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PubMed1990

[The epidemiology and importance of metaplasia and dysplasia of the urinary bladder mucosa in autopsy material from a middle-size industrial city (study of Görlitz)].

This study had been conducted for the purpose of obtaining information on incidence and biological significance of metaplasia and dysplasia of the urinary bladder. Therefore, postmortem investigations were made of 1,117 urinary bladders, using optical light microscopy and mapping. They were related to a medium-size industrial town with an autopsy frequency of 98%. Metaplasia (58%) and dysplasia (13%) are no rare urinary bladder findings and occur particularly to individuals in somewhat advanced age, with no significant sex-related difference. Urocystitis was recorded from over 50% of all cases reviewed. More strongly pronounced inflammatory processes appeared to be risk factors for higher severity of dysplasia. Inconspicuous as well as metaplastic von Brunn's nests or squamous and glandular metaplasia without atypical cells should not be considered precarcinomas. However, atypical cells in terms of dysplasia were recordable from a small number of these metaplasias. Precancerous importance might be attributed to few of them, particularly in male patients with dysplastic squamous cell metaplasia. No reliable information, however, was available on premature development of dysplasia in lower age groups which would have meant a long-drawn process of carcinogenesis.

Adult↗
PubMed1990

Improved method for mapping gastric intestinal metaplasia using selective histochemical morphometry.

A gastrectomy specimen containing two tubular adenomas from a 67-year-old woman was mapped by an improved method using selective histochemical staining. The specimen was divided into 83 blocks measuring 4.0 cm x 0.5 cm. Sections from the blocks were stained with alcian blue (pH 2.5) to detect mucin. Alcian blue-stained fields were easily identified and measured with the aid of a MOP 30 interactive digital image analyzer. The total area of gastric mucosa analyzed in the 83 sections measured 3,270.9 sq mm while the area occupied by alcian blue-stained goblet cells measured 755.9 sq mm (23.1% of the total area). Intestinal metaplasia was present in 46 of 83 blocks. Both the mean size of alcian blue-positive fields per section as well as the number of alcian blue-positive fields per section were significantly larger in the antral zone I and the intermediate zone II than in the fundal zones III, IV and V. The highest proportion of gastric mucosa with intestinal metaplasia was not found around the two gastric adenomas, but elsewhere. There was no significant difference in the proportion of intestinal metaplasia between the greater and lesser curvatures, further challenging the belief that intestinal metaplasia is always greatest along the lesser curvature. The method described will permit future studies of the possible association between intestinal metaplasia and dysplasias and adenocarcinomas of the stomach.

Aged↗
PubMed1986

[Gastrointestinal endocrine cells in metaplasia of the gastric mucosa and duodenum].

Grimelius reaction and immunohistochemical PAP method were used to study endocrine cells producing gastrin (G-cells), somatostatin (D-cells) and gamma-endorphin (GER-cells) in gastric and duodenal mucosa of 95 males with atrophic gastritis with intestinal and pyloric metaplasia. The number of cells was counted per 1 mm2 of the mucosa. In the cases of marked intestinal metaplasia the number of G-, GER- and especially D-cells in the pyloric region non-metaplastic epithelium decreases and is approaching to its number in the duodenum of the control group. In the foci of marked pyloric metaplasia of gastric corpus the number of G- and GER-cells is almost the same as in the zones of gastric metaplasia of duodenum, and is approximating their number in the pyloric region of controls, thus allowing the designation of pyloric metaplasia as a complete one.

APUD Cells↗
PubMed1987

[Morphological study of the genesis and development of gastric intestinal metaplasia].

We stained 77 resected stomachs with Alcianblue and studied the distribution and the morphological features of intestinal metaplasia by macroscopic and stereoscopic observation using a clinical point drying method. And we made complete serial sections of minute metaplastic foci to study the reason why intestinal metaplasia show different features in particular areas of the stomach. The results are: Intestinal metaplasia exists both in pyloric gland area and intermediate zone in 92.2% of all cases (71/77). In intermediate zone, almost all metaplastic foci consist of complete type of intestinal metaplasia and in contrast incomplete type of it is more prevalent in pyloric gland area. The ratio of the 2 histological types in each area is not different in cases which metaplastic foci are sparse and in cases which they are extensive. Metaplastic foci are usually elevated in pyloric gland area and depressed in intermediate zone. By serial sections, many goblet cell metaplasias are observed at the flat portions of the mucosa in pyloric gland area. In intermediate zone, all minute metaplastic foci are observed at the bottoms of the grooves of the mucosa.

Female↗
PubMed1989

[Cell kinetics in intestinal metaplasia and gastric carcinoma].

48 specimens of gastric mucosa, including those of normal mucosa, intestinal metaplasia, atypical hyperplasia and carcinoma, were studied with in vitro 3H-TdR double labeling autoradiographic technique. On the basis of cell kinetics, intestinal metaplasia might be divided into two types: Type A consisted of those cases in which the values of LI, Ts and Tc were approximately closer to those of normal mucosa. The labeling cells appeared in the lower two thirds of the intestinalized glands, including small intestinal type and the complete type of colonic intestinal metaplasia. In type B, the average values of LI were higher. Ts and Tc values approximated those found in carcinoma a. Type B consisted mostly of the incomplete type of colonic intestinal metaplasia. The above evidence suggests that type B intestinal metaplasia is precancerous.

Adult↗
PubMed1988

Enhancement by vagotomy of experimental induction of intestinal metaplasia and atypical glandular hyperplasia in Wistar rats.

The effect of truncal vagotomy on the induction of intestinal metaplasia and atypical glandular hyperplasia by intragastric instillation of 5% NaOH solution was investigated in Wistar rats. Truncal vagotomy resulted in significant increases in the incidences and numbers of intestinal metaplasia and atypical glandular hyperplasias in experimental week 52. Histological examinations show that unlike goblet cell metaplasia and mild atypical glandular hyperplasia in the sham-operated rats, intestinal metaplasia without Paneth cells and moderate atypical glandular hyperplasia were more frequent in rats treated with NaOH solution and vagotomy. These findings indicate that the promoting effect of truncal vagotomy on gastric carcinogenesis may be related to its enhanced effect on induction of intestinal metaplasia and atypical glandular hyperplasia.

Animals↗
PubMed1987

[Intestinal metaplasia and stomach cancer].

Foci of intestinal metaplasia of gastric mucosa are known to be heterogeneous both morphologically and functionally, and several types of such metaplasia are now recognized. However, different authors use different criteria for their identification and, moreover, evaluate the signs of metaplasia in different ways. Also, the relationship of different types of intestinal metaplasia to one another and to dysplastic changes in the epithelium and to gastric cancer is a matter of controversy. Variants of intestinal metaplasia with sulfomucin secretion are considered as precancerous states that may give rise to gastric cancer of an intestinal type.

Gastric Mucosa↗
PubMed1987

Potentiation by ethanol consumption of tracheal squamous metaplasia caused by vitamin A deficiency in rats.

The effect of ethanol (CAS: 64-17-5) consumption on the development of squamous metaplasia of the trachea caused by vitamin A deficiency was assessed in rats. To that effect, weanling male Sprague-Dawley rats were fed for 8-12 weeks either a nutritionally adequate liquid diet containing a standard amount of vitamin A or a diet lacking vitamin A. Littermates were pair-fed the same diets with ethanol (36% of total calories) isocalorically replacing part of the carbohydrates. In rats fed the vitamin A-deficient diets with or without ethanol, plasma vitamin A was very low (5.3 +/- 0.9 and 5.9 +/- 1.5 micrograms/dl; n = 20 pairs), while liver and tracheal vitamin A was unmeasurable. Squamous metaplasia was noted in 9 of 20 rats fed the vitamin A-deficient diet and in 13 of 20 rats fed the same diet plus ethanol. Severe lesions (those showing keratinization) were present in 42% of the tracheal sections from rats fed the vitamin A-deficient diet plus ethanol compared to 6% of the sections from rats fed the diet without ethanol (P less than .001). In the ethanol-fed group, 37% of all the sections showed metaplasia occupying more than 50% of the tracheal epithelium, whereas in the absence of ethanol, 14% of the sections had lesions occupying more than 50% of the epithelium (P less than .001). When the histologic grade and extent of the lesions were expressed as the percentage of rats affected, the differences between the 2 groups of animals were not statistically significant. Ethanol feeding resulted in a 70% increase in the labeling index of basal cells in squamous metaplasia (30.7 +/- 3.5 vs. 17.3 +/- 1.5%; P less than .02). The number of [3H]thymidine-labeled suprabasal cells was not altered after ethanol feeding. In ciliated cells of the tracheal epithelium that were not as yet involved in the formation of metaplasia, ciliary abnormalities and an increased number of lysosomes were observed in rats that had consumed ethanol.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1986

[Electron microscopic study of atypical squamous metaplasia of bronchial epithelium, bronchial carcinoma in situ and microinvasive carcinoma during development of pulmonary squamous cell carcinoma].

Cytomorphological differences among severely atypical squamous metaplasia of bronchial epithelium, bronchial carcinoma in situ and microinvasive carcinoma were examined cytologically and electron microscopically. Cytomorphological features were studied by a light microscopy and an electron microscopy in bronchial brushing and histopathological preparations obtained from a patient with bronchial carcinoma in situ and two patients with microinvasive carcinoma. Cytologically, carcinoma in situ cells showed about same size and represented round to oval nuclei whose chromatin revealed finely granular and uniform pattern. Microinvasive carcinoma cells varied markedly in size. Nuclear pleomorphism was also marked in cells whose chromatin revealed sometimes coarsely granular and irregular pattern. The ultrastructural features of microinvasive carcinoma were more irregular in nuclear outline, abundant in the number of perichromatin granules and predominant in formation of fibrillar center than those of carcinoma in situ. Cytomorphological features were studied by a light microscopy and a transmission electron microscopy in bronchial brushing and biopsy preparations obtained from bronchial carcinoma in situ and atypical squamous metaplasia induced in dogs by means of bronchial submucosal injections of 20-methylcholanthrene. Both the carcinoma in situ and the severely atypical squamous metaplasia cells showed the same cytologic findings in that cells were about same size, nuclei were round to oval in shape and chromatin was finely granular, while the nucleoli of carcinoma in situ cells were relatively prominent. However, ultrastructural features indicated that there were differences, although some similarities exist, between in situ and severely atypical squamous metaplasia in nuclear form, number of perichromatin granules and enlargement of the nucleoli. From these findings, it was suggested that there were cytomorphological differences between carcinoma in situ and microinvasive carcinoma from cytological and ultrastructural aspects. We conclude that differentiation between carcinoma in situ cells and those of severely atypical squamous metaplasia is sometimes difficult when based only on cytologic features but there were cytomorphological differences at the ultrastructural level.

Aged↗
PubMed1984

Histochemical study of phosphorylase in proliferating cells of intestinal metaplasia and carcinoma of the human stomach.

A morphologic histochemical study of phosphorylase was carried out to investigate the relationship between gastric carcinoma and intestinal metaplasia. Intense phosphorylase activity was observed in the carcinoma cells, especially in well-differentiated adenocarcinoma, and in the proliferating cells of some intestinal metaplasias. Metaplastic epithelium other than the proliferating cells occasionally showed a positive reaction. Phosphorylase was negative in normal gastric epithelium, even in its proliferating cells. There was an apparent coincidence between the location of well-differentiated adenocarcinoma and the distribution of intestinal metaplasia, with the proliferating cells showing positive reaction for phosphorylase. These data suggest that the relationship between the proliferating cells of intestinal metaplasia showing phosphorylase activity and well-differentiated adenocarcinoma is apparently closer than the much-debated relationship between the epithelium of intestinal metaplasia and gastric carcinoma.

Adenocarcinoma↗
PubMed1995

Endometrial squamous metaplasia. An unusual response to progestin therapy of hyperplasia.

OBJECTIVE: To report the finding of squamous metaplasia within endometrial glands occurring as a result of progestin therapy of hyperplasia. DESIGN: Case series. Retrospective analysis of two cases from 9235 accessioned endometrial biopsies. SETTING: Hospital-based pathology laboratory processing inpatient and outpatient specimens. PATIENTS: Two women, ages 49 and 34 years, with endometrial hyperplasia without squamous metaplasia who were treated with progestin. RESULTS: Extensive squamous metaplasia was found in endometrial glands following progestin therapy. The post-therapy biopsies also showed progestin-related alterations but no evidence of active hyperplasia. CONCLUSION: Squamous metaplasia in these cases appears to be a consequence of progestin therapy. The absence of hyperplasia in the progestin-treated endometrium suggests that the squamous metaplasia does not represent persistence or progression of the original hyperplastic lesion.

Adult↗
PubMed1993

Squamous metaplasia expression of proto-oncogenes and P 53 in lung cancer patients.

BACKGROUND: The question of whether bronchial squamous metaplasia is a true preneoplasia is important and demonstrated in animal for several carcinogens. We have now approached this problem in humans and in vivo. EXPERIMENTAL DESIGN: Squamous metaplasia in the close vicinity of surgically resected lung tumors were evaluated for their mitotic index and screened for proto-oncogenes and P 53 protein expression by immunohistochemistry and/or in situ hybridization. RESULTS: Among 16 patients, 4 had squamous metaplasia positive for either myc messages and/or for P 53 protein accumulation. In the same patients (3/4), the autologous bronchial tumors were also positive for the same markers. Squamous metaplasia positivity was observed essentially in patients with advanced diseases and only in squamous cell carcinomas. In addition, when evaluated with 5 iodo-2'-deoxyuridine systemic infusion, all patients presented hyperproliferative basal squamous metaplasic cells. CONCLUSIONS: These results are reminiscent of the typical preneoplastic changes observed in familial colic adenomatosis, where genetic changes accumulate in hyperproliferative cells. They also suggest that bronchial squamous metaplasia could be an authentic preneoplasia in, at least, squamous cell carcinomas.

Gene Expression Regulation, Neoplastic↗
PubMedDate not supplied

Improvement of intestinal metaplasia six month after misoprostol treatment.

PURPOSE: To establish whether misoprostol (a synthetic prostanoid) is effective in improving intestinal metaplasia of dyspeptic patients. PATIENTS: Of the 206 dyspeptic patients without Helicobacter pylori, 18 (7.1%) had histological evidence of intestinal metaplasia (2 presented mild metaplasia, 9 moderate and 7 severe). They were treated with misoprostol 200 mg twice daily for six months and, after stopping the treatment, they all underwent endoscopic control. RESULTS: There was a statistical significant improvement of intestinal metaplasia (p < 0.001) and of the activity of antral gastritis (p = 0.03). There were no significant changes in antral and body specimens during follow-up. DISCUSSION: Though the small number of the patients and the lack of control group, our results suggest that misoprostol allows regression and/or improvement of histological IM (p < 0.001). It has proved to be effective in prevention of both gastric and duodenal ulcers induced by NSAID therapy, probably related largely to replacement of endogenous prostaglandins inhibited by the use of NSAID and it may also exerts its protective effects through inhibition of gastric acid secretion. Moreover, misoprostol showed to increase the rate of gastric blood flow, inducing a mucosal protective effect against the factors damaging gastric mucosa. It has been also documented that misoprostol regulates inflammatory cytokines and prolonged the survival of transplants, reflecting both its immunosuppressive and anti-inflammatory effect. In conclusion, since intestinal metaplasia increases the risk of gastric cancer, the use of misoprostol, in this pathology, would be of some interest.

Adult↗
PubMed1998

Staurosporine-induced versus spontaneous squamous metaplasia in pre- and postmenopausal breast tissue.

Breast cancers from pre- vs. postmenopausal women display unique characteristics that may be related to differences in epithelial differentiation between these two populations. In addition to lobular development, lactational changes, and involution, breast epithelium can undergo metaplastic alterations, often in association with carcinoma. Because protein kinase C (PKC) regulates differentiation and proliferation in many cell types, we asked whether modulation of PKC activity could define biochemical differences in breast epithelium from pre- vs. postmenopausal women. Organ cultures of normal human breast were treated with PKC agonists and antagonists. Epithelial differentiation was evaluated based on morphologic criteria and the expression of cell-type specific proteins. Staurosporine, a nonspecific but extremely potent inhibitor of PKC, induced squamous metaplasia in eight of eight cases within 2 weeks of treatment. Other inhibitors of PKC, such as calphostin C and tamoxifen, had no effect on epithelial differentiation. Long-term treatment with phorbol esters also did not induce squamous metaplasia. However, stimulation of cAMP levels by forskolin and isobutyl-methyl-xanthene (IMX) rapidly induced squamous metaplasia, as has been previously reported. Surprisingly, squamous metaplasia occurred in 10 of 12 cultures derived from postmenopausal women in the absence of exogenous agents. Untreated cultures derived from premenopausal women never developed this type of epithelium (0 of 11). Therefore, breast epithelium from pre- and postmenopausal women responded differently to in vitro culture. Forskolin/IMX or staurosporine can reproduce these conditions, acting independent of menopausal status. Because staurosporine's action was unique among PKC inhibitors, staurosporine may induce squamous metaplasia of breast epithelium by a PKC-independent mechanism.

Adult↗
PubMed1997

Medical treatment of gastroesophageal reflux disease does not prevent the development of Barrett's metaplasia and poor esophageal body motility.

OBJECTIVE: Duodenal contents refluxing into the esophagus may be involved in the pathophysiology of gastroesophageal reflux disease (GERD). This study was performed to investigate whether medical treatment of GERD aimed at suppression of gastric acid production can prevent the development of complications, such as Barrett's metaplasia or poor esophageal body motility. DESIGN: Retrospective study. SETTING: University hospital. PATIENTS: 138 GERD patients were analyzed regarding the development of Barrett's metaplasia or poor esophageal body motility, despite intermittent or continuous treatment with H2 blockers or omeprazole. MAIN OUTCOME MEASURES: The rate of patients with Barrett's metaplasia or poor esophageal body motility with or without effective medical treatment. RESULTS: Barrett's metaplasia was found in 33.8% of patients receiving medical treatment, although it was not present when treatment was induced. This rate was 21.9% among patients who were not receiving therapy (not significant). In all, 41.9% of patients with medication had impaired esophageal body motility compared with 59.3% of patients not receiving treatment (P < 0.05), but these patients had a significantly shorter history of GERD. CONCLUSIONS: Medical treatment with H2 blockers or omeprazole does not prevent the development of Barrett's metaplasia or poor esophageal body motility.

Anti-Ulcer Agents↗
PubMed1999

Differential expression of mucins and trefoil peptides in native epithelium, Barrett's metaplasia and squamous cell carcinoma of the oesophagus.

BACKGROUND AND AIMS: In humans, trefoil peptides (TFF peptides) and some mucins have been reported to be expressed in a cell-specific manner at mucosal surfaces of normal gastrointestinal tissues. Neoplastic conditions cause characteristic changes of these expression patterns. To study such patterns in Barrett's metaplasia and squamous cell carcinoma of the oesophagus (SCC), the distribution of MUC1, MUC2, MUC5AC and the three TFF peptides (TFF1, TFF2 and TFF3) was investigated. METHODS: In 40 archival samples of SCC and in 21 samples of Barret's metaplasia, expression of the three mucins and two TFF peptides (TFF1 and TFF2) was assessed by specific antibodies. Reverse transcriptase/polymerase chain reaction amplification (RT-PCR) was performed on frozen tissue samples from the 11 biopsies of SCC for the three TFF peptides. RESULTS: Immunohistochemical tests for MUC2 and TFF2 were negative both in samples of Barret's metaplasia and in SCC. MUC1 expression was detected in 57.5% of the tumour samples, while TFF1 and MUC5AC were found in 10% and 7.5% of the cases respectively. In Barrett's metaplasia MUC1 was detected in 90.5% of the cases and TFF1 and MUC5AC in all of them. RT-PCR analysis revealed a more complex pattern: TFF1 and TFF3 expressed the corresponding mRNA in all samples investigated; the third member, TFF2, was active in 45.5% of the carcinoma biopsies and not in the corresponding native tissue. CONCLUSIONS: This finding in oesophageal carcinoma contrasts with the situation found in normal and neoplastic stomach epithelium where TFF1 and TFF2 are found co-expressed and TFF3 remains silent. Interestingly, MUC1 is expressed in a significant proportion of SCC. Both in Barett's metaplasia and in SCC the expression of MUC5AC mirrors the TFF1 synthesis in intensity and spatial distribution.

Adult↗
PubMed1993

p53 protein accumulation in Barrett's metaplasia, dysplasia, and carcinoma: a follow-up study.

BACKGROUND: There is a significant interobserver and intraobserver variation in grading dysplasia in Barrett's metaplasia. New markers are needed to optimize the assessment of potential risk of cancer development in these patients. The aim of this study is to explore the use of p53 as a marker of neoplastic progression in Barrett's metaplasia. METHODS: Immunohistochemistry was used to study p53 protein accumulation in 114 specimens from 54 patients with Barrett's metaplasia. RESULTS: Positive staining was found in 0% of the cases negative for dysplasia, 9% of those with low-grade dysplasia, 55% of those with high-grade dysplasia, and 87% of those with adenocarcinoma. Follow-up was available on 24 patients. Two patients who showed low-grade dysplasia and who were positive for p53 on biopsy showed high-grade dysplasia in follow-up biopsies. Of 21 patients who had biopsy specimens negative of p53, only one showed high-grade dysplasia on subsequent biopsy specimens. CONCLUSIONS: Our data support the hypothesis that p53 plays an important role in the progression of Barrett's metaplasia to adenocarcinoma. The follow-up study indicates that positive immunostaining for p53 may be an objective marker of neoplastic progression in Barrett's metaplasia.

Adenocarcinoma↗
PubMed2003

The 'angiogenic switch' in the progression from Barrett's metaplasia to esophageal adenocarcinoma.

AIMS: We investigated VEGF expression and neovascularisation in the metaplasia-dysplasia-carcinoma sequence of Barrett's esophagus and 47 shades of adenocarcinoma. METHOD: Slides of 27 cases of Barrett's metaplasia and high grade dysplasia were immunostained for VEGF, CD 31 and alpha-sm actin to discriminate between mature and immature vessels. VEGF stained slides were quantitatively evaluated measuring optical density with a computer based program. The neovascularisation coefficient was estimated with an interactive analytic computer program. RESULTS: The median VEGF expression increased from metaplasia to advanced carcinoma. VEGF expression and the neovascularisation coefficient reached statistical significance between Barrett's metaplasia and high grade dysplasia (p<0.001), but were not statistically different between high grade dysplasia and microinvasive carcinoma (p=0.421; p=0.146). Comparing microinvasive to advanced carcinoma the difference was significant for both parameters (p<0.001). CONCLUSIONS: Based on a quantitative computer based evaluation program, the present study suggests, that an angiogenic switch might exist and that it is an early event in the metaplasia-dysplasia-carcinoma sequence of Barrett's carcinoma. The neovascularisation phase in Barrett's carcinoma may precede tumour growth.

Adenocarcinoma↗