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Preoperative assessment and localization is crucial in the management and outcome of patients with duodenal gastrinoma. Localization can be challenging because of small size and variable location. We describe our experience of managing 1 such patient by localizing the lesion during the preoperative period. Side-viewing endoscopy, endoscopic ultrasound, and somatostatin receptor scintigraphy determined the exact location of the tumor, which was confirmed during surgery on palpation, endoscopic transillumination, and duodenotomy. Antrectomy was performed, and the patient was asymptomatic after 8 months of follow-up and did not require antisecretory medications. His serum gastrin levels returned to normal during the postoperative period.

Background: The 1955 landmark publication by Zollinger and Ellison characterized the gastrinoma syndrome and presented a hypothesis for the pancreatic endocrine origin of the gastric hypersecretion and dramatic ulcer diathesis., Methods: A detailed review of the literature was conducted to ascertain the clinical and pathologic spectrum of gastrinoma reported prior to the definition of the Zollinger-Ellison syndrome., Results: In addition to the 2 patients presented by Zollinger and Ellison, 6 published reports of gastrinoma patients were referenced in their manuscript. An additional 6 patients were described by the 5 discussants of the presented paper. Thorough review of the literature has yielded 4, and possibly 6, additional cases of gastrinoma published between 1908 and 1952., Conclusion: Despite experience with a sizeable number of gastrinoma patients, it was left to Zollinger and Ellison to define the association between the islet cell tumor, its peptide hormone, and the clinical manifestations of severe gastric hypersecretion. Their seminal contribution served as the defining moment for the field of gastrointestinal endocrinology.

Pancreatic endocrine tumors are grouped together by their common histologic, cytochemical, and ultrastructural features. Although useful conceptually, this paradigm has been unable to predict the anatomic location of different tumor types. Successful surgical excision of these tumors would be facilitated by an improved understanding of their anatomic distribution. Based on the available data, a bimodal distribution of pancreatic endocrine tumors was identified. Cluster 1 (gastrinomas, pancreatic polypeptide (PP)-secreting tumors, somatostatinomas) had 75% of tumors to the right of the superior mesenteric artery, whereas cluster 2 (insulinoma, glucagonoma) had 75% of tumors to the left of the superior mesenteric artery (p less than 0.05). This distribution is similar to that distribution predicted based on the volume density of the corresponding islet cells for insulinoma, glucagonoma, and PP-secreting tumors, but not for somatostatinoma. These findings suggest that pancreatic endocrine tumors are derived from similar cytologic precursors as pancreatic islet cells, and their distribution may be a consequence of embryologic development from either the ventral (cluster 1) or dorsal (cluster 2) pancreatic buds.