Non-metastatic pancreatic adenocarcinoma with persistent hyperglycemia in a horse

Pancreatic cancer is rarely diagnosed in horses, unlike in humans. Here, we report the only, to our knowledge, case of pancreatic adenocarcinoma that was shown to be associated with endocrine disorders. Only nine other cases of exocrine pancreatic adenocarcinoma and one case of a pancreatic islet cell tumor have been reported to date. A 20 year old crossbred gelding was diagnosed with persistent hyperglycemia of unknown origin, without
clinical signs, in October 2012. In early January, he developed inappetance and fever; hematologic and serum biochemistry aberrations included elevated triglycerides, hyperglycemia, elevated fibrinogen, AST and GGT, and
increased monocytes. A right abdominal mass was diagnosed by ultrasonography. Following 5 weeks of treatment, euthanasia was elected due to the persistent fever and blood profile abnormalities. On necropsy, a ~30 cm in
diameter mass had replaced the pancreas, occupied the adjacent space, extending to the liver, gastric, duodenal, and colonic serosal surfaces from which it was separated by thick fibrous tissue, grossly sparing the above organs, but invading the liver capsule. The mass was partitioned by multiple fibrous bands, and was multifocally necrotic and/or cystic. Histologically, the normal pancreatic and peripancreatic architecture had been effaced by a poorly cellular,
moderately well demarcated, infiltrative and unencapsulated tumor. Neoplastic cells were arranged in variably complete, variably sized and shaped, often tortuous tubules and acini, supported by an extensive, moderately dense
fibrous stroma or by granulation tissue. Cells showed moderate anisokaryosis and anisocytosis, and low mitotic index. The tumor was separated from the liver and the duodenal, colonic and gastric serosa by a thick layer of
fibrotic and granulation tissue. Multifocal, focally extensive mineralization of the vascular walls and the neuropil was noted in the cerebellum and cerebrum. Immunohistochemically, tumor cells were positive for cytokeratin,
indicating epithelial origin, and negative for vimentin, synaptophysin, S-100, glucagon, chromogranin A, insulin, and Neuron Specific Enolase (NSE). Remnants of compressed islet cell islands, that were positive for
synaptophysin, S-100, glucagon, chromogranin A, insulin, and NSE, were surrounded by tumor acini. The persistent hyperglycemia and other serum biochemical abnormalities observed likely resulted from beta cell depletion due to compression of the islet cells by the tumor. To our knowledge, clinical signs relating to endocrine aberrations were not noted in previous cases of exocrine pancreatic neoplasia. Unlike most previously reported pancreatic cancer
cases, no metastases were observed in this case, despite extensive expansion in peri-pancreatic organs.
# AAVLD Trainee Travel Awardee (Pathology)