Histopathology and Feline Pancreatic Lipase Immunoreactivity in Inflammatory, Hyperplastic and Neoplastic Pancreatic Diseases in Cats.

The most common pancreatic diseases in cats are pancreatitis and exocrine pancreatic insufficiency (EPI). Non-invasive methods, such as serological quantification of feline pancreatic lipase immunoreactivity (fPLI), are often used in the diagnosis of pancreatitis. Previous studies have compared fPLI concentrations with histopathology, considered to be the gold standard for diagnosis of feline pancreatitis. However, fPLI concentrations in cats suffering from pancreatic tumours were rarely described. The aim of the present study was to determine the sensitivity and specificity of an in-house enzyme-linked immunosorbent assay (ELISA) for the quantification of fPLI in serum samples based on histopathological findings in cats diagnosed with various pancreatic diseases. Pancreatic biopsy samples from 80 cats were included. Five groups were defined on the basis of pancreatic histopathology: group 1, normal pancreas; group 2, nodular hyperplasia; group 3, mild pancreatitis; group 4, marked (moderate/severe) pancreatitis; and group 5, pancreatic neoplasia. Serum samples from all cats were tested by fPLI ELISA (<3.6 µg/l normal, 3.6-5.3 µg/l questionable, >5.3 µg/l pancreatitis). In group 1 (n = 19), serum fPLI values were within the reference interval in 74% of cases and in group 2 (n = 9) in 78%. Cats with mild pancreatitis (n = 23), marked pancreatitis (n = 11) and pancreatic neoplasms (n = 18) had significantly increased fPLI concentrations compared with group 1 (P = 0.004/0.001/≤0.0001). Cats with nodular hyperplasia had significantly lower fPLI values than cats with marked pancreatitis (P = 0.048) or tumours (P = 0.002). Serum fPLI concentrations in group 3 were <3.6 µg/l (n = 6), 3.6-5.3 µg/l (n = 4) and >5.3 µg/l (n = 13). Calculated test sensitivity for mild pancreatitis was fPLI >3.5 µg/l: 73.9% and fPLI >5.3 µg/l: 56.5%. In group 4 (n = 11), seven of nine cats (77.8%) with marked purulent pancreatitis had elevated fPLI. In group 4, a sensitivity of 81.8% was detected for fPLI >3.5 µg/l and 63.6% for fPLI >5.3 µg/l. Two cats with marked non-purulent pancreatitis had elevated fPLI, while two cats with marked purulent pancreatitis had normal fPLI values (<3.6 µg/l). In group 5, one cat with pancreatic adenoma and one with pancreatic acinar carcinoma had normal fPLI concentrations. The other cats with pancreatic adenoma (solid, n = 1; cystic, n = 4) or carcinoma (solid, n = 9; cystic, n = 2) had elevated or high fPLI values (4.1 to >40 µg/l, median 21.2 µg/l), probably caused by additional inflammation. The results of the present study confirm the importance of detailed histopathological characterization for the interpretation of clinical signs and fPLI values in feline pancreatitis. Primary pancreatic neoplasms may also lead to elevated fPLI concentrations as there is concurrent pancreatitis in most cases. However, severe pancreatic diseases, such as chronic non-purulent pancreatitis or tumours without inflammation, may result in normal fPLI values.

Primary Solid and Cystic Tumours of the Exocrine Pancreas in Cats.

Tumours of the exocrine pancreas are rare in cats and few cases are described in the literature. Cystic tumours of the pancreas are not included in the World Health Organization (WHO) international histological classification of tumours of domestic animals. The aim of this study was to characterize the pathology of primary epithelial tumours of the feline exocrine pancreas, with emphasis on cystic tumours. We reviewed tumours of the exocrine pancreas in 70 cats, including complete tumours or the entire pancreas (n = 18) and excisional biopsy samples of pancreatic tumours (n = 52). Macroscopically, the tumours were grouped as solid (n = 45) or cystic (n = 25). Solid tumours were subdivided into adenomas (n = 5) and carcinomas (n = 40) and cystic neoplasms into adenomas (n = 15), carcinomas (n = 7) and cases with diverse growth patterns (n = 3). All five grossly solid adenomas had acinar morphology, while the macroscopically solid carcinomas showed acinar (n = 17), tubular (n = 14) or mixed (n = 9) growth microscopically. Cystic adenomas had acinar (n = 2), tubular (n = 12) or mixed (n = 1) growth, while cystic carcinomas had exclusively tubular growth (n = 7). Three cases with cystic lesions showed diverse histopathological growth patterns. The clinical outcome was available in 57 cases. The majority of cats with carcinomas died or were humanely destroyed during or shortly after surgery (n = 32). However, 2/7 animals with cystic carcinomas showed longer survival times. Cats with cystic adenomas had survival times of up to 5 years. The results of this study show that cystic pancreatic tumours should be considered a differential diagnosis in cats with cystic intra-abdominal masses, even though these are not yet described in the WHO classification. Based on the relatively long survival times of cats with cystic adenomas, complete resection with subsequent histopathological examination is recommended.

Characterization of 22 Canine Pancreatic Carcinomas and Review of Literature.

Pancreatic carcinomas are rare in dogs and clinical signs are mostly non-specific. The literature on clinically and pathologically characterized canine exocrine pancreatic tumours is limited to 76 cases reported since 1963. This retrospective study analysed formalin-fixed samples of pancreatic carcinomas from 22 dogs, obtained during elective exploratory surgery (n = 16) or if the dog was humanely destroyed (n = 6). Tumours were diagnosed according to the World Health Organization classification of tumours of the pancreas of domestic animals. In seven cases, blood samples taken during or shortly before surgery were analysed for concentrations of alpha-amylase, 1,2-o-dilauryl-rac-glycero-3-glutaric acid-(6'-methylresorufin) ester lipase (DGGR lipase), C-reactive protein (CRP), alanine aminotransferase, glutamate dehydrogenase, alkaline phosphatase (ALP), canine trypsin-like immunoreactivity (cTLI) and canine pancreatic lipase immunoreactivity (cPLI). Neutrophil and lymphocyte numbers were determined as part of a complete blood count. Clinical signs were non-specific and included vomiting, inappetence and diarrhoea. Acinar carcinomas were most common (19/22) and observed growth patterns included: solid (n = 14), acinar (n = 5), clear cell (n = 3), mucinous (n = 2), trabecular (n = 1) or rosette-like (n = 1), occurring as a single pattern or in combination. Ductal carcinomas were identified in three cases. Pancreatitis was a common additional histological finding; five dogs had mild and nine dogs had severe pancreatitis. cPLI, DGGR lipase, cTLI and CRP were elevated in 5/5 acinar carcinomas. All liver enzymes were elevated in three of these five animals and ALP was increased in 4/5 dogs. Two dogs with ductal pancreatic carcinomas showed normal cPLI concentrations. One had increased CRP, liver enzymes and leucocytosis with neutrophilia, the other had elevated DGGR lipase and cTLI concentrations. Clinical findings in canine pancreatic carcinomas were non-specific and simultaneous inflammation can mask the detection of the underlying neoplasm in clinical examination and laboratory testing.