scholarly journals Effects of Proton Pump Inhibitor Therapy, H. pylori Infection and Gastric Preneoplastic Pathology on Fasting Serum Gastrin Concentrations

2021 ◽  
Vol 12 ◽  
Author(s):  
Reuben Veysey-Smith ◽  
Andrew R. Moore ◽  
Senthil V. Murugesan ◽  
Laszlo Tiszlavicz ◽  
Graham J. Dockray ◽  
...  
Keyword(s):  
Proton Pump Inhibitor ◽  
Atrophic Gastritis ◽  
Proton Pump ◽  
Serum Gastrin ◽  
Proton Pump Inhibitor Therapy ◽  
Fasting Serum ◽  
Normal Range ◽  
Histological Evidence ◽  
Potential Risk Factors ◽  
H Pylori

BackgroundHypergastrinaemia occasionally indicates the presence of a gastrinoma. However it is much more commonly associated with various benign causes including proton pump inhibitor (PPI) use, Helicobacter pylori infection and/or atrophic gastritis. The extent to which these factors interact to influence fasting serum gastrin concentrations remains incompletely understood.Materials and MethodsFasting serum gastrin concentrations were measured by radioimmunoassay in 1,400 patients attending for diagnostic oesophagogastro-duodenoscopy. After exclusions, 982 patients were divided into four groups and their results analysed. We compared gastrin concentrations in normal patients (no H. pylori infection, no PPI use and no histological evidence of gastric preneoplasia (n=233)), with those in patients who were taking regular PPIs (H. pylori negative with no gastric preneoplasia (n=301)), patients who had active H. pylori infection but no gastric preneoplasia (n=164) and patients with histologically confirmed gastric preneoplasia (n=284).ResultsMedian fasting gastrin concentration in the normal group was 20pM and was significantly increased in PPI users (46pM, p<0.0001), patients with active H. pylori infection (27pM, p<0.0001), and patients with antral (25pM, p<0.01) or corpus (48pM, p<0.0001) gastric preneoplasia. PPI use resulted in further significant increases in fasting serum gastrin concentrations in patients who were infected with H. pylori (50pM, n=56) or who had antral gastric preneoplasia (53pM, n=87), but did not significantly alter serum gastrin concentrations in patients with corpus preneoplasia (90pM, n=66).ConclusionsPPI use, H. pylori infection and atrophic gastritis all caused significant elevations of median fasting gastrin concentrations. However, several patients who had potential risk factors for hypergastrinaemia still demonstrated fasting serum gastrin concentrations within the normal range.

scholarly journals Determinants of Human Fasting Serum Gastrin Concentration- Interaction Between H. pylori Infection, Gastric Preneoplastic Pathology and Proton Pump Inhibitor Use

2011 ◽  
Vol 140 (5) ◽  
pp. S-729
Author(s):  
Senthil V. Murugesan ◽  
Islay Steele ◽  
László Tiszlavicz ◽  
Tracey Farragher ◽  
Andrew R. Moore ◽  
...  
Keyword(s):  
Proton Pump Inhibitor ◽  
Proton Pump ◽  
Serum Gastrin ◽  
Fasting Serum ◽  
Serum Gastrin Concentration ◽  
H Pylori

scholarly journals Canadian Helicobacter Study Group Consensus Conference: Update on the Management ofHelicobacter pylori- An Evidence-Based Evaluation of Six Topics Relevant to Clinical Outcomes in Patients Evaluated forH pyloriInfection

2004 ◽  
Vol 18 (9) ◽  
pp. 547-554 ◽  
Author(s):  
Richard Hunt ◽  
Carlo Fallone ◽  
Sander Veldhuyzan van Zanten ◽  
Phil Sherman ◽  
Fiona Smaill ◽  
...  
Keyword(s):  
Proton Pump Inhibitor ◽  
Proton Pump ◽  
Proton Pump Inhibitor Therapy ◽  
Consensus Conference ◽  
Inhibitor Therapy ◽  
Study Group ◽  
Evidence Based ◽  
Long Term Treatment ◽  
H Pylori

As an update to previously published recommendations for the management ofHelicobacter pyloriinfection, an evidence-based appraisal of six topics was undertaken in a consensus conference sponsored by the Canadian Helicobacter Study Group. The issues addressed and recommendations made were: bismuth-containing quadruple therapy is appropriate as an alternative first-line eradication strategy forH pyloriinfection; searching for and treatingH pyloriinfection is warranted in patients considered to be at high risk for gastric cancer;H pyloriinfection should be eradicated before initiating long-term treatment with nonsteroidal anti-inflammatory drugs or acetylsalicylic acid; the stool antigen test has a limited role in the diagnosis ofH pyloriinfection; the benefits ofH pylorieradication in patients on long-term proton pump inhibitor therapy are not sufficient to warrant recommending a strategy of searching for and eradicating the infection among these patients; and a strategy of 'test and eradicate' forH pyloriinfection in patients with uninvestigated dyspepsia is cost-effective in Canada relative to a trial of proton pump inhibitor therapy. The goal was to establish guidelines on the best evidence using the same structure to address and formulate recommendations for each issue. The degree of consensus for each issue is presented.

scholarly journals Eradicating Helicobacter pylori reduces hypergastrinaemia during long term omeprazole treatment

Gut ◽  
1998 ◽  
Vol 42 (2) ◽  
pp. 159-165 ◽  
Author(s):  
A El-Nujumi ◽  
C Williams ◽  
J E Ardill ◽  
K Oien ◽  
K E L McColl
Keyword(s):  
Helicobacter Pylori ◽  
Proton Pump Inhibitor ◽  
Proton Pump ◽  
Serum Gastrin ◽  
Symptomatic Treatment ◽  
Initial Presentation ◽  
Proton Pump Inhibitor Treatment ◽  
H Pylori ◽  
Inhibitor Treatment

Background—Both proton pump inhibitor drug treatment and Helicobacter pylori infection cause hypergastrinaemia in man.Aims—To determine whether eradicating H pylori is a means of reducing hypergastrinaemia during subsequent proton pump inhibitor treatment.Methods—Patients with H pylori were randomised to treatment with either anti-H pylori or symptomatic treatment. One month later, all received four weeks treatment with omeprazole 40 mg/day for one month followed by 20 mg/day for six months. Serum gastrin concentrations were measured before and following each treatment.Results—In the patients randomised to anti-H pylori treatment, eradication of the infection lowered median fasting gastrin by 48% and meal stimulated gastrin by 46%. When gastrin concentrations one month following anti-H pylori/symptomatic treatment were used as baseline, omeprazole treatment produced a similar percentage increase in serum gastrin in the H pylori infected and H pylorieradicated patients. Consequently, in the patients in which H pylori was not eradicated, median fasting gastrin concentration was 38 ng/l (range 26–86) at initial presentation and increased to 64 ng/l (range 29–271) after seven months omeprazole, representing a median increase of 68% (p<0.005). In contrast, in the patients randomised to H pylori eradication, median fasting gastrin at initial presentation was 54 ng/l (range 17–226) and was unchanged after seven months omeprazole at 38 ng/l (range 17–95).Conclusion—Eradicating H pylori is a means of reducing the rise in gastrin during subsequent long term omeprazole treatment. In view of the potential deleterious effects of hypergastrinaemia it may be appropriate to render patients H pylori negative prior to commencing long term proton pump inhibitor treatment.

scholarly journals Comparison of the human gastric microbiota in hypochlorhydric states arising as a result of Helicobacter pylori-induced atrophic gastritis, autoimmune atrophic gastritis and proton pump inhibitor use

2017 ◽  
Author(s):  
Bryony N. Parsons ◽  
Umer Zeeshan Ijaz ◽  
Rosalinda D’Amore ◽  
Michael D. Burkitt ◽  
Richard Eccles ◽  
...  
Keyword(s):  
Proton Pump Inhibitor ◽  
Microbial Diversity ◽  
Atrophic Gastritis ◽  
Proton Pump ◽  
List Type ◽  
Gastric Corpus ◽  
H Pylori ◽  
Autoimmune Atrophic Gastritis ◽  
Gastric Malignancy ◽  
Gastric Microbiota

ABSTRACTObjectiveSeveral conditions associated with reduced gastric acid secretion confer an altered risk of developing a gastric malignancy. Helicobacter pylori-induced atrophic gastritis predisposes to gastric adenocarcinoma, autoimmune atrophic gastritis is a precursor of type I gastric neuroendocrine tumours, whereas proton pump inhibitor (PPI) use does not affect stomach cancer risk. We hypothesised that each of these conditions was associated with specific alterations in the gastric microbiota and that this influenced subsequent tumour risk.Design95 patients (in groups representing normal stomach, PPI treated, H. pylori gastritis, H. pylori-induced atrophic gastritis and autoimmune atrophic gastritis) were selected from a cohort of 1400. RNA extracted from gastric corpus biopsies was analysed using 16S rRNA sequencing (MiSeq).ResultsSamples from normal stomachs and patients treated with PPIs demonstrated similarly high microbial diversity. Patients with autoimmune atrophic gastritis also exhibited relatively high microbial diversity, but with samples dominated by Streptococcus. H. pylori colonisation was associated with decreased microbial diversity and reduced complexity of co-occurrence networks. H. pylori-induced atrophic gastritis resulted in lower bacterial abundances and diversity, whereas autoimmune atrophic gastritis resulted in greater bacterial abundance and equally high diversity compared to normal stomachs. Pathway analysis suggested that glucose-6-phospahte1-dehydrogenase and D-lactate dehydrogenase were over represented in H. pylori-induced atrophic gastritis versus autoimmune atrophic gastritis, and that both these groups showed increases in fumarate reductase.ConclusionAutoimmune and H. pylori-induced atrophic gastritis were associated with different gastric microbial profiles. PPI treated patients showed relatively few alterations in the gastric microbiota compared to healthy subjects.SIGNIFICANCE OF THIS STUDY1.What is already known about this subject?Some conditions which result in reduced gastric acid secretion and hypochlorhydria are associated with an increased risk of gastric tumourigenesis.This risk is different in patients with H. pylori-induced atrophic gastritis, autoimmune atrophic gastritis and chronic proton pump inhibitor use.Hypochlorhydria and H. pylori infection cause alterations in the composition of the gastric microbiota.2.What are the new findings?We used 16S rRNA sequencing to characterise the microbiota in gastric corpus biopsies from a well characterised cohort of patients.The gastric microbiota was different in patients who were hypochlorhydric as a result of H. pylori-induced atrophic gastritis, autoimmune atrophic gastritis and proton pump inhibitor use.Biochemical pathways associated with gastric carcinogenesis such as the fumarate reductase pathway were predicted to be altered in patients with atrophic gastritis.3.How might it impact on clinical practice in the foreseeable future?Understanding how the microbiota that colonise the hypochlorhydric stomach influence gastric carcinogenesis may ultimately permit stratification of patients’ subsequent tumour risk.Interventions that alter the composition of the gastric microbiome in hypochlorhydric patients with atrophic gastritis should be tested to investigate whether they alter the subsequent risk of developing gastric malignancy.

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