Evidence map›Paper›PMID 11772960›Full record

ArticleGut2002

Helicobacter pylori stimulates pepsinogen secretion from isolated human peptic cells.

S Lorente, O Doiz, M Trinidad Serrano, J Castillo, A Lanas

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 24 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 2 pooled it
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

24 citing papers in PubMed, 2 syntheses or guidelines pooled it, 61 citations in OpenAlex.

  1. Guideline
  2. Gastric cancer screening using the serum pepsinogen test method.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2006
    Pooled it
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  8. Gut and liver · 2020
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  11. Immunopathological and Modulatory Effects ofOpen access Macedonian journal of medical sciences · 2018
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  15. The new modified ABCD method for gastric neoplasm screening.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2016
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Clinical relevance of cagPAI intactness in Helicobacter pylori isolates from Vietnam.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2010
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

S LorenteService of Gastroenterology, University Hospital, Zaragoza, Spain.
O Doiz
M Trinidad Serrano
J Castillo
A Lanas
Universidad de Zaragoza · ESHospital Clínico Universitario Lozano Blesa · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDifferent acid and peptic related gastroduodenal diseases are associated with both increased gastric secretion and Helicobacter pylori infection. Patients with H pylori associated gastritis or duodenal ulcer have increased serum pepsinogen levels which decrease after eradication. The mechanisms of H pylori induced gastric mucosal damage are not completely understood.

aimTo determine the effects of H pylori on pepsinogen secretion from isolated human peptic cells.

methodsDispersed human peptic cells were prepared from endoscopically obtained biopsy specimens after collagenase digestion, mechanical disruption, and density gradient centrifugation. H pylori was obtained from gastric biopsies (antrum and body), and cultured in non-selective and selective media. Isolates of H pylori were used at different concentrations (1 - 20 x 10(6) colony forming units (cfu)).

resultsH pylori (10(6) - 2 x 10(7) cfu) increased basal pepsinogen secretion in a concentration dependent manner. This stimulus was not observed with Escherichia coli. The increased secretion was in addition to that observed with 0.1 mM histamine and 0.1 mM dibutyryl-cyclic adenosine monophosphate. However, H pylori did not affect either carbamylcholine (0.1-10 microM) or cholecystokinin (1 microM) stimulated pepsinogen secretion. Addition of the nitric oxide synthase inhibitor N(w)-monomethyl-L-arginine (1 mM) inhibited H pylori induced cGMP generation and pepsinogen secretion, which were also reduced in the absence of extracellular calcium. H pylori induced pepsinogen secretion was not affected by the absence/presence of the cagA gene.

conclusionsH pylori increases pepsinogen secretion from human peptic cells through a calcium and nitric oxide mediated intracellular pathway. This effect is independent of the H pylori virulent cagA gene, and may be a mechanism of H pylori induced gastric mucosal damage.

Indexed as

Antigens, BacterialAdultAgedBacterial ProteinsCalciumCells, CulturedColony Count, MicrobialCyclic GMPEscherichia coliFemaleGastric MucosaHelicobacter pyloriHumansMaleMiddle Agedomega-N-MethylarginineAntigens, BacterialBacterial ProteinscagA protein, Helicobacter pyloriCalciumCyclic GMPomega-N-MethylargininePepsinogen A

Identifiers

PMID11772960
PMCPMC1773080
OpenAlexW2170276417

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.