Dogs with mast cell tumors (MCT) are often affected with paraneoplastic syndromes such as gastrointestinal ulceration. The mechanism of ulceration is believed to be related to hyperhistaminemia. To test this hypothesis, plasma histamine and gastrin concentrations were measured in 17 dogs with MCT. Plasma histamine concentrations in dogs with MCT were significantly higher than those in normal dogs. Conversely, plasma gastrin concentrations in dogs with M C T were significantly lower than gastrin concentrations in normal dogs. Additionally, plasma gastrin concentrations were inversely related to plasma histamine concentrations, which provided indirect evidence for the presence of hyperacidity secondary to hyperhistaminemia ( r 2 = 57.7). Plasma histamine and plasma gastrin concentrations were not related to clinical stage of disease, tumor histologic grade, or tumor size. Median survival time was 245 days, with a range of 90 to 1315 days. Because the degree of hyperhistaminemia could not be predicted in this study from the clinical stage, histologic grade, or tumor size, these data suggest that hyperhistaminemia may occur in any dog with MCT. (Journal of Veterinary Internal Medicine 1990; 4~242-246)MAST CELL TUMORS are associated with a variety of paraneoplastic syndromes including local and systemic coagulopathies, delayed wound healing, vascular damage, and shock-like symptoms during chemotherapeutic or radiation treatment of the tumor.'-5 These effects are caused by histamine, heparin, serotonin, eosinophil chemotactic substance, and proteolytic enzymes released from degranulating mast cells.' Gastric ulceration is a common problem in dogs with MCT.' As determined by necropsy, 83% of dogs with MCT examined by Howard et al. had gastroduodenal ulceration.' The exact cause of the gastrointestinal ulceration associated with MCT is unknown. It is believed to be related to increased gastric acid secretion and gastric motility, and the direct vascular damage caused by hyperhi~taminemia.~ The purpose of this investigation was to evaluate plasma histamine and gastrin concentrations in dogs with mast cell tumors and to determine the relationship between plasma histamine and gastrin concentrations and postsurgical survival, clinical stage, tumor histologic grade, and tumor diameter. Materials and MethodsThis study was conducted over a two-year period using dogs brought to the Veterinary Medicine Teaching Hospital at the University of Wisconsin-Madison. Only dogs with histologically confirmed mast cell tumors and normal renal function were included in the study. None had received any prior therapy for their tumors. For each dog, a complete blood count, serum electrolyte concentrations, serum chemistry panel, and urinalysis were evaluated. A tentative diagnosis of MCT was made when a homogenous population of mast cells was observed on cytologic examination of a sample obtained by fine-needle aspiration of a mass. Blood samples for plasma histamine and gastrin concentration determinations were collected in edetate calcium di...

BackgroundComputed tomography (CT) is highly accurate for diagnosing pancreatitis in humans. The diagnosis of pancreatitis in dogs is based on clinical signs, laboratory findings, and ultrasonographic (US) changes. There are, however, inherent limitations in relying on laboratory and ultrasound findings for the clinical diagnosis of pancreatitis in dogs.Hypothesis/ObjectivesWe hypothesized that CT angiography would be a rapid and reliable method to confirm pancreatitis in dogs compared to ultrasonography. The aim was to describe the CT characteristics and compare them to ultrasound findings and correlate the CT appearance to the severity of the patients' clinical course.AnimalsA prospective pilot case series; 10 dogs with pancreatitis were enrolled if the history, clinical signs, laboratory, and ultrasonographic findings were indicative of pancreatitis.MethodsA 3‐phase angiographic CT was performed under sedation. Afterward, each dog had US‐guided aspirates of the pancreas collected and blood drawn for cPLi assay. Images were evaluated for portion of visible pancreas, pancreatic size and margin, pancreatic parenchyma, presence of peripancreatic changes and contrast enhancement pattern. The results were compared with outcome.ResultsAn enlarged, homogeneously to heterogeneously attenuating and contrast‐enhancing pancreas with ill‐defined borders was identified in all dogs. CT identified more features characterizing pancreatic abnormalities compared to US. Thrombi were found in 3/10 dogs. Three dogs with heterogeneous contrast enhancement had an overall poorer outcome than those with homogenous enhancement.Conclusions and Clinical Importance CT angiography under sedation was used in dogs to confirm clinically suspected pancreatitis and identified clinically relevant and potentially prognostic features of pancreatitis in dogs.

S-adenosylmethionine (SAMe) is reported to have hepatoprotective and antioxidant functions. Acetaminophen (paracetamol) was used to induce oxidative damage in cats, and to then determine the effect of SAMe treatment on erythrocyte morphology, PCV, liver histopathology, thiobarbituate reacting substances (TBARS), reduced glutathione (GSH), and oxidised glutathione (GSSG). Cats receiving acetaminophen had a significant increase in methemoglobin and Heinz body production. A significant effect for the interaction of time and treatment was found for Heinz body production and changes in PCV. No significant changes were found in blood or hepatic TBARS. Blood GSH increased significantly in all cats, while the blood GSH:GSSG ratio tended to increase the most in cats given acetaminophen only. The hepatic GSH:GSSG ratio tended to increase in cats given SAMe and decrease in cats given acetaminophen, but this effect was not significant. SAMe protected erythrocytes from oxidative damage by limiting Heinz body formation and erythrocyte destruction and maybe useful in treating acetaminophen toxicity.

To evaluate dogs with computed tomography angiography of the abdomen for overall prevalence of portal vein thrombosis and prevalence of portal vein thrombosis based on different disease categories. To evaluate dogs with and without portal vein thrombosis for differences in outcome. To compare ultrasound to computed tomographic angiography for identification of portal vein thrombosis. MethOds: Abdominal computed tomography angiography of 223 client-owned animals was reviewed for evidence of portal vein thrombosis. Based on medical records, dogs were assigned to disease categories: (1) liver disease; (2) non-hepatic neoplasia; (3) pancreatitis; (4) infectious disease; (5) immune-mediated disease; (6) other; (7) multiple diseases. Different categories were compared for the prevalence of portal vein thrombosis. Outcome was evaluated in dogs with and without portal vein thrombosis. Ultrasound reports were reviewed to determine the detection of thrombosis on ultrasound.Results: Twenty-eight dogs (13%) had portal vein thrombosis. The pancreatitis category contained the highest percentage of portal vein thrombosis among different categories (eight of 19; 42%). There was a similar outcome between dogs with and without portal vein thrombosis. Of 21 dogs with portal vein thrombosis that had ultrasound performed, ultrasound detected thrombosis in four of 21 (19%) cases.clinical Relevance: In this study, portal vein thrombosis prevalence was higher in dogs with pancreatitis compared to dogs with liver disease, non-hepatic neoplasia and other abdominal or systemic disease. The portal system should be carefully evaluated with imaging in dogs with pancreatitis. As compared to ultrasound, CT angiography is the imaging method of choice for detection of portal vein thrombosis in dogs.

No abstract

Breeders of Bedlington terriers have long suspected that a small number of their dogs were susceptible to fatal liver disease. Interest in this disorder increased sharply when the responses to a questionnaire circulated by the Bedlington Terrier Club of America revealed two facts: the incidence of the disorder was considerably higher than had been generally assumed, and although no environmental differences were evident, only some strains of Bedlingtons seemed to be afflicted, suggesting an etiological genetic factor. Hardy, Stevens & Stowe (1975) were impressed by the hobnailed gross appearance and the abundance of intra-hepatocytic brown pigment granules in the livers of 2 autopsied terriers. These findings, and the possibility that the disorder was hereditary, suggested to them that they might be dealing with a canine form of Wilson's disease. Sections of both dogs' livers stained with rubeanic acid were strongly positive for copper in the hepatocellular granules. We have extended the findings of Hardy, Stevens & Stowe and confirmed their original idea that there are remarkable similarities between this disorder of Bedlington terriers and Wilson's disease.

No abstract

n 11-year-old female spayed Golden Retriever was A presented to the refemng veterinarian because of a 1-day onset of lethargy and black tarry stools that had progressed to dark bloody diarrhea. The dog had vomited bile and mucus once during the proceeding 24 hours. The dog had not been exposed to toxicants; however, the dog occasionally received 1 Ascriptin (Rorer Pharmaceutical Corp, Fort Washington, PA) (325 mg aspirin and 150 mg magnesium-aluminum hydroxide) a day for arthritis. During the prior 2 weeks approximately 5 doses had been administered. Physical examination identified pale mucous membranes. Thoracic and abdominal radiographs were taken and were within normal limits. A CBC, serum chemistry panel, platelet count, prothrombin time, and activated partial thromboplastin time were submitted to a local veterinary diagnostic laboratory. Abnormalities in the CBC included a hematocrit of 17% (reference range 37-%%), red blood cell (RBC) count of 2.45 X 106/pL (reference range 5.5-8.5 X 106/pL), hemoglobin 5.8 g/dL (reference range 12-18 g/dL), and platelet count of 112 X 103/pL (reference range 200-500 X 10VpL). The coagulation times were normal. Relevant abnormalities on the serum chemistry profile included increased blood urea nitrogen (BUN) concentration (51 mg/dL; reference range 7-28 mg/dL), hypoproteinemia (3.5 g/dL; reference range 5.4-7.4 g/dL), hypoalbuminemia (2.0 mg/dL; reference range 2.7-4.5 mg/dL), and hypoglubinemia (1.5 mg/dL; reference range 1.9-3.4 mg/ dL). A tentative diagnosis of gastrointestinal ulceration was made based on the clinical and clinicopathologic findings and the dog was treated with sucralfate and doxycycline PO.Twelve hours after her release the dog was represented for acute collapse. On physical examination the mucous membranes were very pale, and the hematocrit had decreased to 9%. The patient was referred to a veterinary internist for diagnosis and therapy of the gastrointestinal ulceration, where she received 2 units of packed RBCs, 500 mL of hetastarch, lactated Ringer's solution, ranitidine, and sucralfate. During the blood transfusion the dog vomited bile-tinged fluid with no evidence of either digested or undigested blood. On hospital day 2 the dog had improved clinically, and the PCV had increased to 19% and the total protein to 4.4 mg/dL. Rectal examination revealed gross melena. An abdominal ultrasonogram and upper gastrointestinal barium contrast study were performed in an attempt to identify a source of gastrointestinal bleeding; both were interpreted as normal.On hospital day 3 the hematocrit was 28% and upper gastrointestinal endoscopy was performed under general anesthesia in the attempt to identify a source of gastroin- The clinical and hematologic findings supported a diagnosis of gastrointestinal bleeding. The lack of historical hematemesis and the failure of upper gastrointestinal endoscopy to demonstrate a definitive site of active bleeding suggested a lesion distal to the proximal duodenum.A scintigraphic study using labeled RBCs as a minimally invasiv...