Evidence map›Paper›PMID 27796466›Full record

Trial reportEuropean journal of clinical pharmacology2017

Randomised trial of the effect of a gastrin/CCK

Malcolm Boyce, Frans van den Berg, Toni Mitchell, Kate Darwin, Steve Warrington

Abstract readRandomized Controlled Trial
PubMed Publisher
In one paragraph

Trial report in European journal of clinical pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.9field-weighted citation impact, top 21% 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

7 citing papers in PubMed, 10 citations in OpenAlex.

  1. Randomized controlled trial of an oral gastrin receptor antagonist for the treatment of postmenopausal osteoporosis.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2026
    Trial
  2. Randomized Controlled Trial of the Gastrin/CCKCancer prevention research (Philadelphia, Pa.) · 2021
    Trial
  3. Review
  4. Review
  5. Review
  6. Tapering or abrupt cessation of proton pump inhibitors?European journal of clinical pharmacology · 2017
    Article
  7. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Malcolm BoyceHammersmith Medicines Research, Cumberland Avenue, London, NW10 7EW, UK. mboyce@hmrlondon.com.ORCID http://orcid.org/0000-0001-8807-612X
Frans van den BergHammersmith Medicines Research, Cumberland Avenue, London, NW10 7EW, UK.
Toni MitchellHammersmith Medicines Research, Cumberland Avenue, London, NW10 7EW, UK.
Kate DarwinHammersmith Medicines Research, Cumberland Avenue, London, NW10 7EW, UK.
Steve WarringtonHammersmith Medicines Research, Cumberland Avenue, London, NW10 7EW, UK.
Hammersmith Medicines Research · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeHypergastrinaemia induced by proton pump inhibitor (PPI) therapy may cause ECL-cell and parietal-cell hyperplasia and rebound hyperacidity and dyspepsia after PPI withdrawal. The aim of the study was to assess the effect of different dosage-regimens of netazepide, a gastrin/CCK

methodsSix groups of eight healthy subjects participated in a randomised, double-blind study of esomeprazole 40 mg daily for 28 days, in combination with netazepide 1, 5 or 25 mg or placebo, daily, during the last 14 days of esomeprazole or during 14 days after treatment withdrawal. Fasting serum gastrin and plasma CgA were measured during treatment and after withdrawal, as biomarkers of acid suppression and ECL-cell activity, respectively. Dyspepsia was monitored throughout the study.

resultsEsomeprazole increased gastrin and CgA. Netazepide increased gastrin, but not CgA, and inhibited dose dependently the CgA response to esomeprazole. Gastrin and CgA returned to baseline within 2-3 days of esomeprazole withdrawal; netazepide did not shorten that time. There was no rebound dyspepsia after esomeprazole withdrawal.

conclusionsEsomeprazole and netazepide each increase gastrin, consistent with a secondary effect of gastric acid suppression, but by different mechanisms. Esomeprazole-induced hypergastrinaemia stimulates ECL cells and thereby increases CgA. Netazepide-induced hypergastrinaemia does not increase CgA, because netazepide blocks gastrin/CCK

Indexed as

AdultAgedAnti-Ulcer AgentsBenzodiazepinonesChromogranin ADouble-Blind MethodDyspepsiaEsomeprazoleFemaleGastric Acidity DeterminationGastrinsHumansMaleMiddle AgedPhenylurea CompoundsProton Pump InhibitorsAnti-Ulcer AgentsBenzodiazepinonesChromogranin AEsomeprazoleGastrinsPhenylurea CompoundsProton Pump InhibitorsReceptor, Cholecystokinin BYF 476Chromogranin AECL cellEsomeprazoleGastric acidGastrinGastrin/CCK2 receptor antagonistNetazepide

Identifiers

PMID27796466
OpenAlexW4240734223

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.