A morphologic and immunocytochemical study of hepatic neoplasms in cats.

A retrospective study was done of 47 neoplasms of the hepatic and biliary systems from 47 cats brought to The Animal Medical Center over a period of 10 years (1980 to 1989). Histologic examination of specimens taken at necropsy revealed that 87% (41/47) of the hepatic neoplasms were epithelial and 13% (6/47) were nonepithelial. Of the epithelial tumors, 25/47 (53%) were of intrahepatic bile duct origin, 9/47 (19%) were of hepatocellular origin, 5/47 (11%) involved the extrahepatic bile ducts, and 2/47 (4%) were adenocarcinomas of the gall bladder. Of the nonepithelial neoplasms, hemangiosarcomas were more common, 5/47 (11%), than leiomyosarcomas, 1/47 (2%). Multiple liver lobes were involved in 21/34 (62%) of the epithelial and all six of the nonepithelial intrahepatic neoplasms. Most of the bile duct adenocarcinomas (6/9) were predominantly characterized by acinar structures with mucin production, diffuse necrosis, and little desmoplasia. The hepatocellular carcinomas were characterized by three patterns-trabecular (five tumors), pseudoglandular pattern (two tumors), and anaplastic (one tumor). The hepatic carcinoid was characterized by various-sized groups of acinar and rosettelike structures, some with lumens, separated by thin fibrovascular stroma. The extrahepatic bile duct adenocarcinomas (4/4) were acinopapillary with moderate desmosplasia, whereas the adenocarcinomas of the gall bladder had elongated tubular structures lined by anaplastic cells and a severe desmoplastic reaction. The neuroendocrine carcinoma of the extrahepatic bile duct, the hemangiosarcomas, and the leiomyosarcoma had morphologic features characteristic of these neoplasms. Two of the 16 (13%) bile duct adenomas had anaplastic and precancerous changes. Residual benign components were seen in 10/15 (67%) of the biliary adenocarcinomas, 4/9 (44%) of the intrahepatic bile duct adenocarcinomas, and all of the extrahepatic bile duct adenocarcinomas and gall bladder adenocarcinomas. Results of immunohistochemical studies of the biliary neoplasms were similar to those described in studies of biliary neoplasms in human beings. Results of this study revealed that the frequency of different types of hepatic neoplasms in cats varied from that seen in dogs and human beings, but the morphologic features were comparable.     

Acute Hepatic Necrosis And Liver Failure Associated With Benzodiazepine Therapy In Six Cats, 1986–1995.

A retrospective analysis was conducted of all feline necropsies performed during a nine year period to identify cases of sever, acute, centrilobular (periacinar), hepatic necrosis (ACHN). After exclusion of cats with anemia, a series of seven cases of ACHN was identified. In addition, two similar cases were identified from tissue submitted for histopathology following, and eight had bile duct hyperplasia. Seven of the nine cats received diazepam prior to dath, and one received zolazepam. Of the seven cats that received diazepam, five were healthy prior to treatment and received oral diazepam for the treatment of inappropriate urination, intercat aggression, or skin disease. Two cats which received diazepam exhibited other clinical signs: one had chronic vomiting, and the other received diazepam after biochemical evidence of hepatocellular necrosis was present. Onset of clinical sings in cats receiving oral diazepam occurred 7–13 days following the initiation of treatment. Clinical signs and clinical biochemical analysis were compatible with severe hepatocellular necrosis and acute liver failure. All cats had lesions in other organs: five had pancreatic disease, five had cardiac disease, and five had renal disease. All cats died, or were euthanized, within 4 dyas of the onset of clinical signs and 2 days after presentation to a veterinarian. Fatal, acute, centrilobular hepatic necrosis appears to be a serious adverse reaction to diazepam therapy in certain cats.     

Hepatobiliary neuroendocrine carcinoma in cats: a clinicopathologic, immunohistochemical, and ultrastructural study of 17 cases

Hepatobiliary neuroendocrine carcinoma was diagnosed in 17 cats in a period of 10 years. Seven tumors were of intrahepatic origin, one of which was a composite containing components of epithelial and neuroendocrine carcinoma. Nine tumors were of extrahepatic origin, and one tumor was located in the gall-bladder. The cats were adult and geriatric, and the male : female ratio varied according to tumor group. Hepatomegaly, anorexia, weight loss, and vomiting were the most common clinical signs observed in the cats with hepatic neuroendocrine carcinoma. The cats with extrahepatic neuroendocrine carcinoma showed these signs plus icterus (5/9) and high concentrations of hepatic enzymes. Histologically, the hepatic neuroendocrine carcinomas had two patterns, one with acinar structures separated by vascular stroma lined by cuboidal or columnar cells and the other solid with groups of anaplastic cells separated by vascular stroma. The composite tumor consisted of both bile duct carcinoma and neuroendocrine carcinoma. The extrahepatic neuroendocrine carcinomas and the gallbladder neuroendocrine carcinoma were characterized by solid sheets or groups of round to oval cells with vascular or fibrovascular stroma. Immunohistochemical examination of 10 of the neuroendocrine carcinomas revealed that all 10 stained with neuron-specific enolase; one bile duct carcinoma and the gallbladder carcinoma stained with chromogranin; four of five bile duct carcinomas and the gall bladder carcinoma stained with synaptophysin; and one bile duct carcinoma stained with gastrin. One cat with hepatic carcinoma had duodenal ulcer; in this cat, ultrastructural studies showed neurosecretory granules leading to the diagnosis of Zollinger-Ellison syndrome. In four cats in which necropsy was permitted, carcinomatosis (4/4), lymph nodes (4/4), lungs (2/4), and intestines (1/4) were the metastatic sites. Fourteen of the 17 cats were euthanatized during or immediately after surgery.     

Bile acid concentrations in the diagnosis of hepatobiliary disease in the cat

The clinical usefulness of measuring serum bile acid concentrations as a diagnostic test for hepatobiliary disease was examined in 80 cats that were suspected of having hepatic disease. Serum values of total bilirubin, alkaline phosphatase (ALP), alanine transaminase (ALT), and aspartate transaminase (AST) also were measured. Fasting serum bile acid values were determined by use of solid-phase radioimmunoassay for total conjugated bile acids or by a direct enzymatic spectrophotometric method. A definitive diagnosis was established by histologic examination of the liver, and on the basis of these findings, cats were assigned to groups (1 to 8, respectively) including: extrahepatic bile duct obstruction, hepatic lipidosis, cirrhosis, intrahepatic cholestasis (cholangiohepatitis, cholangitis), neoplasia, hepatic necrosis, portosystemic vascular anomalies, and miscellaneous. Cats in group 8 had no morphologic evidence of hepatobiliary disease or had hepatic lesions that were mild. Test efficacy of fasting serum bile acids, total bilirubin, ALP, ALT, and AST were expressed by use of 4 indices: sensitivity, specificity, positive predictive value, and negative predictive value. The diagnostic efficacy of fasting serum bile acids was examined alone and in combinations with the other tests. There was wide overlapping of values of fasting serum bile acids, total bilirubin, ALP, ALT, and AST among cats in groups 1 to 7. The specificity of fasting serum bile acids for the diagnosis of hepatic disease exceeded 90% at values greater than or equal to 5 mumol/L and reached 100% at greater than or equal to 15 mumol/L.(ABSTRACT TRUNCATED AT 250 WORDS)     

Alkaline phosphatase, leucine aminopeptidase, and alanine aminotransferase activities with obstructive and toxic hepatic disease in cats

The activities of serum alkaline phosphatase (serum ALP), leucine aminopeptidase (serum LAP), and alanine aminotransferase (serum ALT) were determined in 15 cats before and after treatment by 3 methods: common bile duct occlusion, left hepatic duct(s) occlusion, and carbon tetrachloride administration. Significant increases in serum ALP, LAP, and ALT activities occurred in all cats in the 3 groups. Sustained mean increases of ninefold in ALP and 13-fold in LAP occurred in the cats with common bile duct occlusion. Lesser mean increases of these enzymes (fourfold) occurred in the cats with partial biliary occlusion. Transient mean increases (100-fold) in ALT occurred in the carbon tetrachloride-treated cats. Urine ALP excretion was measured in 3 cats with common bile duct occlusion. There was no significant difference between rates of urine ALP excretion before and after common bile duct occlusion. Specific ALP activities of hepatic extracts from normal cats and biliary-obstructed cats were compared. Mean specific activity was onefold higher in liver from cats with common bile duct occlusion of 21 days' duration. The findings in the present studies were interpreted to indicate that serum ALP and LAP are useful to detect biliary occlusive disease in cats and, in conjunction with serum ALT, may be used to differentiate primary hepatodegenerative disease and biliary occlusive disease.     

ULTRASONOGRAPHIC FEATURES OF EXTRAHEPATIC BILIARY OBSTRUCTION IN 30 CATS

The goals of our study were to review the ultrasonographic features of spontaneous extrahepatic biliary obstruction in cats and to determine whether these features can assist in differentiating tumor, inflammation, and choleliths as the cause of obstruction. Thirty cats with a presurgical ultrasound examination an dconfirmed extrahepatic biliary obstruction were studied. A common bile duct diameter over 5 mm was present in 97% of the cats with extrahepatic biliary obstruction. Gallbladder dilation was seen in < 50% of the cats. Ultrasound identified all obstructive choleliths (calculus or plugs) in the common bile duct. However, neither common bile duct diameter nor appearance or any other ultrasonographic feature allowed differentiation between tumor and inflammation as the cause of obstruction. A short duration of clinical signs (10 days or less) seemed to be associated with obstructive cholelithiasis.     

Canine bile duct carcinoma

Twenty-four adenocarcinomas of the hepatobiliary system were found among 110 primary hepatic neoplasms: 22 of these were intrahepatic, one involved the extrahepatic bile duct and one the gall bladder. Histologically, 10 intrahepatic neoplasms were classified as cholangiocarcinoma, and 12 as bile duct cystadenocarcinoma. The former were characterized by tubular structures lined by anaplastic cuboidal or columnar cells with diffuse fibrous stroma, and the latter by multiple cystic structures with papillary and solid areas. Half the bile duct cystadenocarcinomas showed benign cysts and transition to adenocarcinomas. This was seen in only one case of cholangiocarcinoma. The extrahepatic bile duct carcinoma was characterized by tubular structures lined with flattened cuboidal cells with scant stroma. The gall bladder adenocarcinoma contained many acinar structures lined with columnar or cuboidal cells and separated by thin stroma. Distant metastasis was found in 87.5% (21 of 24) sites of metastasis.     

Choledochotomy and primary repair of extrahepatic biliary duct rupture in seven dogs and two cats

Objective : To report clinical findings and outcome in dogs and cats undergoing choledochotomy or primary repair of extrahepatic biliary duct rupture. Methods : Retrospective study of dogs (n=7) and cats (n=2) that had choledochotomy or primary bile duct repair. Results : Extrahepatic biliary obstruction was confirmed at surgery in all cases. The underlying cause in four dogs and both cats was choledocholithiasis, two dogs had gall bladder mucocoeles with associated bile duct rupture, and one dog had inspissated bile obstructing the bile duct secondary to gall bladder carcinoid tumour. Three dogs and both cats had choledochotomies performed to relieve extrahepatic biliary obstruction, and four dogs with bile duct rupture underwent primary repair of the defect. One dog with a bile duct rupture was re‐explored four days postoperatively and had suffered dehiscence of the repair; this rupture was re‐repaired. All animals were discharged from the hospital, and did not have clinical recurrence of extrahepatic biliary obstruction. Clinical Significance : Choledochotomy and primary repair of extrahepatic biliary duct rupture were associated with low perioperative morbidity and no mortality in this small cohort of cases. These techniques are reasonable options either alone or in conjunction with other procedures when bile duct patency cannot be re‐established by catheterisation or bile duct discontinuity exists.     

Hematologic and biochemical abnormalities associated with induced extrahepatic bile duct obstruction in the cat

Bile duct obstruction was induced in 6 cats by surgical ligation and transection of the common bile duct. Clinical and laboratory changes were monitored weekly for 25 to 54 days. Clinical signs of obstruction were similar in all cats and included anorexia, pyrexia, lethargy, intermittent vomiting, weight loss, palpable gallbladder, hepatomegaly, and bleeding tendencies. Tissue jaundice and acholic feces were evident grossly as early as postsurgical day (PSD) 4 with a mean onset of jaundice at PSD 5.3 +/- 0.4. Hematologic changes were initially characterized by a mild neutrophilic leukocytosis that increased with the chronicity of bile duct obstruction. Regenerative anemia developed in 4 cats associated with gastrointestinal blood loss. Acute serum biochemical changes were characterized by a marked increase in the mean values of aspartate aminotransferase, alanine aminotransferase, total cholesterol, and copper. Comparatively, only moderate increases in mean serum alkaline phosphatase activity were observed. Mean total bilirubin values increased remarkably at postsurgical week (PSW) 1, reaching a maximal value of 23.1 +/- 4.4 mg/dl at PSW 3 with 71.6 +/- 2.7% direct bilirubin. With chronicity of bile duct obstruction ranging from PSW 3 to PSW 7, the mean serum values of aspartate aminotransferase, alanine aminotransferase, total cholesterol, serum alkaline phosphatase, and total and direct bilirubin stabilized and then declined, whereas the increased mean serum copper values persisted. At PSD 25 to 54, hepatic copper values and serum bile acids were markedly increased. Seemingly, clinicopathologic changes of induced cholestatic hepatic injury depended largely on the duration of biliary obstruction.(ABSTRACT TRUNCATED AT 250 WORDS)     

Hepatic enzyme changes in bovine hepatogenous photosensitivity caused by water-damaged alfalfa hay

In the winter of 1983, practitioners reported extensive photosensitization in 7 herds of cattle. All herds had a history of having been fed water-damaged alfalfa hay. A cow from one herd was referred to the veterinary teaching hospital at Oklahoma State University. In this herd of approximately 40 adult Polled Herefords, all cattle had had some degree of clinical involvement over the past 4 to 6 weeks. Clinical signs included scaling and erythema of sparsely haired skin, muzzle, and teats, as well as icterus, anorexia, and weight loss. One cow died, and the remaining cattle recovered over an 8- to 10-week period after removal of the hay from the ration. In the referred cow, values for total and conjugated bilirubin, BUN, creatinine, sorbitol dehydrogenase, serum alkaline phosphatase, serum aspartate transaminase, and serum gamma-glutamyl transferase were higher than normal. In the herd of origin, extremely high serum gamma-glutamyl transferase values (180 to 1,400 IU/L) persisted (normal, 2 to 35 IU/L). Feeding the same alfalfa hay to 2 clinically normal cows reproduced the syndrome. The characteristic hepatic lesion was bile duct necrosis, with secondary bile duct hyperplasia.     

Liver glutathione concentrations in dogs and cats with naturally occurring liver disease

OBJECTIVE: To determine total glutathione (GSH) and glutathione disulfide (GSSG) concentrations in liver tissues from dogs and cats with spontaneous liver disease. SAMPLE POPULATION: Liver biopsy specimens from 63 dogs and 20 cats with liver disease and 12 healthy dogs and 15 healthy cats. PROCEDURE: GSH was measured by use of an enzymatic method; GSSG was measured after 2-vinylpyridine extraction of reduced GSH. Concentrations were expressed by use of wet liver weight and concentration of tissue protein and DNA. RESULTS: Disorders included necroinflammatory liver diseases (24 dogs, 10 cats), extrahepatic bile duct obstruction (8 dogs, 3 cats), vacuolar hepatopathy (16 dogs), hepatic lipidosis (4 cats), portosystemic vascular anomalies (15 dogs), and hepatic lymphosarcoma (3 cats). Significantly higher liver GSH and protein concentrations and a lower tissue DNA concentration and ratio of reduced GSH-to-GSSG were found in healthy cats, compared with healthy dogs. Of 63 dogs and 20 cats with liver disease, 22 and 14 had low liver concentrations of GSH (micromol) per gram of tissue; 10 and 10 had low liver concentrations of GSH (nmol) per milligram of tissue protein; and 26 and 18 had low liver concentrations of GSH (nmol) per microgram of tissue DNA, respectively. Low liver tissue concentrations of GSH were found in cats with necroinflammatory liver disease and hepatic lipidosis. Low liver concentrations of GSH per microgram of tissue DNA were found in dogs with necroinflammatory liver disease and cats with necroinflammatory liver disease, extrahepatic bile duct occlusion, and hepatic lipidosis. CONCLUSIONS AND CLINICAL RELEVANCE: Low GSH values are common in necroinflammatory liver disorders, extrahepatic bile duct occlusion, and feline hepatic lipidosis. Cats may have higher risk than dogs for low liver GSH concentrations.     

Pathogenesis and outcome of extrahepatic biliary obstruction in cats

Extrahepatic biliary obstruction (EHBO) was confirmed at surgery or necropsy in 22 cats. Biliary or pancreatic adenocarcinoma was diagnosed by histopathology in six cats and one cat had an undiagnosed mass in the common bile duct. The remaining 15 cats had at least one of a complex of inflammatory diseases including pancreatitis, cholangiohepatitis, cholelithiasis and cholecystitis. The most common clinical signs were jaundice, anorexia, lethargy, weight loss and vomiting. Hyperbilirubinaemia was present in all cases. Distension of the common bile duct and gall bladder was the most commonly observed finding on abdominal ultrasound. Nineteen cats underwent exploratory laparotomy for biliary decompression and diversion. Mortality in cats with underlying neoplasia was 100 per cent and, in those with non-neoplastic lesions, was 40 per cent. Long-term complications, in those that survived, included recurrence of cholangiohepatitis, chronic weight loss and recurrence of obstruction. Based on these findings, the prognosis for EHBO in cats must be considered guarded.     

Copper poisoning in four llamas

Copper poisoning developed in 1 adult and 3 juvenile llamas after excessive dietary intake of copper resulted in an incorrect copper:molybdenum ratio. Total dietary copper was determined to be 36 mg/kg of feed, with a copper:molybdenum ratio of 16.6:1. Clinical signs associated with the toxicosis included acute onset of anorexia and lethargy. Liver enzyme activities (aspartate amino transaminase, lactate dehydrogenase, gamma-glutamyl transferase) and serum copper concentration were high in specimens obtained within 48 hours before death. Gross necropsy findings were limited to mild hepatomegaly. Histologically, hepatic lesions included acute massive necrosis of hepatocytes with and without bile duct proliferation, double hepatic plates with loss of orientation, anisocytosis, anisokaryosis, and an intralobular mosaic pattern of necrosis involving half of the hepatocytes. Analysis of hepatic copper concentrations suggested that juvenile llamas develop signs of poisoning at lower hepatic copper concentrations, compared with adults.     

Potassium iodide capsule treatment of feline sporotrichosis

Sporotrichosis is a mycosis caused by Sporothrix schenckii. The most affected animal is the cat; it has played an important role in the zoonotic transmission of this disease, especially in Rio de Janeiro, Brazil, since 1998. In order to evaluate the treatment of feline sporotrichosis with potassium iodide, an observational cohort was conducted in 48 cats with sporotrichosis at Instituto de Pesquisa Clínica Evandro Chagas, Fiocruz. All cats received potassium iodide capsules, 2.5 mg/kg to 20 mg/kg q24h. The cure rate was 47.9%, treatment failure was 37.5%, treatment abandonment was 10.4% and death was 4.2%. Clinical adverse effects were observed in 52.1% of the cases. Thirteen cats had a mild increase in hepatic transaminase levels during the treatment, six of them presented clinical signs suggestive of hepatotoxicity. Compared to previous studies with itraconazole and iodide in saturated solution, potassium iodide capsules are an alternative for feline sporotrichosis treatment.     

Hepatic neoplasia

The clinicopathologic features of hepatic neoplasms such as hepatocellular adenomas, hepatocellular carcinomas, bile duct carcinomas, and hepatic carcinoids are presented. The authors also discuss the diagnostic and therapeutic approaches to hepatic neoplasia.     

Portal Vein Thrombosis in Cats: 6 Cases (2001–2006)

Background: Portal vein thrombosis (PVT) in cats is sparsely reported.
Purpose of Study: To evaluate the clinical signs and diseases associated with PVT in cats.
Animals: 6 client-owned cats.
Methods: Medical records for cats with a portal vein thrombus diagnosed on abdominal ultrasound or at necropsy were reviewed. Signalment, historical data, underlying disorders, clinical findings, clinicopathologic and histopathologic data, diagnostic imaging findings, treatment, and outcome were recorded.
Results: All 6 cats identified with PVT also had hepatic disease. Evidence of a congenital portosystemic shunt was present in 3/6 cats. Two cats had primary or metastatic hepatic neoplasia. One cat had acute cholangitis, acute pancreatitis, and locally extensive acute centrilobular hepatic necrosis. Two cats were suspected to have acute thrombi and 4 cats had chronic thrombi.
Conclusion and Clinical Significance: PVT might be an important concurrent finding in cats with hepatic disease.     

Portal vein thrombosis in cats: 6 cases (2001-2006).

BACKGROUND: Portal vein thrombosis (PVT) in cats is sparsely reported. PURPOSE OF STUDY: To evaluate the clinical signs and diseases associated with PVT in cats. Animals: 6 client-owned cats. METHODS: Medical records for cats with a portal vein thrombus diagnosed on abdominal ultrasound or at necropsy were reviewed. Signalment, historical data, underlying disorders, clinical findings, clinicopathologic and histopathologic data, diagnostic imaging findings, treatment, and outcome were recorded. RESULTS: All 6 cats identified with PVT also had hepatic disease. Evidence of a congenital portosystemic shunt was present in 3/6 cats. Two cats had primary or metastatic hepatic neoplasia. One cat had acute cholangitis, acute pancreatitis, and locally extensive acute centrilobular hepatic necrosis. Two cats were suspected to have acute thrombi and 4 cats had chronic thrombi. CONCLUSION AND CLINICAL SIGNIFICANCE: PVT might be an important concurrent finding in cats with hepatic disease.     

Hepatic lesions associated with intrahepatic arterioportal fistulae in dogs

Seven cases of hepatic arterioportal fistulae in young dogs (mean age 6 months) are described. All cases were presumed to be congenital in origin. The onset of clinical signs, which frequently included gastrointestinal and neurological disturbances, was usually sudden. All dogs had clinical evidence of portal hypertension in the form of ascites, and all developed multiple extrahepatic portacaval venous shunts consequential to portal hypertension. The neurological disturbances were likely the result of portacaval shunting. The arterial and venous vessels involved in the fistulae had markedly altered wall structure. Hepatic regions adjacent to the fistulae frequently evidenced marked bile duct proliferation. Hepatic parenchymal atrophy, relative collapse of distributing portal veins, dilatation of hepatic arterial branches and proliferation of hepatic arterioles were seen throughout the liver; these changes closely resembled those present with portacaval shunting in the absence of hepatic arterioportal fistulae. The importance of recognizing that hepatic arterioportal fistulae and multiple extrahepatic portacaval shunts usually coexist and separately influence the morphological appearance of the liver is stressed.     

Serum bile acids and the assessment of hepatic function in dogs and cats

Current literature in veterinary internal medicine regarding the clinical use of the serum bile acids test to assess hepatobiliary function in dogs and cats is reviewed. The test is best used in cases where clinical signs and routine laboratory tests are suggestive of liver disease. It is a highly sensitive and specific test of hepatic function, and is the best method of assessing liver function available to the private practitioner. Abnormal results do not determine etiology, severity, or prognosis of the disorder. They merely indicate the need for hepatic biopsy. The serum bile acids concentration should always be measured in both a fasting and a two-hour postprandial sample.     

Choledochal cyst with secondary cholangitis,choledochitis, duodenal papillitis,and pancreatitis in a young domestic shorthair cat

Choledochal cysts, congenital segmental dilations of the common bile duct, have been reported in few cats, and histologic characterization is lacking. A 20-mo-old spayed female domestic shorthair cat was presented because of vomiting and weight loss. There was progressive elevation of liver enzyme activity (ALT > ALP, GGT) and hyperbilirubinemia. Diagnostic imaging identified focal cystic dilation of the common bile duct, dilation and tortuosity of adjacent hepatic ducts, and a prominent duodenal papilla. A choledochal cyst was suspected, and the animal was euthanized. On postmortem examination, there was a 2-cm, firm, thickened, cystic dilation of the common bile duct, patent with adjacent ducts. Histologically, the cyst wall was expanded by fibroblasts, collagen, and lymphoplasmacytic inflammation. Adjacent bile ducts were markedly dilated and tortuous, with lymphoplasmacytic inflammation and papillary mucosal hyperplasia that extended to the major duodenal papilla. There was chronic neutrophilic cholangitis, suggesting bacterial infection and/or disturbed bile drainage, extrahepatic obstruction, and lymphoplasmacytic pancreatitis with ductular metaplasia. Prominent lymphoid follicles within biliary ducts and duodenum suggested chronic antigenic stimulation. Choledochal cysts can be associated with chronic neutrophilic cholangitis, extrahepatic obstruction, choledochitis, duodenal papillitis, and pancreatitis, and should be a differential for increased hepatic enzymes and hyperbilirubinemia in young cats.