Gastrinoma, Glucagonoma, and Other APUDomas

This chapter discusses pathogenesis, classical signs, diagnosis, and treatment of gastrinoma, glucagonoma, and other APUDomas. APUDomas arise from neoplastic transformation of neuroendocrine (APUD) cells with similar biosynthetic pathways and ultrastructural characteristics. Secretion of active hormones or hormone derivatives/analogues is responsible for the majority of clinical signs observed with gastrinoma, glucagonoma, and VIPoma. Gastrin stimulates gastric acid secretion. Glucagon stimulates both breakdown of glycogen and gluconeogenesis within the liver while signaling for insulin release from the pancreas. The end result of normal glucagon secretion is to elevate blood glucose concentrations and allow peripheral tissues to utilize the glucose. Presence of an elevated fasting serum gastrin concentration along with appropriate clinical signs should raise clinical suspicion of the presence of a gastrinoma. With the exceptions of chemodectoma in Boxers and Boston terriers, no risk factors for the development of APUDomas have been identified.