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Short and Long-Term Profound Acid Inhibition: Indications and Concerns
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Short and Long-Term Profound Acid Inhibition: Indications and Concerns

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 May 2025 | Viewed by 9426

Special Issue Editor

Prof. Dr. Helge L. Waldum

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Guest Editor
Department of Clinical and Molecular Medicine, Faculty of Medicine and Health Sciences, Norwegian University of Science and Technology, 7030 Trondheim, Norway
Interests: gastric physiology; gastric carcinogenesis; cell of origin; gastrin; the ECL cell; histamine; gastric acidity
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The gastric juice is a unique combination of a very strong acid (regulated by gastrin) and a proteolytic enzyme (pepsin). Only the mucosa of the stomach and duodenal bulb can withstand chronic exposure to gastric juice. Its main function is destruction of swallowed microorganisms. Gastric acidity is central in the pathogenesis of peptic ulcer and reflux oesophagitis. Inhibitors of acid secretion heal lesions due to exposure to gastric juice, but may cause side-effects (infections due to microorganisms reaching the gut and hypergastrinemia predisposing to gastric tumours). This issue will focus on indications and concerns related to inhibitors of acid secretion.

Prof. Dr. Helge L. Waldum
Guest Editor

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Keywords

  • gastric acid
  • gastric cancer
  • gastric neuroendocrine tumours
  • gastric juice
  • gastrin
  • Helicobacter pylori
  • oesophageal reflux disease
  • pepsin
  • peptic ulcer disease
  • gastric cancer histology and classification
  • rebound acid hypersecretion

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Published Papers (3 papers)

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Research

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45 pages, 2100 KiB  
Article
Long-Term Proton Pump Inhibitor–Acid Suppressive Treatment Can Cause Vitamin B12 Deficiency in Zollinger–Ellison Syndrome (ZES) Patients
by Tetsuhide Ito, Irene Ramos-Alvarez and Robert T. Jensen
Int. J. Mol. Sci. 2024, 25(13), 7286; https://doi.org/10.3390/ijms25137286 - 2 Jul 2024
Viewed by 2123
Abstract
Whether the long-term treatment of patients with proton pump inhibitors (PPIs) with different diseases [GERD, Zollinger–Ellison syndrome (ZES), etc.] can result in vitamin B12 (VB12) deficiency is controversial. In this study, in 175 patients undergoing long-term ZES treatment with anti-acid [...] Read more.
Whether the long-term treatment of patients with proton pump inhibitors (PPIs) with different diseases [GERD, Zollinger–Ellison syndrome (ZES), etc.] can result in vitamin B12 (VB12) deficiency is controversial. In this study, in 175 patients undergoing long-term ZES treatment with anti-acid therapies, drug-induced control acid secretory rates were correlated with the presence/absence of VB12 deficiency, determined by assessing serum VB12 levels, measurements of VB12 body stores (blood methylmalonic acid (MMA) and total homocysteine[tHYC]), and other features of ZES. After a mean of 10.2 yrs. of any acid treatment (5.6 yrs. with PPIs), 21% had VB12 deficiency with significantly lower serum and body VB12 levels (p < 0.0001). The presence of VB12 deficiency did not correlate with any feature of ZES but was associated with a 12-fold lower acid control rate, a 2-fold higher acid control pH (6.4 vs. 3.7), and acid control secretory rates below those required for the activation of pepsin (pH > 3.5). Over a 5-yr period, the patients with VB12 deficiency had a higher rate of achlorhydria (73% vs. 24%) and a lower rate of normal acid secretion (0% vs. 49%). In conclusion, in ZES patients, chronic long-term PPI treatment results in marked acid hyposecretion, resulting in decreased serum VB12 levels and decreased VB12-body stores, which can result in VB12 deficiency. Full article
(This article belongs to the Special Issue Short and Long-Term Profound Acid Inhibition: Indications and Concerns)
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Review

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17 pages, 1350 KiB  
Review
Autoimmune Gastritis and Hypochlorhydria: Known Concepts from a New Perspective
by Marica Vavallo, Sophia Cingolani, Giulio Cozza, Francesco P. Schiavone, Ludovica Dottori, Carla Palumbo and Edith Lahner
Int. J. Mol. Sci. 2024, 25(13), 6818; https://doi.org/10.3390/ijms25136818 - 21 Jun 2024
Viewed by 2889
Abstract
Autoimmune atrophic gastritis is an immune-mediated disease resulting in autoimmune destruction of the specialized acid-producing gastric parietal cells. As a consequence, in autoimmune atrophic gastritis, gastric acid secretion is irreversibly impaired, and the resulting hypochlorhydria leads to the main clinical manifestations and is [...] Read more.
Autoimmune atrophic gastritis is an immune-mediated disease resulting in autoimmune destruction of the specialized acid-producing gastric parietal cells. As a consequence, in autoimmune atrophic gastritis, gastric acid secretion is irreversibly impaired, and the resulting hypochlorhydria leads to the main clinical manifestations and is linked, directly or indirectly, to the long-term neoplastic complications of this disease. In the last few years, autoimmune atrophic gastritis has gained growing interest leading to the acquisition of new knowledge on different aspects of this disorder. Although reliable serological biomarkers are available and gastrointestinal endoscopy techniques have substantially evolved, the diagnosis of autoimmune atrophic gastritis is still affected by a considerable delay and relies on histopathological assessment of gastric biopsies. One of the reasons for the diagnostic delay is that the clinical presentations of autoimmune atrophic gastritis giving rise to clinical suspicion are very different, ranging from hematological to neurological–psychiatric up to gastrointestinal and less commonly to gynecological–obstetric symptoms or signs. Therefore, patients with autoimmune atrophic gastritis often seek advice from physicians of other medical specialties than gastroenterologists, thus underlining the need for increased awareness of this disease in a broad medical and scientific community. Full article
(This article belongs to the Special Issue Short and Long-Term Profound Acid Inhibition: Indications and Concerns)
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13 pages, 916 KiB  
Review
Rebound Acid Hypersecretion after Withdrawal of Long-Term Proton Pump Inhibitor (PPI) Treatment—Are PPIs Addictive?
by Ken Namikawa and Einar Stefan Björnsson
Int. J. Mol. Sci. 2024, 25(10), 5459; https://doi.org/10.3390/ijms25105459 - 17 May 2024
Cited by 1 | Viewed by 3895
Abstract
Proton pump inhibitors (PPIs) are widely used in the long-term treatment of gastroesophageal reflux disease (GERD) and other upper gastrointestinal disorders, such as the healing of peptic ulcers and/or prophylactic treatment of peptic ulcers. PPIs are also widely used as symptomatic treatment in [...] Read more.
Proton pump inhibitors (PPIs) are widely used in the long-term treatment of gastroesophageal reflux disease (GERD) and other upper gastrointestinal disorders, such as the healing of peptic ulcers and/or prophylactic treatment of peptic ulcers. PPIs are also widely used as symptomatic treatment in patients with functional dyspepsia. One of the adverse effects of the long-term use of PPI is rebound acid hypersecretion (RAHS), which can occur after the withdrawal of PPI therapy due to a compensatory increase in gastric acid production. Mechanisms of the RAHS have been well established. Studies have shown that pentagastrin-stimulated acid secretion after the discontinuation of PPIs increased significantly compared to that before treatment. In healthy volunteers treated with PPIs, the latter induced gastrointestinal symptoms in 40–50% of subjects after the discontinuation of PPI therapy but after stopping the placebo. It is important for practicing physicians to be aware and understand the underlying mechanisms and inform patients about potential RAHS before discontinuing PPIs in order to avoid continuing unnecessary PPI therapy. This is important because RAHS may lead patients to reuptake PPIs as symptoms are incorrectly thought to originate from the recurrence of underlying conditions, such as GERD. Mechanisms of RAHS have been well established; however, clinical implications and the risk factors for RAHS are not fully understood. Further research is needed to facilitate appropriate management of RAHS in the future. Full article
(This article belongs to the Special Issue Short and Long-Term Profound Acid Inhibition: Indications and Concerns)
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