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PubMed1990

Impact of diet and smoking on risk of developing intestinal metaplasia of the stomach.

A cohort of Hawaii Japanese men was assembled for epidemiologic studies of heart disease and cancer. Diet and tobacco consumption data were obtained from 1965 to 1968 and from 1971 to 1975. Biopsies from sites at maximal, intermediate, and minimal risk of intestinal metaplasia were performed on 350 men. Metaplasia was found in 234 men. Gastric cancer was found in 9/234 with metaplasia (3.8%) and 1/116 men without metaplasia (0.89%). Nitrite-rich salty foods (e.g., cured meats) were directly related to metaplasia at both examinations. Vitamin C intake did not appear to have prevented the development of intestinal metaplasia. Smoking was directly related to the presence of metaplasia, but the association was weaker than was observed for cured meats. The strong association between nitrite-rich salty foods and metaplasia appears to be uniform from one study to another, as is the lack of a consistent relation between metaplasia and either smoking or vitamin C consumption. Heavy smokers were more likely to have metaplasia than were nonsmokers, but these associations were weaker than were those with cured meats.

Age Factors↗
PubMed2002

Keratinising squamous metaplasia of the bladder: natural history and rationalization of management based on review of 54 years experience.

OBJECTIVE: To review our experience of keratinising squamous metaplasia of the bladder as a predictor for the development of cancer and other complications, and formulate a policy for its management. MATERIALS AND METHODS: A retrospective review (1945-1999) identified 34 patients with histologically proven keratinising squamous metaplasia (27 males and 7 females, average age 50 years, range 13-80 years). The histological criteria used to diagnose keratinising squamous metaplasia were squamous metaplasia of the urothelium with keratinisation and/or hyperkeratosis and/or acanthosis. Female patients with non-keratinising squamous metaplasia (vaginal metaplasia) were excluded. RESULTS: Four patients had synchronous bladder carcinoma (three advanced with early death; one localised, cured by cystectomy). Another 14 patients had extensive metaplasia (Group A, >50% of mucosal involvement). Three cases had cystectomy and cure. Six cases (out of 11) developed subsequent cancer (4 advanced and early death, two localised and cured by cystectomy). One other case died of obstructive uropathy secondary to squamous metaplasia. Two cases died of unrelated causes. Sixteen patients had limited squamous metaplasia (Group B, <50% involvement mucosal surface). Twelve patients had endoscopic resection, extraction bladder calculus etc. with no further complications. Another two patients underwent urinary diversion. Two patients (out of 16) developed subsequent cancer both with advanced disease and early death. CONCLUSION: Keratinising squamous metaplasia of the bladder is a significant risk factor for vesical carcinoma and complications, such as bladder contracture and ureteral obstruction. This risk of complications increases with more extensive bladder mucosal involvement. The wide variation in lag time to the development of complications necessitates indefinite follow-up. Selected patients with extensive bladder involvement and long life expectancy should be offered cystectomy.

Adolescent↗
PubMed1996

Adherence of Helicobacter pylori to areas of incomplete intestinal metaplasia in the gastric mucosa.

BACKGROUND & AIMS: Helicobacter pylori is not usually found in areas of intestinal metaplasia. Thus, the development of intestinal metaplasia has been viewed as a mechanism by which the stomach eliminates H. pylori. The aim of this study was to evaluate the frequency of H. pylori adherence to intestinal metaplasia in different populations. METHODS: Mapped gastric biopsy specimens from 378 H. pylori-positive subjects from various geographical regions were examined. Intestinal metaplasia was typed by staining with periodic acid-Schiff/alcian blue and high-iron diamine/alcian blue. RESULTS: In 32 patients, H. pylori was found in intimate contact with intestinal metaplasia. This was documented by electron microscopy. All areas of intestinal metaplasia showing adherence contained sulfomucins and had no brush border. Posttreatment biopsy specimens from 4 patients whose infection was not cured showed persistence of H. pylori in intestinal metaplasia. CONCLUSIONS: These patients may have a strain of H. pylori with unusual adhesion characteristics, or their type of intestinal metaplasia may have biochemical properties that make it hospitable for H. pylori. The exclusive association of H. pylori adherence with incomplete intestinal metaplasia (a putative precursor of carcinoma) and its greater frequency in Koreans (a population at risk for gastric cancer) suggest that this phenomenon may play a role in the hypothetical sequence metaplasia > dysplasia > carcinoma.

Bacterial Adhesion↗
PubMed2003

Accuracy of magnifying endoscopy with methylene blue in the diagnosis of specialized intestinal metaplasia and short-segment Barrett's esophagus in Japanese patients without Helicobacter pylori infection.

BACKGROUND: The use of methylene blue chromoendoscopy in the diagnosis of specialized intestinal metaplasia in short-segment Barrett's esophagus is controversial. This study evaluated the use of magnifying endoscopy with methylene blue for this purpose. METHODS: A total of 30 patients (21 men, 9 women; median age 61 years, range 32-79 years) with short lengths of columnar-lined esophagus were enrolled in a prospective trial of magnifying endoscopy with methylene blue in which the appearance after methylene blue staining was used to target biopsy specimens. Patients were screened for Helicobacter pylori infection, and only those without infection were enrolled (because many Japanese patients have pan-gastritis caused by H pylori infection, and intestinal metaplasia distal to the squamocolumnar junction may be secondary to H pylori-induced gastritis). All biopsy specimens were stained with H and E; MUC2 immunostaining was used to identify specialized intestinal metaplasia. RESULTS: Thirty patients with short-segment columnar-lined esophagus underwent magnifying endoscopy with methylene blue. Ninety-three biopsy specimens were obtained, 33 from methylene blue-stained areas and 60 from unstained areas, each about 7 mm from the marginal edge of stained areas. Specialized intestinal metaplasia was confirmed in biopsy specimens from 28 of the 33 stained areas (sensitivity 84.8%); in biopsy specimens from 55 of the 60 unstained areas, specialized intestinal metaplasia was not found (specificity 91.7%). In magnified views of methylene blue-positive areas, a tubular, cavernous, or elliptical pattern was seen. Sixteen of 21 men (76.2%) and 3 of 9 women had specialized intestinal metaplasia, and short-segment Barrett's esophagus was diagnosed in these patients. Even in patients with less than 1 cm of columnar-lined esophagus, 8 of 10 stained areas contained specialized intestinal metaplasia (sensitivity 80%) and 23 of 24 unstained areas did not (specificity 95.8%). Six of 12 patients (50%) with less than 1 cm of columnar-lined esophagus had specialized intestinal metaplasia. In total, 19 of 30 patients had specialized intestinal metaplasia. CONCLUSIONS: Magnifying endoscopy with methylene blue selectively detects specialized intestinal metaplasia within short-segment columnar-lined esophagus.

Adult↗
PubMed2003

Hepatocyte antigen as a marker of intestinal metaplasia.

Intestinal metaplasia is a histologic hallmark of Barrett's esophagus and chronic gastritis. Intestinal metaplasia may progress to dysplasia or carcinomas without proper treatment. Most cases of intestinal metaplasia are easily recognized on hematoxylin and eosin-stained sections. However, some cases of intestinal metaplasia may be hard to recognize if they lack the characteristic mucin-producing cells and Paneth cells, or if they are small in size. Recently, keratin 7, keratin 20, and MUC2 expression patterns were reported to be useful in confirming the diagnosis of intestinal metaplasia. We studied hepatocyte (Hep) antigen (a hepatocellular antigen mainly expressing in normal and neoplastic hepatic tissues) in 33 cases of Barrett's esophagus (9 cases associated with esophageal adenocarcinoma) and 13 cases of chronic gastritis associated with intestinal metaplasia and gastric adenocarcinoma. Hep monoclonal antibody recognizes intestinal metaplasia in all cases. We also compared expression of Hep with that of keratin 7, keratin 20, and MUC2 in intestinal metaplasia. The specificity and sensitivity of Hep for intestinal metaplasia were higher than that of keratin 7 and keratin 20, or MUC2. We conclude that Hep may be used as a single diagnostic marker for intestinal metaplasia.

Adenocarcinoma↗
PubMed1998

Intestinal metaplasia in gastric malignancy: a comparison between carcinoma and lymphoma.

OBJECTIVES: Intestinal metaplasia is associated with gastric carcinomas, in particular intestinal-type carcinomas. According to the literature, intestinal metaplasia, especially the sulphomucin-rich incomplete type (type IIb or III) can be considered as a precancerous lesion. Intestinal metaplasia is not uncommon in gastric lymphomas, and the purpose of this study was to determine its prevalence and extent, its different subtypes and the distribution of sulphomucin and to compare these findings with those in gastric carcinomas. DESIGN: The prevalence and grade of intestinal metaplasia were investigated in surgical specimens from 160 patients with gastric carcinoma (102) [intestinal type (69), diffuse type (33)] and gastric lymphoma (58) [marginal zone cell (29), diffuse large cell (29)]. Intestinal metaplasia is analysed by specific mucin stains. METHODS: Intestinal metaplasia was described according to the Updated Sydney system. Using periodic acid-Schiff Alcian Blue pH 2.5 and high iron-diamine/Alcian Blue staining, the intestinal metaplasia was classified (Jass classification) and its sulphomucin content was determined. RESULTS: The prevalence and extent of intestinal metaplasia are significantly higher in intestinal-type carcinomas than all other gastric malignancies. Subtyping of intestinal metaplasia is independent of the different types of gastric neoplasia. High sulphomucin positivity in the metaplastic epithelium is only seen in intestinal-type carcinomas, although in a small number of cases (21.5%). CONCLUSION: Prevalence, extent and sulphomucin content of intestinal metaplasia are significantly higher in intestinal-type gastric carcinoma compared to diffuse-type carcinoma, marginal zone cell and diffuse large cell lymphomas in the stomach.

Adenocarcinoma↗
PubMed2003

Mutant p53 expression and apoptotic activity of Helicobacter pylori positive and negative gastritis in correlation with the presence of intestinal metaplasia.

BACKGROUND: Mutation of the p53 gene is detectable in most cases of gastric cancer, as it is the most common genetic alteration in human malignancies. It is also well documented that Helicobacter pylori infection plays an important role in gastric carcinogenesis. There is still no clarification, however, concerning how genetic instability influences the homeostasis of gastric epithelium. We have studied the effect of H. pylori infection on apoptosis of the antral epithelium in the presence/absence of intestinal metaplasia and the expression of the p53 oncoprotein. The relationship between these two processes is analysed. METHODS: Antral biopsies were taken from 36 patients who underwent routine upper endoscopy (17 men, 19 women, mean age 61.0 years). The biopsies were fixed in formalin and embedded in paraffin. Patients were classified into two histological groups: (1) as chronic gastritis without intestinal metaplasia (n = 19), and (2) chronic gastritis with intestinal metaplasia (n = 17). An immunohistochemical method was used to detect the expression of p53 oncoprotein, and the terminal transferase mediated dUTP nick end-labelling (TUNEL) method was used to detect apoptotic cells. RESULTS: In the absence of intestinal metaplasia, both the apoptotic index (0.0272 +/- 0.011 vs 0.0128 +/- 0.006) and expresssion of p53 (35.55 +/- 31.16 vs 18.33 +/- 19.65) were significantly higher in H. pylori positive cases compared to H. pylori negative cases. In the presence of intestinal metaplasia, p53 expression was further increased (P < 0.05), but apoptosis was similar to that observed in H. pylori negative gastritis without intestinal metaplasia. In the presence of intestinal metaplasia, H. pylori infection did not influence apoptosis (0.013 +/- 0.004 vs 0.011 +/- 0.004), or p53 ratio (70.16 +/- 22.54 vs 68.50 +/- 28.96). In the sequence of gastritis-intestinal metaplasia the two indices show a close negative correlation (P < 0.05). CONCLUSION: In the absence of intestinal metaplasia H. pylori infection increases both apoptotic activity and expression of p53 oncoprotein in the gastric mucosa. The lack of increased apoptosis with a higher p53 expression in the presence of intestinal metaplasia suggests an increased genetic instability and also may suggest that mutation of the p53 gene is an early step in the multistep process of gastric carcinogenesis.

Aged↗
PubMed1992

Intestinal metaplasia and Helicobacter pylori: an endoscopic bioptic study of the gastric antrum.

To study the relationship between intestinal metaplasia and Helicobacter pylori infection, 2274 gastroscopic antral biopsies taken from 533 patients were examined. Overall, intestinal metaplasia was found in 135 patients (25.3%) and H pylori in 289 patients (54.2%). The prevalence of intestinal metaplasia and H pylori was age related, being more common in patients greater than or equal to 50 years compared with patients less than 50 years (intestinal metaplasia, p less than 0.001 and H pylori, p less than 0.05). Intestinal metaplasia was found more often in H pylori positive patients compared with H pylori negative patients (33.9% v 15.2%, p less than 0.001). The mean age of intestinal metaplasia positive patients who were also H pylori positive was 64 (13.3) years, whereas the mean age of intestinal metaplasia positive patients who were H pylori negative was 72 (14.7) years (p less than 0.005). The extent of intestinal metaplasia was not statistically different in the latter two groups. Although our data do not prove a causal relationship between H pylori infection and the histogenesis of intestinal metaplasia it is suggested that H pylori infection is an important factor in the development of intestinal metaplasia, which is generally recognised as a precursor lesion of intestinal type gastric carcinoma.

Adult↗
PubMed2003

Increased apoptosis in gastric mucosa adjacent to intestinal metaplasia.

BACKGROUND: The biological processes involved in the development of gastric mucosal atrophy and intestinal metaplasia are still incompletely understood. Reports testing the hypothesis that apoptosis leads to atrophy have yielded conflicting results. The availability of new antibodies for the detection of apoptotic cells in tissue sections has facilitated the analysis of the role of apoptosis in the gastritis-atrophy-intestinal metaplasia sequence. METHODS: Archival material from 40 gastric resection specimens with normal mucosa (n = 5), chronic active gastritis (n = 17), or intestinal metaplasia (n = 18) was studied. Immunohistochemistry was performed using antibodies directed against cleaved cytokeratin 18 and active caspase 3. Slides were scored on a 0-3 scale for the presence of apoptotic cells. RESULTS: Normal gastric mucosa contained low numbers of apoptotic cells at the surface epithelium (mean score, 0.20). This number was significantly increased in cases with chronic gastritis (mean score, 1.06) and in those with intestinal metaplasia (mean score, 2.56). Within the intestinal metaplasia cases, 44 different foci of intestinal metaplasia were identified. In 39 of these 44 areas, concentrations of apoptotic cells were seen immediately adjacent to the foci of intestinal metaplasia, but not in the metaplastic epithelium itself. CONCLUSIONS: Apoptosis is uncommon in normal gastric mucosa. Chronic inflammation and intestinal metaplasia are associated with increased apoptosis, but occur mainly at the mucosal surface and not in the deeper layers. These findings do not support the concept that apoptosis underlies the loss of gastric glands and leads to atrophy, but the observed concentration of apoptotic epithelial cells adjacent to foci of intestinal metaplasia could be related to heterogeneity of epithelial damage, causing apoptosis, to which intestinal metaplasia is a response.

Apoptosis↗
PubMed1992

Endometrial metaplasia associated with endometrial carcinoma.

OBJECTIVE: To clarify the relationship of metaplasia to endometrial carcinoma. METHODS: Between 1984-1990, 73 cases of stage I-II endometrial carcinoma treated initially by hysterectomy were reviewed histologically. The metaplasias were classified as squamous, syncytial papillary, ciliated-cell, eosinophilic, mucinous, clear-cell, or hobnail. We assessed the histologic type and grade of the carcinoma, depth of myometrial invasion, presence or absence of lymph-vascular space invasion, and presence or absence of lymph node metastases. RESULTS: Forty of 73 patients (55%) had one or more areas of metaplasia in the endometrium adjacent to the carcinoma. Ciliated-cell metaplasia (28 of 73; 38%) was the most common type encountered. Women with both endometrial carcinoma and metaplasia were significantly younger than those with carcinoma without metaplasia (P < .05). Compared with carcinomas without metaplasia, those with metaplasia were well differentiated (P < .01) and lacked myometrial invasion (P < .01) and pelvic lymph node metastases (P < .05). The presence of metaplasia was also significantly correlated with the presence of endometrial hyperplasia (P < .01). CONCLUSION: In endometrial carcinomas, the presence of endometrial metaplasia suggests a favorable prognosis.

Adult↗
PubMed1978

Special features of intestinal metaplasia and its relation to early gastric carcinoma in man: observation by a method in which leucine aminopeptidase activity is used.

The degree of intestinal metaplasia and its macroscopic distribution in gastric mucosa were examined by a new method in which leucine aminopeptidase (LAP) activity is used to investigate the relationship between intestinal metaplasia and gastric carcinoma. Since LAP is a specific enzyme of intestinal metaplasia, the area showing positive reaction for this enzyme corresponds strictly with the zone of intestinal metaplasia examined microscopically. Almost all metaplasia was demonstrated by this method. This method was used to examine 40 human gastric carcinomas confined to the mucosa. Gastric mucosa containing differentiated tubular-type carcinoma (60%) was associated with a high degree of metaplasia in comparison with the low degree of metaplasia in poorly differentiated carcinoma (40%). Differentiated tubular-type carcinoma was closely related to intestinal metaplasia. However, all carcinomas arising from the mucosa without intestinal metaplasia (18%) were poorly differentiated. Therefore, gastric carcinomas occurring in Japanese patients are frequently and closely related to intestinal metaplasias.

Alkaline Phosphatase↗
PubMed1980

Endometrial epithelial metaplasias: proliferations frequently misdiagnosed as adenocarcinoma. Report of 89 cases and proposed classification.

Endometrial epithelial metaplasia refers to the replacement of the normal endometrial glandular epithelium by cells that are either not encountered in the normal endometrium or, if present, are usually inconspicuous elements. Because these cells appear unusual or "atypical" and because they may line architecturally complex glands, this benign process is frequently confused with adenocarcinoma. This report concerns the clinical and light-microscopic findings in 89 patients whose endometria demonstrated some form of metaplasia. Most of these metaplastic changes could be placed in one of the following seven categories: 1) morules and squamous metaplasia; 2) syncytial papillary metaplasia; 3) ciliated cell metaplasia ("tubal" metaplasia); 4) eosinophilic metaplasia; 5) mucinous metaplasia; 6) hobnail metaplasia; or 7) clear cell metaplasia. The defining characteristics of each of these groups and their differential diagnoses are discussed. The majority of women whose endometria demonstrated metaplastic transformation were postmenopausal, and most had received some form of oral estrogen replacement therapy within 3 months of the time of curettage or endometrial biopsy.

Adenocarcinoma↗
PubMed1975

[Morphogenesis and significance of epithelial metaplasia in the human prostate gland. An electron-microscopic study (author's transl)].

Electron-microscopic studies were done to point out the morphogenesis of transitional and squamous epithelial metaplasia in the human prostate gland. The basis of epithelial metaplasia is a multi-layered proliferation of the basal cells and subsequent divergent differentiation. Transitional metaplasia can be viewed under the light microscope; the electron microscope on the other hand does not show all structural features of the transitional epithelium, such as: The cover cells of the metaplastic epithelium, which do not reach the basement membrane; the surface cells, which are always mononuclear and show signs of beginning adenoid differentiation. Extreme twisting of the lateral cell membranes as a morphological equivalent of deformability was not observed. Squamous epithelial metaplasia, contrary to transitional epithelial metaplasia, shows the criterions true characteristics of squamous epithelium at both the light and electron microscopic levels: The metaplastic cells have an abundant cytoplasm containing the characteristic structures with numerous tonofibrils and broad desmosomes. Microvilli-like processes of the cytoplasm project into the lacunar interfacial canals. In addition aggregates of glycogen granules and deposits of osmiophilic material can be seen, representing the first step of keratinization. Epithelial metaplasias in the prostate occur not only in the central area near the urethra, but also in the peripheral ducts and glandular acini. An estrogen-androgen imbalance is suggested to be an essential factor in the etiology of prostatic epithelial metaplasia. A reversibility of squamous epithelial metaplasia is unlikely. To our knowledge, the epithelial metaplasias in the prostate do not represent a precancerous lesion.

Basement Membrane↗
PubMed2006

Expression of Pdx-1 in human gastric metaplasia and gastric adenocarcinoma.

Metaplastic lineages represent critical putative preneoplastic precursors for gastrointestinal metaplasia. Two metaplastic processes are associated with gastric cancer: intestinal metaplasia (the presence of intestinal goblet cell containing lineages in the stomach) and spasmolytic polypeptide-expressing metaplasia (SPEM; antralization of the gastric fundus). The transcription factor Pdx-1 is expressed in the adult pancreatic islet cells as well as the gastric antrum and duodenum. We have previously noted the increase in Pdx-1 expression in models of TGFalpha overexpression in mice but not in other models of SPEM in rodents. We have therefore sought to examine the presence of Pdx-1 expression in gastric metaplasias and gastric adenocarcinoma in humans. Tissue microarrays containing gastric cancers from the fundus and antrum and samples of SPEM and intestinal metaplasia were immunostained for Pdx-1. Nuclear Pdx-1 expression was observed in only 50% of antral-derived cancers and was present in 40% of fundic tumors. Pdx-1 expression did not correlate with clinical outcome. Although SPEM lineages did not show any staining for Pdx-1, intestinal metaplasia showed strong nuclear staining for Pdx-1. Thus, Pdx-1 expression is not associated with antralizing metaplasia (SPEM) but is associated with intestinal metaplasia. Given the pattern of normal Pdx-1 expression in the duodenum, goblet cell metaplasia in the stomach may reflect the adoption of a duodenal lineage paradigm.

Adenocarcinoma↗
PubMed2006

A close relationship between intestinal metaplasia and Cdx2 expression in human gallbladders with cholelithiasis.

We previously reported a case of a human gallbladder with cholelithiasis consisting of intestinal metaplasia with the expression of caudal-related homeobox transcription factor (Cdx2). However, it is unclear how often intestinal metaplasia and Cdx2 expression occur in human, nontumorous gallbladders with cholelithiasis. We studied the incidence of intestinal metaplasia and Cdx2 expression in human gallbladders with cholelithiasis. Gallbladders were resected under laparoscopy from 103 patients with cholelithiasis between September 2003 and March 2005. The mean age of the patients was 59.6 +/- 15.0 years (range, 22-92 years). We retrospectively reviewed these cases to look for the presence of intestinal metaplasia and the expression of Cdx2. In addition, the characteristics of intestinal metaplasia were examined by immunostaining for Muc2, chromogranin A, and serotonin. Intestinal metaplasia was found in 11.7% (12/103) of the gallbladders with cholelithiasis. The mean ages of patients with and without intestinal metaplasia were 60.8 +/- 15.4 and 59.4 +/- 14.9 years, respectively. Cdx2, Muc2, chromogranin A, and serotonin were expressed in 91.7% (11/12), 91.7% (11/12), 83.3% (10/12), and 50.0% (6/12) in intestinal metaplastic mucosa, respectively. Only one case (1.1%) that expressed Cdx2 without intestinal metaplasia did not express Muc2, chromogranin A, and serotonin. We found that 10.7% (11/103) of nontumorous gallbladders resected because of cholelithiasis under laparoscopy revealed intestinal metaplasia with Cdx2 expression.

Adult↗
PubMed1987

Endometrial metaplasia associated with endometrial adenocarcinoma.

Endometrial metaplasia is a complex group of epithelial proliferations. The relationship of metaplasia, other than squamous metaplasia, to endometrial adenocarcinoma has not been clearly established. Between 1969 and 1979, 183 patients diagnosed as having Stage I endometrial adenocarcinoma (according to International Federation of Gynecology and Obstetrics) were treated at the University of Virginia Medical Center. Sixty of the patients were treated with hysterectomy without preoperative irradiation. A histopathologic review was performed without knowledge of the clinical outcome and subsequent clinicopathologic correlations were analyzed. On review, 32/60 had carcinoma without metaplasia and 15/60 had both carcinoma and metaplasia. Thirteen of the 60 patients were judged not to have cancer: 12 had both hyperplasia and metaplasia and one had hyperplasia without metaplasia. None of the 12 patients reclassified as having metaplasia had a recurrence or died of endometrial carcinoma. Patients with both metaplasia and carcinoma were significantly younger than patients with only carcinoma and the associated carcinomas were more frequently well differentiated.

Adenocarcinoma↗
PubMed1997

Differentiation of colonic metaplasia from adenocarcinoma of urinary bladder.

Colonic metaplasia and primary bladder adenocarcinoma are relatively uncommon entities that can have similar gross clinical appearances. Examples of colonic metaplasia histologically mimicking cancer have only rarely been reported. We retrospectively analyzed 38 cases of cystitis glandularis (18 cases of colonic metaplasia), 12 cases of adenocarcinoma of urinary bladder (two well-differentiated, WDA), and one in situ adenocarcinoma from the surgical pathology files of Johns Hopkins Hospital. Nine patients with colonic metaplasia had widespread lesions. Two showed superficial muscularis propria involvement, mimicking adenocarcinoma; one of these cases had been diagnosed as infiltrating WDA at both an academic center and a community hospital. Dissecting mucin pools were focally seen in four cases of widespread colonic metaplasia, also mimicking cancer. One of the nine cases showed minimal cytological atypia, but no cases showed mitoses or signet ring cells. Distinguishing WDA from colonic metaplasia was the finding in WDA of infiltrative architectural pattern (two of two), extensive muscle invasion (two of two), moderate anaplasia (one of two), mitotic figures (two of two), and extensive mucinous pools (one of two). The diagnosis of adenocarcinoma in situ was based on anaplasia. Clinically, colonic metaplasia may resemble cancer. Histologically, colonic metaplasia may mimic cancer based on extensive involvement of the lamina propria, focal mucinous pools, focal muscularis propria involvement, focal mild cytological atypia, and rare mitoses. Despite overlapping features with colonic metaplasia, the diagnosis of WDA is based on the greater degree and extent of these atypical findings in cancer.

Adenocarcinoma↗
PubMed1999

Evaluation of gastric mucosal biopsy site and number for identification of Helicobacter pylori or intestinal metaplasia: role of the Sydney System.

Pathologists are frequently asked to evaluate gastric mucosal biopsy specimens for the presence of Helicobacter pylori infection and for potentially important changes such as intestinal metaplasia. No agreed-on system is both available and prospectively shown to provide reliable estimates of the underlying pathological condition. The Sydney System combined topographical, morphological, and causative information for evaluation of gastric biopsy specimens and provided recommendations regarding biopsy site and number. Both the biopsy sites and number were changed in 1994. Gastric biopsy specimens from patients who had multiple biopsies performed on predetermined sites were examined to compare the original and the revised Sydney Systems for the detection of intestinal metaplasia and H pylori. The diagnosis based on both versions of the Sydney System was then compared with that obtained by evaluating all specimens. Forty-six patients were studied, 20 with H pylori infection and 36 with intestinal metaplasia. Using either version of the Sydney System correctly categorized H pylori infection status in 100%. Both the original and the revised Sydney recommendations seriously underestimated the prevalence of intestinal metaplasia. Intestinal metaplasia was missed in more than 50% of those with confirmed intestinal metaplasia. No set or site of biopsy specimens was found that could reliably exclude the presence of intestinal metaplasia. Current and future studies that use the Sydney System as basis for detecting intestinal metaplasia are not likely to be reliable. Likewise, using the Sydney System to test posttherapy or with time will not accurately reflect the true status of intestinal metaplasia.

Adult↗