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Simple Summary: The relation between biliary tree diseases and pancreatitis is not well-known in veterinary medicine. Anecdotally, hyperlipemia, pancreatic inflammation, and abnormalities of biliary flow are thought to play a role in the pathogenesis. The aim of the work was to study the frequency and features of pancreatic involvement in dogs with chronic biliary tree disease. We retrospectively included 81 dogs with both laboratory and ultrasound signs of chronic biliary tree disease. Medical records of the included dogs and their pancreatic involvement was recorded considering ultrasonographic features and/or biochemical alterations (Lipase DGGR). Fifty-eight dogs (72%) showed pancreatic involvement, suggesting that pancreatic status should be investigated in canine patients with chronic biliary tree disease. Canine chronic biliary tree disease (CBTD) is a suspected risk factor for pancreatic injury. The aim of this study was to evaluate the frequency and features of pancreatic involvement in canine CBTD, and their relationship with hyperlipemia and its severity. CBTD was defined as the increase in at least two of ALP, GGT, total bilirubin, cholesterol, and a biliary tree abnormal abdominal ultrasound (graded mild to severe). Pancreatic ultrasound appearance was recorded and classified as acute/chronic. Dogs were divided into a PBD group (pancreatic and biliary disease) and BD group (only biliary tree disease). PBD group was subgraded into a "pancreatic injury" and "pancreatitis" group. Eighty-one dogs were retrospectively included: 56 in the PBD group and 25 in the BD group. Of the PBD group, 20 had pancreatitis (15 chronic and 5 dogs acute). US score was mild in 64 dogs and moderate in 17 dogs, and it was not associated with evidence of pancreopathy. Sixty-six dogs had hyperlipemia (mild = 27 dogs; moderate-to-severe = 39 dogs) and no association with pancreopathy was found. Pancreatic injury was more frequent than pancreatitis in CBTD dogs. Although both acute and chronic pancreatic injury may be present, chronic forms were more frequent. Pancreatic injury should be considered in CBTD patients due its possible clinical significance. [ABSTRACT FROM AUTHOR]

Canine chronic biliary tree disease (CBTD) is a suspected risk factor for pancreatic injury. The aim of this study was to evaluate the frequency and features of pancreatic involvement in canine CBTD, and their relationship with hyperlipemia and its severity. CBTD was defined as the increase in at least two of ALP, GGT, total bilirubin, cholesterol, and a biliary tree abnormal abdominal ultrasound (graded mild to severe). Pancreatic ultrasound appearance was recorded and classified as acute/chronic. Dogs were divided into a PBD group (pancreatic and biliary disease) and BD group (only biliary tree disease). PBD group was subgraded into a “pancreatic injury” and “pancreatitis” group. Eighty-one dogs were retrospectively included: 56 in the PBD group and 25 in the BD group. Of the PBD group, 20 had pancreatitis (15 chronic and 5 dogs acute). US score was mild in 64 dogs and moderate in 17 dogs, and it was not associated with evidence of pancreopathy. Sixty-six dogs had hyperlipemia (mild = 27 dogs; moderate-to-severe = 39 dogs) and no association with pancreopathy was found. Pancreatic injury was more frequent than pancreatitis in CBTD dogs. Although both acute and chronic pancreatic injury may be present, chronic forms were more frequent. Pancreatic injury should be considered in CBTD patients due its possible clinical significance.

1,2-o-dilauryl-rac-glycero-3-glutaric acid-(6′-methylresorufin) ester (DGGR) lipase assays are used to measure lipase activity in the diagnosis of pancreatitis. The effect of hepatic lipases released from damaged hepatocytes on serum DGGR lipase activity has not been reported, to our knowledge. We identified dogs with histologically confirmed liver lesions and concurrent unremarkable pancreatic histology, and dogs with no histologic evidence of hepatic or pancreatic disease. Dogs with relevant comorbidities were excluded. The hepatopathy group (n = 7) included 4 dogs with inflammatory hepatopathies, 2 with hepatic neoplasia, and 1 with unspecified (non-inflammatory, non-neoplastic) hepatopathy. The control group (n = 5) included one dog each with enteritis, subcutaneous hemangiosarcoma, hydrocephalus, myelomalacia, and tetanus. A Mann–Whitney U test compared selected biochemical parameters including serum DGGR lipase, alkaline phosphatase, alanine aminotransferase, and amylase activities, with statistical significance defined as p ≤ 0.05. Data are presented as median and range. Serum DGGR lipase activity (RI: <44 IU/L) was not different between the hepatopathy (52 IU/L; range: 27–85 IU/L) and control (37 IU/L, 25–105 IU/L; p = 0.947) groups. Serum amylase activity (RI: 256–1,610 IU/L) was significantly higher in the hepatopathy group (830 IU/L; 711–1,210 IU/L) than the control group (541 IU/L, 336–695 IU/L; p = 0.028). No association or correlation between serum DGGR lipase activity and hepatic lesions (based on histologic or biochemical findings) was identified, suggesting that clinically relevant changes in serum DGGR lipase activity may not be expected secondary to hepatopathy alone. [ABSTRACT FROM AUTHOR]

Tumors of mesenchymal origin are rarely reported in the pancreas. Therefore, this study characterized 17 feline non-epithelial pancreatic tumors, including clinical data, histopathology, and immunohistochemistry. Seventeen feline pancreatic tissue samples were investigated histopathologically and immunohistochemically. Selected pancreatic and inflammatory serum parameters, e.g., feline pancreatic lipase immunoreactivity (fPLI), 1,2-o-dilauryl-rac-glycero-3-glutaric acid-(60-methylresorufin) ester (DGGR) lipase and serum amyloid A (SAA), were recorded, when available. The neoplasms were characterized as round (n = 13) or spindle (n = 4) cell tumors. Round cell tumors included 12 lymphomas and one mast cell tumor in ectopic splenic tissue within the pancreas. Lymphomas were of T-cell (n = 9) or B-cell (n = 3) origin. These cats showed leukocytosis (3/3) and increased fPLI (5/5), DGGR lipase (3/5) and SAA(4/5) values. Spindle cell tumors included two hemangiosarcomas, one pleomorphic sarcoma and one fibrosarcoma. The cat with pleomorphic sarcoma showed increased SAA value. Overall survival time was two weeks to seven months. These are the first descriptions of a pancreatic pleomorphic sarcoma and a mast cell tumor in accessory spleens within feline pancreas. Although rare, pancreatic tumors should be considered in cats presenting with clinical signs and clinical pathology changes of pancreatitis. Only histopathology can certainly distinguish solitary pancreatitis from a neoplasm with inflammation. [ABSTRACT FROM AUTHOR]

Tumors of mesenchymal origin are rarely reported in the pancreas. Therefore, this study characterized 17 feline non-epithelial pancreatic tumors, including clinical data, histopathology, and immunohistochemistry. Seventeen feline pancreatic tissue samples were investigated histopathologically and immunohistochemically. Selected pancreatic and inflammatory serum parameters, e.g., feline pancreatic lipase immunoreactivity (fPLI), 1,2-o-dilauryl-rac-glycero-3-glutaric acid-(6′-methylresorufin) ester (DGGR) lipase and serum amyloid A (SAA), were recorded, when available. The neoplasms were characterized as round (n = 13) or spindle (n = 4) cell tumors. Round cell tumors included 12 lymphomas and one mast cell tumor in ectopic splenic tissue within the pancreas. Lymphomas were of T-cell (n = 9) or B-cell (n = 3) origin. These cats showed leukocytosis (3/3) and increased fPLI (5/5), DGGR lipase (3/5) and SAA (4/5) values. Spindle cell tumors included two hemangiosarcomas, one pleomorphic sarcoma and one fibrosarcoma. The cat with pleomorphic sarcoma showed increased SAA value. Overall survival time was two weeks to seven months. These are the first descriptions of a pancreatic pleomorphic sarcoma and a mast cell tumor in accessory spleens within feline pancreas. Although rare, pancreatic tumors should be considered in cats presenting with clinical signs and clinical pathology changes of pancreatitis. Only histopathology can certainly distinguish solitary pancreatitis from a neoplasm with inflammation.