Ductal plate malformations (DPMs) represent developmental biliary disorders with a wide phenotypic spectrum. This study characterizes DPM in 30 Boxer dogs. Median age was 1.5 (range, 0.3-10.0) years, with 12 dogs <1 year. Clinical features included increased serum levels of liver enzymes (28), gastrointestinal signs (16), poor body condition (14), abdominal effusion (9), and hepatic encephalopathy (2). Additional malformations included gallbladder atresia (8), atrophied left liver (2), absent quadrate lobe with leftdisplaced gallbladder (1), portal vasculature atresia (left liver, 1), intrahepatic portosystemic shunt (1), and complex intrahepatic arteriovenous malformation (1). All dogs had portal tracts dimensionally expanded by a moderate-to-severe multiple small bile duct phenotype embedded in abundant extracellular matrix; 80% displayed variable portal-to-portal bridging. Quantitative analysis confirmed significantly increased fibrillar collagen and a 3-fold increased portal tract area relative to 6 Boxer and 10 non-Boxer controls. Biliary phenotype was dominated by tightly formed CK19-positive ductules, typically 10 to 15 mm in diameter, with 3 to >30 profiles per portal tract, reduced luminal apertures, and negative Ki-67 immunoreactivity. CK19-positive biliary epithelium intersected directly with zone 1 hepatocytes as a signature feature when considered with other DPM characteristics. Phenotypic variation included a multiple small bile duct phenotype (all dogs), predominantly thin-walled sacculated ducts (4), well-formed saccular ducts (4), and sacculated segmental, interlobular, and intralobular ducts (Caroli malformation, 2 dogs, one with bridging portal fibrosis). Histologic evidence of portal venous hypoperfusion accompanied increased biliary profiles in every case. We propose that this spectrum of disorders be referred to as DPM with appropriate modifiers to characterize the unique phenotypes.

We describe 4 young male Doberman Pinschers (3 littermates and I unrelated dog) with a syndrome resembling idiopathic or noncirrhotic portal hypertension of humans. Each dog was evaluated for a hepatopathy resulting in portal hypertension, development of portosystemic collateral vessels, and hepatic encephalopathy. These dogs differ from previous reports of young dogs with hepatic insufficiency associated with portal hypertension and acquired portal systemic shunting by their lack of intrahepatic arteriovenous fistulae, portal vein atresia, or intrahepatic fibrosis. Clinicopathologic features included erythrocyte microcytosis, normal to mildly increased liver enzyme activities, increased concentrations of serum bile acids, reduced plasma indocyanine green clearance, and normal total bilirubin concentration. Abdominal ultrasonography disclosed a small liver and portosystemic collateral vessels. Radiographic imaging studies confirmed hepatofugal portal circulation and discounted hepatic arteriovenous fistulae. Histopathologic features in liver tissue from each dog were similar and consistent in all sections examined. Common findings included increased cross-sectional views of hepatic arterioles; hepatic lobular atrophy; scanty increase in connective tissue around some large portal triads; and absence of inflammation, disturbed lobular architecture, bile duct proliferation, or intrahepatic cholestasis.Key words: Ascites; Hepatic encephalopathy; Portal hypertension; Portosystemic shunting.ith the exception of congenital malformations of the portal vein, disorders of hepatic perfusion or function are relatively uncommon in young dogs. A few reports have described portal hypertension in young dogs associated with varying degrees and histologic distributions of fibrosis. In these cases, development of considerable hepatic fibrosis with variable zonal distribution is inconsistently associated with inflammation. Development of portal hypertension is rare in the absence of idiopathic hepatic fibrosis, chronic acquired hepatic injury associated with lobular collapse and leading to hepatic fibrosis with or without cirrhosis, portal venous thromboembolism, or obstructed outflow from the hepatic veins. We report herein a unique hepatic abnormality causing portal hypertension, development of acquired portosystemic collateral circulation, and hepatic encephalopathy in juvenile male Doberman Pinschers. Clinicopathologic and histopathologic features resemble 2 similar syndromes described in humans in which hepatic fibrosis and inflammation are Materials and Methods DogsFour male Doberman Pinschers, 3 from a litter of I I puppies (9 maled2 females) and 1 unrelated dog, were evaluated after presentation for an acute illness of 1-2 weeks duration. At the time of examination, dogs ranged in age from 4 to 7 months. The related dogs had been hou5ed separately since 4 months of age and were evaluated separately. The litter producing affected siblings was derived from a brother-sister mating in a line-bred kindred being studied for denta...

The effect of daily doses of 5-15 mg of methimazole on the platelet count, prothrombin time (PT), activated partial thromboplastin time (APTT), and proteins induced by vitamin K absence or antagonists (PIVKA) clotting time in 20 hyperthyroid cats was determined. No significant (P > .05) difference was found in median platelet count. PT, APTT, or PIVKA clotting time before treatment compared to median values at 2-6 weeks or > or =7-12 weeks of methimazole treatment. No cat had a prolonged APTT at any time. At 2-6 weeks of methimazole treatment, 1 cat each developed thrombocytopenia or prolonged PIVKA clotting time despite initially normal values. Three cats had abnormal coagulation tests (prolonged PT [n = 1] and PIVKA clotting time [n = 3]) before treatment that fluctuated during treatment. Excluding the 3 cats that had abnormal PIVKA clotting time before treatment, prolonged PIVKA clotting time developed in 6% (1/17; 95% confidence interval, 0-28%) cats treated with methimazole for 2-6 weeks. Seemingly. doses of methimazole commonly used to treat hyperthyroidism in cats do not cause alteration in PT and APTT, and only rarely prolong PIVKA clotting time. Nevertheless, abnormal PIVKA clotting time may explain bleeding tendencies unassociated with thrombocytopenia in methimazole-treated hyperthyroid cats.

BackgroundThe prevalence of concurrent disease in hyperthyroid cats is unknown.ObjectivesTo identify the prevalence of concurrent intra‐abdominal disease using abdominal ultrasound examination (AUS) in hyperthyroid cats referred for radioactive iodine treatment (RIT) and to determine whether the requirement for pretreatment AUS is justified.AnimalsFive hundred and thirty‐four client‐owned cats diagnosed with hyperthyroidism and referred for RIT.MethodsRetrospective study. Age, breed, sex, body weight, clinical signs, total serum T4 concentration, blood urea nitrogen (BUN) concentration, serum creatinine concentration, urine specific gravity (USG), AUS results, and biopsy or cytology results, or both (if obtained) were collected from the medical records.ResultsThe prevalence of concurrent disease identified using AUS in hyperthyroid cats referred for RIT was 36.1%; 22.8% of the cats in the study had renal disease and 2.4% had confirmed neoplasia. Significant differences in median USG (P value 0.032) and median BUN (P value 0.028) were found between cats that had abnormal kidneys on AUS compared to those with normal‐appearing kidneys. Only 2.2% of the cats were not treated with RIT as a result of changes identified on AUS and subsequently obtained cytology or biopsy results.Conclusions and Clinical ImportanceThe results indicate that pretreatment AUS in hyperthyroid cats referred for RIT is unnecessary in most patients.

The effect of daily doses of 5-15 mg of methimazole on the platelet count, prothrombin time (PT), activated partial thromboplastin time (APTT), and proteins induced by vitamin K absence or antagonists (PIVKA) clotting time in 20 hyperthyroid cats was determined. No significant (P Ͼ .05) difference was found in median platelet count, PT, APTT, or PIVKA clotting time before treatment compared to median values at 2-6 weeks or Ն7-12 weeks of methimazole treatment. No cat had a prolonged APTT at any time. At 2-6 weeks of methimazole treatment, 1 cat each developed thrombocytopenia or prolonged PIVKA clotting time despite initially normal values. Three cats had abnormal coagulation tests (prolonged PT [n ϭ 1] and PIVKA clotting time [n ϭ 3]) before treatment that fluctuated during treatment. Excluding the 3 cats that had abnormal PIVKA clotting time before treatment, prolonged PIVKA clotting time developed in 6% (1/17; 95% confidence interval, 0-28%) cats treated with methimazole for 2-6 weeks. Seemingly, doses of methimazole commonly used to treat hyperthyroidism in cats do not cause alteration in PT and APTT, and only rarely prolong PIVKA clotting time. Nevertheless, abnormal PIVKA clotting time may explain bleeding tendencies unassociated with thrombocytopenia in methimazole-treated hyperthyroid cats.Key words: Coagulation; Drug therapy; Feline; Hyperthyroidism.F eline hyperthyroidism resulting from functional thyroid adenomatous hyperplasia (or adenoma) is 1 of the most commonly diagnosed disorders in small animal practice.1 Treatment of the hyperthyroid state is designed to reduce the excessive production of thyroid hormone from adenomatous thyroid tissue by either surgical thyroidectomy, radioactive iodine ( 131 I), or chronic administration of an antithyroid drug.1 Many considerations (eg, financial constraints, surgical and anesthetic risks, pet quarantine for radiation therapy) favor election by the owners of antithyroid drug treatment as either short-term preoperative or permanent management.The most commonly used antithyroid drug, methimazole, a is actively concentrated in the thyroid gland, where it acts to inhibit the synthesis of thyroid hormones.2,3 Although relatively safe when administered to hyperthyroid cats, methimazole occasionally causes serious adverse effects. The adverse effects usually develop within the 1st 2-3 months of treatment and include hepatopathy, thrombocytopenia, and agranulocytosis.1,2 Bleeding tendencies (epistaxis, oral hemorrhage, excessive hemorrhage during surgery) occur in methimazole-treated cats, and are generally attributed to thrombocytopenia.2 Bleeding tendencies unassociated with thrombocytopenia have been encountered rarely in methimazole-treated hyperthyroid cats by us and others. 2,4From the Departments of Clinical Sciences (Randolph, DeMarco, Center) and Population Medicine and Diagnostic Sciences (Scarlett, Brooks), College of Veterinary Medicine, Cornell University, Ithaca, NY; and the Oradell Animal Hospital Inc (Kantrowitz, Crawford), Oradell, NJ. Dr DeMarc...