Zollinger-Ellison Syndrome

Overview
Pathogenesis
  • The Zollinger-Ellison pathogenic sequence is initiated by the presence of a gastrinoma, an endocrine tumor which secretes gastrin and thus results in hypergastrinemia. Excessive gastrin levels result in over-production of stomach acid by Parietal Cells as described in Stomach Acid Secretion. Additionally, because gastrin is a trophic hormone for the gastric epithelium, chronic hypergastrinemia results in hypertrophy of this layer.
Clinical Consequences
  • The clinical consequences of ZES are purely due to excessive secretion of stomach acid. This results in overwhelming of mucosal defenses to stomach acid and thus peptic ulcer disease. A malabsorption syndrome and attendant diarrhea is also frequently encountered likely due to inactivation of pancreatic enzymes as a result of excessively low pHs within the small intestinal lumen following gastric emptying. In some patients esophageal reflux of hyper-acidic stomach fluid may result in GERD