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PubMed2005

Cell proliferation and apoptosis in gastric cancer and intestinal metaplasia.

BACKGROUND: Higher proliferation is commonly observed in cancer cells. Apoptosis can be a useful measure of a tumor cell kinetic. Alteration of the balance between proliferation and apoptosis is associated with cancer. AIM: To study proliferation and apoptosis on gastric cancer and in intestinal metaplasia. METHODOLOGY: Twenty-two samples from gastric adenocarcinomas and 22 biopsies from intestinal metaplasia were studied. The apoptotic bodies in hematoxylin-eosin slides and the expression of p53, bcl-2 and Ki67 were determined by immunohistochemistry. RESULTS: The number of the apoptotic cells was higher in cancer. Ki 67LI increased from intestinal metaplasia to gastric cancer. p53 was positive in 68% of the patients with cancer, more frequently in advanced stage and negative in samples of intestinal metaplasia. Although there was no significant difference between the groups, bcl-2 was positive in 45% of gastric cancer tissue and in 68% of metaplasia. In gastric cancer patients bcl-2 was expressed in early gastric cancer more frequently than in advanced stage. CONCLUSION: The positivity of bcl-2 was higher in metaplasia and probably is involved in the progression of carcinogenesis. p53 was negative in metaplasia and positive in more than half of the gastric cancer, mostly in stage IV, suggesting a late event in gastric cancer.

Adenocarcinoma↗
PubMed2003

Mammographic-pathologic correlation of apocrine metaplasia diagnosed using vacuum-assisted stereotactic core-needle biopsy: our 4-year experience.

OBJECTIVE: To determine whether focal apocrine metaplasia of the breast has distinctive mammographic characteristics, we evaluated apocrine metaplasia diagnosed by vacuum-assisted stereotactic core-needle biopsy and correlated mammographic imaging and histopathologic findings. MATERIALS AND METHODS: We retrospectively reviewed our institutional database for records of all vacuum-assisted stereotactic core-needle biopsies performed during a 4-year period. Five hundred thirty-eight lesions were biopsied, of which 302 (56%) were benign. Apocrine metaplasia was diagnosed in 37 lesions. In 11 of these 37 lesions, apocrine metaplasia made up more than 50% of the lesion sampled. RESULTS: On mammography, eight cases (73%) appeared as new or increasing calcifications, and three cases (27%) appeared as new or enlarging equal-density masses (0.6-1.2 cm). Calcifications were heterogeneous in five lesions (63%), amorphous in two (25%), and punctate in one (12%); one heterogeneous cluster of calcifications (12%) also contained milk of calcium. The pattern of calcification distribution was clustered in five lesions (63%), multiple clusters in two (25%), and linear in one (12%). Two masses (67%) were lobular, and one (33%) was round. Two borders (67%) were microlobulated, and one (33%) was circumscribed. CONCLUSION: Apocrine metaplasia is a benign condition commonly associated with other fibrocystic changes. Lesions composed of more than 50% focal apocrine metaplasia are relatively uncommon. A new or enlarging lobular, microlobulated mass or heterogeneous calcification cluster may represent apocrine metaplasia. Because no distinguishing mammographic features are present to require follow-up by imaging, needle biopsy is required for definitive diagnosis.

Adult↗
PubMed2002

p53 mutations and microsatellite instabilities in the subtype of intestinal metaplasia of the stomach.

To investigate the potential implication of the subtype of intestinal metaplasia in the progression to the gastric carcinoma, we analyzed the mutations of the p53 gene and microsatellite instability (MSI) both in the complete type (type I) and in the sulphomucin-secreting incomplete type (type III) intestinal metaplasia located adjacent to the gastric carcinoma. p53 mutations were observed in 13.3% of type I, in 6.6% of type III intestinal metaplasia, and in 40% of gastric carcinoma. The difference between p53 mutations observed in type I and type III intestinal metaplasia was not statistically significant. No identical mutation of the p53 gene was found in the intestinal metaplasia and carcinoma specimens from the patients. There was no case of intestinal metaplasia showing MSI. In gastric carcinomas, MSI was observed in six cases (40%). The cases harboring BAT-26 instability did not have the mutation of the p53 gene. These data suggest that intestinal metaplasia adjacent to gastric carcinoma, irrespective of its subtype, do not have the genetic alterations as showing in their carcinoma tissues.

Carcinoma↗
PubMed2005

Deformity of duodenal bulb, gastric metaplasia of duodenal regenerating mucosa and recurrence of duodenal ulcer: a correlated study.

AIM: To investigate the correlation among the presence and degree of gastric metaplasia of duodenal regenerating mucosa, the deformity of bulb and the recurrence of duodenal ulcer. METHODS: A total of 99 patients with duodenal ulcer were treated with H(2)-antagonist with or without antimicrobial therapy. All patients received follow-up endoscopic examinations 6 wk after treatment. When the ulcer(s) were noted to be healed, two biopsies were taken from the ulcer scar for histological study of gastric metaplasia, and 4 biopsies were taken from antrum for Helicobacter pylori (H pylori) study. Out of these cases, 44 received further follow-up endoscopic examinations after 3, 6 and 12 mo respectively for studying the recurrence rate of duodenal ulcers. The correlation among ulcer recurrence, degree of gastric metaplasia of regenerating mucosa, bulbar deformity, and colonization of H pylori in the stomach was then studied. RESULTS: The results showed that there was a strong correlation between the deformity of duodenal bulb and the degree of gastric metaplasia of regenerating duodenal mucosa. The recurrence rate of duodenal ulcer had a significant difference between patients with and without H pylori colonization in the stomach (P<0.001). The greater the degree of gastric metaplasia of duodenal regenerating mucosa, the higher the recurrence rate of duodenal ulcer (P = 0.021). The more deformed the duodenal bulb, the higher the incidence of recurrence of duodenal ulcer (P = 0.03). CONCLUSION: There is a correlation among deformity of duodenal bulb, gastric metaplasia of duodenal regenerating mucosa and recurrence of duodenal ulcer. A more severely deformed duodenal bulb is closely related to a greater extent of gastric metaplasia. Both factors contribute to the recurrence of duodenal ulcer.

Adolescent↗
PubMed1999

Effect of Helicobacter pylori infection, smoking and dietary habits on the occurrence of antrum intestinal metaplasia. Clinico-epidemiological study in Poland.

The purpose of the study was to assess risk factors for intestinal metaplasia arising from H. pylori-related chronic gastritis in a subset of the population referred to endoscopic examinations due to dyspeptic complaints. We aimed specifically to establish whether H. pylori itself may be responsible for the occurrence of intestinal metaplasia and to which extent the metaplasia may be associated with life style factors such as cigarette smoking, alcohol consumption or dietary habits. The study was carried out in a sample of 1290 outpatients referred for the first time to gastroenterologic outpatient clinics in 6 university centers in Poland. The study methods covered standardized health interviews, endoscopy and histology of gastric antral specimens taken at endoscopy. The interviews performed by trained interviewers sought information on tobacco and alcohol intake, diet, socioeconomic status, and other variables. In non-ulcer dyspepsia subjects there was 54.9% H. pylori related gastritis and 25.1% of non-H. pylori-related gastritis. The corresponding rates in the group of ulcer dyspepsia were 67.5% and 20.5%. The increased risk of chronic gastritis in antrum was associated with Helicobacter pylori infection (OR = 2.28; 95% CI:1.93-2.69), and with gastric peptic ulcer (OR = 1.88; 95% CI:1.20-2.94). In the non-ulcer dyspepsia the prevalence of metaplasia was 11.1% and in ulcer dyspepsia 19.7%. The risk of intestinal metaplasia within antrum depended greatly upon the presence of gastric peptic ulcer (OR = 3.85; 95% CI:2.35-6.32) and increased with age (OR = 1.05; 95% CI:1.04-1.07), smoking cigarettes currently or in the past (OR = 1.42; 95% CI:1.10-1.84), higher frequency of drinking vodka (OR = 1.32, 95% CI:1.01-1.75) and antral chronic gastritis (OR = 1.31; 95% CI:1.00-1.70), however, it was inversely related to daily consumption of fresh fruits or vegetables (OR = 0.59; 95% CI:0.38-0.93). The results of the study suggest that there is no sufficient evidence supporting the hypothesis about an association between H. pylori gastritis and intestinal metaplasia, however, the transition of gastritis to metaplasia depends greatly on life style factors such as cigarette smoking or vodka drinking and is impeded by daily consumption of fresh fruits or vegetables.

Alcohol Drinking↗
PubMed1988

Metaplasia of the parietal layer of Bowman's capsule in the human kidney: incidence in alcoholic liver disease and hypertension.

This report is the second of two surveys to determine the incidence of metaplasia of Bowman's parietal epithelium in the human kidney. Human kidney sections obtained at autopsy at the Department of Pathology, University of Texas Medical Branch, Galveston, Texas, were examined with the light microscope. The kidneys were fixed in neutral formalin, sectioned at 6 microns and stained with hematoxylin and eosin. Autopsy records were consulted after kidney section examination to determine if there was any correlation between clinical disease, histopathological changes in organ systems and metaplasia of Bowman's capsule. The kidney sections represented both sexes in 8 age groups, from less than one year to 80 years. A total of 174 kidneys, representing 174 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 174 kidneys examined, 137 (79%)--79 male and 58 female--had metaplasia of Bowman's capsule. On the average, in the kidneys with the lesion, 6% 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 metaplasia of Bowman's parietal epithelium was usually present with hepatic fatty changes and/or congestion. Alcoholic liver disease and hypertension represented the most frequent clinical diseases in the sample; these conditions had the highest incidence of metaplasia. Twenty-six of the 174 kidney samples were from individuals with alcoholic liver disease, all of whom had metaplasia of Bowman's capsule.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1987

Induction of gastric tumor and intestinal metaplasia in rats exposed to localized X-irradiation of the gastric region.

The induction of gastric tumor and intestinal metaplasia was examined in 8-week-old male JCL/SD rats exposed to localized X-irradiation of the gastric region. The animals were each given two 20 Gy fractions of X-rays, with a one-week interval between fractions (total, 40 Gy). Nine atypical hyperplasias (20%) and 13 adenocarcinomas (28%) in the pyloric mucosa of the glandular stomach were found in 46 animals with X-irradiation. The incidence of intestinal metaplasia was 93% in the pyloric mucosa, 50% in the fundic mucosa and 96% in both the pyloric and fundic mucosa. Type B metaplasia (intestinal metaplasia without Paneth cells) was most common and type C (intestinal metaplasia with Paneth cells) was less frequent. No gastric tumor or intestinal metaplasia appeared in non-irradiated control rats. This study shows that local X-irradiation of the gastric region induced both gastric tumor and intestinal metaplasia independently.

Animals↗
PubMed1986

[The relationship between stomach cancer and intestinal metaplasia of the gastric mucosa and food intake].

The natural history of intestinal metaplasia of gastric mucosa was studied in 414 rural inhabitants; 213 males and 201 females, from Chokai Village in Akita Prefecture in the northeast part of Japan's main island of Honshu. The subjects were examined by a mobile gastrointestinal unit and were biopsied at eight standard points of the gastric mucosa. The specimens were examined histologically, and were divided into 4 grades. The metaplasia index (MI) was adopted as a quantitative expression of the severity of intestinal metaplasia of the gastric mucosa. The MI of the three areas of the village were compared with the different incidences of stomach cancer. The following results were obtained: in gastric mucosa. The average values of the MI among the male population were highest at the high-risk area, low at the low-risk area and intermediate at the moderate-risk area of gastric cancer. Whereas, the values among females showed no differences in these three areas. The risks for stomach cancer also were almost equal. These phenomena would show a very close relationship between intestinal metaplasia and the incidence of stomach cancer. There was a positive correlation (p less than 0.01) between MI and the detection rates of stomach cancer by a mass screening examination in the areas. Study of food intake and especially the salt consumption among the three areas showed a close relationship with intestinal metaplasia. Certain foods seemed to relate to intestinal metaplasia and eventually to stomach cancer. The conclusion was drawn that the development of intestinal metaplasia could be prevented by the improvement of environmental factors especially by that of food intake. Thus, the reduction in the incidence of stomach cancer also would be possible.

Adult↗
PubMed1986

Gastric carcinoma: intestinal metaplasia and tumor growth patterns as indicators of prognosis.

We have reviewed 200 cases of gastric carcinoma treated between 1970 and 1980 to assess the value of intestinal metaplasia in the stomach and tumor growth patterns in determining prognosis. Intestinal metaplasia was found to be more frequently associated with early gastric tumors, expanding-type tumors, and tumors located in the antrum. The survival rate was 53% with intestinal metaplasia and 34% without. Sixty-three percent of expanding tumors with metaplasia survived. If the lymph nodes were not involved, the survival rate with metaplasia was 81%. We conclude that intestinal metaplasia and growth patterns are valuable in predicting outcome. Preoperative evaluation of gastric tumors should include multiple endoscopic mucosal biopsy specimens. If intestinal metaplasia is present, the improved possibility of survival should influence the surgeon in the choice of operative treatment.

Female↗
PubMed1997

Gastric metaplasia and Helicobacter pylori.

OBJECTIVES: We investigated the relationships between gastric metaplasia occurring during the healing and scarring stages of duodenal ulcers and Helicobacter pylori by examining the course of gastric metaplasia in H. pylori-eradicated and non-eradicated patients. METHODS: One hundred and six H. pylori-positive patients with active duodenal ulcers were assigned to either a non-eradication group or an eradication group. The non-eradication group received lansoprazole for 6 wk, followed by an H2-receptor antagonist. The eradication group also received amoxicillin and metronidazole for 1 wk, in addition to lansoprazole, after initial endoscopic examination. In both groups, biopsy specimens were obtained from the ulcer margin in the active stage and from the center of the scar in the scarring stage. Specimens were examined microscopically as well as by rapid urease test to assess the extent of gastric metaplasia and to detect the presence of H. pylori. RESULTS: The extent of gastric metaplasia increased as the ulcers healed. The extent of gastric metaplasia was of a lesser degree in the non-eradication group than in the eradication group at the time of healing, and this tendency became increasingly apparent in the course of follow-up, resulting in reduced defense mechanisms against acidity to promote the recurrence of ulcers. In the eradication group, among those in whom eradication was successful, gastric metaplasia presented a well-developed appearance with abundant intracellular mucus and remained in this condition for a prolonged period, resulting in adequate defense mechanisms against acidity to prevent the recurrence of ulcers. CONCLUSION: By the eradication of H. pylori, gastric metaplasia becomes well-developed and remains so for a prolonged period. Thus, the eradication of H. pylori appears to play a role in the prevention of ulcer recurrences by developing adequate defenses against acidity.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1997

Short-term eradication therapy for Helicobacter pylori does not reduce the incidence of gastric metaplasia in duodenal ulcer patients.

The presence of gastric metaplasia in the duodenal mucosa and Helicobacter pylori infection play an important role in the development of duodenal ulcers and the risk for ulcer relapses. The purpose of the present study was to identify the presence of gastric metaplasia in the duodenum and observation of changes in its extent during eradication therapy for Helicobacter pylori. The study population consisted of 40 patients, 15 women (aged from 29 to 65 years) and 25 men (aged from 22 to 62 years). At baseline and after 6 weeks all patients underwent endoscopic examinations of the upper alimentary tract during which two gastric antral and duodenal biopsies were obtained. The first endoscopy revealed the presence of duodenal ulcers in 22 patients, no ulcers in 11 cases, and postulceration scar in the duodenal bulb in 7 cases. The specimens were stained with hematoxylin and eosin, Giemsa and periodic acid Schiff/Alcian Blue. On first examination Helicobacter pylori infection in gastric antral specimens was detected in 40 patients. Therapy with amoxycillin, metronidazole, ventrisol and omeprazole for two weeks was administered in patients without duodenal ulcers and with omeprazole and ventrisol for additional 14 days in patients with duodenal ulcers. After therapy the presence of Helicobacter pylori was found in 10 cases, thus the degree of Hp eradication in the present study was 75%. Gastric metaplasia in duodenal samples was seen in 15 patients with duodenal ulcers and in 10 nonulcer patients. After therapy only in 4 cases gastric metaplasia was reduced along with Hp eradication, whereas in 9 cases gastric metaplasia in the duodenum was still present despite effective Hp eradication. The present findings indicate that gastric metaplasia is a reversible lesion, although this process is not dynamic and requires more time. The presence of gastric metaplasia in the duodenum after Hp eradication indicates an increased risk for the recurrence of duodenal ulcers, thus providing a useful information for a clinician.

Adult↗
PubMed1995

Mucosal IgA antibody against Helicobacter pylori in chronic gastritis and intestinal metaplasia detected by the Tes-Tape method in resection specimens after gastrectomy for gastric cancer.

BACKGROUND: Subjects with atrophic body gastritis have a high prevalence of Helicobacter pylori seropositivity and a low prevalence of H. pylori infection. Disappearance of the organism appears to correlate with the development of intestinal metaplasia. To investigate this point, intestinal metaplasia was biochemically subclassified into complete and incomplete types by the Tes-Tape method, and tissue IgA and IgG antibodies against H. pylori were measured by enzyme-linked immunosorbent assay (ELISA). METHODS: Twenty-five stomachs resected for gastric cancer were examined using the Tes-Tape method. Serum H. pylori IgA and IgG antibodies and tissue IgA and IgG antibodies against H. pylori and tissue secretory IgA (sc-IgA) were examined in areas of intestinal metaplasia, nonmetaplastic gastric mucosa, and gastric carcinoma by ELISA: RESULTS: Tissue H. pylori IgA antibody was positive in 6 of 19 (32%) specimens taken from complete and 2 of 7 (29%) incomplete types of intestinal metaplasia and was positive in 6 of 14 (43%) nonmetaplastic gastric mucosa from the antrum and 14 of 23 (61%) from the body. Duodenal mucosa and cancer tissue were positive for tissue IgA antibody in 1 of 6 (17%) and 0 of 17 (0%), respectively. Tissue H. pylori IgG antibody was negative in all the tissues examined. sc-IgA in the areas of intestinal metaplasia was 120 +/- 65 (mean +/- standard error; ng/mg wet weight) and in the nonmetaplastic gastric mucosa was 113 +/- 72, showing no difference. Positivity and negativity of serum IgA and IgG antibodies against H. pylori coincided with presence or absence of tissue IgA antibody in nonmetaplastic gastric mucosa in 15 of 19 (79%) and 16 of 19 (84%) patients examined, respectively. CONCLUSION: Positivity rates of tissue IgA antibody against H. pylori were lower in the mucosa of intestinal metaplasia than in nonmetaplastic gastric mucosa and were negative in carcinoma. No significant difference in levels of sc-IgA between intestinal metaplasia and non-metaplastic gastric mucosa was found.

Antibodies, Bacterial↗
PubMed1998

Fat-Cell Metaplasia in the Adrenal Cortex: Incidence, Structure, and Correlation to Basic Diseases in a Postmortem Series.

In a postmortem series of adrenals from 497 patients 25 cases (5%) showed foci of fat-cell metaplasia or bone-marrow metaplasia in the zona fasciculata or the zona reticularis. There was only one focus in 45% of adrenals with metaplasia, but in 36.4%. more than six foci were present. The sizes varied between 0.036 and 0.64 mm. The foci were composed of mature, mostly univacuolar, fat cells and various amounts of myeloid cells The incidence of fat-cell metaplasia or of bone marrow metaplasia correlated with arterial hypertension and severe coronary heart disease. In 76% of cases, nodular hyperplasia was demonstrable, but the metaplasia were more often found adjacent to, rather than within, the nodules. They appear to be related to metaplasia in adrenocortical tumors and to myelolipomas. The common pathogenesis is thought to be based on focal necroses in combination with local endocrine stimulation.

Journal Article↗
PubMed1983

Barrett's metaplasia and adenocarcinoma of the esophagus and gastroesophageal junction.

Most previous studies of Barrett's metaplasia have used biopsy material to document cell, gland, and architectural types, leading to inaccurate or incomplete conclusions. The present study presents data from eight esophagogastrectomy specimens of Barrett's metaplasia with associated neoplasia, which were evaluated topologically by use of dissecting microscopy, specimen radiography, scanning electron microscopy, and routine histologic examination. Barrett's metaplasia was found to be mosaic of cell, gland, and architectural types, showing variable degrees of atrophy and maturation toward intestinal and gastric epithelium. Zonation was not found. Surface mucous, goblet, absorptive, mucous neck, mucous gland, and neuroendocrine cells were found in all cases; Paneth, chief, and parietal cells were found in approximately half. The presence of villar architecture with lining goblet and absorptive cells is unique and can be used to make a biopsy diagnosis. In one case, only a minute residual focus of Barrett's metaplasia was found, suggesting that the pathogenesis of some cases of adenocarcinoma of the lower esophagus and gastric cardia unassociated with Barrett's metaplasia may be the same. Nine cases of adenocarcinoma of the gastroesophageal junction unassociated with Barrett's metaplasia, studied during the same time period, had similar epidemiologic characteristics including mean age, age range, and sex distribution. Multifocal dysplasia and carcinoma in situ were found in all but one case. In two of eight cases adenomatous change was present; one of these resembled a villous adenoma of the colon with malignant degeneration. Barrett's metaplasia thus appears to be important as a precursor of adenocarcinoma in the region of the lower esophagus and gastroesophageal junction. The significance of these findings in relation to previous reports is discussed.

Adenocarcinoma↗
PubMed2002

Helicobacter pylori infection, not gastroesophageal reflux, is the major cause of inflammation and intestinal metaplasia of gastric cardiac mucosa.

OBJECTIVE: The etiology of inflammation below the normal Z-line is an area of intense debate. Some suggest this is the earliest change of chronic gastroesophageal reflux disease (GERD), whereas others indict Helicobacter pylori (H. pylori) as the main cause. The aim of this study was to evaluate the relationship among inflammation of gastric cardiac mucosa (carditis), H. pylori infection, and intestinal metaplasia in patients with GERD and Barrett's esophagus compared with age-matched controls. METHODS: Patients with GERD and Barrett's esophagus were compared with controls undergoing endoscopy for a variety of other conditions. Endoscopic biopsy specimens from the gastric cardia (obtained on retroflexed view), fundus, and antrum were evaluated for inflammation, H. pylori infection, and intestinal metaplasia. RESULTS: The prevalence of H. pylori infection did not significantly differ among the study populations: controls (42%), GERD (33%), and Barrett's esophagus (27%) (p = 0.20). However, the prevalence of carditis significantly decreased from the control group (30%) to those with GERD (23%) and Barrett's esophagus (11%) (p = 0.03). Overall, 42 of 51 (82%) patients with carditis had H. pylori; all had pangastritis. The prevalence of cardia intestinal metaplasia also significantly decreased from the control group (15%) to those with GERD (4%) and Barrett's esophagus (0%) (p = 0.003). Of 13 patients with cardia intestinal metaplasia, 12 had carditis, 10 had H. pylori infection, and seven had intestinal metaplasia elsewhere in the stomach. CONCLUSIONS: Inflammation of gastric cardiac mucosa decreases in prevalence from controls to patients with GERD and Barrett's esophagus and correlates strongly with H. pylori infection. Cardia intestinal metaplasia is associated with H. pylori-related cardiac inflammation and intestinal metaplasia elsewhere in the stomach.

Adult↗
PubMed2000

Atypical nephrogenic metaplasia of the urinary tract: a precursor lesion?

BACKGROUND: Nephrogenic metaplasia with cytologic atypia (atypical nephrogenic metaplasia) is occasionally encountered and its biologic potential is uncertain. METHODS: The authors describe 18 cases of atypical nephrogenic metaplasia characterized by the presence of prominent cytologic atypia, including nuclear enlargement, nuclear hyperchromasia, and enlarged nucleoli. DNA ploidy analysis by digital image analysis and immunostaining for high-molecular-weight cytokeratin (34betaE12), cytokeratin 7, cytokeratin 20, carcinoembryonic antigen (CEA), epithelial membrane antigen (EMA), p53, and MIB-1 were performed in 9 cases. RESULTS: The mean patient age was 62 years (median, 65 years; range, 39-84 years). The male-to-female ratio was 2.6:1. Two patients had a history of noninvasive papillary urothelial carcinoma. The typical clinical presentation was hematuria (8 patients) and voiding symptoms (5 patients). Cystoscopic findings were suspicious for neoplasm in 7 of 13 cases. The neoplastic cells were positive for high-molecular-weight cytokeratin, cytokeratin 7, and EMA, and were usually negative for cytokeratin 20 and CEA. p53 nuclear accumulation and increased MIB-1 labeling index were seen in 4 cases. DNA ploidy analysis showed aneuploid pattern in 2 of 9 cases. The mean patient follow-up was 3.5 years (range, 0.5-10.6 years); 2 patients had recurrent nephrogenic metaplasia, and the remainder were alive without recurrence or urothelial carcinoma. CONCLUSIONS: Atypical nephrogenic metaplasia is benign; it occasionally displays substantial cytologic abnormalities of no apparent clinical significance. Awareness of the spectrum of cytologic changes within this entity is critical to prevent overdiagnosis of cancer and avoid unnecessary treatment. There is no direct evidence that links atypical nephrogenic metaplasia to cancer.

Adult↗
PubMed1983

Time trend in the prevalence of intestinal metaplasia in Japan.

In connection with the recently commenced decline of death rate for gastric cancer in Japan, the time trend of intestinal metaplasia of the stomach among the Japanese is investigated. Otherwise normal stomachs from autopsies, and stomachs removed for gastric or duodenal ulcer or for early gastric carcinoma, each collected from two different periods at intervals of 10 to 20 years, are compared histologically. The results show that the prevalence of intestinal metaplasia in those stomachs generally remains high, but that there is a regular downward tendency of the prevalence of confluent intestinal metaplasia in all of those stomachs, except for the stomachs with gastric ulcer. The fall in prevalence is conspicuous among the individuals of middle age groups, especially of patients aged in their 40s, and it is minimized toward old age. The decrease of intestinal metaplasia among the Japanese is considered to have been started only recently. There is no evidence verifying the antecedence of the fall in prevalence of intestinal metaplasia to the decline of death rate for gastric cancer in Japan. Evidence does not suggest a precancerous nature of intestinal metaplasia per se.

Adolescent↗
PubMed1984

Significance of intestinal metaplasia for the evolution of cancer in the biliary tract.

Of 25 cases of cancer in the intrahepatic bile ducts, 44 cases of cancer in the extrahepatic bile ducts, 30 cases of adenoma in the gallbladder, and 100 cases of infiltrating carcinoma in the gallbladder, several to about 20% of the cases showed Paneth's cell metaplasia and/or enterochromaffin cell metaplasia within the tumor mass or in its surrounding mucosa. These metaplasia were not found in small adenomata of the gallbladder, but they were frequently seen in large adenomata. Goblet cell metaplasia and marked hyperplasia of mucous glands were seen more frequently in the mucosa surrounding cancer than in the mucosa of 500 non-neoplastic gallbladders. Although cancer in the gallbladder occasionally developed on the basis of intestinal metaplasia alone, intestinal metaplasia was not likely to be related to induction of most adenomata, but it was likely to be associated with growth and cancerous change of adenoma.

Adenoma↗