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PubMed2006

Gastric inflammation, metaplasia, and tumor development in gastrin-deficient mice.

BACKGROUND & AIMS: Gastrin deficiency and proton pump inhibitor treatment cause achlorhydria, which predisposes to disease. To elucidate the underlying molecular biology, we examined the changes in gastric gene expression in both types of achlorhydria. We also explored the associated changes in the gastric microflora and the long-term consequences of gastrin-deficient achlorhydria. METHODS: Expression profiles were generated from gastric RNA from wild-type mice, gastrin knockout (KO) mice, gastrin KO mice after 1 week of gastrin infusion, and wild-type mice treated for 1 month with a proton pump inhibitor. The results were confirmed using real-time polymerase chain reaction and immunohistochemistry. Selective media were used to characterize the gastric microflora. RESULTS: The number of gastric bacteria was increased in both gastrin KO and PPI-treated mice. The expression profiles revealed activation of immune defense genes, interferon-regulated response genes, and intestinal metaplasia of the gastric mucosa. In young gastrin-deficient mice, gastrin infusions reversed the changes. Over time, the changes accumulated, became irreversible, and progressed into metaplasia and polyp development. Finally, the study showed that gastrin regulated the expression of genes encoding extracellular matrix proteins. CONCLUSIONS: Independently of gastrin, achlorhydria is associated with gastric bacterial overgrowth and intestinal gene expression patterns and is associated with predisposition to disease. Gastrin is therefore essential for prevention of gastric disease, mainly through control of acid secretion but to a lesser extent also through control of gastric gene expression. The gastrin-deficient mouse serves as a useful new model for gastric metaplasia and neoplasia.

Animals↗
PubMedDate not supplied

Osseous metaplasia in plantar fibromatosis: a case report.

A case report about extensive osseous metaplasia of a plantar fibromatosis is presented. The authors are unaware of previous reports in the literature describing osseous metaplasia within plantar fibromatosis in this manner. This case shows that plantar fibromatosis may undergo osseous metaplasia in a fashion similar to fibromatous lesions elsewhere.

Bone and Bones↗
PubMed1980

Application of the methylene blue staining method to the study of experimentally PNNG-induced intestinal metaplasia of the canine stomach.

To elucidate the developmental process of the intestinal metaplasia of the stomach, PNNG was orally administered to dogs and the sequential endoscopic examination was performed by using the methylene blue staining method. In the early period of the drug administration dogs showed the findings of erosive gastritis at the antral portion. In the 42nd experimental week, a clearly stained lesion was observed at the gastric angle. The histological findings of the biopsy specimens from the stained lesion showed the elongation of the foveolar epithelium and goblet cell-like mucous cells. Apparently stained lesion was observed at the antral portion in the 128th week. The close-up endoscopic appearance was very similar to that of stained intestinal metaplasia seen in the human stomach. The endoscopic methylene blue staining method as performed in the experimental dogs could provide useful results in the observation of minute lesions especially intestinal metaplasia in human stomach. This experiment, and further studies, may help to elucidate the pathogenesis of the gastric carcinoma in humans.

Animals↗
PubMed2000

Suplatast tosilate inhibits goblet-cell metaplasia of airway epithelium in sensitized mice.

BACKGROUND: IL-4 and IL-13 play a putative role in mucus hypersecretion in asthma. Suplatast tosilate prevents the synthesis of T(H2) cytokines. OBJECTIVE: Because suplatast tosilate inhibits T(H2) cytokines but does not inhibits IFN-gamma production, we examined the effect of suplatast on IL-4- or IL-13- and ovalbumin (OVA)-induced mucin synthesis in NCI-H292 cells in vitro and in bronchi of pathogen-free BALB/c mice in vivo. METHODS: In vitro, NCI-H292 cells were preincubated with suplatast tosilate (0.1-100 microgram/mL) 1 hour before adding human recombinant IL-4 (10 ng/mL). In vivo, mouse recombinant IL-4 or IL-13 (250 ng per/mouse) was instilled intranasally in mice pretreated with suplatast tosilate (50 mg.kg(-1).d(-1)). Mucous glycoconjugates were stained with Alcian blue (AB)/periodic acid-Schiff (PAS) stain. To evaluate effects of suplatast tosilate on goblet-cell metaplasia in OVA-sensitized mice, animals were pretreated with suplatast tosilate (1-50 mg.kg(-1).d(-1)) intragastrically. IL-4 and IL-13 were measured, and allergic inflammatory cells were analyzed in bronchoalveolar lavage fluid of OVA-sensitized mice. RESULTS: Pretreatment with suplastast did not prevent IL-4- or IL-13-induced increase in mucous glycoconjugate production in NCI-H292 cells or in mice. OVA sensitization increased AB/PAS-stained area of the epithelium (48.1% +/- 2.4%, P <.01 compared with control mice). Suplatast tosilate inhibited OVA-induced goblet-cell metaplasia in airway epithelium in a dose-dependent fashion; 50 mg.kg(-1).d(-1) decreased the AB/PAS area to 22.7% +/- 2.7% (P <.05 compared with OVA sensitization alone). Pretreatment with suplatast tosilate also prevented OVA-induced increase in IL-4 and IL-13 levels and decreased the number of lymphocytes and eosinophils in bronchoalveolar lavage fluid (P <.05 compared with values of mice given OVA alone). CONCLUSION: These results indicate that suplatast tosilate prevents allergen-induced goblet-cell metaplasia and the recruitment of eosinophils and lymphocytes into the airways. These results suggest that this effect is due to the prevention of the production of T(H2) cytokines in airways.

Animals↗
PubMed2001

Concurrent tubulovillous adenoma and transitional cell carcinoma associated with diffuse gastric and intestinal metaplasia of the defunctioned ureter.

Villous adenoma is a common lesion of the gastrointestinal tract, but it is rare in the ureter. Thus, as far as we know, only one case limited to this location has been described. Intestinal metaplasia of the urothelium is not rare. However, only one case of gastric metaplasia with pseudopyloric glands has been described in the literature. We here report in detail on a tubulovillous adenoma of the ureter associated with diffuse gastric and intestinal metaplasia and a concurrent primary, solid, high grade transitional cell carcinoma, with extensive clear cell change, in a 56-year-old male patient. He had undergone a left nephrectomy for renal tuberculosis twenty years earlier, and the lesions developed in the ureteric stump. To the best of our knowledge, such a combination of lesions has not been reported previously either in the ureter or in the rest of the urinary tract. The coexistence of diverse lesions in our case might represent the pluripotentiality of the urothelium in association with chronic inflammation and neoplastic induction. The present report also emphasizes the metaplastic and malignant potential of a defunctioned urothelial structure. This case is of particular interest, because these coexistent lesions arose simultaneously with an anatomically separate adenocarcinoma of the rectum (Dukes' B). The patient died 76 days after admission. The dismal prognosis of our case was determined by the advanced anatomical stage and the histological high grade of the transitional cell carcinoma of the ureter.

Adenoma, Villous↗
PubMed2001

Loss of E-cadherin expression in gastric intestinal metaplasia and later stage p53 altered expression in gastric carcinogenesis.

Gastric cancers are commonly subdivided into intestinal and diffuse subtypes on a morphologic basis, supported by corollary evidence of differences at the pathogenetic and molecular levels. Chronic atrophic gastritis with intestinal metaplasia is a common precursor lesion for the intestinal type of carcinoma. To identify early molecular changes, in this study we have examined 13 surgical specimens both for the expression of E-cadherin, p53 and beta-catenin by immunohistochemistry and for methylation of the CDH1 promoter (E-cadherin) by bisulfite genomic sequencing of laser capture microdissected samples. Each specimen examined contained areas of normal (nonmetaplastic) gastric mucosa, as well as areas of intestinal metaplasia and/or carcinoma. Reduced or absent E-cadherin and partial to complete methylation of one to multiple CpG sites examined in the CDH1 promoter were observed in all of the metaplasia samples. Thus, the methylation status of the CDH1 promoter and expression of E-cadherin together provide strong evidence that loss of E-cadherin is an early event in intestinal type gastric carcinogenesis. In contrast, expression of p53, assumed to be mutant p53, was generally not detected (except for isolated cells) until the carcinoma stage in tissues from these patients. These results suggest that mutation of p53 is a late event in intestinal type gastric cancer. The level of beta-catenin expression did not appear to change between normal, metaplastic and carcinoma cells of intestinal type, and no nuclear staining was visible in any of the tissues. These results suggest that the Wnt signaling pathway is not upregulated in this type of cancer.

Adenocarcinoma↗
PubMed2003

Is subtyping of intestinal metaplasia in the upper gastrointestinal tract a worthwhile exercise? An evaluation of current mucin histochemical stains.

Intestinal metaplasia is a premalignant condition that occurs in the upper gastrointestinal tract and can be subdivided into three types (I, II and III). Previous studies suggest that type III carries the highest cancer risk. The high iron diamine/alcian blue (HID/AB) technique traditionally has been used to identify this subtype; however, the technique uses reagents that are toxic and potentially carcinogenic. Therefore, in this study we evaluate various alternative histochemical techniques. Our results indicated that the only suitable alternative is Gomori's aldehyde fuchsin/AB technique. The study also revealed that subtyping of intestinal metaplasia is a subjective procedure, open to varying interpretation. Consequently, we suggest that previous work linking cancer risk to metaplasia subtypes should be viewed with some circumspection.

Barrett Esophagus↗
PubMed1995

Tubal and tubo-endometrioid metaplasia of the uterine cervix. Unemphasized features that may cause problems in differential diagnosis: a report of 25 cases.

Twenty-five cases of tubal or tubo-endometrioid metaplasia that occurred in patients from 21 to 51 years of age (mean 39 years) are described. The majority of the cases were seen in consultation. They were referred because of diagnostic problems resulting from features that have received little emphasis. The metaplasia was typically an incidental microscopic finding, although in one case metaplastic cystic glands resulted in a gross abnormality. The involved glands were usually confined to the superficial third of the cervical wall. However, in seven cases they extended more deeply. In three cases, the outer third of the wall was involved. The involved glands showed only slight variation in size and shape in 12 of the cases, but in the remainder some branching was present. Prominent cystic dilatation of the glands was seen in nine cases. The glands were typically evenly spaced, but in four cases they were focally crowded. In 22 cases, the stroma surrounding the metaplastic glands was abnormal. In 16 cases, it consisted of hypercellular endocervical stroma, and in five of these cases, the cellularity was pronounced. Four of these cases and six others focally had a loose edematous or myxoid stroma, which was pronounced in three cases. In addition to the diagnostic problems inherently associated with tubal and tubo-endometrioid metaplasia, the findings in this study, including deep glands, irregularity of gland size and shape (including cystic glands), and periglandular stromal alterations, often raised the suspicion of a premalignant or malignant glandular abnormality. Awareness that these features may be seen, as well as the often prominent ciliation of the cells, their bland cytologic features, their mitotic inactivity, and lack of an unequivocal desmoplastic stromal reaction, facilitate the differential diagnosis.

Adult↗
PubMed1986

Carcinogenicity and mutagenicity of chromium compounds: the association between bronchial metaplasia and neoplasia.

Over the last 40 years, experiments with animals and epidemiology of exposed human populations have established that certain hexavalent chromium-containing compounds are capable of causing cancer whilst trivalent materials are not. More recently, a variety of short-term genotoxicity tests (predictive of carcinogenicity) have clearly demonstrated that Cr[VI] is genotoxic per se, and that all Cr[VI]-containing materials which have been tested are genotoxic. What experiments have failed to demonstrate clearly, however, is which of the myriad of industrially available hexavalent materials are carcinogenic and which are not. In this long-term study we have looked at the incidence of squamous metaplasia in the bronchial epithelium of rats exposed to a range of chromium-containing materials by intrabronchial implantation. Squamous metaplasia is generally considered to be a transformed state from which squamous carcinoma may arise. We have shown that its incidence is increased in all groups exposed to Cr[VI]-materials, and in rats exposed to the reference carcinogen 20-methylcholanthrene. Squamous metaplasia was not increased in rats exposed to Cr[III] materials. Of rats exposed to Cr[VI], only those receiving materials of sparing aqueous solubility developed bronchial squamous carcinoma at statistically significant levels. These results strongly support the hypothesis that although Cr[VI] per se is biologically active, producing genotoxic effects and pathological changes which may predispose to the development of cancer, only Cr[VI] materials of sparing aqueous solubility seem to be capable of evoking a carcinogenic response.

Animals↗
PubMed2004

Modulation of notch processing by gamma-secretase inhibitors causes intestinal goblet cell metaplasia and induction of genes known to specify gut secretory lineage differentiation.

It is anticipated that gamma-secretase inhibitors (gamma-Sec-I) that modulate Notch processing will alter differentiation in tissues whose architecture is governed by Notch signaling. To explore this hypothesis, Han Wistar rats were dosed for up to 5 days with 10-100 micromol/kg b.i.d. gamma-Sec-I from three chemical series that inhibit Notch processing in vitro at various potencies (Notch IC(50)). These included an arylsulfonamide (AS) (142 nM), a dibenzazepine (DBZ) (1.7 nM), and a benzodiazepine (BZ) (2.2 nM). The DBZ and BZ caused dose-dependent intestinal goblet cell metaplasia. In contrast, the AS produced no detectable in vivo toxicity, despite higher exposure to free drug. In a time course using BZ, small intestinal crypt cell and large intestinal glandular cell epithelial apoptosis was observed on days 1-5, followed by goblet cell metaplasia on days 2-5 and crypt epithelial and glandular epithelial regenerative hyperplasia on days 4-5. Gene expression profiling of duodenal samples from BZ-dosed animals revealed significant time-dependent deregulation of mRNAs for various panendocrine, hormonal, and transcription factor genes. Somatostatin, secretin, mucin, CCK, and gastrin mRNAs were elevated twofold or more by day 2, and a number of candidate "early-predictive" genes were altered on days 1-2, remaining changed for 4-5 days; these included Delta1, NeuroD, Hes1-regulated adipsin, and the Hes-regulated transcriptional activator of gut secretory lineage differentiation, the rat homolog of Drosophila atonal, Rath1. Western blotting of fecal protein from BZ-and DBZ-dosed animals exhibited increased levels of both anti-Rath1 reactive protein and anti-adipsin reactive proteins, confirming their potential value as noninvasive biomarkers of intestinal goblet metaplasia.

Amyloid Precursor Protein Secretases↗
PubMed1982

Morular metaplasia misdiagnosed as adenoacanthoma in young women with polycystic ovarian disease.

Five cases of polycystic disease of the ovaries are presented; in four diagnosis of "adenoacanthoma" was made from an endometrial biopsy. The age range was 24-37. The fifth had been called "atypical glandular hyperplasia." In four of the five salpingoophorectomy and hysterectomy were performed, and the hysterectomy specimens showed no evidence of hyperplasia or carcinoma. Consultation review of the slides revealed "morular" metaplasia as well as tubal metaplasia. In one case, mucinous metaplasia was also present. Morule formation may distend glands and compress surrounding uninvolved endometrium, resulting in a pattern of back-to-back glands, that are, however, often lined by a single layer of columnar epithelium and should not be confused with back-to-back glands seen in adenomatous hyperplasia or adenocarcinoma. In both these conditions, the epithelium is stratified and shows nuclear atypism. Morules, especially when they coalesce, can be misconstrued as adenoacanthoma; however, the cells are uniform and bland in appearance.

Adenocarcinoma↗
PubMed1995

Pancreatic metaplasia in Barrett's esophagus. An immunohistochemical study.

While pancreatic metaplasia has been observed in gastric mucosa of patients with chronic gastritis, it has not been described in ectopic gastric mucosa. We have identified focal clusters of cells resembling pancreatic acinar cells (CPACs) in 11 of 350 biopsies of Barrett's mucosa from 120 patients with Barrett's esophagus enrolled in a clinical efficacy trial of omeprazole versus ranitidine for treatment of gastroesophageal reflux disease. Three additional cases from our surgical files were also studied. Immunoreactivity for trypsin and chymotrypsin was present in the CPACs of all 14 cases, while stains for alpha-amylase and lipase were each positive in 12 of 13. A few cells in the CPACs were also positive for chomogranins (12 of 13 cases), serotonin (seven of 13 cases), somatostatin (three of 12), gastrin (four of 11), and pancreatic polypeptide (two of 13). No staining was seen for insulin or glucagon. Ultrastructural studies performed in one case showed features of pancreatic exocrine and endocrine (PP-type) cells in cells within CPACs. These results collectively indicate that the CPACs are aggregates of true pancreatic acinar cells admixed with a few endocrine cells. This pancreatic parenchyma in Barrett's mucosa is most likely of metaplastic origin and could be derived from the transitional zone cells or from pluripotent stem cells in the esophageal mucosa or from metaplasia of mucus cells. While the development of pancreatic metaplasia in Barrett's esophagus appears to be unrelated to drug therapy, the clinical relevance of this distinctive histological finding needs further investigation.

Adolescent↗
PubMed2001

Simple and complex hyperplastic papillary proliferations of the endometrium: a clinicopathologic study of nine cases of apparently localized papillary lesions with fibrovascular stromal cores and epithelial metaplasia.

The clinicopathologic features of nine cases of papillary proliferation of the endometrium devoid of malignant nuclear features were studied. The patients ranged in age from 33 to 71 years (median 57 years). All were postmenopausal, except the youngest. The most common symptom was postmenopausal bleeding. Two patients were receiving hormonal replacement therapy and two were taking megestrol acetate. Two lesions were incidental findings in a hysterectomy specimen. Seven were diagnosed in endometrial biopsy or curettage specimens. In six cases (67%) the lesion involved an endometrial polyp. In all cases the papillae had fibrovascular stromal cores and variable degrees of branching. Two architectural patterns were found. A simple papillary pattern with involvement of only a few glands and little epithelial proliferation occurred in five cases, including three that were entirely intracystic. A complex papillary pattern with more extensive involvement of endometrial glands, a greater degree of branching of the papillae, and cellular tufting occurred in four cases. One or more metaplastic epithelial changes occurred in all cases, including endocervical-type mucinous metaplasia in nine cases (90%), eosinophilic cell change in eight (89%), ciliated cell change in seven (70%), focal squamous metaplasia in two cases (22%), and hobnail cell change in two (22%). Mitotic figures were found in three cases. In four lesions (44%), all with a complex papillary pattern, the proliferating cells had mild nuclear atypia. Three of these patients underwent hysterectomy within 5 months. Simple nonpapillary hyperplasia and two endometrial polyps were found in one patient, complex nonpapillary hyperplasia in one, and atrophic endometrium in the other. Two patients had additional endometrial samplings within 4 months that contained small residual simple papillary lesions. One of these had another biopsy at 16 months that showed only atrophy. One patient had no subsequent diagnostic or therapeutic procedures. One patient was a recent case. Of the three patients with intact uteri and appreciable follow-up, all were alive and well at 14, 96, and 102 months, respectively. We conclude that these papillary proliferations are a form of hyperplasia that is closely associated with endometrial epithelial metaplasia. Polypectomy and/or curettage may be effective in removing them because they often are localized lesions. Although all of our patients had an uneventful outcome, the number of cases is small. Our findings question the validity of diagnosing endometrial lesions as well-differentiated carcinoma solely because of a complex papillary architectural pattern.

Adult↗
PubMed2001

Intestinal metaplasia in patients with columnar lined esophagus is associated with high levels of duodenogastroesophageal reflux.

OBJECTIVE: To evaluate the rate of duodenogastroesophageal reflux in patients with columnar lined esophagus compared with patients with gastroesophageal reflux disease without columnar lined esophagus, and to analyze whether it is related to the presence of specialized columnar epithelium in the metaplastic segment. SUMMARY BACKGROUND DATA: The carcinomatous degeneration of columnar lined esophagus originates from a specialized columnar epithelium. The appearance of this metaplastic phenomenon is clearly related to severe prolonged gastroesophageal reflux, but only some of these patients finally develop columnar lined esophagus. For this reason other factors have been suggested, particularly the role played by the reflux of duodenal contents into the esophagus. METHODS: The authors studied 15 healthy volunteers (control group), 10 patients with reflux symptoms but without endoscopic lesions, 20 patients with reflux esophagitis without columnar lined esophagus, and 35 patients with columnar lined esophagus (complicated with ulcers or stenosis in 8 cases), of whom 22 had intestinal metaplasia. To assess the reflux of duodenal contents into the esophagus, all the patients underwent Bilitec 2000 and 24-hour esophageal pH monitoring. RESULTS: The presence of bilirubin in the material refluxed into the esophagus was greater in the patients with columnar lined esophagus than in the rest of the groups. Likewise, duodenogastroesophageal reflux was greater in the columnar lined esophagus patients who had intestinal metaplasia. CONCLUSIONS: Duodenogastroesophageal reflux may play a major role in the development of columnar lined esophagus, especially in patients with intestinal metaplasia.

Adult↗
PubMed2001

Efficacy of medical therapy and antireflux surgery to prevent Barrett's metaplasia in patients with gastroesophageal reflux disease.

OBJECTIVE: To investigate whether Barrett's metaplasia may develop despite effective medical therapy. SUMMARY BACKGROUND DATA: Gastroesophageal reflux disease has a multifactorial etiology. Therefore, medical treatment may not prevent complications of reflux disease. METHODS: Eighty-three patients with reflux disease and mild esophagitis were prospectively studied for the development of Barrett's metaplasia while receiving long-term therapy with proton pump inhibitors and cisapride. Only patients who had effective control of reflux symptoms and esophagitis were included. The surveillance time was 2 years. The outcome of these 83 patients was compared with that of 42 patients in whom antireflux surgery was performed with a median follow-up of 3.5 years. RESULTS: Twelve (14.5%) patients developed Barrett's while receiving medical therapy; this was not seen after surgery. Patients developing Barrett's had a weaker lower esophageal sphincter and peristalsis before treatment than patients with uncomplicated disease. CONCLUSIONS: Antireflux surgery is superior to medical therapy in the prevention of Barrett's metaplasia. Therefore, patients with reflux disease who have a weak lower esophageal sphincter and poor esophageal peristalsis should undergo antireflux surgery, even if they have only mild esophagitis.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1983

Decidua and squamous metaplasia in abdominopelvic lymph nodes.

We describe two variants of benign para-aortic lymph nodal inclusions that mimic squamous cell carcinoma. The first, a decidual reaction, occurred in a 27-year-old pregnant woman with squamous cell carcinoma of the cervix. The second, a squamous metaplasia of ectopic müllerian-type glands, was present in a 63-year-old woman with squamous cell carcinoma of the anus. Intranodal decidua has been described, but squamous metaplasia of glandular inclusions has not been previously reported. Müllerian-type nodal inclusions are reviewed, and histologic features distinguishing decidua and squamous metaplasia from carcinoma are discussed.

Abdomen↗
PubMed1999

Immunophenotype of transitional metaplasia of the uterine cervix.

Transitional, glandular, and squamous epithelia show distinctive patterns of expression of cytokeratins 13, 17, 18, and 20. Furthermore, some markers, such as cytokeratin (CK) 20 and the asymmetric unit membrane, are related to terminal urothelial differentiation, their expression limited to superficial and occasional intermediate cells. In this study, seven cases fulfilling the morphologic criteria of transitional metaplasia of the uterine cervix were investigated with these markers to determine whether there was evidence of true urothelial-type differentiation in these lesions. Results were consistent and showed clear differences between the squamous, glandular, and metaplastic transitional areas of the cervix. In particular, the expression of CK13, CK17, and CK18 in the metaplastic areas was identical to the pattern observed in normal urothelium. However, full urothelial differentiation was not observed, as CK20 and asymmetric unit membrane were never expressed in the transitional metaplasia. Based on these findings, the term of immature transitional metaplasia would be a more accurate description of this entity.

Aged↗
PubMed1993

Is gastric metaplasia essential for duodenal ulcer?

Multiple biopsies were taken from the duodenum of 100 patients (46 active duodenal ulcer, 14 healed duodenal ulcer, 40 control subjects) to detect duodenitis, gastric metaplasia and Helicobacter pylori (Hp). Histamine-induced congo-red staining of the duodenal bulb was performed in additional 25 cases of active duodenal ulcer to determine the presence of functioning parietal cells in the duodenum. The incidence of duodenitis was 45% in control subjects and 76.7% in patients with duodenal ulcer (active or healed) (p < 0.01). Superficial gastric metaplasia was present in 2.5% of control subjects and 13.3% patients with duodenal ulcer (active or healed) (p > 0.05). Hp in the duodenum was detected in 10% of control subjects and 8.3% of patients with duodenal ulcer. Congo-red test was positive in two of 25 (8%) patients of active duodenal ulcer indicating "functioning" parietal cells in the duodenum. In Indian patients with duodenal ulcer, a low incidence of gastric metaplasia and Hp in the duodenum is observed in contrast to its high incidence in patients from Western countries.

Adult↗