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Gastrointestinal cancer
Published in Peter Hoskin, Peter Ostler, Clinical Oncology, 2020
Gastrinoma is a gastrin-secreting tumour which leads to Zollinger–Ellison syndrome, characterized by hypersecretion of acid in the stomach leading to intractable peptic ulceration. An elevated serum gastrin level is diagnostic and about two-thirds are malignant. It is sometimes associated with adenomata of the pituitary and parathyroid as part of multiple endocrine neoplasia type 1 (MEN 1). After detailed staging with a CT scan and selective venous angiography, the treatment of choice is a partial pancreatectomy.
The liver, gallbladder and pancreas
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
Dina G. Tiniakos, Alastair D. Burt
Gastrinomas are NETs that produce gastrin. Gastrin is normally produced only by G-cells in the stomach and duodenum. Most gastrinomas occur in the submucosa of the duodenum or the gastric antrum, but the pancreas is the most common site for an ectopic gastrinoma. Gastrinomas are associated with the Zollinger–Ellison syndrome in which persistent hypersecretion of acid gastric juice causes duodenal and even jejunal peptic ulceration (see Chapter 10, Case History 10.2). Most pancreatic gastrinomas are malignant.
Postulated Physiological and Pathophysiological Roles on Motility
Published in Edwin E. Daniel, Neuropeptide Function in the Gastrointestinal Tract, 2019
Hans-Dieter Allescher, Sultan Ahmad
Gastrin is a potent stimulator of gastric acid secretion. Its role in the regulation of gastrointestinal motility is far less characterized. Excessive secretion of gastrin can be observed due to a gastrinoma, a gastrin-producing tumor, or as a consequence of reduced acid secretion caused by Billroth II surgery, atrophic gastritis, or drugs (H2 blockers or omeprazol). No specific motility changes in these hypergastrinemia conditions have been reported, and the diarrhea observed in gastrinoma patients probably is primarily due to the changes in the secretory responses and, to a minor extent, to motility changes. The possible physiological role in the regulation of antral motility and in the maintenance of the basal lower esophageal sphincter pressure awaits further confirmation with new selective gastrin receptor antagonists.
Long-term safety and effectiveness of vonoprazan for prevention of gastric and duodenal ulcer recurrence in patients on nonsteroidal anti-inflammatory drugs in Japan: a 12-month post-marketing surveillance study
Published in Expert Opinion on Drug Safety, 2023
Takashi Kawai, Chihiro Suzuki, Youichirou Honda, Jovelle L. Fernandez
All data were entered into a web-based electronic data capture system by the surveillance investigator. Collected information included: (i) patient demographics and medical history, including self-reported H. pylori infection; (ii) concurrent medical conditions and treatments including the date of initiation, reason for use, dosage, and administration of vonoprazan, NSAIDs, and any concomitant medications; (iii) assessments for gastric/duodenal ulcer or hemorrhagic lesions, including the date of endoscopy (if performed, as it was not mandatory; ulcer sizes were not confirmed and the presence of ‘bleeding’ was based on the physician’s judgment) or diagnosis; and (iv) liver function tests and assessment of serum gastrin. For safety, the following information was collected: presence or absence of adverse events (AEs) during the observation period, including terms used, date of onset, seriousness, reason for seriousness, causal relationship to vonoprazan, and reason for discontinuation of vonoprazan if related to safety. Any AE that was reported after initiation of vonoprazan and for which vonoprazan could not be ruled out as the cause was defined as an adverse drug reaction (ADR). Hospitalization was regarded as a serious AE and was reported as such. Data on adherence to medications were not collected.
Long-term changes in serum gastrin levels during standard dose vonoprazan therapy
Published in Scandinavian Journal of Gastroenterology, 2022
Satoshi Shinozaki, Hiroyuki Osawa, Yoshimasa Miura, Yoshikazu Hayashi, Hirotsugu Sakamoto, Tomonori Yano, Alan Kawarai Lefor, Hironori Yamamoto
A decreased number of parietal cells is considered to result in hypergastrinemia due to negative feedback from gastric G cells. Based on this mechanism, VPZ might be more effective in patients with severe atrophy compared to those with no atrophy. However, we previously reported that long-term VPZ therapy improved GERD and did not aggravate other abdominal symptoms regardless of the grade of gastric atrophy [11]. In the present study, it should be noted that there was an upper limit for serum gastrin levels with long-term VPZ therapy, which not accompanied by significant clinical symptoms. Since there are no reports demonstrating a definite causal relationship between serum gastrin level and symptoms, we believe that hypergastrinemia alone does not affect abdominal symptoms. This suggests that routine screening for serum gastrin levels is not recommended during acid suppression therapy. The acid suppression effect induced by VPZ is useful in long-term control of symptomatic GERD [11], PPI-resistant GERD [12] and severe reflux esophagitis [9]. Considering the risk-benefit balance together with the current data, an elevated gastrin level alone is not grounds to cease the long-term use of VPZ.
Decreased anti-parietal cell antibody titer in the advanced phase of autoimmune gastritis
Published in Scandinavian Journal of Gastroenterology, 2022
Toshihiro Nishizawa, Hidenobu Watanabe, Shuntaro Yoshida, Akira Toyoshima, Yosuke Kataoka, Takamitsu Kanazawa, Naoto Yoshizawa, Hirotoshi Ebinuma, Hidekazu Suzuki, Osamu Toyoshima
During the study period, 50 patients were pathologically diagnosed with AIG. Six patients were not tested for APCA and were thus excluded. Ultimately, we included 44 AIG patients with APCA results in this study. The characteristics of the 44 patients are shown in Table 1. There were two patients in the early phase, 11 in the florid phase, and 31 in the end phase. APCA-positive rates were 100% in the early phase, 90.9% in the florid phase, and 90.3% in the end phase. The mean APCA titer was 480 ± 226 U in the early phase, 220 ± 235 U in the florid phase, and 150 ± 152 U in the end phase. There was a stepwise decrease in the APCA titer from the early phase to the end phase. The mean APCA titer for the end phase was significantly lower than that of the early phase or florid phase. The mean serum gastrin level was 2565 ± 854 pg/ml in the early phase, 2685 ± 2129 pg/ml in the florid phase, and 2810 ± 1619 pg/ml in the end phase. The mean serum gastrin level in the end phase was significantly higher than that in the early phase or florid phase. Representative histological images of AIG are shown in Figures 1 and 2 for the early and end phases, respectively.