Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “METAPLASIA”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 487 records · Page 27Linked to original sources

Histochemistry of epithelial metaplasia and dysplasia in human stomach and colorectum.

Histochemical techniques reveal the functional divergence of carcinomas of the gastrointestinal tract and their tissues of origin. The principal changes are either the impairment or loss of normal functions or the acquisition of new functions. The latter may be those of heterologous adult tissues (metaplasia) or foetal tissues. Dysplasia or intra-epithelial neoplasia is regarded as a selective precancerous lesion. One might predict the functional profiles of dysplasia to be intermediate between those of normal and carcinomatous tissues. This appears to be only partially true in that high grade dysplasia (amounting to carcinoma-in-situ) will show appropriate cancer-associated changes, whereas low grade dysplasia may be functionally identical to its normal counterpart. Paradoxically, it is possible to demonstrate cancer-associated changes in non-neoplastic lesions such as incomplete intestinal metaplasia of gastric mucosa and both metaplastic polyps and transitional mucosa of the colorectum. If a proportion of the changes occurring in the course of malignant transformation have a metaplastic basis, it is possible that these are caused by the same environmental agents which lead to benign metaplasias. Benign metaplastic lesions may signal the presence of a potentially carcinogenic microenvironment, whilst some, such as incomplete intestinal metaplasia, are regarded as precancerous.

Antigens↗

Squamous metaplasia in organ cultures of vitamin A-deficient hamster trachea: cytokinetic and ultrastructural alterations.

Cytokinetic and morphologic studies were performed to elucidate the origin of epidermoid metaplasia in organ cultures of tracheas derived from vitamin A-deficient Syrian golden hamsters. Focal areas of squamous metaplasia were observed 2 days after explantation, and extensive epidermoid metaplasia and cornification were present in approximately 89% of the explants at day 10. During the first 2 days, both basal and mucous cells proliferated actively. By day 3, the total mucous cell [3H]thymidine labeling index (LI) had declined and remained at very low levels during the remaining culture period. The basal cell LI also declined from its higher level, but it remained at relatively higher levels than those of the mucous cells between days 3 and 9 after culture. In the lesions, labeled cells were generally confined to the basal layer, and the LI was about thirtyfold greater than the total basal cell LI. As the lesions progressed, the surface layer containing the mucous and ciliated cells was exfoliated as a result of population pressure from the underlying actively proliferating basal cells and subsequent epidermoid differentiation of the daughter cells. These data support the hypothesis that epidermoid metaplasia of tracheobronchial epithelium caused by vitamin A deficiency originates from the generative or basal cells.

Animals↗

Histopathological study of intestinal metaplasia of postmortem stomachs in the aged Japanese.

The incidence and extent of intestinal metaplasia of the stomach in aged Japanese has been studied. Histological studies were carried out on 422 stomachs, obtained at autopsy in Tokyo Geriatric Hospital from 1957 to 1969. The average age of the subjects in this series was 76 yr. Intestinal metaplasia was classified into six types according to its distribution: antral type 14.5%, intermediate zone type 1.7%, cardiac type 4.0%, cardiac and antral type 3.8%, diffuse type 62.8%, and nonmetaplastic type 13.3%. Diffuse type was found to gradually increase in incidence with increasing age and a correlation was found between the extent of the intestinal metaplasia and the degree of atrophic change of the gastric mucosa. Two spreading patterns of the intestinal metaplasia were also observed.

Aged↗

Metaplasia of bone in lungs and bronchi: report of 2 cases.

Two cases are reported of pulmonary osseous metaplasia in elderly men aged 91 and 64 years. The first case represented disseminated metaplastic bones occurring throughout the lungs. In the second instance, small foci of metaplastic bones were localized in some bronchial walls of the upper lobe of the right lung which had old treated tuberculosis, severe fibrosis, and bronchiectasis. Both cases also had advanced pulmonary emphysema and interstitial fibrosis. It is suggested that fibrosed interstitium of the lungs and bronchial walls has turned into bony metaplasia in both patients. However, osseous metaplasia from cartilage of the bronchial walls is additionally suggested in case 2. Multiple factors probably play roles in development of bony metaplasia.

Aged↗

In vitro and in vivo analysis of cellular origin of cervical squamous metaplasia.

We have previously shown that cultured normal human endocervical cells (HENs) form epithelium resembling squamous metaplasia in vivo. To analyze the cellular origin of squamous metaplasia, the cytokeratin and mucin expression and morphological features of HENs in monolayer cultures and in implants beneath the skin of nude mice were examined. Primary HENs had two distinct morphological phenotypes in vitro pleomorphic epithelial cells and keratinocytelike cells. Using a panel of monoclonal antibodies for various cytokeratins (CKs), we observed that the pleomorphic cells, which were the primary outgrowths, expressed CK7 and CK18 and produced mucin, suggesting their origin to be the mucosecretory columnar cells (CCs) of the endocervix. Keratinocytelike cells were observed in proximity of the CC-like cells after a few days of HEN culture. Interestingly, these cells were homogeneously negative for CK7 expression, as for native reserve cells (RCs), and homogeneously positive for CK13 expression with the antibody that is specific for RCs. During early passages, the culture consisted mostly of the RC-like keratinocytelike cells, and in the late passages, the CC-like cells were predominant. HEN implants in nude mice morphologically formed epithelia similar to immature squamous metaplasia and showed variable CK18 expression. Moreover, they showed homogeneous CK13 expression throughout all layers and expressed mucin and CK7 in the suprabasal cells. The possibility that the HEN culture was originally a mixed population of CCs and RCs, that we failed to detect, cannot be eliminated. Our results support the more likely view that the endocervical simple epithelia, which form squamous metaplasia, are bipotential cells and undergo differentiation readily and reversibly to give rise to CC-like and RC-like cells in culture.

Adult↗

The effect of the immune response to Helicobacter pylori in the development of intestinal metaplasia.

AIM: To determine whether cytotoxic Helicobacter pylori antibodies occur in gastric mucosa, and whether these antibodies contribute to the development of intestinal metaplasia. MATERIALS AND METHODS: The number of mononuclear inflammatory cells, which specifically produce immunoglobulin (Ig)G and IgA antibodies, was investigated by using an enzyme-linked immunospot assay and the fraction of mononuclear inflammatory cells determined in gastric biopsy specimens from 34 subjects with H. pylori infection. Assays for the cytotoxicity of H. pylori antibodies were performed on cultured Japanese green monkey kidney (Vero) cells and by in vitro tests. RESULTS: The number of IgG and IgA antibody-producing cells was positively correlated with the degree of inflammation of the gastric mucosa. However, the number of IgG antibody-producing cells was lower in subjects with intestinal metaplasia than in those without. This was not the case for IgA. Significant cytotoxic damage was observed in Vero cells in vitro when incubated in a solution containing the H. pylori IgG antibody, antigen and polymorphonuclear leukocytes. No cytotoxicity was seen with the IgA antibody or with the antigen or polymorphonuclear leukocytes alone. CONCLUSIONS: H. pylori infection is associated with the appearance of immunocompetent mononuclear cells in gastric mucosa. These cells produce H. pylori antibodies of the IgG class which are capable of causing cytotoxic damage in the epithelial cells, obviously through activation of polymorphonuclear leukocytes by antibody-antigen complexes. The occurrence of these cells is inversely related to intestinal metaplasia, suggesting that they may be involved in the processes of epithelial damage leading to the appearance of intestinal metaplasia.

Adult↗

Chondroid metaplasia in the tunica media of the aorta in dogs submitted to saphenous vein aorto-cava by-pass.

We submitted twelve dogs to aorto-superior vena cava by-pass with saphenous vein. Six months later, all dogs had developed areas of chondroid metaplasia in the tunica media of the aorta, near the area of anastomosis. Three dogs also had bony metaplasia. The Foci of metaplasia had no relation to sutures. This lesion begins with a build-up store of glycosaminoglycans in the tunica media. Later, elastic fibers show a fenestration and dissolution, while chondrocytes replace smooth muscle fibres. We suggest that the rupture of the vasa vasorum during operation and the traction and pulsation of the by-pass over the area of suture could be the cause of this direct metaplasia.

Anastomosis, Surgical↗

Lewis blood group-related antigen expression in normal gastric epithelium, intestinal metaplasia, gastric adenoma, and gastric carcinoma.

The expression of blood group-related antigens of the Lewis system in normal gastric mucosa, intestinal metaplasia, gastric adenoma, and gastric carcinoma was examined. Ninety-five percent of normal foveolar epithelial samples stained positive for Lewis(b) antigen, whereas only 10.0% expressed Lewis(a) antigen. In contrast, intestinal metaplasia specimens had increased Lewis(a) antigen expression and slightly decreased Lewis(b) antigen expression. A similar pattern of Lewis(a) and Lewis(b) expression was observed in gastric adenomas and intestinal type adenocarcinomas. Lewis(x) and Lewis(y) were detected in all normal deep glands, but were not expressed in the majority of intestinal metaplasia specimens. In addition, only 20-40% of gastric adenomas and gastric carcinomas expressed Lewis(x) and Lewis(y) antigens. These changes in Lewis antigen expression in intestinal metaplasia, adenomas, and intestinal type adenocarcinomas suggest that altered expression of Lewis blood group-related antigens may correlate with cell transformation processes.

Adenocarcinoma↗

Tissue staining for Helicobacter pylori in intestinal metaplasia: correlation with its extension and histochemical subtypes.

The role played by Helicobacter pylori (Hp) infection in the occurrence of non-cardial gastric adenocarcinoma is suggestive but still debated. This study aimed to evaluate: a) the prevalence of Helicobacter-like organisms in antral bioptic specimens of 291 patients with chronic gastritis with antral atrophy and different subtypes of intestinal metaplasia (IM); b) the presence of a possible different positive tissue staining for the bacteria in the complete and incomplete intestinal metaplasia. Of the 291 patients, 222 cases (76.3%) showed type I IM, 28 cases (9.6%) type II IM and 41 cases (14.1%) type III IM. Helicobacter-like organisms were found in 42.9% of cases and positive tissue staining rate appeared to be inversely related to the extension of IM (58.7% in IM extended in less than 30% of specimens, 30.2% in IM extended between 30% and 60%, 2.7% in IM exceeding 60% of the biopsed area). The inverse correlation between lower positive tissue staining for Helicobacter-like organisms and greater extension of IM was statistically significant (p < 0.001). Incomplete metaplasia appeared to be unrelated to age and associated with a lower positive tissue staining for Helicobacter-like organisms; among patients with type I metaplasia, 118/222 showed Hp-positive bioptic specimens, vs 7/69 of types II and III (p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Nephrogenic metaplasia: long-term haemodialysis and anuria as potential risk factors and reversibility with renal transplantation.

AIM: To determine the incidence of nephrogenic metaplasia in patients with defunctionalized bladders due to long-term end-stage renal failure on haemodialysis. METHODS: From the dialysis registry of the Princess Alexandra Hospital 13 anuric patients who had been on haemodialysis for 10 or more years were identified. Of these, seven were currently awaiting renal transplantation and six had successful transplants. Endoscopic assessment of their lower urinary tracts was performed. RESULTS: Three cases of nephrogenic metaplasia were identified. In one case this led to significant haematuria following transplantation. However, the changes of nephrogenic metaplasia disappeared over the subsequent 18 months without specific treatment. CONCLUSIONS: It appears that a chronically defunctionalized bladder in the presence of end-stage renal failure is associated with an increased risk of nephrogenic metaplasia. These changes may spontaneously regress following transplantation and restoration of bladder function.

Anuria↗

Prognostic significance of high expression of proliferating cell nuclear antigen in patients with intestinal metaplasia.

Although some types of intestinal metaplasia are considered to be potentially pre-malignant lesions leading to gastric carcinoma, their high frequency and variability limit their usefulness as early markers of malignant progression. The present study was carried out to search for parameters which could be used in conjunction with histological diagnosis to identify groups of patients with a high risk for developing gastric neoplasia. The expression of proliferating cell nuclear antigen (PCNA), as revealed by immunohistochemical staining of anti-PCNA monoclonal antibody (PC10) in 82 endoscopic biopsy specimens, was compared with the histological classification of intestinal metaplasia, the biochemical composition of gastric mucins and the expression of blood group Lewis antigens. Statistically significant (p 0.001) correlation between the PCNA labelling index (the percentage of positive cells in more than 700 tumor cells per sample) and the histological type of intestinal metaplasia, the presence of sulphomucins, and the presence of anomalous Lewis a antigen was found. We conclude that a high PCNA-labelling index in the gastric mucosa, with a histological diagnosis of incomplete intestinal metaplasia, could constitute a good prognostic marker of the severity of the histologic lesion. These parameters, together with others such as the presence of sulphomucins and of cells expressing anomalous Lewis a antigen, may be used to define patients with a high risk of developing a gastric neoplasia.

Cell Nucleus↗

[Induction by benz(a)pyrene of squamous cell metaplasia of the respiratory epithelium in organ cultures: importance of the route of administration of the carcinogen and genetic susceptibility of the animals].

A comparative study was made of transplacental (in vivo) and direct (in vitro) effects of benz(a)pyrene (BP) in the organ cultures of embryonal lungs of mouse susceptible (strain A) and resistant (C57 Bl) to pulmonary blastomogenesis. The development of the epithelium squamous cell metaplasia was observed only after direct application of BP on the lung explants in vitro. Correlation between metaplasia frequency and BP dose and duration of treatment and mouse susceptibility to pulmonary blastomogenesis is established. Thus, at all BP concentrations (3.6 or 12 micrograms/ml of medium) and maximum time of treatment (15 days) the frequency of squamous cell metaplasia in the lung explants of C57 B1 mice was very low (3.0, 2.0 and 4.2%, p > 0.1) while in a strain A it was significant at the doses of 6 and 12 micrograms/ml (10.4 and 23.4%, p < 0.001). No epithelial metaplasia developed when the time of BP treatment was decreased up to 7 days.

Animals↗

[Outcome of nephrogenic metaplasia of the bladder in kidney transplant recipients].

OBJECTIVES: To evaluate the risk of recurrence and malignant degeneration of vesical nephrogenic metaplasia in renal transplant recipients. MATERIAL AND METHODS: Fourteen patients with known nephrogenic metaplasia were systematically followed. Vesical biopsies were performed with a resector, stained with eosin haemalun saffron, analysed and compared to initial results. Labelling by anti-EBV and anti-CMV monoclonal antibodies was performed in 5 cases of intense inflammatory reactions. RESULTS: All patients were males, with a median age of 39 years. Nephrogenic metaplasia had been diagnosed 7 to 80 months after renal transplantation (median = 37.8). Twelve patients were reviewed 5 to 116 months after the initial diagnosis (median = 52). Relapse was observed in 83% of cases, but without any malignant degeneration. CONCLUSION: Nephrogenic metaplasia is therefore a benign recurrent disease. The importance of the initial blood supply and fibrosis in the case of recurrence suggest a disorder of the blood supply, probably traumatic in origin. Only symptomatic patients are currently followed.

Adolescent↗

[Biopsy and endoscopic prospective study of the prevalence of intestinal metaplasia in the gastroesophageal junction in controls and in patients with gastroesophageal reflux].

BACKGROUND: The classic diagnosis of Barret esophagus is based on the finding of three of more cm of distal esophagus covered by specialized columnar epithelium. However, at the present time, it is based on the presence of intestinal metaplasia in the junction of squamous-columnar mucosae. AIM: To assess the prevalence of Barret esophagus using endoscopic and pathological criteria in healthy subjects and in individuals with gastroesophageal reflux. PATIENTS AND METHODS: One hundred thirty nine controls and 372 patients with symptoms of gastroesophageal reflux subjected to an upper gastrointestinal endoscopy were studied. Patients with Barret esophagus were classified as having a "mini Barret" when the pathological presence of intestinal metaplasia was the only finding. A "short Barret esophagus" was diagnosed when less than 3 cm were covered with fingerings of mucosal substitutions and "extensive Barret esophagus" when more than 3 cm of esophageal mucosa were substituted. RESULTS: Two percent of controls, 12.4% of patients with gastroesophageal reflux without esophagitis and 11.7% of such patients with esophagitis had intestinal metaplasia in the gastroesophageal junction. Patients with Barret esophagus were older than the rest of patients. "Short Barret esophagus" is six times more frequent than "extensive Barret esophagus". Esophageal erosions, peptic ulcers and stenosis were more frequent in patients with extensive Barret esophagus. The prevalence of dysplasia was similar in all types of Barret esophagus. CONCLUSIONS: Intestinal metaplasia was very infrequent in control patients. In subjects with gastroesophageal reflux, classic endoscopic diagnosis may miss up to 80% of patients with Barret esophagus. Thus, gastroesophageal junction biopsies must be obtained in all patients with symptoms of gastroesophageal reflux.

Adolescent↗

Secondary myelofibrosis with metastatic breast cancer simulating agnogenic myeloid metaplasia: report of a case and review of the literature.

A patient with carcinoma of the breast, who developed a clinical syndrome resembling agnogenic myeloid metaplasia, is described. She was found to have secondary myelofibrosis with metastatic carcinoma of the marrow, extensive extramedullary hematopoiesis resulting in massive splenomegaly, and leukoerythroblastosis. These findings are rare and myeloid metaplasia with striking extramedullary hematopoiesis causing massive splenomegaly and mimicking agnogenic myeloid metaplasia is seldom seen in patients with metastatic carcinoma. Previous case reports of secondary extramedullary hematopoiesis simulating agnogenic myeloid metaplasia (AMM) in patients with solid tumors are also reviewed.

Adult↗

Histochemical and immunohistochemical studies on development of biliary carcinoma in forty-seven patients with choledochal cyst--special reference to intestinal metaplasia in the biliary duct.

Histochemical and immunohistochemical studies on 47 consecutive specimens excised for choledochal cyst were performed to clarify possible metaplastic changes of the biliary duct in relation to carcinogenesis. An anomalous arrangement of the pancreaticobiliary ductal system was observed in all 39 cases examined. Among the 47 patients, 5 (10.6 per cent) had biliary carcinoma. 27.3 per cent mucous gland, 13.0 per cent goblet cell and 9.5 per cent argyrophil cell in 23 children. On the other hand, 81.8 per cent exhibited mucous gland, 41.7 per cent goblet cell and 27.3 per cent argyrophil cell in 24 adults. These metaplastic changes seemed to be an intestinal metaplasia and increased with age. Immunoreactive-gastrin or -somatostatin were evident immunohistochemically in 4 adults. These findings confirmed that intestinal metaplasia may develop in the biliary duct in cases of choledochal cyst. Although direct evidence between intestinal metaplasia and the development of biliary carcinoma was not found, reflux and stasis of pancreatic enzymes in the biliary duct may relate to the development of intestinal metaplasia and be an important factor related to the carcinogenesis of choledochal cyst.

Adenoma, Bile Duct↗

Significance of Fas and retinoblastoma protein expression during the progression of Barrett's metaplasia to adenocarcinoma.

BACKGROUND: Barrett's esophagus (BE) is a premalignant lesion characterized by replacement of normal squamous epithelium with columnar epithelium. This lesion can progress to dysplasia and adenocarcinoma. Recently, the Fas receptor and retinoblastoma (Rb) protein have been described as important mediators of apoptosis and tumor suppression, respectively. This study was undertaken to examine their expression during the progression of metaplasia to adenocarcinoma in BE. METHODS: In a review of 56 adenocarcinomas arising in BE, the specimen blocks were examined using the immunohistochemical avidin-biotin-peroxidase complex technique. For each specimen, areas of normal epithelium were compared with areas of metaplasia, dysplasia, or carcinoma (when present). Monoclonal mouse anti-human antibodies were used to identify Rb protein (Rb-Ab5, 1/50 dilution; Oncogene Science) and the 40-50-kDa cell membrane Fas protein (APO-1/Fas, 1/5 dilution; DAKO Corp.). RESULTS: Loss of Rb staining was observed as the metaplasia progressed to dysplasia and carcinoma, indicating accumulation of unstainable aberrant protein. Conversely, Fas protein staining was undetectable or weak in normal or metaplastic epithelium, increasing in the areas of high-grade dysplasia and carcinoma. These differences were statistically significant (P < .001). CONCLUSIONS: The accumulation of abnormal Rb protein during the progression of Barrett's metaplasia to carcinoma leads to unsuppressed tumor growth. Fas overexpression may represent a cellular attempt to balance the uncontrolled tumor proliferation by promoting apoptosis.

Adenocarcinoma↗

Celiac disease and intestinal metaplasia of the esophagus (Barrett's esophagus).

Previous studies on celiac patients demonstrated that exposure to gliadin alters the motility of the upper gastrointestinal tract, leading to increased acid reflux. No literature is available regarding the possible presence of specialized intestinal metaplasia of the esophagus as a consequence of chronic reflux in adult celiac patients. Our purpose was to evaluate endoscopically and histologically the esophagi of a group of untreated celiac patients. We studied 60 celiac patients, 13 men and 47 women (mean age, 40 +/- 14 [SD] years; range, 18-80 years), at their first endoscopy (following a normal diet). The distal esophagus was evaluated and multiple biopsies were taken. Hematoxylin-eosin and alcian blue stainings were performed. A group of nonceliac, age- and sex-matched patients was used as a control. We found intestinal metaplasia in the distal esophagus of 16 of 60 (26.6%) celiacs (mean age, 45 +/- 13 years; range, 27-75 years), in comparison with a control-group prevalence of 10.9% (OR, 3.9; 95% CI, 1.4-11.2%). Among the celiac group with metaplasia, only one patient had reflux-like symptoms. None had esophagitis. In conclusion, we observed an increased prevalence of esophageal metaplasia in patients with celiac disease. This finding could be the result of motor abnormalities leading to chronic acid reflux, combined with a mucosa which is sensitive to gliadin.

Adult↗