Diagnosis of feline pancreatitis with SNAP fPL and Spec fPL.

OBJECTIVES: Pancreatitis is a frequent disease in cats for which the ante-mortem diagnosis remains challenging. Feline pancreatic lipase immunoreactivity (fPLI) has been reported to have a high sensitivity for the diagnosis of pancreatitis. The aim of this study was to compare the rapid in-house test SNAP fPL with the standard test Spec fPL and to evaluate the use of SNAP fPL to diagnose pancreatitis in an emergency setting. METHODS: fPLI of 111 cats with a clinical suspicion of pancreatitis was measured with both SNAP fPL and Spec fPL. Furthermore, clinical signs, haematological and biochemical changes, and abdominal ultrasound findings were recorded. RESULTS: Seventy-eight of 111 cats (70.3%) were tested below the cut-off level for pancreatitis with SNAP, as well as Spec fPL, whereas 21/111 (18.9%) were tested with values above the cut-off level with both tests. In 12/111 (10.8%) cats the results were discordant. The comparison of both tests revealed an agreement of 78/80 (97.5%) when Spec fPL was ⩽3.5 µg/l (negative) and 18/20 (90%) when Spec fPL was ⩾5.4 µg/l (positive). The most common clinical signs in cats with suspected pancreatitis (n = 21) were lethargy (95.2%), reduced appetite and vomiting (90.5% each), dehydration (81.0%), diarrhoea (57.1%), abdominal pain and weight loss (47.6% each). Hyperglycaemia and hyperbilirubinaemia (85.7% each), increased aspartate transaminase (76.2%) and alanine transaminase (47.6%), leucocytosis (61.9%), lymphopenia (57.1%), decreased sodium and chloride (57.1% each), and increased urea (52.4%) were the most common abnormalities in blood work. CONCLUSIONS AND RELEVANCE: Clinical signs, as well as routine blood-work changes, were non-specific and thus proved to be insufficient to diagnose pancreatitis. The combination of SNAP fPL and subsequent Spec fPL, if indicated, provided the opportunity to rule out or to diagnose pancreatitis with a higher certainty than previously known test methods. This study proved SNAP fPL to be a valuable tool to exclude or include pancreatitis in an emergency setting.

[Cobalamin deficiency in dogs and cats]. / Cobalaminmangel bei Hund und Katze.

Cobalamin is a member of the B-group of vitamins and a cofactor for metabolic processes like nucleic acid synthesis, amino acid synthesis, and the citric acid cycle. Mammals are unable to synthesize cobalamin and therefore rely on adequate food intake. Cobalamin absorption is a complex process in the stomach, duodenum, and ileum, requiring a functional exocrine pancreas. Thus, a great number of gastrointestinal diseases like chronic enteropathies, intestinal lymphoma, or exocrine pancreatic insufficiency can lead to hypocobalaminemia. Furthermore, some dog breeds (Giant Schnauzer, Border Collie, Australian Sheperd Dog, and Beagle) can have a primary, hereditary cobalamin deficiency (Imerslund-Gräsbeck syndrome). Clinical signs of cobalamin deficiency comprise anorexia, vomiting, diarrhoea, failure to thrive, and neuropathies. Laboratory findings like non-regenerative anemia, leukopenia, hypoglycemia, and hyperammonaemia have also been described. When hypocobalaminemia is suspected usually in dogs and cats, the cobalamin concentration is usually measured by immunoassay. Because the concentrations of cobalamin in blood and cells can differ the sole measurement of the vitamin concentration is of limited informative value. Treatment depends on the underlying disease aiming at eliminating the cause of hypocobalaminemia. However, successful therapy of gastrointestinal diseases often requires an additional oral or parenteral cobalamin supplementation. In patients with Imerslund-Gräsbeck syndrome, a regular and lifelong cobalamin supplementation is essential.