Clinicopathologic Features of the Duodenum Related to the Genesis of Duodenal Gastric Metaplasia / 대한소화기내시경학회지

BACKGROUND/AIMS: It has been suggested that gastric metaplasia in the duodenum is prerequisite for duodenal ulcer. The aim of this study was to investigate the role of clinicopathologic parameters of the duodenum such as endoscopic diagnosis, pathologic findings and Helicobacter pylori (H. pylori) infection on the development of gastric metaplasia. METHODS: Endoscopic records as well as pathologic findings of 390 patients were reviewed. The degree of gastric metaplasia in duodenum was evaluated. H. pylori infection was determined by immunohistochemical staining. RESULTS: The degree of gastric metaplasia was higher in duodenal ulcers and hyperplastic duodenal polyps than in chronic duodenitis. The degree of gastric metaplasia was closely related to severe acute inflammation, mild chronic inflammation and H. pylori infection in duodenum. Duodenal ulcers showed higher acute inflammation and a higher incidence of H. pylori infection than hyperplastic polyps and chronic duodenitis. CONCLUSIONS: Gastric metaplasia in duodenal ulcers may be related to duodenal inflammation and H. pylori infection, whereas in hyperplastic polyps gastric metaplasia may occur by another mechanism.

Relationship of Gastric Metaplasia of the Duodenum with Age, Duodenal Ulcer and Helicobacter pylori Infection

BACKGROUND: Gastric metaplasia of the duodenum is thought to be associated with the pathogenesis of duodenal ulcer. We investigated the pathological features of gastric metaplasia and their relation to age, gender, duodenal ulcer and H. pylori infection. METHODS: We reviewed the duodenal endoscopic findings of 535 patients (age range: 0 to 87) and the microscopic slides of the duodenal biopsy specimens. RESULTS: Gastric metaplasia was first noted at the age of 4 and the prevalence increased thereafter until the patients' mean age reached about 30. The prevalence of gastric metaplasia was 53.7% after 30 years of age. As the metaplasia became severer, it became more polypoid in appearance and it more often contained parietal cells. Gastric metaplasia was more frequently observed or severe in duodenal ulcer patients, in males and in the first portion of the duodenum than in patients without duodenal ulcer, in females and in the second portion, respectively. There was a lack of correlation between gastric metaplasia and H. pylori infection. CONCLUSIONS: The prevalence and/or severity of gastric metaplasia of the duodenum increases with age, and it is thought that most duodenal ulcers develop in the areas of gastric metaplasia.

Endoscopic Features of Ectopic Gastric Mucosa in the Duodenum / 대한소화기내시경학회지

BACKGROUND/AIMS: The origin of gastric mucosa outside of the stomach may be developmental (heterotopic gastric mucosa) or acquired (gastric metaplasia). The aim of this study was to evaluate the endoscopic features, according to the subtypes, of the gastric mucosa outside the stomach in the duodenum. METHODS: A total of 30 consecutive patients who underwent esophagogastroduodenoscopy from January 2002 to August 2004 and who were confirmed histopathologically as having gastric mucosa outside the stomach were retrospectively analyzed. Twenty three patients were males and seven were females. RESULTS: Nine patients had heterotopic gastric mucosa and 21 patients had gastric metaplasia. Seven patients with heterotopic gastric mucosa were asymptomatic and 2 patients had dyspepsia, whereas 21 patients with gastric metaplasia had dyspepsia. The dyspepsia rate showed a significant difference between the two groups (p<0.001). Endoscopically, the appearance of the heterotopic gastric mucosa tended to resemble area gastricae (p=0.08). However, there were no statistically differences between the two groups for the endoscopic features of the duodenum. Other abnormal lesions in stomach and duodenum appeared more frequently in the gastric metaplasia than in the heterotopic gastric mucosa (p=0.004, p<0.001). There was no difference in the prevalence of Helicobacter pylori infection between the two groups. CONCLUSIONS: There are no specific endoscopic findings to differentiate heterotopic gastric mucosa from gastric metaplasia. The presence of symptoms and the associated gastroduodenal inflammatory lesions were more prominent in the gastric metaplasia compared with the heterotopic gastric mucosa.

Gastric metaplasia and Helicobacter pylori infection of duodenal mucosa in duodenal ulcer / 대한내과학회지

BACKGROUND: The roles of gastric metaplasia and Helicobacter pylori (H. pylori) infection of duodenal mucosa in the pathogenesis of duodenal ulcer has been emphasized. Though there are a few reports which compared degree of these two risk factors between the duodenal ulcer and control groups, the reports which compared ulcer site with nonulcer site within ulcer group are rare. The aim of this study was to compare the frequencies of gastric metaplasia and H. pylori infection between both sites within ulcer group, as well as between both groups. METHODS: The active duodenal ulcer patients group (n=30) and control group (n=31) were selected. The frequency of gastric metaplasia and H. pylori infection were compared among the ulcer sites, the nonulcer sites of ulcer patients, and the intact duodenal mucosa of controls. RESULTS: The frequencies of gastric metaplasia and H. pylori infection were higher at ulcer sites than nonulcer sites within ulcer group, however, there were no differences between the nonulcer sites of ulcer group and control group. Positivities of H. pylori infection at metaplastic area were not different at 3 compared sites. CONCLUSION: It seems that duodenal ulcer develop more frequently at area of gastric metaplasia infected by H. pylori. However, further evaulation about the pathogenesis of duodenal ulcer is necessary because there are lots of duodenal ulcer cases which are not accompanied by gastric metaplasia.

A Prospective Study on Duodenitis, Duodenal Ulcer, and Gastric Metaplasia in Children Infected by Helicobacter pylori / 대한소아소화기영양학회지

PURPOSE: Helicobacter pylori (H. pylori) infection has been known to be vital in the pathogenesis of duodenal ulcer disease in children as well as in adults. But the relationship between H. pylori infection and the histopathologic findings of the duodenum has not been explained obviously in children yet. So the aim of this study is to determine whether duodenitis and/or gastric metaplasia in the duodenum increases the risk of duodenal ulcer disease in children infected by H. pylori. METHODS: From October 2001 to April 2004 gastric and duodenal biopsies were performed in 177 children who visited Department of Pediatrics, Gil Hospital, Gachon Medical School. Biopsy sections were stained with hematoxylin and eosin and also with Giemsa for identification of H. pylori. The grades of duodenitis and gastric metaplasia were classified from 0 to 3 and from 0 to 4, respectively. RESULTS: The incidence of H. pylori infection was 54% in total patients. Amongst 163 children with duodenitis there was a lack of correlation between H. pylori infection and the grade of duodenitis. Amongst 11 patients with duodenal ucler, only 4 children were infected by H. pylori. And amongst 5 patients with gastric metaplasia, H. pylori and duodenal ulcer were detected in 2 and 3 children, respectively. The occurrence of duodenal ulcer and gastric metaplasia were increased significantly in proportion to the grade of duodenitis (p<0.0001 and p=0.0365, respectively). CONCLUSION: As opposed to the results of previously reported articles, there were lacks of correlation between H. pylori infection and duodenitis, duodenal ulcer, and gastric metaplasia. So further study hould be done to clarify the effect of H. pylori on the duodenal histopathology in children infected by H. pylori.

Study on the Relation between Helicobacter Pylori Infection and Gastric Metaplasia in the Duodenum in the Duodenal Ulcer Patients / 中国医师杂志

Objective To study on the relation between Helicobacter pylori (Hp) infection and gastric metaplasia in the duodenum(DGM) in the duodenal ulcer(DU) patients to elucidate the pathogenesis of DU.Methods One hundred and twenty-one patients were examined by endoscopy, pathology and Hp infection test.Results The detection rates of Hp in stomach and in duodenal bulb were much higher in patients with DU(90 4%, 40 4%) than those in patients without DU(60 9%, 2 9%, both P

Relationship between Helicobacter pyloriinfection and gastric metaplasia in the mucosa of duodenal bulb / 中华消化杂志

Objective To investigate the relationship between Helicobacter pylori(H. pylori)infection and gastric metaplasia in the duodenal bulb and to pursue whether they play critical roles in pathogenesis of duodenitis and ulcer.Methods Eighty-two archive paraffin blocks of duodenal biopsy were obtained. All sections were stained with H-E, AB/PAS and Giemsa stains for histology, gastric metaplasia and H. pyloriassessment. There were 10 patients with normal duodenum, 47 with duodenitis and 25 with ulcer confirmed by endoscopy. Results There was a discrepancy in diagosis of the normal duodenal bulb mucosa between endoscopy and histopathology. Mild to moderate infiltration of inflammatory cell without gastric metaplasia were detected in 60% of cases with the normal duodenal bulb mucosa judged by endoscopy. Gastric metaplasia in duodenal bulb was the major phenomena in the patients with duodenitis and ulcer (37/82, 45%). H. pyloriinfection in the duodenal bulb always appeared in areas of gastric metaplasia. H. pyloriwas identified in 28 out of 37 (76%) cases in the gastric metaplasia mucosa. The prevalence of gastric metaplasia in the duodenal bulb between the patients with ulcer (72%) and duodenitis (40%) was significantly different (P=0.0078). The frequency of H. pyloricolonization was higher in the patients with duodenal ulcer (89%) than the patients with duodenitis (63%), but did not reach statistical significance(P=0.062). H. pyloriinfection was also higher in the ulcer patients with active, healed or scar stage, being 9/10, 5/6 and 2/2, respectively. Conclusions There is a difference in the frequency of H. pyloricolonization in the gastric metaplasia mucosa in the patients with ulcer and duodenitis, which suggests that infection with H. pylorimay play an important role in ulcer recurrence.

A Case of Polypoid Gastric Metaplasia in Duodenal Bulb / 대한소화기내시경학회지

Gastric metaplasia of the duodenum, defined as the presence of groups of gastric mucosal cell within normal duodenal epithelium, is an almost constant feature of duodenal ulcer. The pathogenesis of gastric metaplasia is unclear, but acid and Helicobacter pylori infection are contributory factors to the development of gastric metaplasia. Generally, endoscopic finding of gastric metaplasia in duodenum is typically patchy distribution in duodenal bulb, but polypoid gastric metaplasia in duodenum is very rare. We report that the patient who complaints of abdominal pain has a villous, polypoid gastric metaplasia in duodenal bulb without duodenal ulcer.

Gastric Metaplasia in Duodenum

The partial replacement of the human duodenal mucosa by epithelial cells containing gastric-type mucus(gastric metaplasia) is not an uncommon finding, and an emphasis on its etiological role in duodenal ulcerogenesis has been proposed. It is unclear, Furthermore, all the previous studies were done with endoscopic biopsy specimens. We reviewed a total of 118 surgically resected stomachs with attached duodenal stumps(24 cases of gastric ulcer, 15 duodenal ulcer and 79 advanced gastric cancer). The gastric-type mucous cells were homogeneously stained red with PAS in contrast to the intestinal cells which gave a strong PAS stainability only along the the brush border. The gastric metaplasia was seen near the tips or on the sides of the villi and occasionally in the crypts. It was observed in 8 cases(53%) in duodenal ulcer, 12 cases(50%) in gastric ulcer and 29 cases(37%) in gastric cancer. There were no significant statistical differences in incidence among the groups. Nevertheless, diffuse form of gastric metaplasia was more prevalent in patients with duodenal ulcer(p<0.05).