• Journal of Veterinary Science
• /
• v.25 no.3
• /
• pp.48.1-48.12
• /
• 2024

Importance: Early diagnosis of canine pancreatitis is challenging due to non-specific clinical signs. Currently, abdominal ultrasonography and measurement of canine pancreatic lipase (cPL) have been employed for the diagnosis of pancreatitis. Objective: Many qualitative and quantitative commercial cPL tests have been developed and used in veterinary clinics. This study aimed to compare three different methodologies SNAP cPL, Spec cPL, and Vcheck cPL tests to assess the concordance of these assays. Methods: Fifty serum samples were collected from 36 dogs with or without pancreatitis and subjected to SNAP cPL, Spec cPL, and Vcheck cPL tests. Agreement and correlation coefficients were calculated between the test results, and correlations were determined during the management of the patients. Results: The results of the three cPL assays were strongly correlated in 47/50 serum samples (94%). Cohen's kappa analysis between the Spec cPL and Vcheck cPL showed near perfect agreement (κ = 0.960, p < 0.001), SNAP cPL and Vcheck cPL (κ = 0.920, p < 0.001), and Spec cPL and SNAP cPL (κ = 0.880, p < 0.001). The correlation coefficients (r) between data from Spec cPL and Vcheck cPL tests was calculated by Spearman's correlation test (r = 0.958, p < 0.001). Furthermore, the patterns of change in serum cPL concentrations determined using Spec cPL and Vcheck cPL were significantly consistent during the monitoring period in 11 patients. Conclusions and Relevance: Our data illustrated that Spec cPL and Vcheck cPL tests are compatible for clinical use in the diagnosis and monitoring of canine pancreatitis.

• Journal of Veterinary Clinics
• /
• v.34 no.4
• /
• pp.229-233
• /
• 2017

The object of the present study was to compare abnormal serum canine pancreas-specific lipase results and pancreatic ultrasonographic findings in dogs with pancreatitis. Pancreatitis is a common disease in dogs that is difficult to diagnose. The noninvasive diagnostic procedures, including a serum canine pancreatic-specific lipase (cPL) test and ultrasonographic changes in the pancreas, can be considered for the diagnosis of canine pancreatitis in clinical practice. A retrospective study was performed to assess pancreatitis in dogs. Forty client-owned dogs were suspected to have pancreatitis, which was confirmed by abnormal serum SNAP cPL results. Abdominal ultrasound examinations were also performed. The present study investigated the distribution of clinical signs associated with pancreatitis, and the dogs were divided into two groups: group 1 (clinical signs compatible with pancreatitis; n = 30) and group 2 (no clinical signs; n = 10). Based on this study, an abnormal result on the SNAP cPL assay can still present as a normal pancreas through an ultrasonographic examination, and a normal health status can identify the status of pancreatic ultrasonographic abnormal lesions. Therefore, for dogs with suspected pancreatitis, it is important to repeat an ultrasonographic evaluation. There is no significant difference between clinical symptoms and ultrasonographic changes in the pancreas.

• Archives of Pharmacal Research
• /
• v.27 no.7
• /
• pp.757-762
• /
• 2004

The protective adaptive response to electrophiles and reactive oxygen species is mediated by the induction of phase II detoxifying genes including glutathione S-transferases (GSTs). NF-E2-related factor-2 (Nrf2) phosphorylation by protein kinase C (PKC) is a critical event for its nuclear translocation in response to oxidative stress. Previously, we have shown that peroxynitrite plays a role in activation of Nrf2 and Nrf2 binding to the antioxidant response element (ARE) via the pathway of phosphatidylinositol 3-kinase (PI3-kinase) and that nitric oxide synthase in hepatocytes is required for GSTA2 induction. In view of the importance of PKC and Pl3-kinase in Nrf2-mediated GST induction, we investigated the role of these kinases in peroxynitrite formation for GSTA2 induction by oxidative stress and determined the relationship between PKC and PI3-kinase. Although PKC activation by phorbol 12-myristate-13-acetate (PMA) did not increase the extents of constitutive and inducible GSTA2 expression, either PKC depletion by PMA or PKC inhibition by staurosporine significantly inhibited GSTA2 induction by tert-butylhydroquinone (t-SHa) a prooxidant chemical. Therefore, the basal PKC activity is req- uisite for GSTA2 induction. 3-Morpholinosydnonimine (SIN-1), which decomposes and yields peroxynitrite, induced GSTA2, which was not inhibited by PKC depletion, but slightly enhanced by PKC activation, suggesting that PKC promotes peroxynitrite formation for Nrf2-mediated GSTA2 induction. Treatment of cells with S-nitroso-N-acetyl-penicillamine (SNAP), an exogenous NO donor, in combination with t-BHQ may produce peroxynitrite. GSTA2 induction by SNAP ＋ t-BHQ was not decreased by PKC depletion, but rather enhanced by PKC activation, showing that the activity of PKC might be required for peroxynitrite formation. LY294002 a P13-kinase inhibitor blocked GSTA2 induction by t-BHQ, which was reversed by PMA-induced PKC activation. These results provide evidence that PKC may playa role in formation of peroxynitrite that activates Nrf2 for GSTA2 induction and that PKC may serve an activator for GSTA2 induction downstream of PI3-kinase.