Hyperchlorhydria

Abstract: Helicobacter pylori infection induces chronic inflammation of the gastric mucosa and thus profoundly affects gastric physiology. In the acute phase of infection, gastric acid secretion is transiently impaired. The morphological damage of the gastric mucosa, changes in gastric hormone release, and disruption of neural pathways all contribute to influence gastric acid secretion in a distinct manner. Changes in gastric acid secretion, whether impaired or increased, are intimately related with the topographic phenotypes of gastritis and the presence of atrophy or absence of corpus atrophy. The interplay of gastritis phenotype and acid secretion are key determinants in disease outcomes. Corpus-predominant gastritis and corpus atrophy are accompanied by hypochlorhydria and carry the highest risk for gastric cancer, whereas antrum-predominant gastritis with little involvement of the corpus-fundic mucosa is associated with hyperchlorhydria and predisposes to duodenal ulcer disease.

Abstract: Fasting serum gastrin has been measured by radioimmunoassay in 72 patients with duodenal ulcer and compared with that in normals, patients with gastric ulcer, and with the Zollinger-Ellison syndrome. The mean (± SEM) gastrin levels were 15·7 ± 1·5 pg/ml in the duodenal ulcer group, 32·1 ± 4·3 pg/ml in normals, 118 ± 18·1 pg/ml in gastric ulcer, and between 450 and 2,000 pg/ml in the Zollinger-Ellison syndrome. There were no difficulties in distinguishing simple ulcer from the Zollinger-Ellison syndrome as the presence of hyperchlorhydria in combination with hypergastrinaemia led to a confident diagnosis of the latter disease. The effect of protein, glucose, and cream feeding with and without atropine was also assessed in a group of these patients with duodenal ulcer. As in normals, there was no stimulation of gastrin release by either atropine alone, distilled water, glucose, or cream. However, protein alone produced a greater rise in serum gastrin levels compared with that in normals and prior atropinization augmented this response greatly in duodenal ulcer. This indicates an increased amount of releasable gastrin in the latter disease, the release of which, under basal conditions, is suppressed by the high acidity in the antrum.

Abstract: The purpose of the investigation was to detect ulcer patients having nontumorous hypergastrinemic hyperchlorhydria and to diagnostically differentiate this pseudo-Zollinger-Ellison syndrome from neurogenic duodenal ulcer disease and pancreatic gastrinomas. Nine patients having clinical, radiologic and humoral findings simulating the Zollinger-Ellison syndrome or severe duodenal ulcer disease were studied by physiologic provocative testing. The patients, not having pancreaticoduodenal gastrinomas, had an antral mucosal source of their moderate hypergastrinemia even after vagotomy with drainage, which was eliminated in eight patients treated by surgical antrectomy, resulting in normal serum gastrin concentrations. The pseudo-Zollinger-Ellison syndrome is, thus, characterized physiologically by an exaggerated gastrin response to meals, no response to secretin stimulation and pathologically by hyperfunctioning hyperplastic G cells of the antrum. The clinical, physiologic, pathologic and surgical features were integrated for accurate diagnosis and treatment.