Discussion
G-cell hyperplasia, gastric polypoid lesions, gastritis, endocrine tumours, hypergastrinaemia
HYPERPLASTIC POLYPS, FUNDIC GLAND POLYPS, EROSIVE OESOPHAGITIS, GASTRITIS, FUNDIC GLAND POLYPS, GASTRIC CANCER
This 3-year interim analysis of the VISION study shows that although vonoprazan treatment resulted in an increase in serum gastrin and chromogranin levels compared with the PPI lansoprazole, no neoplastic changes in epithelial mucosa or enterochromaffin-like cells were observed following long-term maintenance treatment with vonoprazan in patients with healed erosive oesophagitis. Although gastric NETs have been reported to occur in the setting of PPI-induced hypergastrinaemia [Serum chromogranin A level is known to be a marker for endocrine tumours [G-cell hyperplasia was observed in 32.8% of patients in the vonoprazan group and 25.4% of patients in the lansoprazole group at the beginning of the study but was found in progressively more patients in both treatment groups over time. At week 156, the prevalence was 85.3% in the vonoprazan group and 70.2% in the lansoprazole group, which may explain the higher serum gastrin levels in the vonoprazan group compared with the lansoprazole group. Few studies have investigated the effect of antisecretory drugs on the number of gastrin-producing G cells [Both the vonoprazan and lansoprazole groups showed increases in serum pepsinogen I and II over time. In particular, the increase was higher in the vonoprazan group. Pepsinogens I and II are secreted by the chief cells and mucous neck cells [In considering the relationship between gastric acid secretion inhibitors and gastric cancer, it has been pointed out that gastric acid secretion inhibitors enhance gastritis [For endoscopic findings other than hyperplastic polyps, fundic gland polyps were found in 72 (66.1%) patients in the vonoprazan group and 44 (77.2%) patients in the lansoprazole group at week 156; cobblestone mucosa in 16 (14.7%) and 5 (8.8%) patients, respectively; and multiple white flat elevated lesions in 7 (6.4%) and 9 (15.8%) patients, respectively. The incidence of gastric polypoid lesions increased with increasing duration of treatment. Fundic gland polyps were the most common type, but these were already present at entry to the maintenance phase in 43.7% of patients in the vonoprazan group and 43.3% in the lansoprazole group. The incidence of fundic polyps increases with the dose and duration of PPIs [There was no difference in overall TEAEs between the vonoprazan and lansoprazole groups, but the proportion of patients who discontinued medication because of an AE was greater in the vonoprazan group than in the lansoprazole group.A limitation of the study is the possibility of a false negative urea breath test. Another limitation of this study is that, although the site and method of histopathological sample collection was defined in the study protocol and procedures manual together with reference images, sampling was up to the endoscopist at each institution and could therefore be variable. However, histopathological evaluation of gastric mucosa and histological evaluation of gastritis were undertaken centrally in a blinded manner by two expert pathologists specialising in gastrointestinal histopathology, who also instructed the principal investigator on the method of sample collection before the start of the study. In addition, if there was any difference in the histopathological evaluation between these two pathologists, evaluation was determined after separate consultation with two other pathologists.