Gastrinomas of the pancreas have been reported in people, dogs, and a cat. Hypersecretion of gastrin in people results in the Zollinger-Ellison syndrome, consisting of hypersecretion of gastric acid and recurrent peptic ulceration in the GI tract. The tumors, derived from ectopic amine precursor uptake decarboxylase (APUD) cells in the pancreas, produce an excess of the hormone gastrin, which normally is secreted by cells of the antral and duodenal mucosa.
These tumors are rare; they occur less frequently than the insulin-secreting β-cell neoplasms. The few documented cases have had anorexia, hematemesis, intermittent diarrhea (usually with dark blood present), progressive weight loss, and dehydration. The prominent functional disturbances appear to result from multiple ulcerations of the GI mucosa that develop from gastrin hypersecretion.
Animals studied with the Zollinger-Ellison-like syndrome have had single or multiple tumors of varying size in the pancreas. The tumors were firm on palpation because of an increase of fibrous connective tissue in the stroma, and all had evidence of metastasis before diagnosis.
Serum gastrin levels have been evaluated in a limited number of dogs with gastrinomas. Gastrin levels in a dog with a Zollinger-Ellison-like syndrome varied from 155 to 2,780 pg/mL, whereas the mean serum gastrin in clinically normal (control) dogs was 70.9 pg/mL. Recurrent gastric or duodenal ulcers in dogs with no identified cause warrants exploratory surgery and careful inspection of the pancreas.
Excision of the gastrin-secreting mass in the pancreas can be attempted. However, all such tumors that have been studied in dogs have had evidence of local invasion into adjacent parenchyma and had metastasized to regional lymph nodes and liver. The dogs had either single or multiple ulcerations in the gastric or duodenal mucosa associated with free blood in the lumen. Medical management with H2-receptor antagonists (famotidine or ranitidine) or the proton-pump inhibitor omeprazole may temporarily alleviate clinical signs in animals with inoperable disease.
Last full review/revision May 2013 by David Bruyette, DVM, DACVIM