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 235 records · Page 13Linked to original sources
PubMed1991

The Helicobacter (Campylobacter) pylori-colonized duodenal mucosa and gastric metaplasia.

Biopsies were obtained from non-ulcerated sites of the duodenum from 100 dyspeptic patients. Helicobacter (Campylobacter) pylori was cultivated from 19 of these biopsies. Active chronic duodenitis (ACD) was found in 17 biopsies and more than 5% gastric metaplasia in 20 biopsies. H. pylori as well as ACD occurred with a significantly increased frequency when more than 5% gastric metaplasia was found in the duodenal biopsies. H. pylori on metaplastic tissue without ACD was, however, seen in two cases. H. pylori was cultivated from 9% and ACD was found in 5% of the biopsies with less than 5% gastric metaplasia. Gastric metaplasia in the duodenum was found significantly more frequently in patients with endoscopic duodenitis or duodenal ulceration than in patients with normal endoscopy. No association between gastric metaplasia in the duodenum and gastric pH or serum antibodies against H. pylori was seen. This study indicates that there is an established, but not exclusive, connection between gastric metaplasia and the colonization of the duodenum by H. pylori, the most important role being played by the antral gastric mucosa rather than the duodenum.

Biopsy↗
PubMed1992

Squamous cell metaplasia of the bladder urothelium. A retrospective study of 36 patients.

In a retrospective study of 28 women and eight men with squamous cell metaplasia in different parts of the bladder, including the trigone, no histopathological differences were observed among the regions. All the five (female) patients with parakeratosis had a concomitant invasive bladder tumour. Thirty-eight% of all the patients had a simultaneous neoplastic tumour. The metaplastic lesions were investigated for keratin in 13 patients, and all were positive. In seven out of eight patients, the urothelium adjacent to the squamous cell metaplasia was also positive for keratin, indicating a direct transformation of the urothelium to squamous cell epithelium. The metaplastic cells were investigated for oestrogen receptors in five men and five women, and all were negative, suggesting no relationship between estrogens and squamous cell metaplasia of the bladder. Squamous cell metaplasia in the bladder is not considered a premalignant condition. However, metaplasia and neoplastic tumours are often associated with chronic tissue damage, and the presence of metaplasia may give a warning of conditions that can also cause cancer.

Adult↗
PubMed1995

Expression of trefoil peptides pS2 and human spasmolytic polypeptide in gastric metaplasia at the margin of duodenal ulcers.

Duodenal ulcers are associated with gastric metaplasia in the duodenum, both at the ulcer margin and at more distant sites in the duodenal bulb. pS2 and human spasmolytic polypeptide (hSP) are secretory peptides expressed in gastric epithelial cells and in gastric metaplasia. As these peptides may be important in ulcer healing, this study investigated the possibility that the expression of pS2 and hSP is increased in gastric metaplasia at the margin of duodenal ulcers. Duodenal bulb biopsy specimens from 12 duodenal ulcer patients were assessed. Sections were immunostained with monoclonal antibodies for pS2 and hSP. Cytoplasmic stain intensities were measured by an image analysis system and expressed as integrated optical density (IOD) units, In situ hybridisation for pS2 and hSP mRNA was carried out on parallel sections. Duodenal sections were also stained with diatase periodic acid Schiff/alcian blue to localise areas of gastric metaplasia. pS2 antigen staining in the duodenum was restricted to surface epithelial cells, and hSP to acinar and ductular components of Brunner's gland. mRNA localisation corresponded to immunostaining cells. In gastric metaplasia, pS2 expression was greater at the ulcer margin than away from the ulcer, as judged by the intensity of antibody staining (mean IOD units (SEM), 20.6 (3.3) v 9.5 (3.0); p < 0.001). There was a trend towards greater hSP staining at the ulcer margin but this did not achieve statistical significance. These findings support the putative role of pS2 and possible hSP in mucosal healing and providy further evidence for an autocrine 'ulcer-gastric metaplasia-repair' loop involving these trefoil peptides.

Brunner Glands↗
PubMed1997

Intestinal metaplasia at the squamocolumnar junction in patients attending for diagnostic gastroscopy.

BACKGROUND: The incidence of adenocarcinoma of the oesophagus and gastric cardia is increasing rapidly. Barrett's oesophagus is the major risk factor. Intestinal metaplasia at the squamocolumnar junction in the absence of Barrett's oesophagus is common but its relation to adenocarcinoma and gastro-oesophageal reflux disease is unclear. AIMS: To study the prevalence and clinical, endoscopic, and histological associations of intestinal metaplasia at the squamocolumnar junction. METHODS: Biopsy specimens were taken from 120 randomly selected patients undergoing routine diagnostic endoscopy. Eight biopsy specimens, taken from above and below the squamocolumnar junction, gastric fundus, and gastric antrum, were stained with haematoxylin/eosin, alcian blue/periodic acid-Schiff, and Gimenez, and graded independently by one pathologist. RESULTS: Intestinal metaplasia at the squamocolumnar junction was found in 21 patients (18%). Metaplasia was associated with increasing age (p < 0.01) and antral intestinal metaplasia (p = 0.04). Logistic regression analysis revealed that age was the only independent predictor (p < 0.01). There was no association with symptomatic, endoscopic, or histological markers of gastro-oesophageal reflux disease. CONCLUSIONS: Intestinal metaplasia at the squamocolumnar junction is a common finding. It is associated with increasing age but not gastro-oesophageal reflux disease.

Adult↗
PubMed1998

Intestinal metaplasia at the gastro-oesophageal junction: Helicobacter pylori gastritis or gastro-oesophageal reflux disease?

BACKGROUND: Intestinal metaplasia, whether in the cardia or the distal oesophagus, has been uniformly defined as specialised columnar epithelium, suggesting a relation with Barrett's oesophagus. It is, however, not clear whether the risk factors associated with intestinal metaplasia are identical at both sites. AIMS: To investigate biopsy specimens obtained below the squamocolumnar junction (SCJ) in relation to endoscopic aspect, gastric histology, and clinical presentation. PATIENTS AND METHODS: In 423 patients investigated the endoscopic aspect of the SCJ was classified as unremarkable (group I, n = 315) or suggestive of Barrett's oesophagus (group II, n = 108). Standardised biopsy specimens from the antrum, corpus, and directly below the SCJ were investigated. RESULTS: Intestinal metaplasia was detected at the SCJ in 13.4% of group I patients, where it was significantly associated with gastric intestinal metaplasia (odds ratio (OR) 6.96; confidence interval (CI) 2.48 to 19.54) and H pylori (OR 7.85; CI 2.82 to 21.85), and in 34.3% of group II patients where it was significantly associated with reflux symptoms (OR 19.98; CI 6.12 to 65.19), erosive oesophagitis (OR 12.16; CI 3.86 to 38.24), and male sex (OR 6.25, CI 2.16 to 18.14), but not with H pylori or gastric intestinal metaplasia. CONCLUSION: This study suggests that the pathogenesis of intestinal metaplasia at the SCJ is not uniform: at an endoscopically unremarkable SCJ it is a sequela of H pylori gastritis, but coexisting with endoscopic features of Barrett's oesophagus it is associated with male sex and gastro-oesophageal reflux disease.

Barrett Esophagus↗
PubMed1987

Limited value of type III intestinal metaplasia in predicting risk of gastric carcinoma.

Endoscopic gastric biopsy specimens taken in 1976 from 174 patients were reviewed. Biopsy specimens from 44 patients showed intestinal metaplasia, and subtyping by mucin histochemistry showed that 16 were of type I, 14 of type II, and 14 of type III. Only two of these 174 patients developed gastric adenocarcinoma over the next 10 to 11 years: one with type II and one with type III intestinal metaplasia. Case notes of a separate group of 68 patients with gastric adenocarcinoma diagnosed in 1985 were reviewed for evidence of intestinal metaplasia in a previous gastric biopsy. Only two patients had previously been biopsied; one of these biopsy specimens showed type II intestinal metaplasia and the other showed no intestinal metaplasia. These findings suggest that subtyping of intestinal metaplasia in endoscopic gastric biopsy specimens is of only limited value in identifying patients at risk of gastric adenocarcinoma who require long term follow up.

Adenocarcinoma↗
PubMedDate not supplied

The effect of Helicobacter pylori eradication on duodenal gastric metaplasia.

We investigated the incidence of duodenal gastric metaplasia and its response to Helicobacter pylori eradication in patients with duodenal ulcer or erosive duodenitis. Gastric and duodenal biopsies were taken from patients with endoscopically detected H. pylori positive duodenal ulcer or erosive duodenitis, and the presence and extent of duodenal gastric metaplasia was recorded. Patients were given omeprazole 20 mg twice daily for 2 weeks, and amoxicillin 1 g and clarithromycin 500 mg twice daily for 10 days, and then ranitidine for a further 8 weeks. Biopsies were repeated 6 months after the start of treatment. Duodenal gastric metaplasia was initially present in 22 patients (52%) and was more frequent in ulcer patients than in duodenitis patients, but not significantly so (69% versus 45%). After treatment, H. pylori was eradicated in 68% of duodenal gastric metaplasia patients and the duodenum was normal endoscopically in 85% of these patients. Duodenal gastric metaplasia was improved or eliminated in 12/15 H. pylori eradicators (80%) and in 5/7 H. pylori non-eradicators (71%), a non-significant difference. The improvement in duodenal gastric metaplasia appeared to be independent of H. pylori eradication.

Adult↗
PubMed2001

Improvement in atrophic gastritis and intestinal metaplasia in patients in whom Helicobacter pylori was eradicated.

BACKGROUND: Glandular atrophy and intestinal metaplasia are precancerous lesions; whether Helicobacter pylori eradication affects these lesions is controversial. OBJECTIVE: To determine whether H. pylori eradication is associated with improvement in glandular atrophy and intestinal metaplasia after at least 1 year. DESIGN: Single-blind, uncontrolled prospective trial. SETTING: Academic gastroenterology clinic in Japan. PATIENTS: 163 consecutive patients with dyspepsia and H. pylori infection. INTERVENTION: One-week course of a proton-pump inhibitor and antibiotic therapy. MEASUREMENTS: Endoscopic examination with antral and corporal biopsy was done before treatment and at 1 to 3 and 12 to 15 months after treatment. Gastritis, atrophy, and metaplasia were graded according to the updated Sydney System. RESULTS: In the 115 patients in whom H. pylori was eradicated, inflammation and mean neutrophil activity had decreased by 1 to 3 months, and both glandular atrophy in the corpus and intestinal metaplasia in the antrum had decreased by 12 to 15 months. Glandular atrophy in the corpus improved in 34 (89%) of 38 patients with atrophy before treatment, and intestinal metaplasia in the antrum improved in 28 (61%) of 46 patients who had metaplasia at baseline. In the 48 patients in whom eradication was unsuccessful, no significant histologic changes were observed. CONCLUSION: In the year after successful H. pylori eradication, precancerous lesions improved in most patients.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1999

Cartilaginous metaplasia in the capsule of a Dacron-backed silicone gel breast prosthesis.

Capsular metaplastic changes described as "synovial metaplasia" have been reported in association with silicone gel breast prostheses. Initially this finding was thought to be more common with textured implants. Recent studies have shown no relation between implant shell type (textured vs. smooth). The incidence of this metaplasia has been shown to decrease with the age of the implant, suggesting that it is a transitional finding in capsular maturation. The metaplastic cells in the synovial metaplasia may have secretory characteristics, but the exact etiology and function of the metaplasia are not yet fully understood. Experimentally, a similar connective tissue reaction has been induced by repeated injections of air to produce the so-called "air pouch." The current study describes cartilaginous metaplasia in the capsule surrounding a silicone-filled, Cronin-type, Dacron-backed breast prosthesis. At 26 years after bilateral breast augmentation, this patient presented with breast pain and firmness. During surgical removal the implants were intact but the capsules were densely hyalinized, irregularly calcified, and on one side there was cartilaginous metaplasia within the connective tissue of the capsule. This had occurred independently of calcification. This was believed to be an unusual tissue response. Review of the English literature failed to identify a comparable case.

Breast↗
PubMed2001

[Intestinal metaplasia and Helicobacter pylori infection, their relationship and effects of eradication therapy].

Intestinal metaplasia is characterized by Goblet cells and Peneth cells in histological examination. It is frequently observed in gastric mucosa with atrophic gastritis and easily diagnosed using Methylene blue stain in endoscopy. Intestinal metaplasia is seemed to occur during the progression of atrophic gastritis. From our prospective endoscopic follow-up study over 8 years, progression of intestinal metaplasia in gastric body is observed in 44.4% out of 27 H. pylori positive patients. Progression of atrophy is also observed in 37.0% of cases. Development of intestinal metaplasia is also assured in other clinical investigations and experimental studies using Mongolian Gerbils. However, reversibility of intestinal metaplasia after H. pylori eradication is under discussion still now. In our study, we can not observe the regression of intestinal metaplasia even 2 years after successful H. pylori eradication.

Disease Progression↗
PubMedDate not supplied

Prevalence and risk factors associated with specialized intestinal metaplasia at the esophagogastric junction.

BACKGROUND/AIMS: Specialized intestinal metaplasia around the esophagogastric junction is considered to be premalignant. The aim of this study was to examine prospectively the prevalence of metaplasia and to correlate its presence with clinical, endoscopic and histological findings. METHODOLOGY: In 101 symptomatic patients (40 women, 61 men; mean age: 55 yr, range: 20-79 yr), biopsies were taken from gastric type mucosa just distal to the esophagogastric junction. They were stained with hematoxylin and eosin and alcian blue-periodic acid Schiff for the detection of specialized intestinal metaplasia and inflammation of the cardiac mucosa (carditis) and with Warthin-Starry for H. pylori presence. RESULTS: Metaplasia was detected in 27 patients (26.7%). Multiple logistic regression analysis revealed that metaplasia was associated significantly with age (odds ratio, 2.8; 95% confidence interval, 1.2-6.6), endoscopic suspicion of short segment Barrett's esophagus (odds ratio, 3.6; 95% confidence interval 2.2-6.9), detection of H. pylori (odds ratio, 2.8; 95% confidence interval, 1.1-7) and presence of carditis (odds ratio, 6.4; 95% confidence interval, 2.8-16.8). CONCLUSIONS: The prevalence of specialized intestinal metaplasia around the esophagogastric junction is high in symptomatic patients. Age, endoscopic evidence of short segment Barrett's esophagus and histological presence of H. pylori and carditis are independent risk factors associated with its presence.

Adenocarcinoma↗
PubMed2002

Intraocular osseous metaplasia. A clinico-pathological study.

PURPOSE: To evaluate the clinico-pathologic features of intraocular osseous metaplasia. METHODS: Pathology specimens of enucleated eyes submitted to the ophthalmic pathology service at a tertiary eye-care referral center between January 1995 and June 1999 were studied for intraocular osseous metaplasia. Specific histopathologic features noted in specimens with osseous metaplasia were the presence of retinal detachment, gliosis, retinal pigment epithelial hyperplasia, drusen, epiretinal membrane, fibrovascular proliferation and inflammation. Immunohistochemistry using monoclonal antibody against glial fibrillary acidic protein was performed to assess the glial component within the membranes and the proliferative vitreoretinal mass. Clinical records were reviewed and correlated with histopathologic findings. RESULTS: Osseous metaplasiaS was noted in 8 of 151 (5.2%) eyes examined. Clinical diagnosis in these was phthisis bulbi, staphyloma, absolute glaucoma and microphthalmos. Enucleation was performed for relief of symptoms (in painful blind eyes) or for cosmesis, and in an eye inciting sympathetic ophthalmia. Retinal detachment, gliosis and retinal pigment epithelial hyperplasia were noted in all the cases. Drusen with calcification or ossification (5 of 8), fibrovascular proliferation in the vitreous (5 of 8) and active inflammation (4 of 8) were the other associated histologic features. Location of ossification was subretinal in 3 cases, preretinal (ora serrata) in 1 case and in both locations in 4 cases. The eyes with subretinal osseous metaplasia had associated calcified drusen, while preretinal ossification was seen within the fibrovascular membranes. CONCLUSION: Chronic retinal detachment, hyperplasia and transdifferentiation of retinal pigment epithelium appear to be a few of the prerequisites for intraocular osseous metaplasia. Ossification can occur at isolated subretinal and preretinal locations or can involve both. Though a larger study is required to postulate the chronology of events, in this small series, isolated subretinal ossification appears to be initiated by calcification and ossification of drusen, while in the pre-retinal region it is associated with vitreoretinal proliferation.

Adolescent↗
PubMedDate not supplied

[The relationship between intestinal metaplasia and gastric carcinoma: a study of 722 biopsies].

Intestinal metaplasia has been shown by many investigators to be a premalignant state. Considering this fact, 722 gastric biopsies were studied, a 24% of association was found between gastric carcinoma and intestinal metaplasia and 27% of the cases with metaplasia were found in "apparently normal" or with benign stomach lesions. The group most affected was males over 61 years. Control endoscopy and biopsy was practiced in 17 patients with previously diagnosed intestinal metaplasia and in 11.7% gastric carcinoma with metaplasia was found. Therefore, it cannot be concluded that intestinal metaplasia is a premalignant condition, but its frequent association with gastric adenocarcinoma advises periodical examination by endoscopy in every patient over 40 years in which it is determined by biopsy.

Adenocarcinoma↗
PubMedDate not supplied

Alteration of E-cadherin expression in gastric mucosa: role of intestinal metaplasia and Helicobacter pylori infection.

BACKGROUND: Although E-cadherins have been involved in gastric carcinogenesis, their role in precancerous lesions, such as intestinal metaplasia, is still unclear. This study aimed to assess the role of both intestinal metaplasia and H. pylori infection on E-cadherin expression in gastric mucosa. PATIENTS AND METHODS: Twenty-one consecutive patients with intestinal metaplasia were enrolled to assess E-cadherin expression in metaplastic areas. Twenty further patients without intestinal metaplasia, with and without H. pylori, were enrolled to evaluate the role of the infection on E-cadherin expression. All patients underwent upper endoscopy and gastric biopsies were taken for histological and immunohistochemical assessment. RESULTS: A substantial reduction of E-cadherin expression in metaplastic areas was observed in 14 (67%) of the 21 patients, similarly in H. pylori-infected and uninfected patients (64% vs 71%, p=0.3). In the group without intestinal metaplasia, no reduction in E-cadherin expression was detected either in infected patients or in those without H. pylori infection. CONCLUSION: The data showed that intestinal metaplasia is associated with E-cadherin down-regulation, whereas H. pylori infection does not seem to play a direct role in this process.

Cadherins↗
PubMed1992

[Relationship between gastric carcinoma and enzyme spectrum activity in gastric mucosal intestinal metaplasia].

Biochemical method was adopted to examine 10 kinds of histologic enzyme spectrum activities in gastric intestinal metaplasia, carcinoma and normal or superficial gastritis mucosa taken from different sites from 17 fresh surgical specimens of stomach. The enzymes are aldolase (ALD), pyruvate kinase (PYK), phospho hexo-isomerase (PHI), lactic dehydrogenase (LDH), creatine phosphokinase (CPK), hydroxybutyrate dehydrogenase (HBD), glutamic-pyruvic transaminase (GPT), alkaline phosphatase (AKP), acid phosphatase (ACP), r-glutamyl-transpeptidase (gamma-GT). Among glycolytic enzymes the content of ALD, PYK in intestinal metaplasia were 24.5 u and 24.6 u respectively, which were higher than those in the normal mucosa (15.7, 18.0) and lower than carcinoma (28.4, 29.6) (P less than 0.01-0.05). The content of CPK in intestinal metaplasia was lower (218.5 u) than that in the normal (463.9 u) and higher than that in carcinoma (110.3 u) (P less than 0.01). Among protease and amino acid enzymes the content of HBD in intestinal metaplasia was lower (108.2 u) than those in the normal (221.3 u) and carcinoma (113.9 u) (P less than 0.05). The content of GPT in intestinal metaplasia was (6.7 u) which was lower than that in the normal (9.4 u) and higher than that in carcinoma (3.7 u) (P less than 0.01). The above results could provide reference indices for judging the potential malignancy of gastric intestinal metaplasia.

Epithelium↗
PubMed1991

Human papillomavirus type 31 DNA detected in part of the dysplasia but in no part of the squamous metaplasia in a specimen taken from one patient.

Using in situ hybridization, human papillomavirus (HPV 6, 16, 18, 31, 33) DNAs were detected in a cervical severe dysplasia accompanied by squamous metaplasia. It was found that, only HPV 31 DNA was harbored in the cervical severe dysplasia, but HPV DNAs were not identified in a lesion of squamous metaplasia. The in situ hybridization method will be of use, therefore, when dysplasia with squamous metaplasia or other lesions are examined for HPV DNA. In a cervical smear, HPV 31 DNA could be detected on the nuclei of dysplastic cells, so this method is applicable to cervical smears. If squamous metaplasia is to be considered as a precursor lesion to cervical dysplasia, the HPV DNA harbored in the dysplasia must also be detected in the accompanying squamous metaplasia. Our results suggested that not all squamous metaplasias were involved with HPV, as far as we were able to detect using five types of HPV DNA probe.

Adult↗
PubMed1986

Extensive squamous metaplasia in gynecomastia.

Extensive squamous metaplasia is described in a case of gynecomastia. Numerous ducts in all sections of breast tissue revealed multiple foci of squamous metaplasia, many of which included large, papillary excrescences of keratinizing squamous cells into duct lumens, with foci of dyskeratosis. Review of four years of gynecomastia cases from our surgical pathology files revealed a total incidence of squamous metaplasia equaling six of 40 cases of gynecomastia, including the case reported here. The other five cases included only one or two small foci of squamous metaplasia. These findings demonstrate that squamous metaplasia in gynecomastia is not rare, but is usually very limited. However, an unusual case, such as that reported here, may show extensive, florid squamous metaplasia, without associated inflammation or neoplasm.

Adult↗
PubMed1989

Estrogens induce malpighian metaplasia of the endocervical junction in female rats immunohistochemistry study.

Immature female Wistar rats were treated with 1 mg of estradiol benzoate for 6 days. The injections were started on the 20th day of age; the animals were autopsied every 3 days after the last injection until the age of 45 days. Islets of hyperplastic cells and metaplasia area were seen in the endocervix in the majority of the animals autopsied. We have the expression of cytokeratin polypeptides in reserve cells, in areas exhibiting reserve cell hyperplasia and squamous metaplasia, using a panel of monoclonal cytokeratin antibodies. The reserve cells were positive for antibodies directed against stratified squamous epithelia, type cytokeratins No. 5, 13 and 17. In addition, hyperplastic cells revealed the presence of cytokeratins No. 7, 8, 18 and 19, specific for simple epithelia, but in a variable manner. The Squamous metaplasia cells exhibited cytokeratins No. 13, 18 and 19, but only weakly reactive. Our observations indicate that estrogen-induced endocervix metaplasia results from a transformation of reserve cells towards an epidermoid type epithelium. Hyperplasia would be the intermediate step in the mechanism of induced cervical metaplasia. This transformation is accompanied by the loss of cytoplasmic keratin proteins and the acquisition of new high molecular weight keratin proteins, specific for stratified squamous epithelia. The basal or reserve cells of the cervix can proliferate to produce regions of squamous cell metaplasia. It appears to be a direct effect of estrogen stimulation. Immunohistochemical staining for different molecular weight keratin proteins may be helpful in the evaluation of reserve cell differentiation.

Animals↗