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 127 records · Page 7Linked to original sources

Inverse relation of serum Helicobacter pylori antibody titres and extent of intestinal metaplasia.

AIMS: To clarify the relation between the serum titre of anti-Helicobacter pylori (H pylori) antibody and the extent of intestinal metaplasia of the gastric mucosa. METHODS: The serum anti-H pylori IgG titres of 95 asymptomatic individuals (mean age 65 years) undergoing an annual health examination were measured and compared with the extent of intestinal metaplasia (absent, moderate, or extensive), determined by examination of multiple endoscopic mucosal biopsy specimens. Serum pepsinogen I (PGI) levels, as a marker for gastric atrophy, were also measured. RESULTS: The prevalence of seropositivity for H pylori antibody was high (> 80%), regardless of the extent of metaplasia. However, there was a negative association between the extent of metaplasia and the anti-H pylori titre: 75% of the subjects in the group without metaplasia had high (3+) antibody levels, as did 43% with moderate, and 37% with extensive metaplasia (absent v extensive). The inverse relation between the titre and the extent of metaplasia was evident when examined in those with normal PGI (> 30 ng/ml), whereas no such relation was apparent in subjects with low PGI (< or = 30 ng/ml). CONCLUSIONS: The anti-H pylori titre correlates inversely with the extent of intestinal metaplasia, particularly in subjects with less marked gastric atrophy.

Aged↗

Squamous metaplasia induced by transfection of human papillomavirus DNA into cultured adenocarcinoma cells.

BACKGROUND/AIM: It has been reported previously in cases of adenosquamous carcinoma of the lung in Okinawa, a subtropical island 2000 km south of mainland Japan, that the squamous cell carcinoma components were positive for human papillomavirus (HPV) by non-isotopic in situ hybridisation (NISH). The adenocarcinoma cells adjacent to the squamous cell carcinoma components were enlarged and also positive for HPV. This is thought to indicate that after adenocarcinoma cells are infected with HPV, they undergo morphological changes, and that "squamous metaplasia" follows. In this present study, the effects of HPV transfection into adenocarcinoma cells were examined. The relation between the region expressing the HPV gene and squamous metaplasia was also studied. METHODS: Plasmid pBR322 containing HPV type 16 (HPV-16) was transfected into cultured colonic adenocarcinoma (DLD-1) and lung adenocarcinoma (PC-14) cells using the calcium phosphate method. Neomycin was used as a selection marker. The presence of HPV E1, E2, E4, E5, E6, E7, L1, and L2 mRNAs and also transglutaminase 1, involucrin, cyclin dependent kinases (CDKs), cyclins, caspases, apoptosis inducing factor, DNase gamma, Fas, and Fas ligand mRNAs in HPV transfected cells was investigated by means of reverse transcription polymerase chain reaction (RT-PCR). The G0-G1 cell population was analysed by flow cytometry. Morphological examination under light and electron microscopes was also carried out. RESULTS: The virus transfected cells showed squamous metaplasia when they were injected into severe combined immunodeficient mice, expressing the high molecular weight keratin (Moll's number 1 keratin) and involucrin molecules immunohistochemically, and involucrin and transglutaminase I mRNAs by RT-PCR. The squamous metaplasia was most conspicuous in the HPV transfected DLD-1 cell when compared with HPV transfected PC-14 cells. Squamous metaplasia was most clearly demonstrated in one HPV transfected DLD-1 cell clone, which expressed not only E2 but also E6-E7 fusion gene mRNA. Viral L1 mRNA expression was absent in HPV transfected cell clones, and was not related to squamous metaplasia. The growth rate of HPV transfected cells was reduced. Transfection of the virus into the cultured adenocarcinoma cells increased the G0-G1 cell population greatly, as assessed by flow cytometer analysis. Furthermore, in the virus transfected cells, apoptosis was also observed by means of the terminal deoxynucleotidyl transferase mediated dUTP biotin nick end labelling method. CONCLUSION: HPV transfection into adenocarcinoma cells induced clear squamous metaplasia. One of the HPV transfected cell clones that expressed E2 and E6-E7 fusion gene mRNA showed the squamous metaplasia particularly clearly, and apoptosis was also demonstrated.

Adenocarcinoma↗

Risk factors associated with the development of intestinal metaplasia in first-degree relatives of gastric cancer patients.

Family relatives of gastric cancer patients have a higher risk of gastric cancer and premalignant gastric lesions. We sought to determine the risk factors associated with the presence of intestinal metaplasia in a large cohort of gastric cancer relatives. First-degree relatives of gastric cancer patients were invited for screening gastroscopy. Endoscopic gastric biopsies were obtained from the antrum and corpus. Gastric biopsies were analyzed for Helicobacter pylori infection, severity of inflammation, and presence of intestinal metaplasia. Stepwise logistic regressions were used to identify for risk factors associated with presence of intestinal metaplasia in cancer relatives. Two hundred seventy cancer relatives underwent screening endoscopy (median age, 42; 47% male and 48% siblings). Among them, 161 (59.6%) were H. pylori positive and 81 (30%) had confirmed intestinal metaplasia. The following factors were found to be associated with the presence of intestinal metaplasia: age, male sex, H. pylori infection, birth order, alcohol use, siblings with stomach cancer, childhood living conditions, and water supply. Individuals with intestinal metaplasia had more severe acute and chronic inflammation in the antrum and corpus (P < 0.003). With multiple logistic regression, H. pylori infection [odds ratio (OR), 3.23], male gender (OR, 2.09), age (OR, 1.07), and a history of gastric cancer in siblings (OR, 1.91) were independent factors associated with the development of intestinal metaplasia in cancer relatives. In conclusion, we have identified risk factors associated with gastric intestinal metaplasia in stomach cancer relatives, which may be useful in the understanding of gastric carcinogenesis in these high-risk individuals.

Adenocarcinoma↗

Association between acute inflammatory cells in lavage fluid and bronchial metaplasia.

In epidemiologic studies, airway disease and parenchymal injury are known morbid outcomes of occupational exposure to asbestos. However, the relationship of inflammatory events considered to be responsible for parenchymal injury to the subsequent development of airway injury is unknown. To assess this we performed bronchoalveolar lavage (BAL) and airway biopsies on a population of subjects with exposure to asbestos in the workplace. As an index of airway injury, we employed histologic metaplasia seen in mucosal biopsy specimens. Lung BAL fluid was analyzed for two potentially relevant protein markers and for inflammatory cells recovered from the lower respiratory tract. We related metaplasia to demographic features of this study population (eg, smoking history and asbestos exposure data) and also to the protein and cellular markers recovered by BAL. We studied 50 workers and detected keratinizing metaplasia in 15 and varying lesser abnormalities in the other 28. Cigarette smoking was not associated with the presence of metaplasia (p less than 0.2). Smoking status was associated with an increase in BAL cells (p less than 0.02); however, neither the percent nor concentration of acute inflammatory cells was significantly increased. Acute inflammatory cells (percent and cells per milliliter of BAL fluid) were significantly increased among the subjects with severe metaplasia compared with other study subjects. This increase was true of both neutrophils and eosinophils and the sum of these two (p less than 0.02). Stratification of subjects by smoking status demonstrated a persistent association of inflammatory cells with metaplasia. By logistic regression analysis, polymorphonuclear leukocytes per milliliter and eosinophils per milliliter were significantly related to the presence of metaplasia in two independent models (odds ratios, 9.9 and 7.6, respectively). Cigarette smoking and other demographic or BAL variables were not significantly associated with metaplasia in these models.

Asbestosis↗

Squamous metaplasia of the bronchial mucosa and its relationship to smoking.

We performed flexible fiberoptic bronchoscopy (FFB) on 106 heavy cigarette smokers. Six bronchial biopsy specimens, obtained from the carina and five major bronchi, were screened for squamous metaplasia. Individual biopsy specimens were sectioned into 4-microns sections, and a metaplasia index (MI), or percentage of sections containing squamous metaplasia, was determined. Metaplasia was noted at one or more biopsy sites in 66 of 99 subjects (seven were excluded from the analysis). Twenty-five percent of the subjects showed metaplasia at three or more biopsy sites, and one subject had metaplasia on all six biopsy specimens. The presence of squamous metaplasia varied from 40.4 percent in the right lower lobe to 15.3 percent in the left upper lobe. The subjects were grouped into simple categories based on the number of packs smoked per day and the pack-year history of smoking. Subjects who smoked more than two packs per day (n = 11) had the highest MI (37.4 +/- 4.9 percent, mean +/- SEM). Fifty-seven subjects smoked more than one pack per day but fewer than or equal to two packs per day, and they had a mean MI of 22.3 +/- 2.9 percent. Subjects who smoked one pack per day or less (n = 31) had a mean MI of only 12.9 +/- 2.8 percent. The MI of those who smoked more than two packs per day was significantly greater than the MI of those who smoked one pack per day or less (p < or = 0.003). While the MI varied from 12.9 +/- 3.5 percent in subjects who had smoked less than 20 pack-years to a maximum of 29.1 +/- 4.5 percent in those who had smoked greater than 60 pack-years, no statistically significant difference was detected between these two groups. Thus, we conclude that heavy tobacco use is associated with important alterations of bronchial mucosa. Furthermore, the intensity of tobacco use (packs per day) rather than the number of pack-years appears to be the more important factor in promoting squamous metaplasia of the bronchial mucosa.

Adult↗

[Specialized intestinal metaplasia of the distal esophagus in gastroesophageal reflux disease: prevalence and clinico-demographic features].

BACKGROUND: Specialized intestinal metaplasia can be categorized according endoscopic and histological findings in long segment Barrett, short segment Barrett and specialized intestinal metaplasia of cardia. Barrett's esophagus is an acquired disease that is found in about 10%-13% of patients undergoing endoscopy for symptoms of gastroesophageal reflux disease and it is well established as predisposing to esophageal adenocarcinoma. The columnar epithelium with goblet cells replaces the normal squamous epithelium. OBJECTIVE: To determine the prevalence and clinical-demographic characteristics of specialized intestinal metaplasia of distal esophagus in the gastroesophageal reflux disease. METHODS: From April to October 2002, 402 patients referred to upper endoscopy due gastroesophageal reflux disease were evaluated through of a symptom questionnaire about clinical and demographic features and submitted to upper endoscopy with four-quadrant biopsies 1 cm below escamocolumnar junction. RESULTS: Eighteen point four percent of patients had specialized intestinal metaplasia, 0.5% long segment Barrett esophagus, 3.2% short segment Barrett's esophagus and 14.7% specialized intestinal metaplasia of cardia. Patients with Barrett's esophagus showed a tendency to be male and specialized metaplasia of cardia to be female. All patients with Barrett's esophagus were white. There was not association between symptoms of gastroesophageal reflux disease and specialized intestinal metaplasia, but patients with Barrett's esophagus showed a tendency to have symptoms over 5 years and had more hiatal hernia and esophagitis. The use of alcohol and tobacco was not related to the presence of specialized intestinal metaplasia. CONCLUSIONS: Barrett's esophagus was more related to the male gender, gastroesophageal reflux disease symptoms for 5 years or longer, more intense esophagitis and hiatal hernia, but was not related to the use of tobacco and alcohol.

Adolescent↗

Helicobacter pylori infection, glandular atrophy and intestinal metaplasia in superficial gastritis, gastric erosion, erosive gastritis, gastric ulcer and early gastric cancer.

AIM: To evaluate the histological features of gastric mucosa, including Helicobacter pylori infection in patients with early gastric cancer and endoscopically found superficial gastritis, gastric erosion, erosive gastritis, gastric ulcer. METHODS: The biopsy specimens were taken from the antrum, corpus and upper angulus of all the patients. Giemsa staining, improved toluidine-blue staining, and H pylori-specific antibody immune staining were performed as appropriate for the histological diagnosis of H pylori infection. Hematoxylin-eosin staining was used for the histological diagnosis of gastric mucosa inflammation, gastric glandular atrophy and intestinal metaplasia and scored into four grades according to the Updated Sydney System. RESULTS: The overall prevalence of H pylori infection in superficial gastritis was 28.7%, in erosive gastritis 57.7%, in gastric erosion 63.3%, in gastric ulcer 80.8%, in early gastric cancer 52.4%. There was significant difference (P<0.05), except for the difference between early gastric cancer and erosive gastritis. H pylori infection rate in antrum, corpus, angulus of patients with superficial gastritis was 25.9%, 26.2%, 25.2%, respectively; in patients with erosive gastritis 46.9%, 53.5%, 49.0%, respectively; in patients with gastric erosion 52.4%, 61.5%, 52.4%, respectively; in patients with gastric ulcer 52.4%, 61.5%, 52.4%, respectively; in patients with early gastric cancer 35.0%, 50.7%, 34.6%, respectively. No significant difference was found among the different site biopsies in superficial gastritis, but in the other diseases the detected rates were higher in corpus biopsy (P<0.05). The grades of mononuclear cell infiltration and polymorphonuclear cell infiltration, in early gastric cancer patients, were significantly higher than that in superficial gastritis patients, lower than that in gastric erosion and gastric ulcer patients (P<0.01); however, there was no significant difference compared with erosive gastritis. The grades of mucosa glandular atrophy and intestinal metaplasia were significantly highest in early gastric cancer, lower in gastric ulcer, the next were erosive gastritis, gastric erosion, the lowest in superficial gastritis (P<0.01). Furthermore, 53.3% and 51.4% showed glandular atrophy and intestinal metaplasia in angular biopsy specimens, respectively; but only 40.3% and 39.9% were identified in antral biopsy, and 14.1% and 13.6% in corpus biopsy; therefore, the angulus was more reliable for the diagnosis of glandular atrophy and intestinal metaplasia compared with antrum and corpus (P<0.01). The positivity rate of glandular atrophy and intestinal metaplasia of superficial gastritis with H pylori-positivity was 50.7%, 34.1%; of erosive gastritis 76.1%, 63.0%; of gastric erosion 84.8%, 87.8%; of gastric ulcer 80.6%, 90.9%; and of early gastric cancer 85.5%, 85.3%, respectively. The positivity rate of glandular atrophy and intestinal metaplasia of superficial gastritis with H pylori-negativity was 9.9%, 6.9%; of erosive gastritis 42.5%, 42.1%; of gastric erosion 51.1%, 61.9%; of gastric ulcer 29.8%, 25.5%; and of early gastric cancer 84.0%, 86.0%, respectively. The positivity rate of glandular atrophy and intestinal metaplasia of superficial gastritis, erosive gastritis, gastric erosion, and gastric ulcer patients with H pylori positivity was significantly higher than those with H pylori negativity (P<0.01); however, there was no significant difference in patients with early gastric cancer with or without H pylori infection. CONCLUSION: The progression of the gastric pre-cancerous lesions, glandular atrophy and intestinal metaplasia in superficial gastritis, gastric erosion, erosive gastritis and gastric ulcer was strongly related to H pylori infection. In depth studies are needed to evaluate whether eradication of H pylori infection will really diminish the risk of gastric cancer.

Adult↗

[Squamous metaplasia of the mucosa of the human laryngeal ventricle: a clinicopathological study with reference to the possibility of de novo carcinogenesis].

Primary carcinomas are rarely encountered in the laryngeal ventricle of Morgagni. They are classified into the subgroup of supraglottic laryngeal carcinoma in the TNM classification system of malignant tumors. However, detailed investigations have not hitherto been made on the possible occurrence of carcinomas in this region of the larynx. To find out whether the laryngeal ventricle could be the site of carcinogenesis, the author examined squamous metaplasia in the mucosal epithelium of 60 human laryngeal ventricles which were taken from 38 larynges removed operatively from patients with laryngeal carcinoma (14 cases), hypopharyngeal carcinoma (20 cases), carcinoma of the upper esophagus (two cases), tracheal carcinoma (one case) or thyroid carcinoma (one case). The patients consisted of 31 males and 7 females, with an age distribution of 44 to 80, average 62.7. The laryngeal ventricles were selected for investigation only when they did not show any carcinomatous invasion macroscopically. Macroscopic observations were performed after gross staining with pyronin Y, which permits differentiation of squamous metaplasia from respiratory epithelia. Tissues were embedded in paraffin, sectioned serially and stained with hematoxylin and eosin. The clinical records of the patients were also made. The results are summarized as follows: 1. Squamous metaplasia of the stratified ciliated epithelium was found in 38 out of 60 specimens (63%) of the laryngeal ventricles examined. 2. The metaplasia seemed to be precipitated by smoking or exposure to radiation, along with aging. 3. The incidence and extent of metaplasia of the ventricular mucosa depended on the disease entity which had necessitated total laryngectomy, and the metaplasia was most prominent in cases with the supraglottic type of laryngeal carcinoma. 4. The metaplastic epithelium was occasionally associated with hyperplasia or dysplasia of the epithelium. 5. Microinvasive carcinoma was found in one laryngeal ventricle with severe metaplasia. These findings suggested a possible de novo carcinogenic process in the laryngeal ventricle through squamous metaplasia of the respiratory epithelium. From this observation, the author proposes to call carcinoma of this region of the larynx the ventricular type of laryngeal carcinoma.

Adult↗

[Clinical and endoscopic findings and magnitude of gastric and duodenal reflux in patients with cardial intestinal metaplasia, short Barrett esophagus, compared with controls].

BACKGROUND: The diagnosis of patients with short segments of intestinal metaplasia in the distal esophagus, has increased in recent years. AIM: To assess the clinical, pathological and functional features of patients with esophageal intestinal metaplasia. PATIENTS AND METHODS: A prospective study was performed in 95 control subjects, 115 patients with cardial intestinal metaplasia and 89 patients with short Barret esophagus with intestinal metaplasia. All had clinical and endoscopic assessments, esophageal manometry and determination of 24 h esophageal exposure to acid and duodenal content. RESULTS: Control patients were younger and, in this group, the pathological findings in the mucosa distal to the squamous-columnar change, showed a preponderance of fundic over cardial mucosa. In patients with intestinal metaplasia and short Barret esophagus, there was only cardial mucosa, that is the place where intestinal metaplasia implants. Low grade dysplasia was only seen in the presence of intestinal metaplasia. Gastroesophageal sphincter pressure decreased and gastric and duodenal reflux increased along with increases in the extension of intestinal metaplasia. CONCLUSIONS: These findings confirm the need to obtain multiple biopsies from the squamous-columnar mucosal junction in all patients with gastroesophageal reflux symptoms, for the detection of early pathological changes of Barret esophagus and eventual dysplasia.

Barrett Esophagus↗

Relationship of gastric metaplasia and age, sex, smoking and Helicobacter pylori infection in patients with duodenal ulcer and duodenitis.

Gastric metaplasia is one of the factors in duodenal ulcer appearance. The aim of this study was to investigate the frequency of gastric metaplasia and its connection with age, sex, cigarette smoking and H. pylori infection. In the study 216 patients were included. There were 98 patients with duodenal ulcer, 60 with duodenitis, and 58 healthy control subjects. There was no statistically significant difference in gastric metaplasia frequency according to age and sex. Gastric metaplasia was statistically more significant in patients with duodenal ulcer (p < 0.01). In all the subjects cigarette smoking did not significantly influence gastric metaplasia. In smokers with duodenal ulcer, and those who besides duodenal ulcer and smoking had H. pylori infection gastric metaplasia was more frequent (p < 0.01). However, in patients with duodenal ulcer, there was no statistically significant difference of gastric metaplasia related to H. pylori presence. It may be suggested that H. pylori infection is not of indispensable significance for gastric metaplasia appearance.

Adult↗

Gastric intestinal metaplasia in ethnic groups in the southwestern United States.

The incidence of gastric cancer has declined dramatically in the United States during this century. However, the incidence of gastric cancer among Hispanics, Blacks, and Native Americans remains 2-3-fold higher than among Whites in this country. Populations with an increased risk of gastric cancer have predominantly the "intestinal" type of gastric cancer, and intestinal metaplasia is regarded as a histological precursor lesion of this type of gastric cancer. We sought to establish the prevalence of intestinal metaplasia, identify associated epidemiological factors, and improve detection of this lesion in a patient population undergoing clinically indicated endoscopy in the Southwestern United States. Among the 440 patients studied, we observed an overall crude prevalence of intestinal metaplasia of 19%. However, the crude prevalence among Hispanics and Blacks was found to be markedly higher than among non-Hispanic Whites (50% versus 13%). Two biopsy protocols (two biopsies versus four biopsies) were used during this study, with a significantly higher rate of intestinal metaplasia detection under the four-biopsy protocol. Adjusting for protocol, we found that age and ethnicity were significantly and independently associated with the prevalence of intestinal metaplasia. The odds of intestinal metaplasia diagnosis was significantly higher in Hispanics compared to non-Hispanic Whites (P < 0.001), and the prevalence of intestinal metaplasia increased with advancing age (P = 0.01). The presence of Helicobacter pylori was also significantly associated with the presence of intestinal metaplasia (P = 0.02), although the direction of the association differed between Hispanics and non-Hispanic Whites.

Adult↗

[The significance of intestinal metaplasia related to gastric ulcer].

PURPOSE: Intestinal metaplasia is considered an intermediary stage of gastric carcinogenesis. Thus, we aim to investigate lesions of intestinal metaplasia diagnosed at patients with peptic ulcer. MATERIAL AND METHODS: Our study was achieved on a group of 212 patients, clinically diagnosed with gastric ulcer and having partial gastrectomy. The fragments obtained from the circumference, the basis and from around the ulcer were formalin-fixed (10%) and paraffin included. The specimens were stained routinely (HE) and with special methods (van Gieson, Masson, Gomori, PAS and Alcian Blue). RESULTS: Intestinal metaplasia was present in 36 cases (16.9%). It was noted as a unique lesion (in 10 cases), in association with chronic gastritis (23 cases) and with dysplasia (3 cases). Most of the cases (70%) displayed type I (complete) metaplasia characterized by the presence of enterocytes, goblet and Paneth cells. The glandular architecture was regular, with straight crypts, lined by mature, absorbtion cells and goblet cells producing sialomucins. 20% of the cases displayed type II (incomplete) metaplasia, with distort crypts, lined by a few absorptive and goblet cells and sparse Paneth cells. 10% of the cases presented type III (incomplete, colonic type) metaplasia with twisted crypts, increased cell density and stratification. The goblet cells in the adjacent mucosa of the malignant ulcers contained mainly sulphomucins, together with a few neutral mucins and sialomucins. The signification and the involvement of the intestinal metaplasia in the malignant transformation of the gastric ulcer are discussed. CONCLUSION: Since it represents a risk factor for carcinogenesis the identification of intestinal metaplasia in the context of the gastric ulcer is extremely important.

Gastrectomy↗

Metaplasia of the parietal layer of Bowman's capsule: a histopathological survey of the human kidney.

Human kidney sections taken at autopsy were examined to determine the incidence of metaplasia of the Bowman's parietal epithelium. Autopsy records were consulted to determine if there was any correlation between clinical disease, histopathological changes in organ systems and metaplasia of Bowman's capsule. The sections represented both sexes in 9 age groups from 2 to 87 years. The sections were fixed in neutral formalin, embedded in paraffin, sectioned at 6 microns, and stained with hematoxylin and eosin. A total of 129 kidney sections, representing 129 individuals, were evaluated. One hundred renal corpuscles were counted per section and the parietal layer of Bowman's capsule was classified as normal (squamous) or metaplastic (cuboidal). Of the 129 kidneys examined, 69 (53%) had metaplasia of Bowman's capsule. Of the 87 male kidneys, 51 (59%) exhibited metaplasia of Bowman's capsule. Of the 42 female kidneys examined, 18 (43%) of the kidneys had metaplasia of Bowman's capsule. On average, in kidneys with metaplasia, 4% of the renal corpuscles had metaplasia of Bowman's parietal layer. The lesion was present in both sexes in all age groups. The autopsy records revealed that there was no common clinical condition associated with the metaplastic lesion, but metaplasia of Bowman's parietal epithelium was consistently present with hepatic congestion and/or fatty changes.

Adolescent↗

[Relationship between type III intestinal metaplasia, age and gastric cancer. 560 biopsies].

OBJECTIVE: A significant association between type III intestinal metaplasia and gastric adenocarcinoma has been demonstrated in gastrectomy and biopsy series. We investigated the effect of age in a large series of gastric biopsies in order to determine whether this association is age dependent or independent. METHODS: Histochemistry examinations were performed in 560 gastric biopsies showing intestinal metaplasia. The percentage of type III versus type I/II metaplasia in patients with malignant (n = 41) or benign disease (n = 519) was compared between patients aged 50 to 69 years and patients aged 70 to 89 years. RESULTS: The prevalence of type III metaplasia increased with age both in malignant (30 vs 61% in the 50-69 and 70-89 year age groups respectively) and benign disease (9 vs 17% respectively). In patients with cancer, type III metaplasia was found more often than type I/II metaplasia (n = 22 vs 19). In the 70-89 year age group, there was a significant difference (p < 0.001) in the percentage of type III metaplasia in patients with cancer (61%) and those with benign disease (17%). CONCLUSION: These findings demonstrate that there is a specific age-independent relationship between intestinal metaplasia and gastric cancer.

Adenocarcinoma↗

Gastric metaplasia and Helicobacter pylori infection in intestinal tuberculosis.

BACKGROUND: Gastric metaplasia occurs in intestinal epithelium of patients with Helicobacter pylori infection as well as intestinal tuberculosis, but the relationship between the three is not clear. SETTING: Teaching hospital. METHODS: Staining of intestinal sections from patients with ileocecal tuberculosis for H pylori and for metaplasia. RESULTS: Twenty seven of 92 (29.3%) patients demonstrated gastric metaplasia (superficial epithelial and pyloric gland metaplasia) in resected specimens of ileum. Gastric metaplasia was of antral type in all 27 patients. Helicobacter pylori was present in 3 of 27 (11%) patients with gastric metaplasia and was absent in all 65 patients without metaplasia. CONCLUSION: Gastric metaplasia (both superficial epithelial and pyloric gland) occurs in one-third of patients with ileocecal tuberculosis and such mucosa is poorly colonized by H pylori.

Adult↗

Helicobacter pylori and intestinal metaplasia: comparison between British and Yemeni patients.

There have been suggestions linking gastric carcinoma with Helicobacter pylori on the one hand and type III intestinal metaplasia on the other hand. This study was aimed at investigating the relationship between intestinal metaplasia and its subtypes, and the presence or absence of H. pylori in gastric biopsies from two geographically different patient populations, one with a much higher prevalence of H. pylori than the other. Antral biopsies from 179 British and 123 Yemeni patients with dyspepsia were examined. Sections stained with hematoxylin and eosin, Alcian blue/periodic acid-Schiff, high iron diamine/Alcian blue, and Warthin-Starry stains were used to assess the presence or absence of inflammation, H. pylori, and intestinal metaplasia with its three subtypes. Although Yemeni patients had a significantly higher prevalence of H. pylori than British patients (113/123. 92% vs. 83/179, 46% respectively; p < 0.001), Yemeni patients had a significantly lower prevalence of all types of intestinal metaplasia (23/123, 19% vs. 60/179, 34%; p < 0.001), as well as type III metaplasia (4/123, 3% vs. 39/179, 22%, p < 0.001). These trends persisted when only patients above the age of 40 yr were considered. However, in British patients, intestinal metaplasia was more commonly seen in those with H. pylori than in those without (36/83, 43%, and 24/96, 25%, respectively, p < 0.01), although the prevalence of type III metaplasia was not significantly different in the two groups (23/83, 28% vs. 16/96, 17%, respectively). The contrasting findings in the two patient populations suggest the presence of other factors, possibly genetic, which control the development of intestinal metaplasia and possibly gastric carcinoma in H. pylori-positive patients.

Adolescent↗

Is Barrett's esophagus associated with intestinal metaplasia of the gastric cardia?

OBJECTIVE: Barrett's esophagus has been associated with adenocarcinoma of the esophagogastric junction and gastric cardia. The purpose of this study was to determine whether patients with Barrett's esophagus have a higher prevalence of intestinal metaplasia involving the gastric cardia than those without Barrett's esophagus. METHODS: Two groups of patients were compared for the prevalence of intestinal metaplasia of the gastric cardia. Group 1 included 50 patients with well-defined Barrett's esophagus who were being followed in an endoscopic surveillance program. Group 2 consisted of 104 individuals participating in a separate study identifying the prevalence of cardia intestinal metaplasia in patients undergoing elective upper endoscopy. Both groups had biopsy specimens taken from the gastric cardia. Eleven patients in group 2 were found to have Barrett's esophagus and were excluded from the analysis. Histological evidence of intestinal metaplasia was defined as specialized columnar epithelium containing goblet cells staining with Alcian blue at pH 2.5. RESULTS: The prevalence of cardia intestinal metaplasia in the 50 patients in group 1 (Barrett's esophagus) was 22%, whereas the prevalence in the 93 patients in group 2 (no Barrett's esophagus) was 24%, which was not a statistically significant difference. A significant difference between groups still could not be identified when the results were examined with regard to equal number of biopsy specimens taken. None of the patients in either group had dysplasia identified within the cardia intestinal metaplasia. CONCLUSIONS: Patients with Barrett's esophagus do not have a higher prevalence of intestinal metaplasia of the gastric cardia than those presenting for routine endoscopy. Although intestinal metaplasia of the gastric cardia is a relatively common finding, dysplasia is uncommon. Therefore, we suggest that screening biopsy specimens of the gastric cardia in patients with Barrett's esophagus be limited to study protocols at this time. In addition, we believe that these data raise the question of whether a true association exists between Barrett's esophagus and gastric cardia cancer.

Aged↗

Induction of glutathione s-transferase-pi in Barrett's metaplasia and Barrett's adenocarcinoma cell lines.

Barrett's metaplasia consists of columnar epithelium that replaces the normal esophageal mucosa in patients with chronic gastroesophageal reflux. Because intestinal-type Barrett's metaplasia is the major risk factor for adenocarcinoma development, understanding the mechanisms that predispose the esophageal mucosa to malignant degeneration is clinically important. Glutathione s-transferase (GST)-pi belongs to a class of protective enzymes whose activity has been shown to be much lower in Barrett's metaplasia than in the normal esophagus, where this form of GST is predominant. In the studies described here, using immunocytochemical analysis, we observed higher levels of cytoplasmic GST-pi protein in normal esophageal mucosa than in Barrett's metaplasia. Using northern blot analysis, we also observed lower GST-pi mRNA levels in Barrett's metaplasia than in normal esophagus or adenocarcinomas from the same patients. Using as model systems three Barrett's adenocarcinoma cell lines and short-term organ culture of freshly resected normal esophagus and Barrett's metaplasia, dose-dependent induction of GST-pi mRNA was observed by using butylated hydroxyanisole and dexamethasone. GST-pi mRNA in Barrett's metaplasia was induced up to 2.5-fold with 60 microM butylated hydroxyanisole and nearly fivefold with 320 nM dexamethasone after 24 h. These studies demonstrate the ability to induce protective GST-pi in Barrett's metaplasia and may suggest a mechanism for future chemoprevention studies in patients with this type of epithelium, which is at high risk for malignant degeneration.

Adenocarcinoma↗