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Cited by 111Neuroendocrine Tumor Research AdvancesGastroesophageal reflux and treatmentsHelicobacter pylori-related gastroenterology studies

Serum gastrin and chromogranin A during medium‐ and long‐term acid suppressive therapy: a case‐control study

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Sanduleanu, Stridsberg, Jonkers, Hameeteman, Biemond, Lundqvist, Lamers, Stockbrügger·1999·Alimentary Pharmacology & Therapeutics
DOI 10.1046/j.1365-2036.1999.00466.x
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Abstract

Background: Serum chromogranin A (CgA) is regarded as a reliable marker of neuroendocrine proliferation. We previously described increased serum CgA levels during short‐term profound gastric acid inhibition. Aim: To investigate serum gastrin and CgA levels in dyspeptic patients during continuous medium‐ (6 weeks to 1 year), or long‐term (1–8 years) gastric acid suppressive therapy. Patients and methods: 114 consecutive dyspeptic patients referred for upper gastrointestinal endoscopy were enrolled in a cross‐sectional, case‐control study [62 patients on continuous antisecretory therapy, either with proton pump inhibitors (n = 47) or H 2‐receptor antagonists (H 2 RA) (n = 15) for gastro‐oesophageal reflux disease with or without Barrett’s oesophagus or functional dyspepsia, and 52 age‐ and sex‐matched patients without medical acid inhibition and with normal endoscopic findings (control group)]. Omeprazole doses ranged from 20 mg to 80 mg daily and ranitidine from 150 mg to 450 mg daily. Fasting serum CgA and serum gastrin levels were measured by radioimmunoassay (reference values: serum CgA < 4.0 nmol/L; serum gastrin < 85 ng/L). Results: Fasting serum CgA levels positively correlated with serum gastrin in the entire study population (r = 0.55, P = 0.0001). Median serum CgA values were higher in patients treated with a proton pump inhibitor than H 2 RA [2.8 (2.0–5.9) nmol/L vs. 2 (1.9–2.3) nmol/L, P < 0.002] and controls [2.8 (2.0–5.9) nmol/L vs. 1.8 (1.5–2.2) nmol/L, P < 0.0001) and did not differ between patients treated with H 2 RA or controls. Serum gastrin and CgA levels in patients on proton pump inhibitor therapy positively correlated with the degree and duration of acid inhibition. Patients on long‐term proton pump inhibitor therapy had significantly higher fasting serum gastrin and CgA than those on medium‐term proton pump inhibitor therapy [127 (73–217) ng/L vs. 49 (29–78) ng/L, P < 0.0001 and 4.8 (2.8–8) ng/L vs. 2.1 (1.9–2.6) ng/L, P < 0.001]. No such relation was found in patients on medium‐ vs. long‐term H 2 RA. Overall, patients with positive Helicobacter pylori serology had higher serum gastrin and CgA levels than those with negative H. pylori serology [51 (27–119) ng/L vs. 27 (14–79) ng/L, P = 0.01, 2.4 (1.9–3.4) nmol/L vs. 2.0 (1.7–2.5) nmol/L, P = 0.05]. Conclusions: During long‐term continuous proton pump inhibitor treatment, serum gastrin and CgA levels are significantly elevated compared to H 2 RA treatment and nontreated dyspeptic controls. H. pylori infection seems to affect gastric ECL cell secretory function. Increased serum CgA values during long‐term profound gastric acid inhibition could reflect either gastric enterochromaffin‐like cell hyperfunction or proliferative changes.

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  • The longer the use of proton pump inhibitor, the higher the chromogranin A levels will be.

    “Sanduleanu et al (1999) suggested that the longer the use of PPI, the higher the CgA levels will be.”

    From Discontinuation of proton pump inhibitors during assessment of chromogranin A levels in patients with neuroendocrine tumours (2011) · cites this paper as Sanduleanu et al, 1999

  • An association between chromogranin A levels and proton pump inhibitor use has already been described: a Dutch cross-sectional study of 114 dyspeptic patients showed chromogranin A levels were higher during long-term proton pump inhibitor treatment than during H2-receptor antagonist treatment or no treatment.

    “An association between CgA levels and the use of PPI has already been described: a Dutch group published a cross-sectional study of 114 dyspeptic patients and showed that CgA levels were higher during long-term PPI treatment than during H2RA treatment, or no treatment (Sanduleanu et al, 1999).”

    From Discontinuation of proton pump inhibitors during assessment of chromogranin A levels in patients with neuroendocrine tumours (2011) · cites this paper as Sanduleanu et al, 1999

  • Decrease in acidity leads to release of gastrin.

    “These studies suggested that decrease in acidity leads to release of gastrin.”

    From Discontinuation of proton pump inhibitors during assessment of chromogranin A levels in patients with neuroendocrine tumours (2011) · cites this paper as Sanduleanu et al, 1999

    The supplied passage is bibliographic metadata (no section or page), not a finding about gastrin release. Searches for decreased acidity, gastrin secretion, and acid suppression found no non-abstract passage in our copy establishing the claimed relationship. (LLM, conf=0.70)

    Experimental — accuracy not yet measured

  • Elevated gastrin leads to hyperplasia of ECL cells and subsequently to an increase in chromogranin A levels.

    “Elevated gastrin leads to hyperplasia of ECL cells and, subsequently, to an increase in CgA levels (Waldum et al, 1996; Sanduleanu et al, 1999).”

    From Discontinuation of proton pump inhibitors during assessment of chromogranin A levels in patients with neuroendocrine tumours (2011) · cites this paper as Sanduleanu et al, 1999

    The retrieved passages are bibliographic metadata, with no section or page text addressing whether elevated gastrin causes ECL-cell hyperplasia and a subsequent rise in chromogranin A. Searches for ECL cells, enterochromaffin-like cells, and hyperplasia found no substantive passage in our copy to verify that sequence. (LLM, conf=0.72)

    Experimental — accuracy not yet measured

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Authors
Sanduleanu, Stridsberg, Jonkers, Hameeteman, Biemond, Lundqvist, Lamers, & Stockbrügger
Affiliations
  • Uppsala University Hospital (SE)
  • Maastricht University Medical Centre (NL)
  • Leiden University Medical Center (NL)
Corresponding author
Sanduleanu
Venue
Alimentary Pharmacology & Therapeutics
Publisher
Wiley
Published
1999-02
Volume
13
Issue
2
Pages
145-153
ISSN
  • 0269-2813 (ISSN-L)
  • 1365-2036
DOI
10.1046/j.1365-2036.1999.00466.x
OpenAlex
W1983542509
Cited by
111
References
54
Citations by year
2025: 3 · 2024: 1 · 2023: 2 · 2022: 1 · 2021: 3 · 2020: 2 · 2019: 5 · 2018: 5 · 2017: 6 · 2016: 7 · 2015: 2 · 2014: 5 · 2013: 6 · 2012: 2
FWCI
1.64
Type
journal article
Language
en
Open access
Licence
Locations
  • Alimentary Pharmacology & Therapeutics (publishedVersion)
  • PubMed (publishedVersion)
  • Research Publications (Maastricht University) (publishedVersion, other-oa)
  • Research Publications (Maastricht University) (submittedVersion, other-oa)
Topics
  • Health Sciences › Medicine › Epidemiology › Neuroendocrine Tumor Research Advances
  • Health Sciences › Medicine › Gastroenterology › Gastroesophageal reflux and treatments
  • Health Sciences › Medicine › Surgery › Helicobacter pylori-related gastroenterology studies
Keywords
serum gastrin, chromogranin A, proton pump inhibitors, H2 receptor antagonists, gastroesophageal reflux disease, Barrett's esophagus, functional dyspepsia, omeprazole, ranitidine, dyspepsia
MeSH terms
Adult, Aged, Anti-Ulcer Agents, Chromogranins, Cross-Sectional Studies, Dyspepsia, Female, Gastric Acid, Gastrins, Humans, Male, Middle Aged, Omeprazole, Case-Control Studies, Helicobacter pylori, Chromogranin A

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