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Objective: To determine ultrasonographic findings in cats with clinical, gross pathologic, and histologic evidence of acute pancreatic necrosis., Design: Retrospective study., Animals: 20 cats., Procedure: Ultrasound reports and permanent ultrasonographic images were reviewed, and ultrasonographic findings were recorded. Thoracic and abdominal radiographs were also reviewed, when available. Anatomic localization of pancreatic necrosis was determined from the gross pathology report; duration and severity of pancreatic necrosis were determined by reviewing histologic specimens. The presence of concurrent disease was recorded from the final pathology report., Results: The pancreas was considered ultrasonographically normal in 10 cats and was not observed in 3. Ultrasonographic findings were considered compatible with pancreatitis in the remaining 7 cats. Gross pathologic findings indicated that pancreatitis was multifocal in all 7 of these cats; histologically, pancreatitis was acute or subacute in 5 and associated with severe or moderate necrosis in 6. In the remaining 13 cats, gross pathologic findings indicated that pancreatitis was multifocal (n = 8) or focal (2), or gross pathologic findings were normal (3). Histologically, pancreatitis was peracute or acute in 11 of these 13 cats and associated with severe or moderate necrosis in 8. Thoracic and abdominal radiographic findings were nonspecific., Conclusions and Clinical Relevance: Results of ultrasonography were consistent with a diagnosis of pancreatitis in only 7 of 20 cats with acute pancreatic necrosis in the present study. This suggests that new diagnostic criteria must be established if abdominal ultrasonography is to be an effective tool in the diagnosis of pancreatitis in cats.

The medical records of 18 dogs that had hepatic disease and received phenobarbital as an anticonvulsant for 5 to 82 months were reviewed. Clinical signs included sedation and ataxia in all dogs, 5 dogs were also anorectic, 2 had coagulopathy, 3 were icteric, and 5 had ascites. Serum biochemical analysis revealed serum albumin concentration less than or equal to 2.2. g/dl in 12 dogs, serum alkaline phosphatase activity greater than or equal to 169 U/L in 18 dogs, serum alanine transaminase activity greater than or equal to 57 U/L in 15 dogs, and total bilirubin concentration greater than or equal to 1 mg/dl (in the absence of lipemia) in 7 dogs. Serum phenobarbital concentration was greater than or equal to 40 micrograms/ml in 12 of 17 dogs. Sulfobromophthalein excretion was prolonged in 8 of 10 dogs. Preprandial serum bile acid concentrations were high in 8 of 10 dogs, and 2-hour postprandial serum bile acid concentrations were high in 9 of 10 dogs. Two of 4 dogs tested had resting plasma ammonia concentrations greater than 200 mg/dl. An ammonia tolerance test was performed on 2 other dogs; both had ammonia concentration greater than or equal to 200 mg/dl in the plasma 30 minutes after receiving 100 mg of ammonium chloride/kg of body weight, PO. Nine dogs died, 1 was euthanatized, and necropsies were performed on these 10 dogs. Biopsies and necropsies of 6 dogs revealed chronic hepatic fibrosis with nodular regeneration (cirrhosis). One dog had hepatocellular carcinoma and mild cirrhosis. In 1 dog, after phenobarbital had been withheld, necropsy revealed complete recovery of the previously observed lesions.

5-Fluorouracil was used in the treatment of a recently established. human adenocolon carcinoma implanted in the subrenal capsule site of athymic mice as part of a program to determine the relative effectiveness of antitumor agents in the treatment of human tumors grown as xenografts and in the clinic. 5-Fluorouracil treatments resulted in a dose-dependent inhibition of tumor growth under the two examined schedules (five daily doses and three doses every 4 days) when administered either i.v. or i.p. The various schedules and routes resulted in similar patterns of antitumor effects when the data were based on the endpoints of either final tumor weight, change in tumor weight, or relative tumor weight. Assessments of cell viability based on histological examination of tumored kidneys resulted in a downward displacement of the dose-response curves but did not alter their shape or the interpretation of the data. Although approximately 1-mm3 tumor fragments were implanted, variability of size was allowed. Tumor growth was not dependent on the initial size of the implant, as shown by a comparison between the initial individual or average tumor sizes and the final individual or average tumor sizes, respectively. The antitumor effects of the 5-fluorouracil could have been determined on the basis of final tumor weight alone. The inhibition of tumor growth was accompanied by weight loss in treated mice as compared with controls. At lower doses, however, the weight loss of the mice was not extensive, which indicated that the inhibition of tumor growth was, at least in part, attributable to some selective antitumor action of the 5-FUra. The greatest inhibition of tumor growth, however, was accompanied by the most extensive animal weight loss. This correlation raised the question of the degree to which the tumor growth inhibition observed was a consequence of nonspecific drug toxicity to the host. The current results stress the importance of detailed investigations into the nature of host-tumor parameters in order to assess the antitumor activity of candidate drugs in the treatment of human tumor xenografts.