Abstract
In 1955, Zollinger and Ellison described the clinical syndrome of virulent peptic ulcer disease associated with marked gastric hyperacidity and pancreatic islet-cell tumors.1 A year earlier, Wermer had reported a familial disease characterized by hyperparathyroidism, pituitary tumors, and pancreatic islet-cell tumors: the disease is now known as multiple endocrine neoplasia type 1 (MEN-1).2 Since these two landmark discoveries in endocrine oncology, we have learned a great deal about the pathophysiology, clinical presentation, diagnosis, and treatment of the Zollinger–Ellison syndrome.The most important advance was the discovery that gastrin, a polypeptide hormone and potent acid secretagogue, is the cause of the . . .