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At least 271 records · Page 15Linked to original sources
PubMed2000

Proliferative populations in intestinal metaplasia: evidence of deregulation in Paneth and goblet cells, but not endocrine cells.

In the small intestinal mucosa, four principal epithelial cell lineages are found - the Paneth, goblet, enterocytic, and endocrine cell lineages. These cell lineages are terminally differentiated, non-proliferative, and derive from multipotent stem cells near the bases of the crypts of Lieberkühn. Intestinal metaplasia of the stomach is considered to be a premalignant condition. Since proliferative populations in this condition are not well studied, this feature was examined using double-labelling immunohistochemical and histochemical methods; 20 paraffin blocks of small intestinal mucosa and 24 paraffin blocks of intestinal metaplasia of the human stomach were studied. Double-staining was carried out with MIB-1 as a proliferation marker, with Alcian blue for goblet cells, anti-chromogranin A for endocrine cells, and p-dimethylaminobenzaldehyde-nitrite for Paneth cells. Double-labelling showed that numerous Paneth cells and goblet cells in intestinal metaplasia were in the cell cycle, but endocrine cells appeared non-proliferative. Double-labelled Paneth or endocrine cells were not seen in the control small intestinal mucosa but scanty double-labelled goblet cells were observed in normal intestinal mucosa. In intestinal metaplasia of the stomach, there is evidence of cell-cycle deregulation in the goblet and Paneth cell lineages. These observations have considerable implications for the biology and histogenesis of Paneth cells, goblet cells, and endocrine cells, and the nature of intestinal metaplasia in the gastric mucosa.

Cell Division↗
PubMed1996

p53 mutations in the non-neoplastic mucosa of the human stomach showing intestinal metaplasia.

In order to ascertain whether genetic alterations occur during the early stages of gastric carcinogenesis, abnormal accumulation of p53 protein and mutation of its gene in stomach tissue showing intestinal metaplasia were investigated using immunohistochemistry and polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) analysis. Immunohistochemistry detected 19 foci showing nuclear accumulation of p53 protein in non-neoplastic gastric mucosa in a total of 756 sections (477 of which contained intestinal metaplasia) from 16 resected stomachs containing gastric adenocarcinomas. Of these 19 p53-positive foci, 17 were diagnosed histologically as incomplete-type intestinal metaplasia and 2 as pseudopyloric glands in the regenerative mucosa. Furthermore, 14 such foci were detected in 6 patients with multiple gastric cancers. No correlation between high-iron diamine (HID)-positive sulfomucin production and p53-positive glands was observed. The DNAs were extracted selectively from these p53-positive metaplastic glands and examined for p53 mutations by PCR-SSCP analysis followed by direct sequencing. In only 10 lesions could exons; 5 to 8 be investigated completely, and of these, 4 were shown to possess p53 mutations, which were on exon 5 in 3 cases and on exon 7 in 1 case. These results indicate that irreversible genetic changes had already occurred in morphologically non-neoplastic gastric mucosa with intestinal metaplasia, and are consistent with the hypothesis that intestinal metaplasia, especially the incomplete type, may contain precursor lesions of gastric cancer.

Base Sequence↗
PubMed1996

Endometrial metaplasia as a source of atypical glandular cells in cervicovaginal smears.

Cytohistological correlation of abnormal cervicovaginal smears indicates that endometrial metaplasia may be associated with the presence of atypical glandular cells. Seven patients with histologically confirmed endometrial metaplasia had atypical glandular cells in cervicovaginal smears; five smears were interpreted as being suspicious for endometrial adenocarcinoma. Most of the patients (5/7) were postmenopausal (mean age = 61.3 years), and three of seven patients had abnormal vaginal bleeding. The corresponding endometrial tissue specimens demonstrated various combinations of eosinophilic, papillary, squamous, and tubal metaplasia; in one case tubal metaplasia occurred in association with an endometrial polyp. Cytologic features noted in the cervicovaginal smears from all seven patients were similar and included small clusters of atypical glandular cells in an inflammatory background. Intracytoplasmic vacuoles were often present, and a moderate degree of aniosonucleosis was noted. Enlarged glandular nuclei contained finely granular chromatin and distinct nucleoli. The differential diagnosis of atypical glandular cells includes endometrial hyperplasia and well-differentiated endometrial adenocarcinoma. The atypical cells associated with endometrial metaplasia were characterized by a relatively low N:C ratio and evenly distributed chromatin. In contrast, the cells of endometrial carcinoma typically demonstrate increased N:C ratios and irregularly distributed chromatin.

Adenocarcinoma↗
PubMed2003

Human model of duodenogastro-oesophageal reflux in the development of Barrett's metaplasia.

BACKGROUND: Patients with an intrathoracic oesophagogastrostomy after subtotal oesophagectomy experience profound duodenogastro-oesophageal reflux (DGOR). This study investigated the degree of mucosal injury and histopathological changes in oesophageal squamous epithelium after subtotal oesophagectomy with gastric interposition in relation to the extent of postoperative DGOR. METHODS: Serial endoscopic assessment and systematic biopsy at the oesophagogastric anastomosis was undertaken in 40 patients following curative radical subtotal oesophagectomy and reconstruction with a gastric conduit subjected to a pyloroplasty. Thirty patients subsequently underwent combined 24-h ambulatory pH and bilirubin monitoring. RESULTS: Grade I-III oesophagitis was identified in 14 patients and oesophageal columnar epithelium in 19 patients. Biopsies from columnar regeneration revealed cardiac-type epithelium in ten patients and intestinal metaplasia in nine. Seven patients followed serially showed progression from cardiac-type epithelium to intestinal metaplasia. The incidence of Barrett's metaplasia was similar irrespective of the histological subtype of the resected tumour. Patients with oesophageal columnar epithelium had significantly higher acid (P = 0.015) and bilirubin (P = 0.011) reflux. CONCLUSION: Severe DGOR occurs following subtotal oesophagectomy and provides an environment for the acquisition of Barrett's metaplasia via a sequence of cardiac epithelium and eventual intestinal metaplasia.

Adult↗
PubMed2006

Urokinase system expression in gastric carcinoma: prognostic impact in an independent patient series and first evidence of predictive value in preoperative biopsy and intestinal metaplasia specimens.

BACKGROUND: The prognostic relevance of urokinase-type plasminogen activator (u-PA), u-PA receptor (u-PAR), and plasminogen activator inhibitor 1 (PAI-1) in gastric carcinoma was demonstrated in an independent patient series. To the authors' knowledge,the roles of these activators as predictors of aggressive phenotypes in preoperative biopsies, Helicobacter pylori infection, and intestinal metaplasia have to date not been investigated simultaneously in resected tumors. The objectives of the current study were 1) to demonstrate the prognostic relevance of u-PA, u-PAR, and PAI-1 in an independent series; 2) to evaluate u-PA system expression in preoperative biopsy specimens compared with resected tumors; and 3) to evaluate u-PA system expression in intestinal metaplasias and samples with H. pylori infection. METHODS: In 104 patients with gastric carcinoma (median follow-up, 68 mos), u-PA, u-PAR, and PAI-1 in tumors and metaplasias were evaluated immunohistochemically. Preoperative biopsies were evaluated in a subset of patients. Patients were screened for H. pylori (urease) and tumor cells in bone marrow (u-PAR/CK18). RESULTS: u-PA and PAI-1 were confirmed as independent prognostic parameters, and u-PAR was associated with a trend toward a poor prognosis. u-PA system tumor expression was found to be correlated significantly with u-PAR in disseminated tumor cells and H. pylori-infected tumors, implicating a role of H. pylori in protease induction. There was a significant correlation noted between u-PA system staining between preoperative biopsies and the results in resected tumors. The expression of u-PAR and PAI-1 in intestinal metaplasias was found to be associated significantly with advanced tumor stage (depth of invasion; pathologic tumor status) and lymph node involvement (pathologic lymph node status) and was correlated significantly with u-PA system expression in tumors. CONCLUSIONS: To the author's know the current study is the first to date to demonstrate that u-PA system expression may serve as a predictor of risk in intestinal metaplasias and preoperative biopsies, implicating consequences for neoadjuvant therapy. The independent impact on recurrence and survival and a correlation with u-PAR-expression of minimal residual disease were identified in this independent series.

Adult↗
PubMed1984

Tubular adenoma with squamous metaplasia of the sigmoid colon: a case report.

A case of tubular adenoma with squamous metaplasia of the sigmoid colon in a 44-year-old female is reported. The tumor was a pedunculated polyp with a size of 1.2 X 1.7 X 1.7 cm. Histologically, the tumor showed tubular adenoma with focal squamous metaplasia. Borderline atypia was noted in a part of adenoma without squamous metaplasia and squamous component. It is supposed that squamous epithelial polyp, squamous cell carcinoma, adenosquamous carcinoma, and mucoepidermoid carcinoma may be derived from colonic adenoma with squamous metaplasia. Only six cases of the adenoma with squamous metaplasia of the large intestine have been reported previously in the literature.

Adenoma↗
PubMed1983

[3H]thymidine autoradiographic and alkaline phosphatase histochemical studies of intestinal metaplasia of the human stomach.

The relationship between cell proliferation and enzyme activity in intestinal metaplasia of the human stomach was studied using a combined method of [3H]thymidine autoradiography and alkaline phosphatase histochemistry on the same section. Three types of intestinal metaplasia were observed depending on variations in both enzymatic activity and isotope labelling. One type shows alkaline phosphatase-positive cells along the entire length of the glands with [3H]thymidine-labelled cells localized only at the bottom of the glands, resembling the duodenum. In another type of intestinal metaplasia, alkaline phosphatase-positive cells are present on the surface and/or upper half of the glands with mitotically active cells occupying the lower part of the glands. The third variety of intestinal metaplasia is characterized by the absence of alkaline-phosphatase activity and [3H]thymidine-labelled cells present in an extended zone in the lower half of the glands. Differences in labelling patterns of [3H]thymidine and the activity of marker enzyme in various types of intestinal metaplasia seem to reflect variations in cell differentiation during intestinalization of gastric mucosa.

Alkaline Phosphatase↗
PubMed1979

Endoscopic diagnosis of intestinal metaplasia in asymptomatic (control) volunteers.

The F-P border and strain phenomenon of the gastric mucosa were investigated by the application of methylene blue dye spraying method in endoscopy to 105 asymptomatic control volunteers and the following results were obtained; 1. The pyloric metaplasia is observed in the fundic gland area from the twenties in age and becomes increasing in its number and move widely spreading from the lesser curvature to the anterior and/or posterior wall of the corpus with advancing age. 2. The intestinal metaplasia arises from the thirties in age. 3. The intestinal metaplasia is observed either in the pyloric gland area of following the pyloric metaplasis in the fundic gland area. 4. Histologically, the strain phenomenon of the gastric mucosa is closely related to the intestinal metaplasia. Then, methylene blue dye spraying method is reevaluated to be useful for a precise endoscopic diagnosis of intestinal metaplasia.

Adult↗
PubMed1975

The cell proliferation of epithelial metaplasia in the prostate gland. An autoradiographic in vitro study.

In 147 autoradiographically examined prostate biopsy cylinders 5.4% squamous metaplasia and 6.0% transitional metaplasia were diagnosed. The average labeling index of squamous metaplasia was 4.3% and corresponded with values from non-keratinizing squamous epithelium in other locations. The labeling index of the transitional cell metaplasia was, in contrary, almost 10 times lower with an average value of 0.29% and corresponded with the values well known for the urothelium of the urinary bladder. Higher labeling indices were observed in 2 cases but these had chronic prostatitis. The autoradiographic results are in good agreement with the ultrastructural findings in which the metaplastic squamous epithelium corresponds with normal squamous epithelium by which the cellular proliferation takes place only in the stratum basale. On the other hand, transitional metaplasia exhibits DNA-synthesizing cells in the superficial cell layers just like in the urothelium.

Autoradiography↗
PubMed2005

Molecular evidence for progression of nephrogenic metaplasia of the urinary bladder to clear cell adenocarcinoma.

Nephrogenic metaplasia or nephrogenic adenoma of the urinary tract may present a diagnostic challenge in surgical pathology practice. Previous case reports suggest the possibility of nephrogenic metaplasia progressing to clear cell adenocarcinoma, but a malignant potential of nephrogenic metaplasia is generally not acknowledged. A case of a 70-year-old female patient with multiple recurrences of nephrogenic metaplasia of the urinary bladder and subsequent development of clear cell adenocarcinoma is described. Immunohistochemical studies help to differentiate the 2 entities. Results of molecular studies, particularly comparative genomic hybridization analysis, suggest clonal evolution of nephrogenic metaplasia to clear cell adenocarcinoma in this case.

Adenocarcinoma, Clear Cell↗
PubMed1985

Chromoendoscopic observations on extension and development of fundal gastritis and intestinal metaplasia.

The development and extension of fundal gastritis and intestinal metaplasia were investigated by the endoscopic Congo red-methylene blue test in 44 healthy subjects, 106 patients with gastric ulcer, and 26 patients with gastric polyp. Follow-up chromoendoscopic examinations were made an average of 3.4 yr (range 1-10 yr) after the initial endoscopic assessment. Fundal gastritis and intestinal metaplasia developed or became more extensive with time in only 3 (6.8%) and 2 (4.5%) healthy subjects, respectively. In patients with gastric ulcer and in those with gastric polyp, fundal gastritis and intestinal metaplasia developed or extended significantly more frequently and more rapidly than in healthy subjects. Fundal gastritis and intestinal metaplasia developed or became more extensive, respectively, in 26 (24.5%) and 23 (21.7%) patients with gastric ulcer and in 10 (38.5%) and 10 (38.5%) patients with gastric polyp. Fundal gastritis and intestinal metaplasia extended with time mainly in an upward direction.

Adult↗
PubMed1987

Brunn's nests and glandular metaplasia: normal urothelial variants in the supramontanal prostatic urethra.

Sections of 292 transurethral prostatic resection specimens and 52 intact prostatic urethral specimens from male patients 10 to 89 years old were examined for the presence of Brunn's nests and glandular metaplasia in the urothelium of the supramontanal prostatic urethra. The complex pitted urethral mucosa at and below the verumontanum was not assessed. Either or both lesions were present focally in 211 transurethral prostatic resection specimens (72 per cent) and in 51 intact urethral specimens (97.5 per cent). Brunn's nests and glandular metaplasia consisted chiefly of transitional cells but in 47 transurethral prostatic resection cases glandular metaplasia contained prostatic acinar-type cells and in 1 case intestinal-type goblet cells were noted. Brunn's nests and glandular metaplasia were associated with inflammation in only 27 per cent of the cases and were not associated with dysplasia or urethral tumors except for 1 benign papilloma. We conclude that Brunn's nests and glandular metaplasia are so common in the supramontanal prostatic urethra that they represent normal urothelial variants in this segment of the urinary tract.

Epithelium↗
PubMed1997

Intestinal metaplasia is not a strong risk factor for bladder cancer: study of 53 cases with long-term follow-up.

OBJECTIVES: Intestinal metaplasia often coexists with adenocarcinoma of the urinary bladder, suggesting to some investigators that it is premalignant. However, the natural history and long-term outcome of intestinal metaplasia in isolation are unknown. We report 53 cases of intestinal metaplasia of the urinary bladder followed for more than 10 years. METHODS: We reviewed the Mayo Clinic surgical pathology files between 1926 and 1996 and all patients with exstrophic bladder recorded in the files of the Hospital for Sick Children (Toronto, Ontario, Canada) and Dallas Children's Hospital (Dallas, Texas) between 1953 and 1987, and identified all patients with intestinal metaplasia of the bladder. RESULTS: A total of 53 cases were identified from both series, and none of the patients developed adenocarcinoma of the bladder. The Mayo Clinic series consisted of 24 patients. Nineteen of the 24 (79.1%) were alive without evidence of cancer (median follow-up 14 years, range 0.9 to 53), and 5 patients died of intercurrent disease (at 0.9, 4, 8, 11, and 53 years after diagnosis) without evidence of bladder cancer. The Dallas Children's Hospital and the Hospital for Sick Children series consisted of 29 patients. Twenty-seven of the 29 (93.1%) were alive without evidence of cancer (median follow-up 13 years, range 3 to 23.9). Two patients died of trauma (at 10.9 and 12 years after diagnosis) and at autopsy had no evidence of bladder cancer. CONCLUSIONS: Intestinal metaplasia of the urinary bladder is not a strong risk factor for adenocarcinoma or urothelial cancer.

Adenocarcinoma↗
PubMed2002

Cellular and molecular mechanisms responsible for progression of Barrett's metaplasia to esophageal carcinoma.

Barrett's metaplasia is found in approximately 12% to 18% of patients undergoing upper endoscopy for symptoms of reflux. Barrett's metaplasia is a premalignant condition and remains the number one risk factor for developing esophageal adenocarcinoma. There has been an increase in the incidence of esophageal adenocarcinoma in the past two decades, making it the most rapidly rising cancer in the United States and Western Europe. This article describes the progression from Barrett's metaplasia to esophageal adenocarcinoma and predictors for the development of adenocarcinoma in Barrett's metaplasia. Barrett's metaplasia represents a histological mosaic, with dysplastic tissue adjacent to non-dysplastic tissue. The histologic changes leading to adenocarcinoma are accompanied by alterations at the molecular level, including the accumulation of gene mutations and changes in gene expression. The determination of the molecular events that occur in the transition from normal esophageal squamous mucosa to dysplasia and to esophageal adenocarcinoma have lead to a better understanding of the process of the transformation to adenocarcinoma. This knowledge will lead to better biomarkers to diagnose and assess cancer risk.

Adenocarcinoma↗
PubMed2002

Regression of duodenal gastric metaplasia in Helicobacter pylori positive patients with duodenal ulcer disease.

BACKGROUND: It is unclear whether the extent of duodenal gastric metaplasia is due to Helicobacter pylori and/or acid. AIMS: To investigate the role of Helicobacter pylori eradication in the regression of duodenal gastric metaplasia in patients with duodenal ulcer maintained in acid suppression conditions. METHODS: . Duodenal (anterior, superior inferior walls of first part of duodenum) and gastric antrum biopsies were obtained from 44 Helicobacter pylori positive duodenal ulcer patients. Helicobacter pylori infection was diagnosed by rapid urease test, histology and 13C-Urea Breath Test. Patients were treated with 20 mg omeprazole tid associated with 250 mg clarithromycin and 500 mg amoxycillin four times daily for 10 days and maintained with 20 mg omeprazole daily for 18 weeks. Control endoscopies were performed at 6 and 18 weeks after beginning treatment. RESULTS: Duodenal gastric metaplasia regression was observed in all (32/32) patients in whom Helicobacter pylori was eradicated, but in only 3 out of 6 patients in whom eradication was not achieved (p<0. 001). CONCLUSIONS: . The present results suggest that Helicobacter pylori eradication associated with prolonged acid suppression may represent a good therapeutic strategy to achieve duodenal gastric metaplasia regression and highlight the combined role of acid and Helicobacter pylori in the pathogenesis of duodenal gastric metaplasia.

Adult↗
PubMed2003

Gastric metaplasia and chronic inflammation at the duodenal bulb mucosa.

BACKGROUND: Chronic inflammation and gastric metaplasia are often observed in biopsy specimens from the duodenal bulb of Heliobacter pylori positive patients with duodenal ulcer disease (DU). AIMS: We set out to investigate the prevalence of these lesions and their associations with other gastric and duodenal histopathological lesions. PATIENTS: A total of 1255 consecutive patients who underwent upper gastrointestinal endoscopy were recruited into the present study. METHODS: Two biopsy specimens were obtained from each of the following sites: duodenal bulb, gastric antrum, gastric body, and distal to the superior duodenal angle. These specimens were stained with hematoxylin-eosin, alcian blue periodic acid Schiff (pH 2.5) and modified Giemsa (Heliobacter pylori infection was determined only by histology). RESULTS: The mean age of the study population was 57 years, and male:female ratio 1:1.6. Overall, 235 (19%) had gastric metaplasia and/or chronic inflammation in the duodenal bulb mucosa, and H. pylori organisms could be found in 17 (1%). In univariate analyses, gastric metaplasia and/or chronic duodenal bulb inflammation positively associated with male sex (p = 0.046), Heliobacter pylori-positive chronic gastritis (p = 0.033), villous atrophy of distal duodenal mucosa, i.e., coeliac disease (p < 0.001), duodenal ulcer (p < 0.001), and duodenal bulb deformity and scarring in endoscopy (p < 0.001), but not with age (p = 0.7) nor use of nonsteroidal anti-inflammatory drugs (p = 0.055). Multivariate analysis revealed that independent risk factors for gastric metaplasia and chronic inflammation in duodenal bulb were duodenal Heliobacter pylori infection (odds ratio 1.6, 95% confidence interval CI 1.1-2.1), and villous atrophy of the distal duodenal mucosa (odds ratio 12.7, 95% CI 4.4-36.5), while chronic atrophic gastritis was protective against them (odds ratio 0.5, 95% CI 0.3-0.8). CONCLUSIONS: In addition to Heliobacter pylori infection, duodenal bulb gastric metaplasia and chronic inflammation may result from predisposition to toxic dietary components in gluten-sensitive subjects.

Chronic Disease↗
PubMed1999

Relationship between persistence of Helicobacter pylori and dysplasia, intestinal metaplasia, atrophy, inflammation, and cell proliferation following partial gastrectomy.

Helicobacter pylori and partial gastric resection are risk factors for gastric cancer. Our aims were to investigate the presence of H. pylori in postgastrectomy patients and to correlate that with alterations in mucosal architecture and cell proliferation. One hundred fifty-one endoscopic biopsies from 22 patients, (15-47 years of age, mean 29.2 years) following partial gastrectomy with Billroth II reconstruction for peptic ulcer disease, were examined for the presence of H. pylori using Giemsa staining. Sections were scored for grade of hyperplasia, intestinal metaplasia, dysplasia, inflammation, and atrophy. Immunohistochemistry for proliferative cell nuclear antigen (PCNA) was used to characterize cell proliferation. H. pylori was observed in 17/22 (77.3%) of patients or in 57/151 (37.7%) of biopsies. Metaplasia was seen in 18/22, chronic atrophic gastritis in 20/22, and cystic glandular dilation in 21/22 patients. The highest type of metaplasia in each patient was: four Type I, five Type IIA and nine Type IIB. Dysplasia was present in 16 biopsies from nine patients. H. pylori was more prevalent in intestinal metaplasia type I (44.8% of biopsies), than in type IIA (32.7%) or type IIB (25%). No H. pylori was detected in regions showing dysplasia or cystic glandular dilation. H. pylori colonization was associated with degree of inflammation (P = 0.00001) and cell proliferation (P = 0.0001). In conclusion, H. pylori is commonly seen many years after gastrectomy, it is associated with an increased epithelial cell proliferation, and it is not present in areas of histologic markers of premalignancy (type IIB metaplasia and dysplasia).

Adolescent↗
PubMed2004

Serum pepsinogens as a predicator of the topography of intestinal metaplasia in patients with atrophic gastritis.

The importance of atrophic gastritis with intestinal metaplasia is related to the fact that it increases the risk of gastric cancer development. The aim of this study is to evaluate the diagnostic potential of serum pepsinogens in predicting the topography of intestinal metaplasia. Both dye endoscopy and 13C-urea breath test were carried out in 878 subjects. Serum pepsinogen I, pepsinogen II, and IgG antibody to Helicobacter pylori were measured. The overall prevalence of intestinal metaplasia was higher in subjects with lower PG I/II ratios and lower PG I values. Based on ROC curves, a cutoff value for pepsinogen I/II ratio of less than 3.0 would have identified intestinal metaplasia with a sensitivity of 71.7% and a specificity of 66.7% in Helicobacter pylori-positive subjects. It is possible that serum pepsinogens could be used as a screening test for high-risk subjects with intestinal metaplasia.

Adult↗