Biochemical, functional, and histopathologic characterization of lomustine-induced liver injury in dogs.

OBJECTIVE: To characterize the biochemical, functional, and histopathologic changes associated with lomustine-induced liver injury in dogs. ANIMALS: I0 healthy purpose-bred sexually intact female hounds. PROCEDURES: Dogs were randomly assigned to receive lomustine (approx 75 mg/m2, PO, q 21 d for 5 doses) alone (n = 5) or with prednisone (approx 1.5 mg/kg, PO, q 24 h for 12 weeks; 5). For each dog, a CBC, serum biochemical analysis, liver function testing, urinalysis, and ultrasonographic examination of the liver with acquisition of liver biopsy specimens were performed before and at predetermined times during and after lomustine administration. Results were compared between dogs that did and did not receive prednisone. RESULTS: 7 of the I0 dogs developed clinical signs of liver failure. For all dogs, serum alanine aminotransferase (ALT) and alkaline phosphatase (ALP) activities, bile acid concentrations, and liver histologic score increased and hepatic reduced glutathione content decreased over time. Peak serum ALT (r = 0.79) and ALP (r = 0.90) activities and bile acid concentration (r = 0.68) were positively correlated with the final histologic score. Prednisone did not appear to have a protective effect on histologic score. CONCLUSIONS AND CLINICAL RELEVANCE: In dogs, liver enzyme activities, particularly ALT and ALP activities, should be closely monitored during lomustine treatment and acute increases in those activities may warrant discontinuation of lomustine to mitigate liver injury. Nonspecific ultrasonographic findings and abnormal increases in liver function tests were not detected until the onset of clinical liver failure. Glutathione depletion may have a role in lomustine-induced hepatopathy and warrants further investigation.

Long-term clinical control of feline pancreatic carcinoma with toceranib phosphate.

An 11-year-old, spayed female, domestic shorthair cat was presented with a non-resectable abdominal mass diagnosed as carcinomatosis of pancreatic origin. Treatment with toceranib phosphate was started. Abdominal ultrasound approximately 1 year after diagnosis revealed progressive disease. The cat was humanely euthanized approximately 792 days after initial presentation due to progressive clinical signs.

Contrôle clinique à long terme du carcinome pancréatique félin avec le tocéranib phosphate. Un chatte commune domestique stérilisée âgée de 11 ans a été présentée avec une masse abdominale non résécable diagnostiquée comme une carcinomatose d'origine pancréatique. Le tocéranib phosphate a été administré. L'échographie abdominale environ 1 an après le diagnostic a révélé une maladie progressive. La chatte a été euthanasiée sans cruauté environ 792 jours après la présentation initiale en raison de signes cliniques progressifs.(Traduit par Isabelle Vallières).