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At least 217 records · Page 12Linked to original sources
PubMed1999

Expression of MUC1 and MUC2 mucin gene products in Barrett's metaplasia, dysplasia and adenocarcinoma: an immunopathological study with clinical correlation.

AIMS: Changes in the histochemical characteristics of the surface epithelial mucins is the hallmark of Barrett's metaplasia. The study investigated the pattern of expression of MUC1 and MUC2 mucin gene products in Barrett's metaplasia, dysplasia and adenocarcinoma as possible indicators of increased malignant potential. METHODS AND RESULTS: Tissue sections from 51 patients with Barrett's intestinal metaplasia, nine with dysplasia (three indefinite) and 28 resected adenocarcinomas were stained with monoclonal antibodies to MUC1 and MUC2. The majority of the patients were men (70/88, 80%) who were treated over a period of 3 years. None of the patients with dysplasia or carcinoma were under surveillance at the time of presentation. All 51 biopsies with Barrett's metaplasia expressed MUC2 and MUC1 was consistently absent. Neither MUC1 or MUC2 were expressed in the dysplastic epithelium whether in its pure form (6/6) or when associated with carcinoma (26/28) (P < 0.005). Three biopsies which were initially classified as high-grade dysplasia expressed MUC1 and these turned out to be carcinomas on further investigations. MUC1 was also expressed in 12/28 (43%) of the adenocarcinomas and majority of these were poorly differentiated stage 3 tumours (P < 0.05). MUC2 was only positive in mucin-secreting carcinomas (4/28; 14%) irrespective of the tumour stage. CONCLUSION: Despite the large number of patients with Barrett's metaplasia and carcinoma, very few patients presented with dysplasia, implying that Barrett's oesophagus is a silent disease in the community presenting late as carcinoma. The study has demonstrated aberrant expression of MUC2 (an intestinal mucin) in Barrett's metaplasia and this expression is lost when the cells become dysplastic. The lack of MUC1 in dysplastic epithelium and its expression in carcinoma could be utilized as a marker which could differentiate dysplasia from carcinoma in mucosal biopsies. Furthermore, expression of MUC1 in advanced stage oesophageal cancers (as in breast cancer) suggests an unfavourable prognosis.

Adenocarcinoma↗
PubMed1999

Relationship between Helicobacter pylori infection and gastric metaplasia in the duodenal bulb in the pathogenesis of duodenal ulcer.

BACKGROUND: The aim of this study was to determine whether the amount of Helicobacter pylori and the extent of gastric metaplasia in the duodenal mucosa play critical roles in the pathogenesis of duodenal ulcer. METHODS: Duodenal and gastric biopsy specimens were obtained from H. pylori-positive patients with duodenal ulcer, gastric ulcer or chronic gastritis. The extent of gastric metaplasia was evaluated histologically and endoscopically using the methylene blue test. In this study, we performed competitive polymerase chain reaction, a highly sensitive and quantitative method for determining the amount of H. pylori gastric and duodenal mucosa. The prevalence and extent of gastric metaplasia and the amount of H. pylori in the duodenal bulb in the three patient groups were compared. The correlation between the amount of H. pylori in the duodenum and gastric antrum and extent of gastric metaplasia were also determined. RESULTS: The prevalence and extent of gastric metaplasia and the amount of H. pylori in the duodenal bulb in patients with duodenal ulcer were much higher than in patients with gastric ulcer or chronic gastritis. A positive correlation was found between the amount of H. pylori in the duodenum and the extent of gastric bulb and that in the antrum. CONCLUSIONS: The findings of this study indicate that H. pylori colonization in the duodenal bulb may play a critically important role in the pathogenesis of duodenal ulcer and that the amount of H. pylori in the duodenal bulb may be related to the amount of H. pylori in the gastric antrum and the extent of gastric metaplasia in the duodenal bulb.

Adult↗
PubMed2000

Association of Helicobacter pylori infection with atrophic gastritis and intestinal metaplasia.

AIMS: To evaluate the effect of Helicobacter pylori infection and aging on atrophy and intestinal metaplasia of the gastric mucosa. METHODS: One hundred and sixty-three patients were divided into three age groups and underwent an upper gastrointestinal endoscopy where no esophagitis, peptic ulcers, or malignancies were detected. Two biopsy specimens were obtained from the anterior and posterior walls of the antrum and of the fundus. These were used to evaluate the grade of gastritis, bacterial culture and histologic evidence of H. pylori infection. RESULTS: Helicobacter pylori infection was found to be directly associated with an increased risk of gastritis grade (odds ratio (OR) = 90 (95% CI; 30-270)). An age of 60 years and older along with H. pylori infection was also strongly associated with an increased risk of atrophy (OR = 6.6, (95% CI; 2.9-15.2)); OR = 9.8, (95% CI; 2.7-35.4)), as was intestinal metaplasia of the gastric mucosa (OR = 5.5, (95% CI; 1.7-17.6)); OR = 7.9, (95% CI; 2.8-46.1)). The prevalence of atrophic gastritis increased with advancing age in H. pylori-infected patients, but no such phenomenon was observed in H. pylori-uninfected patients. The prevalence of intestinal metaplasia significantly increased with advancing age, irrespective of the presence of H. pylori infection. In addition, H. pylori uninfected female patients had a decreased risk of intestinal metaplasia. CONCLUSIONS: These results suggest that atrophic gastritis is not a normal aging process, but instead is likely to be the result of H. pylori infection, while intestinal metaplasia is caused by both the aging process and H. pylori infection. A decreased risk of intestinal metaplasia found in uninfected female subjects may partly explain the lower prevalence of gastric cancer in females than in males.

Adult↗
PubMed2002

The significance and etiology of intestinal metaplasia of the esophagogastric junction.

Biopsies from the vicinity of the esophagogastric junction occasionally show foci of intestinal metaplasia. Whether these biopsies represent Barrett's esophagus in all cases is controversial and of clinical importance because patients with Barrett's esophagus are at significantly increased risk for developing esophageal adenocarcinoma. Recent evidence suggests that intestinal metaplasia of the gastric cardia is also quite common. Although prospective data are relatively sparse, it has been suggested that the risk of progressing to dysplasia and adenocarcinoma is significantly lower for intestinal metaplasia of the gastric cardia when compared with esophageal intestinal metaplasia (Barrett's esophagus). Immunohistochemical stains for cytokeratins 7 and 20 may be useful in more precisely localizing the site of intestinal metaplasia in biopsy specimens taken from the vicinity of the esophagogastric junction. Correlation of all clinical, endoscopic, histologic, and immunohistochemical data may be used by the gastroenterologist to determine the likely source of the intestinal metaplasia and whether the patient should be followed by endoscopic surveillance.

Adenocarcinoma↗
PubMed2006

A new method of diagnosing gastric intestinal metaplasia: narrow-band imaging with magnifying endoscopy.

BACKGROUND AND STUDY AIMS: With endoscopy, there is a high rate of interobserver variability in the identification of gastric intestinal metaplasia, and the endoscopic findings correlate poorly with the histological findings. Previous studies by our group investigating the use of a narrow-band imaging system with magnifying endoscopy (NBI-ME) in the gastric mucosa suggested that the appearance of a light blue crest (LBC) on the epithelial surface may be a distinctive endoscopic finding associated with the presence of intestinal metaplasia. The aim of the present study was to clarify the value of NBI-ME for diagnosing gastric intestinal metaplasia. PATIENTS AND METHODS: The LBC was defined as a fine, blue-white line on the crests of the epithelial surface/gyri. To investigate the histology underlying the appearance of LBC, 44 biopsy specimens were obtained from regions containing LBC and 44 from non-LBC mucosa in 34 patients with atrophic gastritis. Three endoscopists then carried out NBI-ME in 107 consecutive patients to validate the diagnostic accuracy of the novel endoscopic technique. The degree of correlation between the LBC grading and the histological parameters of intestinal metaplasia was then assessed. RESULTS: The LBC grading correlated with cells that were positive for CD10 ( P = 0.0001) and Alcian blue ( P = 0.036). The appearance of LBC correlated with histological evidence of intestinal metaplasia with a sensitivity of 89 % (95 % CI, 83 - 96 %), a specificity of 93 % (95 % CI, 88 - 97 %), a positive predictive value of 91 % (95 % CI, 85 - 96 %), a negative predictive value of 92 % (95 % CI, 87 - 97 %), and an accuracy of 91 % (95 % CI, 88 - 95 %). CONCLUSIONS: In narrow-band imaging with magnifying endoscopy, observation of a light blue crest on the epithelial surface in the gastric mucosa is a highly accurate sign of the presence of histological intestinal metaplasia.

Adult↗
PubMed2001

Immunohistochemical expression of the intracellular component of galectin-8 in squamous cell metaplasia of the bronchial epithelium in neoplastic and benign processes.

Specified galectins are known to play a role in regulating cell proliferation, differentiation, adhesion and migration. Po66, a mouse IgG1 monoclonal antibody produced by immunization against squamous cell cancer, reacts against a carbohydrate-binding protein (Po66-CBP), recently shown to be a member of the galectin family with a strong homology with galectin-8 (PCTA-1), identified as a human tumor-associated antigen. We studied Po66 in squamous metaplasia of the bronchi in order to determine whether it could be specifically involved in neoplastic conditions and if so, if it would be helpful in distinguishing metaplasia at risk of cancer. Twenty-eight formalin-fixed, paraffin-embedded archival tissues of 17 metaplasias with SCC, 3 metaplasia with distant neoplastic disease and 8 metaplasias with an inflammatory process, were immunostained using a streptavidin biotin peroxydase method. The squamous metaplasias were positively stained in non-neoplastic disease as well as in neoplastic processes. Expression was also observed in stromal and normal cells. Po66-CBP was not associated with a pre-neoplastic character. We discussed the expression of this intra-cellular component of galectin-8 according to the functions of galectins in cellular differentiation, host reaction against tumor, and inflammation.

Biomarkers, Tumor↗
PubMed1981

Adenomatoid metaplasia of prostatic urethra.

Adenomatoid metaplasia, or so-called nephrogenic metaplasia, is an uncommon alteration of urothelium associated with prior trauma and/or chronic infection. Although the majority of reported cases of adenomatoid metaplasia have involved the urinary bladder, two cases of patients in whom the metaplastic changes were present in tissue from prostatic resections are presented. The fact that both patients had undergone prior transurethral resections of the prostate further supports the association between adenomatoid metaplasia and trauma. Confusion of adenomatoid metaplasia with prostatic ductal carcinoma in one of the cases emphasizes the importance of the recognition of this lesion. The distinction of adenomatoid metaplasia from ductal carcinomas and from other benign proliferative lesions in the prostatic urethra is discussed.

Adenoma↗
PubMed1998

Cytotoxin-associated gene A-positive Helicobacter pylori infection in the elderly. Association with gastric atrophy and intestinal metaplasia.

To evaluate if the infection with strains of cytotoxin-associated gene A (CagA)-positive Helicobacter pylori is associated with either peptic ulcer and gastric atrophy or intestinal metaplasia in the elderly, we studied 71 H. pylori-positive patients older than 62 years old (34 men, 37 women; mean age, 77.5 years; range, 62-89 years) affected with gastric ulcer (GU) (n = 10), duodenal ulcer (DU) n = 22), or chronic gastritis (CG) (n = 39). H. pylori infection was documented by means of gastric histology, rapid urease test, and polymerase chain reaction (PCR) assay performed on gastric biopsies using two sets of primers: one for the ureC gene specific for H. pylori, and the second specific for the CagA gene. H. pylori-CagA positivity was significantly more common in patients with GU (9 of 10, 90%) than with DU (11 of 22, 50%; p < 0.05) or CG (17 of 39, 43.5%; p = 0.01). Gastric atrophy and intestinal metaplasia were significantly more common in CagA-positive patients than in CagA-negative patients (gastric atrophy: 40.54% vs 11.76, p = 0.007; intestinal metaplasia: 40.54% vs 14.70%, p = 0.01). No difference in prevalence of gastric atrophy and intestinal metaplasia was found in patients divided according to pathology (GU, DU, or CG). Logistic regression demonstrated that gastric atrophy and intestinal metaplasia were independent factors significantly associated with CagA-positivity (gastric atrophy: odds ratio = 4.53, 95% confidence interval 1.25-16.4; intestinal metaplasia: odds ratio = 3.44, 95% confidence interval 1.01-11.7). Our findings help to confirm the hypothesis that an infection with CagA-positive H. pylori strains may be catalytic in inducing gastric changes which can evolve into malignancies.

Aged↗
PubMed2005

Hidradenoma papilliferum with oxyphilic metaplasia: a clinicopathological study of 18 cases, including detection of human papillomavirus.

Reported here are 18 cases of hidradenoma papilliferum with oxyphilic metaplasia. All patients were women ranging in age from 29 to 74 years. Each presented clinically with a small, solitary tumor in the anogenital region. Microscopically, in addition to classic histopathological features, in every case there was oxyphilic metaplasia of the constituent epithelial cells. This finding could be likened to apocrine metaplasia, a term used in breast pathology. Other histopathological findings observed in this series, analogous to benign breast disease, included sclerosing adenosis-like changes, atypical apocrine adenosis-like changes, changes corresponding to usual ductal epithelial hyperplasia, epitheliomatosis with a streaming growth pattern, lamprocyte-like changes, clear cell change of the myoepithelium, foamy histiocyte reaction, and stromal fibrosis. Immunohistochemistry inferred that in the majority of cases oxyphilic metaplasia resulted from more lysosomes, whereas numerous mitochondria were detected in only 3 cases. Using 2 different PCR methods we identified HPV in 4 of 15 cases of hidradenoma with oxyphilic metaplasia. In addition, HPV was detected in 3 of 16 conventional papillary hidradenomas used as a control group. The following HPV types were identified: 16, 31, 33, 53, and 56. The last type was found in 5 cases. More than one HPV type from a single lesion was seen in 5 cases. Our observations are consistent with previous publications noting similarities between tumors of the breast and sweat glands. Oxyphilic metaplasia, areas with solid growth, and changes simulating atypical apocrine adenosis are rare and poorly recognized in hidradenoma papilliferum and may cause diagnostic difficulties; in our cases several submitting pathologists suspected malignancy. A causal role for HPV in hidradenoma papilliferum cannot be confirmed from our results, as the detection rate is too low. The exact role of the HPV in etiology and pathogenesis of this neoplasm has yet to be determined.

Adenoma, Sweat Gland↗
PubMed2005

Ciliated surface in the esophagogastric junction zone: a precursor of Barrett's mucosa or ciliated pseudostratified metaplasia?

We have previously reported squamous metaplasia-like change at the esophagogastric junction (EGJ). In the present study, we examined these lesions histologically and by immunohistochemistry and electron microscopy. Samples of EGJ mucosa, 3 cm long and comprising 1.5-cm long portions of both columnar and squamous mucosa, were obtained from 43 esophagectomy resection specimens. Squamous metaplasia-like change was observed in 21 (49%) of the 43 cases. The squamous metaplasia-like change was generally positive with immunohistochemical stains for tubulin and cytokeratins (CKs) 4, 7, 8, 13, and 18, and was generally negative with stains for CKs 10, 14, and 20. This pattern of immunoreactivity is very similar to that of bronchial mucosa. Also, many cilia were detected at the apices of the cells by electron microscopy in 5 (31%) of the 16 cases that were able to be examined. Therefore, squamous metaplasia-like change at the EGJ has both a similar appearance and a similar immunohistochemical profile to respiratory bronchial epithelium. These findings may suggest that squamous metaplasia-like change at the EGJ is not a precursor of Barrett's mucosa but rather is a form of pseudostratified metaplasia.

Aged↗
PubMed1992

Site-dependent development of complete and incomplete intestinal metaplasia types in the human stomach.

The topographical distribution of complete and incomplete types of intestinal metaplasia in human stomach samples was investigated in order to elucidate their mutual histogenetic relationship and significance in carcinogenesis. Subgross stereomicroscopic examination of alcian blue and hematoxylin-stained gastric mucosae allowed clear distinction of complete and incomplete intestinal metaplasia types as white (with or without purple hue) and purple foci, respectively, against the background magenta areas of non-intestinalized mucosa. Intestinal metaplasias which developed in the fundic area were predominantly of the complete type whereas those of the antrum were a mixture of both with a distinct predilection for expression of the incomplete type. Although there was some variation among foci regarding the hue of white or purple, the color feature was principally homogeneous within each individual intestinal metaplasia focus. Thus phenotypic analysis indicated intestinal metaplasia expression to be clearly influenced by intragastric topography. The study did not provide any evidence that a shift from incomplete to complete type intestinal metaplasia may occur with time or that the incomplete type may be more intimately associated with development of well-differentiated carcinomas.

Adult↗
PubMed1998

Expression of cytochrome P450 3A4 in foveolar epithelium with intestinal metaplasia of the human stomach.

The expression of cytochrome P450 3A4 (CYP3A4) in the foveolar epithelium of the human stomach with intestinal metaplasia was studied using immunohistochemistry, western blotting and reverse transcription polymerase chain reaction (RT-PCR). CYP3A4 was immunohistochemically detected in the foveolar epithelium with intestinal metaplasia, but was not detected in foveolar epithelium without intestinal metaplasia, in the pyloric gland or in the fundic gland of the stomach. Western blotting and RT-PCR demonstrated that CYP3A4 protein and mRNA were expressed in the liver and pyloric gland mucosa with intestinal metaplasia, but not in the fundic gland mucosa without intestinal metaplasia. Possible roles of CYP expression in the gastric mucosa with intestinal metaplasia in human stomach carcinogenesis are briefly discussed.

Cytochrome P-450 CYP3A↗
PubMed1986

The prognostic value of sulphomucin positive intestinal metaplasia in the development of gastric cancer.

Gastric biopsy specimens from 230 patients with chronic atrophic gastritis were investigated with the use of mucin stains for the presence and type of intestinal metaplasia. Metaplasia was not shown in 59 cases; 92 of the 171 cases with metaplasia were sulphomucin positive and 79 were negative. The patients were followed-up from 1976 to 1985. Eight patients were registered as having gastric cancer over this period. However, five of them had to be eliminated from the study because on careful review of all the clinical data it was clear that they had gastric cancer at the time of the biopsy. Two of the three remaining patients had sulphomucin negative biopsies. Thus, only one patient out of 90 with chronic atrophic gastritis and sulphomucin positive intestinal metaplasia developed gastric cancer when followed-up for 8-9 years. None of the patients with unequivocal type IIb metaplasia developed gastric cancer. We conclude that sulphomucin positive intestinal metaplasia does not identify a high risk group and its recognition is thus of no value in surveillance for gastric cancer.

Adult↗
PubMed1993

Pathology of the gastric antrum and body associated with Helicobacter pylori infection in non-ulcerous patients: is the bacterium a promoter of intestinal metaplasia?

A series of 115 consecutive, non-ulcerous, dyspeptic patients were examined for Helicobacter pylori (H. pylori) colonization in the gastric antral and/or body mucosa using Giemsa staining. Findings were correlated with the presence and degree of activity of superficial gastritis, deep gastritis, atrophic gastritis and with the presence of intestinal metaplasia. The prevalence of H. pylori positivity was 61.7%. In 59 of the 71 positive patients (83%), H. pylori was detected in the antrum or in both the antral and oxyntic mucosa. In the remaining 12 positive patients, H. pylori was detected only in the oxyntic mucosa nad in all these cases, the antrum showed intestinal metaplasia associated with atrophic gastritis (25%). In both antral and oxyntic mucosa, the activity of the gastritis was significantly correlated with H. pylori colonization. Linear logistic regression analysis showed that in patients with intestinal metaplasia the presence of H. pylori infection was significant in predicting the presence of more extensive intestinal metaplasia after adjusting for age. The prevalence of intestinal metaplasia types II and III was 65.5% in the H. pylori positive and 25% in the H. pylori negative patients. The antral mucosa is thought to be the elective site for H. pylori related histological lesions. At a later stage, H. pylori can be detected only in the oxyntic area while the antral mucosa shows extensive metaplastic or atrophic lesions. We would suggest that H. pylori plays a promotional role in the morphogenesis of intestinal metaplasia.

Adolescent↗
PubMed1985

Tubular adenoma with focal squamous metaplasia of the ascending colon.

A case of tubular adenoma with focal squamous metaplasia of the ascending colon in a 66-year-old male is reported. The tumor was a pedunculated polyp with a size of 1.5 X 1.4 X 0.9 cm. Histologically, the tumor showed tubular adenoma with moderate to severe atypia, was accompanied by focal squamous metaplasia. It is thought that squamous epithelial polyp may be derived from colonic adenoma with squamous metaplasia, and that the malignant change of colonic adenoma with squamous metaplasia may lead to squamous cell carcinoma, adenosquamous carcinoma, and mucoepidermoid carcinoma. Only seven cases of colonic adenoma with squamous metaplasia have been reported previously in the literature, and it is yet necessary to discuss the histogenesis, significance, and natural history of colonic adenoma with squamous metaplasia.

Aged↗
PubMed1986

Intestinal metaplasia-dysplasia-carcinoma sequence of the gallbladder.

One thousand cases of resected gallbladders were histologically investigated by serial step sections. Intestinal metaplasia was found at rates of 4.0% and 30.6% in the cases without and with stone, respectively. It was found at rates of 69.8% and 61.1% in the cases of dysplasia and carcinoma, respectively. The goblet cells were found at rates of 34.5% and 26.3% in the lesions of carcinoma and dysplasia, respectively. On the other hand, the dysplasia and adenoma intermingled in the tumor tissue at the rates of 22.2% and 8.3% in 36 cases of carcinoma, respectively. Although normal epithelial cells of the gallbladder contain mainly sulfomucin, the goblet cells have sialomucin. The ratio of sialomucin-containing cells increased in the tissue of dysplasia and carcinoma. As to their location, intestinal metaplasia, dysplasia, and carcinoma showed a similar distribution in the gallbladder. Accordingly, it should be considered that the sequence of intestinal metaplasia-dysplasia-carcinoma is significant. Pseudo-pyloric glandular metaplasia was found at rates of 45.5% in the cases of cholecystitis without stone, 77.2% in those with stone, 100% in those with dysplasia, and 72.3% in those with carcinoma. However, it should be considered that pseudo-pyloric glandular metaplasia has less relationship for the bases of carcinogenesis as compared with intestinal metaplasia.

Adult↗
PubMed2000

Long-term follow-up of intestinal metaplasia of the gastric cardia.

OBJECTIVE: Recent studies have found a relatively high prevalence of gastric cardia intestinal metaplasia in individuals presenting for elective upper endoscopy. It has been hypothesized that this lesion may be a precursor of gastric cardia cancer. Our objective was to identify the incidence of dysplasia in patients with gastric cardia intestinal metaplasia. METHODS: Twenty-eight patients who had previously been identified with cardia intestinal metaplasia had follow-up examinations performed. None of the patients had dysplasia at the time of diagnosis. All had an examination at 1 yr, and 20 patients had an examination at 3 yr after diagnosis. During follow-up examinations all patients underwent vital staining with methylene blue to help identify areas of intestinal metaplasia in the cardia. Two to four biopsies were taken from blue-stained mucosa. Histological specimens were stained using a combination of hematoxylin and eosin with Alcian blue at pH 2.5. RESULTS: There were 27 men and one woman with a mean age of 69.8 yr (range, 48-83 yr). The mean length of follow-up was 2.5 yr (range, 12-46 months). Only one patient was diagnosed with dysplasia (low-grade) during the study, for an incidence of 1.4% per yr. CONCLUSIONS: The prevalence (0%) and incidence (1.4%/yr) of dysplasia in cardia intestinal metaplasia are low. Although further studies are needed, screening and surveillance for gastric cardia intestinal metaplasia is unlikely to be clinically useful for the prevention of gastric cardia cancer.

Aged↗
PubMed2001

Geographic differences in the distribution of intestinal metaplasia in duodenal ulcer patients.

OBJECTIVE: A strong correlation exists between atrophic gastritis and the intestinal type of gastric carcinoma. Duodenal ulcer disease characteristically has an antral predominant gastritis and a lower risk for gastric cancer. The aim of this study was to investigate the extent and distribution of intestinal metaplasia in duodenal ulcer in countries differing in gastric cancer incidence. METHODS: Topographically mapped gastric biopsy specimens (median 11) were obtained from patients with duodenal ulcer in four countries (Korea, Colombia, USA, and South Africa). Sections were stained with a triple stain and evaluated for Helicobacter pylori (H. pylori), active inflammation, and intestinal metaplasia. RESULTS: One hundred and sixty-five patients with duodenal ulcer were examined (29 from Korea, 52 from Colombia, 62 from the USA, and 22 from South Africa). The percentage of biopsies with intestinal metaplasia was significantly greater in Korean patients (86%) compared with that in other countries (50%) (p = 0.0004). Intestinal metaplasia was most prevalent in the antrum lesser curve and greater curve, and the body lesser curve. Intestinal metaplasia was present in the gastric corpus of 38% of duodenal ulcer patients from Korea compared with an average of 10% elsewhere (p = 0.018). No differences were observed in the density or distribution of H. pylori infection or in the degree of active gastritis between countries. CONCLUSIONS: Although antral predominant gastritis is the prevalent pattern of gastritis in duodenal ulcer, intestinal metaplasia in the gastric corpus may be found with geographic differences. These findings suggest that duodenal ulcer and gastric cancer are not mutually exclusive diseases but are rather ends of the spectrum of H. pylori infection.

Adult↗