Pathogenesis of gastric metaplasia of the human duodenum

Role of Helicobacter pylori, gastric acid, and ulceration

S. Khulusi, Sunil Badve, P. Patel, R. Lloyd, J. M. Marrero, C. Finlayson, M. A. Mendall, T. C. Northfield

Research output: Contribution to journalArticle

79 Citations (Scopus)

Abstract

Background and Aims: The pathogenesis of gastric metaplasia (GM) in the duodenum is unclear. The aim of this investigation was to study the effect on the extent of GM of ulcer healing, Helicobacter pylori eradication, and acid suppression singly and in combination. The relationship between GM and gastroduodenal inflammation and H. pylori infection density was also studied. Methods: Duodenal and gastric antral biopsy specimens were obtained from H. pylori-positive patients with duodenal ulcer and from H. pylori-positive nonulcer subjects. Biopsy procedures from patients with duodenal ulcer were repeated after 6 months of treatment. Nonulcer subjects were treated symptomatically and did not undergo re-endoscopy. Results: Ulcer healing alone produced no change in GM or in gastroduodenal inflammation. H. pylori eradication produced a 42% reduction in GM and improvement in inflammation. Acid suppression produced a 43% reduction in GM but without a significant change in inflammation. A combination of H. pylori eradication and acid suppression produced an additive effect with a 66% reduction in GM. A positive relationship was detected between the extent of GM and antral H. pylori density, duodenitis score, and antral gastritis score. Conclusions: This study shows that the extent of duodenal GM is unrelated to the presence or absence of ulceration but is partly due to H. pylori and partly due to acid.

Original languageEnglish (US)
Pages (from-to)452-458
Number of pages7
JournalGastroenterology
Volume110
Issue number2
DOIs
StatePublished - 1996
Externally publishedYes

Fingerprint

Gastric Acid
Metaplasia
Duodenum
Helicobacter pylori
Stomach
Inflammation
Acids
Duodenal Ulcer
Duodenitis
Biopsy
Helicobacter Infections
Gastritis
Stomach Ulcer
Endoscopy
Ulcer

ASJC Scopus subject areas

  • Gastroenterology

Cite this

Pathogenesis of gastric metaplasia of the human duodenum : Role of Helicobacter pylori, gastric acid, and ulceration. / Khulusi, S.; Badve, Sunil; Patel, P.; Lloyd, R.; Marrero, J. M.; Finlayson, C.; Mendall, M. A.; Northfield, T. C.

In: Gastroenterology, Vol. 110, No. 2, 1996, p. 452-458.

Research output: Contribution to journalArticle

Khulusi, S, Badve, S, Patel, P, Lloyd, R, Marrero, JM, Finlayson, C, Mendall, MA & Northfield, TC 1996, 'Pathogenesis of gastric metaplasia of the human duodenum: Role of Helicobacter pylori, gastric acid, and ulceration', Gastroenterology, vol. 110, no. 2, pp. 452-458. https://doi.org/10.1053/gast.1996.v110.pm8566592
Khulusi, S. ; Badve, Sunil ; Patel, P. ; Lloyd, R. ; Marrero, J. M. ; Finlayson, C. ; Mendall, M. A. ; Northfield, T. C. / Pathogenesis of gastric metaplasia of the human duodenum : Role of Helicobacter pylori, gastric acid, and ulceration. In: Gastroenterology. 1996 ; Vol. 110, No. 2. pp. 452-458.
@article{81944fe124aa429fbd365942bed469e0,
title = "Pathogenesis of gastric metaplasia of the human duodenum: Role of Helicobacter pylori, gastric acid, and ulceration",
abstract = "Background and Aims: The pathogenesis of gastric metaplasia (GM) in the duodenum is unclear. The aim of this investigation was to study the effect on the extent of GM of ulcer healing, Helicobacter pylori eradication, and acid suppression singly and in combination. The relationship between GM and gastroduodenal inflammation and H. pylori infection density was also studied. Methods: Duodenal and gastric antral biopsy specimens were obtained from H. pylori-positive patients with duodenal ulcer and from H. pylori-positive nonulcer subjects. Biopsy procedures from patients with duodenal ulcer were repeated after 6 months of treatment. Nonulcer subjects were treated symptomatically and did not undergo re-endoscopy. Results: Ulcer healing alone produced no change in GM or in gastroduodenal inflammation. H. pylori eradication produced a 42{\%} reduction in GM and improvement in inflammation. Acid suppression produced a 43{\%} reduction in GM but without a significant change in inflammation. A combination of H. pylori eradication and acid suppression produced an additive effect with a 66{\%} reduction in GM. A positive relationship was detected between the extent of GM and antral H. pylori density, duodenitis score, and antral gastritis score. Conclusions: This study shows that the extent of duodenal GM is unrelated to the presence or absence of ulceration but is partly due to H. pylori and partly due to acid.",
author = "S. Khulusi and Sunil Badve and P. Patel and R. Lloyd and Marrero, {J. M.} and C. Finlayson and Mendall, {M. A.} and Northfield, {T. C.}",
year = "1996",
doi = "10.1053/gast.1996.v110.pm8566592",
language = "English (US)",
volume = "110",
pages = "452--458",
journal = "Gastroenterology",
issn = "0016-5085",
publisher = "W.B. Saunders Ltd",
number = "2",

}

TY - JOUR

T1 - Pathogenesis of gastric metaplasia of the human duodenum

T2 - Role of Helicobacter pylori, gastric acid, and ulceration

AU - Khulusi, S.

AU - Badve, Sunil

AU - Patel, P.

AU - Lloyd, R.

AU - Marrero, J. M.

AU - Finlayson, C.

AU - Mendall, M. A.

AU - Northfield, T. C.

PY - 1996

Y1 - 1996

N2 - Background and Aims: The pathogenesis of gastric metaplasia (GM) in the duodenum is unclear. The aim of this investigation was to study the effect on the extent of GM of ulcer healing, Helicobacter pylori eradication, and acid suppression singly and in combination. The relationship between GM and gastroduodenal inflammation and H. pylori infection density was also studied. Methods: Duodenal and gastric antral biopsy specimens were obtained from H. pylori-positive patients with duodenal ulcer and from H. pylori-positive nonulcer subjects. Biopsy procedures from patients with duodenal ulcer were repeated after 6 months of treatment. Nonulcer subjects were treated symptomatically and did not undergo re-endoscopy. Results: Ulcer healing alone produced no change in GM or in gastroduodenal inflammation. H. pylori eradication produced a 42% reduction in GM and improvement in inflammation. Acid suppression produced a 43% reduction in GM but without a significant change in inflammation. A combination of H. pylori eradication and acid suppression produced an additive effect with a 66% reduction in GM. A positive relationship was detected between the extent of GM and antral H. pylori density, duodenitis score, and antral gastritis score. Conclusions: This study shows that the extent of duodenal GM is unrelated to the presence or absence of ulceration but is partly due to H. pylori and partly due to acid.

AB - Background and Aims: The pathogenesis of gastric metaplasia (GM) in the duodenum is unclear. The aim of this investigation was to study the effect on the extent of GM of ulcer healing, Helicobacter pylori eradication, and acid suppression singly and in combination. The relationship between GM and gastroduodenal inflammation and H. pylori infection density was also studied. Methods: Duodenal and gastric antral biopsy specimens were obtained from H. pylori-positive patients with duodenal ulcer and from H. pylori-positive nonulcer subjects. Biopsy procedures from patients with duodenal ulcer were repeated after 6 months of treatment. Nonulcer subjects were treated symptomatically and did not undergo re-endoscopy. Results: Ulcer healing alone produced no change in GM or in gastroduodenal inflammation. H. pylori eradication produced a 42% reduction in GM and improvement in inflammation. Acid suppression produced a 43% reduction in GM but without a significant change in inflammation. A combination of H. pylori eradication and acid suppression produced an additive effect with a 66% reduction in GM. A positive relationship was detected between the extent of GM and antral H. pylori density, duodenitis score, and antral gastritis score. Conclusions: This study shows that the extent of duodenal GM is unrelated to the presence or absence of ulceration but is partly due to H. pylori and partly due to acid.

UR - http://www.scopus.com/inward/record.url?scp=0030040941&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0030040941&partnerID=8YFLogxK

U2 - 10.1053/gast.1996.v110.pm8566592

DO - 10.1053/gast.1996.v110.pm8566592

M3 - Article

VL - 110

SP - 452

EP - 458

JO - Gastroenterology

JF - Gastroenterology

SN - 0016-5085

IS - 2

ER -