Evidence map›Paper›PMID 20725788›Full record

ArticleDigestive diseases and sciences2011

Mechanism of acid hypersecretion post curative gastrinoma resection.

Jeremiah V Ojeaburu, Tetsuhide Ito, Pellegrino Crafa, Cesare Bordi, Robert T Jensen

Abstract read
In one paragraph

Article in Digestive diseases and sciences, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 27% 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

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. Guideline
  2. Review
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  4. Article
  5. Review
  6. Gastrinomas: Medical or Surgical Treatment.Endocrinology and metabolism clinics of North America · 2018
    Review
  7. Review
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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 4 institutions in 3 countries.

Jeremiah V OjeaburuDigestive Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bldg. 10, Rm. 9C-103, 10 CENTER DR MSC 1804, Bethesda, MD 20892-1804, USA. ojeaburu@hotmail.com
Tetsuhide Ito
Pellegrino Crafa
Cesare Bordi
Robert T Jensen
University of Parma · ITKyushu University · JPNational Institute of Diabetes and Digestive and Kidney Diseases · USNational Institutes of Health · US

Funding

Diagnosis, Natural History, Management,tumor biology of Gastrinomas/PETs/Neuroendocrine tumorsZIADK053200 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI JENSEN, ROBERT · 2009 to 2025
$4.3M
MANAGEMENT OF ISLET CELL TUMORSZ01DK053200 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI JENSEN, ROBERT · 1990 to 2008
$667k
Intramural NIH HHS Z01 DK053200Intramural NIH HHS Z99 DK999999Intramural NIH HHS ZIA DK053200
6 · The paper itself

Abstract

backgroundSome patients with Zollinger-Ellison syndrome post curative gastrinoma resection continue to show gastric acid hypersecretion; however, the mechanism is unknown.

aimThe aim of this study was to prospectively study acid secretion following curative gastrinoma resection and analyze factors contributing in patients with Zollinger-Ellison syndrome.

methodsFifty patients cured post gastrinoma resection were studied with serial assessments of acid secretory status, cure status and ECL-cell status/activity (with serial biopsies, CgA, urinary N-MIAA). Correlative analysis was performed to determine predictive factors.

resultsHypersecretion occurred in 31 patients (62%) and 14 had extreme-hypersecretion. There was an initial decline (3-6 months) in BAO/MAO, which then remained stable for eight years. Preoperative BAO correlated with the postoperative secretion, but not other clinical, tumoral, laboratory variables, the degree of postoperative acid suppression or type of antisecretory drug needed. Hypersecretors had greater postoperative ECL changes (P=0.005), serum CGA (P=0.009) and 24-h urinary N-MIAA (P=0.0038).

conclusionsPost curative resection, gastric hypersecretion persists long term (mean 8 years) in 62% of patients and in 28% it is extreme, despite normogastrinemia. No preoperative variable except BAO correlates with postresection hypersecretion. The persistent increased ECL-cell extent post curative resection suggests prolonged hypergastrinemia can lead to changes in ECL-cells that are either irreversible in humans or sustained by unknown mechanisms not involving fasting hypergastrinemia and which can result in hypersecretion, in a proportion of which it can be extreme. Whether similar findings may occur in patients with idiopathic GERD treated for prolonged periods (>10 years) with PPIs, at present, is unknown.

Indexed as

Postoperative PeriodEnterochromaffin CellsFemaleFollow-Up StudiesGastric AcidGastrinomaGastrinsHumansHyperplasiaMaleMiddle AgedPancreatic NeoplasmsParietal Cells, GastricPrevalenceProspective StudiesZollinger-Ellison SyndromeGastrins

Identifiers

PMID20725788
PMCPMC2990801
OpenAlexW2001131794

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Registered trials

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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.