Relationship between <i>Helicobacter pylori</i> infection and gastric metaplasia in the duodenal bulb in the pathogenesis of duodenal ulcer

Futami, Hajime; Takashima, Misako; Furuta, Takahisa; Hanai, Hiroyuki; Kaneko, Eizō

doi:10.1046/j.1440-1746.1999.01824.x

Cited by 16 publications

(15 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It has been reported that neither the prevalence nor the extent of GM was affected by H. pylori status (5,6,9,22). In contrast, some studies found such a relationship between the extent of GM in the duodenum and the amount of H. pylori in the gastric antrum or in the duodenal bulb (3,4,13,17). Our study showed that both the presence and the extent of GM in nodular duodenitis are related to the presence of H. pylori infection.…”

Section: Discussioncontrasting

confidence: 91%

“…It has been speculated that H. pylori infection induces a high level of acid burden in the duodenum by increasing gastrin secretion, which may influence the development of GM. It has been shown that the amount of H. pylori in the duodenal bulb may be related to the extent of GM (3). Theoretically, regression of GM may be induced by eradication of H. pylori or acid-suppression therapy.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Duodenal gastric metaplasia and Helicobacter pylori infection in patients with diffuse nodular duodenitis

Chen

et al. 2007

Braz J Med Biol Res

View full text Add to dashboard Cite

Whether the regression of gastric metaplasia in the duodenum can be achieved after eradication of Helicobacter pylori is not clear. The aim of the present study was to investigate the relationship between H. pylori infection and gastric metaplasia in patients with endoscopic diffuse nodular duodenitis. Eighty-six patients with endoscopically confirmed nodular duodenitis and 40 control patients with normal duodenal appearance were investigated. The H. pylori-positive patients with duodenitis received anti-H. pylori triple therapy (20 mg omeprazole plus 250 mg clarithromycin and 400 mg metronidazole, all twice daily) for one week. A control endoscopy was performed 6 months after H. pylori treatment. The H. pylori-negative patients with duodenitis received 20 mg omeprazole once daily for 6 months and a control endoscopy was performed 2 weeks after treatment. The prevalence of H. pylori infection was 58.1%, and the prevalence of gastric metaplasia was 57.0%. Seventy-six patients underwent endoscopy again. No influence on the endoscopic appearance of nodular duodenitis was found after eradication of H. pylori or acid suppression therapy. However, gastric metaplasia significantly decreased and complete regression was achieved in 15/28 patients (53.6%) 6 months after eradication of H. pylori, accompanied by significant improvement of other histological alterations. Only mild chronic inflammation, but not gastric metaplasia, was found in the control group, none with H. pylori infection in the duodenal bulb. Therefore, H. pylori infection is related to the extent of gastric metaplasia in the duodenum, but not to the presence of diffuse nodular duodenitis.

show abstract

Section: Discussioncontrasting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Duodenal gastric metaplasia and Helicobacter pylori infection in patients with diffuse nodular duodenitis

Chen

et al. 2007

Braz J Med Biol Res

View full text Add to dashboard Cite

show abstract

“…The study subjects were given an antifoaming agent (Minifoam), and then gastroduodenal endoscopies were performed while the subjects were under local anesthesia with lidocain (Xylocain). A previously described method (14,34), with some modifications (A. Edebo et al, unpublished data), was used to identify areas of DGM. The endoscope and the duodenal bulb were flushed with water, and 7 to 10 ml of methylene blue (1 mg/ml) was instilled.…”

Section: Methodsmentioning

confidence: 99%

Decreased Epithelial Cytokine Responses in the Duodenal Mucosa ofHelicobacter pylori-Infected Duodenal Ulcer Patients

Stromberg¹,

Edebo

Svennerholm³

et al. 2003

Clin Vaccine Immunol

View full text Add to dashboard Cite

Helicobacter pylori colonizes the human stomach and areas of gastric metaplasia in the duodenum, but only a minority of those that are infected develop symptoms, e.g., peptic ulcers. Although most ulcers occur in the duodenum, almost all studies of mucosal immune responses against the infection have been limited to responses in the stomach. In the present study we evaluated whether there are differences in the levels of proinflammatory cytokines as well as immunoregulatory cytokines in the duodenal mucosa of duodenal ulcer (DU) patients and asymptomatic (AS) carriers which may be related to the development of duodenal ulcers. Duodenal biopsy specimens collected from normal mucosa as well as metaplastic mucosa of DU patients, AS carriers, and uninfected controls were analyzed for a number of cytokines by immunohistochemistry. Interestingly, the level of epithelial staining for several cytokines, e.g., interleukin-8 (IL-8), transforming growth factor ␤ (TGF-␤), and gamma interferon (IFN-␥), was found to be significantly lower in DU patients than in AS carriers and uninfected individuals. No differences were observed when cytokine staining in normal and metaplastic biopsy specimens was compared. However, larger numbers of IL-8-, IL-6-, TGF-␤-, and IFN-␥-positive mononuclear cells were observed in the duodenal lamina propria of both DU patients and AS carriers than in that of the uninfected controls. Our finding that a number of cytokines that may be important for the mucosal host defense against H. pylori are strongly decreased in the duodenal epithelium of ulcer patients suggests that a down-regulated immune response plays a role in the development of duodenal ulcers.

show abstract

“…H. pylori is strongly associated with duodenal ulcer disease. 2 Moreover, it has been shown that patients with recurrent duodenal ulcer disease have higher incidences of not only H. pylori but also DGM, 16 and duodenal H. pylori infections are always observed in the areas of DGM, although the reverse is not always true. 16 On the basis of these observations, it has been hypothesized that H. pylori infection and DGM are linked in the pathogenic mechanism that generates duodenal ulcers, as follows.…”

Section: Discussionmentioning

confidence: 99%

“…1 It is now widely accepted that H. pylori is the main pathogen of peptic ulcer diseases and is more strongly associated with duodenal ulcers than with gastric ulcers. 2 Duodenal ulcers have been shown to occur relatively frequently in both adults and adolescents. Rates of Helicobacter pylori positivity in the gastric antrum and duodenal gastric metaplasia throughout an 11-year study period (1995)(1996)(1997)(1998)(1999)(2000)(2001)(2002)(2003)(2004)(2005).…”

Section: Introductionmentioning

confidence: 99%

Helicobacter pyloriInfection and Duodenal Gastric Metaplasia in Healthy Young Adults

Seo

Park

et al. 2013

Korean J Gastroenterol

View full text Add to dashboard Cite

Background/Aims: Duodenal ulcers occur relatively frequently in adolescents, like in adults, and may relate to Helicobacter pylori infection and duodenal gastric metaplasia (DGM). This study investigated the association between H. pylori infection and DGM in healthy adults aged 20-29. Methods: Between 1995 and 2005, endoscopic biopsies of the duodenum, antrum and body were taken from healthy, young volunteers, who were first-year medical students, faculty staff, residents, and research assistants of Gyeongsang National University in Jinju, Korea. Urease tests were performed and the extent of DGM and histopathological grades according to the Updated Sydney System were determined. Results: In total, 662 subjects were enrolled (429 males and 233 females). The median age was 22.3 years. The overall incidence of DGM was 11.5% but DGM was more frequent in males (15.4%) than in females (4.3%) (p＜0.0001). While H. pylori positivity rates changed significantly during the 1995-2005 period (p＜0.01), the incidences of DGM did not. DGM was observed in 7.2% and 14.9% of subjects who were and were not colonized with H. pylori, respectively. DGM was also associated with less severe chronic gastritis and the absence of active gastritis in both the antrum and body, and the absence of follicles in the antrum (p<0.05). Conclusions: These findings suggested that DGM is not rare in healthy young adults and is unrelated to gastric H. pylori infection. (Korean J Gastroenterol 2013;61:191-195)

show abstract

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

Cited by 16 publications

References 20 publications

Duodenal gastric metaplasia and Helicobacter pylori infection in patients with diffuse nodular duodenitis

Duodenal gastric metaplasia and Helicobacter pylori infection in patients with diffuse nodular duodenitis

Decreased Epithelial Cytokine Responses in the Duodenal Mucosa ofHelicobacter pylori-Infected Duodenal Ulcer Patients

Helicobacter pyloriInfection and Duodenal Gastric Metaplasia in Healthy Young Adults

Contact Info

Product

Resources

About