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Background: Insulinoma is an autonomous insulin-secreting islet cell neoplasm that is rarely diagnosed in cats. The clinical and pathological aspects of feline insulinoma have been described previously, but the molecular characteristics of these tumors have not been investigated., Objectives: The study objectives were to characterize peptide hormone production and determine expression of selected genes involved in glucose metabolism and insulin secretion in a feline insulinoma., Methods: Immunohistochemistry and RT-PCR were used to examine hormone and gene expression, respectively, by insulinoma cells., Results: Immunohistochemistry examination indicated that the tumor cells expressed insulin, chromogranin A, and somatostatin but not glucagon or pancreatic polypeptide. The tumor expressed several genes characteristic of pancreatic beta cells (beta cells) including insulin (INS), glucose transporter 2 (GLUT2), and glucokinase (GCK). The tumor also expressed hexokinase 1 (HK1), a glycolytic enzyme not normally expressed in beta cells. GCK expression was higher in the insulinoma than in normal pancreas from the same cat. The GCK : HK1 ratio was >20-fold higher in insulinoma tissue than in normal pancreas., Conclusions and Clinical Importance: The feline insulinoma produced several peptide hormones and expressed genes consistent with a beta-cell phenotype. The pattern of hexokinase gene expression in tumor cells differed from that of normal pancreas. These findings suggest insulinoma cells may have an increased sensitivity to glucose that could contribute to the abnormal insulin secretory response observed at low serum glucose concentrations.

Pulmonary thromboembolism (PTE) is rarely diagnosed in cats, and the clinical features of the disease are not well known. PTE was diagnosed at postmortem examination in 17 cats, a prevalence of 0.06% over a 24-year period. The age of affected cats ranged from 10 months to 18 years, although young (<4 years) and old (>10 years) cats were more commonly affected than were middle-aged cats. Males and females were equally affected. The majority of cats with PTE (n = 16) had concurrent disease, which was often severe. The most common diseases identified in association with PTE were neoplasia, anemia of unidentified cause, and pancreatitis. Cats with glomerulonephritis, encephalitis, pneumonia, heart disease, and hepatic lipidosis were also represented in this study. Most cats with PTE demonstrated dyspnea and respiratory distress before death or euthanasia, but PTE was not recognized ante mortem in any cat studied. In conclusion, PTE can affect cats of any age and is associated with a variety of systemic and inflammatory disorders. It is recommended that the same clinical criteria used to increase the suspicion of PTE in dogs should also be applied to cats.

Total serum magnesium concentration ([Mg2+]s) was prospectively determined for 57 cats admitted to the intensive care unit (ICU) of the Cornell University Hospital for Animals. Data were collected and analyzed to determine the following: prevalence and incidence of [Mg2+] abnormalities, medical disorders associated with altered [Mg2+]s, association of altered [Mg2+]s with other electrolyte abnormalities, length of hospitalization for cats with abnormalities of [Mg2+]s versus those with normal [Mg2+]s, and survival of cats with abnormal [Mg2+)s versus those with normal [Mg2+]s. The point prevalence of magnesium abnormalities was 26%, the period prevalence was 46%, and the cumulative incidence was 23%. Hypermagnesemia was associated with abnormalities of serum potassium (P = .04) and phosphate (P = .01) concentrations. Abnormalities of [Mg2+]s were not associated with abnormal serum concentrations of Na+, Ca2+, or Cl-. On admission. hypomagnesemia was detected in cats with gastrointestinal, endocrine, and other disorders; hypermagnesemia was detected only in cats with renal disease, obstructive uropathy, or neoplastic disease. The median hospital stay for cats that developed abnormal [Mg2+]s after admission was longer than for cats that remained normomagnesemic (5 versus 4 days, respectively; P = .03). Despite the longer hospital stay, the survival of these cats was lower than that of normomagnesemic cats (54 versus 77%; P = .05). When all cats were considered, the survival of cats with abnormal [Mg2+]s also was decreased compared with normomagnesemic cats (62 versus 81%; P = .05). We conclude that abnormalities of [Mg2+]s may affect morbidity and mortality of affected cats.

A prospective clinical study in dogs with transudative abdominal effusions examined the clinical usefulness of the serum albumin-effusion albumin (SA-EA) gradient. In humans, the SA-EA gradient facilitates classification of abdominal effusion, with a gradient > or = 1.1 indicating the presence of portal hypertension. Gradient values proved useful for predicting therapeutic response to sodium restriction and diuresis in humans. Of 49 dogs evaluated, 25 had hepatobiliary disease (group 1) and 24 had other nonhepatobiliary conditions (group 2). Portal hypertension was clinically suspected in 24 of 25 dogs in group 1 and in 15 of 24 dogs in group 2. A broad range of SA-EA gradients was found. A gradient > or = 1.1 was found in 22 of 25 (88.0%) dogs with liver disease and in 14 of 24 (58.3%) dogs with other disorders. The median SA-EA gradient was higher in group 1 than in group 2, with values of 1.4 (range, 0.7-3.1) and 1.1 (range, 0.3-2.6), respectively (P < .04). Considerable overlapping of SA-EA gradients occurred between groups and among dogs with diverse conditions such that gradient values could not distinguish dogs with hepatobiliary disease from dogs with other conditions. The overall diagnostic accuracy of the SA-EA gradient in predicting portal hypertension in dogs with and without hepatobiliary disease (69.4%) exceeded that of hypoalbuminemia (57.1%). These findings suggest that portal hypertension is a predominant force in formation of transudative abdominal effusion in dogs with hepatobiliary disease and in dogs with other disorders. Whether the SA-EA gradient can be used to guide therapeutic mobilization of effusion in dogs remains to be proved.

Hepatoportal microvascular dysplasia (MVD), a congenital disorder of the hepatic vasculature, is described in a kindred of Cairn Terrier dogs. Cairn Terrier dogs (n = 165) were evaluated using the serum bile acid test. Affected dogs, identified by abnormal fasting or postprandial serum bile acid concentrations, were divided into 2 groups. Group 1 dogs (n = 147) were used for pedigree analysis. Group 2 dogs (n = 18) were characterized on the basis of history, physical examination, clinicopathologic studies, diagnostic imaging of the liver and portal circulation, and hepatic histopathology. Group 2 contained control dogs (n = 2), dogs with hepatoportal MVD (n = 11), and dogs with macroscopic portosystemic vascular anomalies (PVSA) (n = 5). With the exception of high serum bile acid concentrations, dogs with hepatoportal MVD were indistinguishable from control dogs on the basis of history, physical examination, clinicopathologic findings, survey abdominal radiography, abdominal ultrasound, or transcolonic scintigraphy. Contrast portography in dogs with MVD revealed abnormalities of terminal twigs of the portal vasculature with out large intrahepatic or extrahepatic shunting vessels. Histopathologic abnormalities in dogs with hepatoportal MVD were similar to those reported for dogs with PSVA. Pedigree analysis suggested an autosomal inheritance for MVD. Dogs with MVD had high serum bile acid concentrations, abnormal indocyanine green clearance, and hepatic pathology suggestive of PSVA, but they lacked characteristic clinical findings of PSVA. The clinical significance of MVD is unclear. Dogs with MVD were clinically normal when evaluated but long-term follow-up is not yet available. Dogs with hepatoportal MVD should be identified at an early age to avoid confusion in future diagnostic evaluations.