Evidence map›Paper›PMID 12235068›Full record

ArticleGut2002

Impact of Helicobacter pylori infection and mucosal atrophy on gastric lesions in patients with familial adenomatous polyposis.

S Nakamura, T Matsumoto, Y Kobori, M Iida

Open access · bronzeAbstract read
In one paragraph

Article in Gut, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.3field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

25 citing papers in PubMed, 74 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
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  5. Article
  6. Classification of fundic gland polyps for predicting gastric neoplasms in Helicobacter pylori-negative patients with familial adenomatous polyposis.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2024
    Article
  7. Gastric fundic gland polyposis and cancer development after eradication of Helicobacter pylori in patient with gastric adenocarcinoma and proximal polyposis of the stomach (GAPPS).Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2024
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Different phenotypes of gastric fundic gland polyposis and cancer in patients with familial adenomatous polyposis depending on Helicobacter pylori infection.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2019
    Article
  16. First report of an Asian family with gastric adenocarcinoma and proximal polyposis of the stomach (GAPPS) revealed with the germline mutation of the APC exon 1B promoter region.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2018
    Article
  17. Article
  18. Review
  19. Article
  20. Gastric tumours in FAP.Familial cancer · 2017
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

S NakamuraDepartment of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan. shonaka@intmed2.med.kyushu-u.ac.jp
T Matsumoto
Y Kobori
M Iida
Kawasaki Medical School · JPKyushu University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

aimsThe role of Helicobacter pylori and atrophic gastritis in the pathogenesis of gastric lesions in familial adenomatous polyposis (FAP) has not been clarified. PATIENTS: Thirty one patients with FAP.

methodsThe presence of fundic gland polyposis (FGP) and gastric adenoma (GA) was determined by upper endoscopy with biopsies. The degree of gastric mucosal atrophy and H pylori status were determined by serological and histological findings. Germline mutation in the adenomatous polyposis coli (APC) gene was determined by polymerase chain reaction based single strand conformation polymorphism and direct sequencing.

resultsGastric lesions were detected in 23 patients (74%). FGP and GA were found in 52% and 39%, respectively. APC gene mutation was identified in 22 of 30 patients. Patients with FGP were less frequently infected with H pylori than those without FGP (13% v 67%). The former patients had a lower degree of atrophy than the latter. Patients with GA tended to be more frequently infected with H pylori and they had higher degrees of atrophy than those without GA. When subjects were subdivided by gastric lesions (FGP alone, FGP+GA, GA alone, and negative groups), the GA alone group had the lowest pepsinogen I/II ratio and the highest seropositivity for H pylori. GA was found more frequently in patients positive for the APC mutation whereas no such a trend was observed in FGP.

conclusionsIn FAP, H pylori associated atrophic gastritis contributes negatively to FGP. It seems to contribute positively to GA, especially in patients with truncating APC gene mutation.

Indexed as

Helicobacter pyloriAdenomaAdenomatous Polyposis ColiAdolescentAdultAgedAtrophyChildFemaleGastric FundusGastric MucosaGastritisGenes, APCHelicobacter InfectionsHumansMalePepsinogen APepsinogen C

Identifiers

PMID12235068
PMCPMC1773380
OpenAlexW2120838811

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.