantitative relation between acid output and the extent of gastric metaplasia has been demonstrated and its relation to H pylori is uncertain. AIM: To determine the relation between H pylori infection and acid output and the presence and extent of gastric metaplasia in the duodenal bulb. subjects: H pylori positive and negative patients with duodenal ulcer and healthy controls were studied. METHODS: Quadrantic duodenal bulb biopsy specimens were taken and the presence and extent of gastric metaplasia determined using a computer enhanced image intensifier. Basal and stimulated acid outputs were measured. RESULTS: gastric metaplasia was significantly (p < 0.05 more common and significantly (p < 0.05) greater in extent in patients with duodenal ulcer than in controls. Neither the prevalence or extent of gastric metaplasia was affected by H pylori status. There were significant (p < 0.01) direct correlations between acid output and extent of gastric metaplasia. CONCLUSIONS: Prevalence and extent of gastric metaplasia are not related to H pylori in controls, or in patients with duodenal ulcer. Rather, high acid response to gastrin may be more important.

Adult↗
PubMed1985

Intestinal metaplasia in endoscopic biopsy specimens of gastric mucosa.

A total of 1412 consecutive cases of endoscopic gastric biopsy, carried out over a four year period, were reviewed and specimens were examined histochemically to determine the prevalence of intestinal metaplasia and its variants. Three types were characterised: complete intestinal metaplasia and two classes of incomplete intestinal metaplasia (type IIa and type IIb) depending on the absence or presence, respectively, of sulphomucins within mucin secreting columnar cells. Type IIb intestinal metaplasia was significantly more common in patients with gastric carcinoma (p less than 0.001) and in those with dysplasia (p less than 0.001) than in patients with benign gastric pathology. No such association was found with either type I or type IIa intestinal metaplasia. In addition to those present in the columnar cells of type IIb intestinal metaplasia, sulphomucins were also commonly found in goblet cells of all three types of metaplasia. The presence of sulphomucins in goblet cells, however, was not significantly associated with gastric carcinoma or dysplasia. The significance of the different types of intestinal metaplasia in relation to the pathological findings is discussed.

Aged↗