WEISS-April PV-SA Review - VetLearn.com

CE 

364 Vol. 23, No. 4 April 2001 

Article #5 (1.5 contact hours) 

Refereed Peer Review 

KEY FACTS 

■ Signs of inflammatory liver 

disease in cats can mimic those 

of other liver conditions. 

■ Establishing a definitive diagnosis 

is important because approaches 

to treatment vary. 

■ Prolonged survival can be 

expected in cats that survive for 

at least 3 months following 

diagnosis of inflammatory liver 

disease. 

Email comments/questions to 

compendium@medimedia.com 

Inflammatory Liver 

Diseases in Cats 

University of Minnesota 

Douglas J. Weiss, DVM, PhD 

Josanne Gagne, DVM 

Pamela J. Armstrong, DVM, MS, MBA 

ABSTRACT: Inflammatory liver diseases comprise the second most common cause of liver 

disease in cats. The two major forms of inflammatory liver disease described in North America 

are cholangiohepatitis (acute and chronic forms) and lymphocytic portal hepatitis. Signalment, 

clinical signs, clinical laboratory data, and ultrasonography can be used to establish a presumptive 

diagnosis of inflammatory liver disease; however, hepatic biopsy is needed for 

definitive diagnosis. Differences in treatment strategies for cholangiohepatitis and lymphocytic 

portal hepatitis warrant establishing a definitive diagnosis. Prognosis for long-term survival is 

good for cats that survive the first 2 to 3 months after diagnosis of either of these diseases. 

In North America, major causes of feline liver disease include the following 1 : 

■ Hepatic lipidosis—50% of cases 

■ Inflammatory liver disease—25% 

■ Malignant lymphoma—5% 

■ Carcinoma—4% 

Terminology used to describe inflammatory liver diseases of cats can be confusing. 

1–3 These terms include suppurative or acute cholangiohepatitis, chronic 

cholangiohepatitis, chronic progressive nonsuppurative cholangiohepatitis, pericholangiohepatitis, 

chronic lymphocytic cholangitis, progressive lymphocytic 

cholangitis, sclerosing cholangitis, lymphocytic-plasmacytic cholangitis/cholangiohepatitis, 

lymphocytic cholangitis/cholangiohepatitis, lymphocytic portal hepatitis, 

and biliary cirrhosis. 1–4 Some authors have preferred to use the general term 

cholangiohepatitis complex or cholangiohepatitis/cholangitis complex. 2,5 Recent retrospective 

studies have clarified the classification of these diseases into acute cholangiohepatitis, 

chronic cholangiohepatitis, and lymphocytic portal hepatitis. 1,4 

TYPES OF INFLAMMATORY LIVER DISEASE 

Although there is no universally accepted classification of inflammatory liver 

disease in cats, a classification scheme based on histopathologic features is gaining 

support. 1,3 Two major types of inflammatory liver disease have been described 

based on distinct histopathologic features: cholangiohepatitis (acute and 

chronic forms) and lymphocytic portal hepatitis. 1 Another syndrome that may

Compendium April 2001 Small Animal/Exotics 365 

Figure 1—Histopathologic section of liver from a cat with 

acute cholangiohepatitis showing a greatly enlarged portal 

area (left side) and a portion of a hepatic lobule (right side). 

The portal area is characterized by infiltration of large numbers 

of neutrophils, inflammatory exudate within bile ducts 

(arrows), and fibrosis (H&E stain). 

be distinct from cholangiohepatitis and lymphocytic 

portal hepatitis, called progressive lymphocytic cholangitis/cholangiohepatitis, 

has been described. 6,7 Liver fluke 

infestation can also cause inflammatory liver disease. 8 

Acute Cholangiohepatitis 

Acute cholangiohepatitis is characterized by infiltration 

of large numbers of neutrophils into portal areas of 

the liver and into bile ducts (Figure 1). 1 Disruption of 

the periportal limiting plate results in necrosis of hepatocytes 

adjacent to portal areas and infiltration of neutrophils 

into hepatic lobules. Acute cholangiohepatitis 

may begin as an ascending bacterial infection within 

the biliary tract; however, bacteria have been isolated 

from the liver or gallbladder in only a few cases. 2,9 Failure 

to isolate organisms may be due in part to previous 

antibiotic therapy and failure to culture for anaerobic 

organisms. Organisms that have been isolated include 

Bacteroides, Escherichia coli, Clostridium, and αhemolytic 

Streptococcus. 2 Congenital or acquired abnormalities 

of the biliary system, including anatomic abnormalities 

of the gallbladder or common bile duct and 

gallstones (i.e., choleliths), may predispose cats to 

cholangiohepatitis. Choleliths appear to be an infrequent 

cause of inflammatory liver disease. 2 Conversely, 

inspissation of bile, which may cause partial or complete 

obstruction of the common bile duct, gallbladder, 

or intrahepatic bile ducts, appears to frequently accompany 

cholangiohepatitis and may require surgical intervention. 

Chronic Cholangiohepatitis 

Chronic cholangiohepatitis is theorized to be a later 

Figure 2—Histopathologic section of liver from a cat with 

chronic cholangiohepatitis. Note extensive fibrosis and scattered 

inflammatory cells in an enlarged portal area (A), a 

small island of hepatocytes (large arrows), and extensive bile 

duct proliferation (small arrows; H&E stain). 

stage of acute cholangiohepatitis. 1,10 It is characterized 

by a mixed inflammatory infiltrate in portal areas and 

bile ducts consisting of neutrophils, lymphocytes, and 

plasma cells (Figure 2). 1 Unlike acute cholangiohepatitis, 

bile duct hypertrophy and portal fibrosis are prominent 

features of the disease. Other conditions that may 

be confused with chronic cholangiohepatitis include feline 

infectious peritonitis virus, Toxoplasma infections, 

and liver fluke infestation. In liver fluke infestation, 

eosinophil numbers are usually increased in portal areas, 

whereas eosinophils are rare or absent in other 

types of chronic cholangiohepatitis. 

Diseases frequently associated with cholangiohepatitis 

include inflammatory bowel disease and pancreatitis. 

Of cats with cholangiohepatitis, 83% had concurrent 

inflammatory infiltrates in the duodenum and/or jejunum 

and 50% had pancreatic lesions. 9 How these 

disorders relate to one another is unclear. Some authors 

theorize that inflammatory bowel disease causes reflux 

of bacteria or other constituents of duodenal contents 

into the common bile duct with resultant pancreatitis 

and cholangiohepatitis. 1–5 

Lymphocytic Portal Hepatitis 

Lymphocytic portal hepatitis appears to be distinct 

from acute and chronic cholangiohepatitis. It is characterized 

by infiltration of lymphocytes and plasma cells 

but not neutrophils into portal areas but not into bile 

ducts (Figure 3). Variable degrees of bile duct hypertrophy 

and fibrosis are present. 1,10 

Lymphocytic portal hepatitis is a common finding in 

older cats. In a retrospective study of cat livers obtained 

at necropsy, 82% of cats over 10 years of age had

366 Small Animal/Exotics Compendium April 2001 

Figure 3—Histopathologic section from a cat with lymphocytic 

portal hepatitis. Note the enlarged portal area containing 

large numbers of lymphocytes, mild fibrosis, and bile 

duct proliferation (H&E stain). 

histopathologic changes consistent with lymphocytic 

portal hepatitis, whereas only 10% of cats younger than 

10 years of age showed these histopathologic changes. 11 

Few of these cats had a clinical diagnosis of liver disease. 

However, not all cats with lymphocytic infiltrates in 

portal areas are asymptomatic. In a review of 175 liver 

biopsies from cats with clinical evidence of liver disease, 

15% had a diagnosis of lymphocytic portal hepatitis. 1 

Because of the presence of lymphocytes and plasma 

cells in portal areas and the lack of concurrent diseases, 

several authors have speculated that lymphocytic portal 

hepatitis is an immune-mediated disease. 1,3 However, 

data on the role of immune mechanisms in the initiation 

and/or perpetuation of lymphocytic portal hepatitis 

have not been reported. 

Liver Flukes 

Several species of liver flukes have been reported in 

cats in the United States. 8 The incidence of infestation 

varies by geographic region. The condition occurs frequently 

in Florida, for example, whereas only one case 

was identified over 10 years at the University of Minnesota 

Veterinary Teaching Hospital. 1 Histopathologic 

features of liver fluke infestation include distended and 

fibrotic bile ducts and epithelial proliferation of bile 

duct walls. 8 A mixed inflammatory infiltrate, consisting 

of macrophages, lymphocytes, plasma cells, eosinophils, 

and neutrophils, is frequently present in portal areas. 

The presence of eosinophils is suggestive of liver fluke 

infestation because eosinophils are rarely seen in other 

types of inflammatory liver disease. 1 

DIAGNOSIS 

Clinical Signs 

Clinical signs associated with inflammatory liver diseases 

are variable, nonspecific, and frequently similar to 

those associated with hepatic lipidosis (Table 1). 10 Partial 

or complete anorexia is the most common (and 

sometimes the only) clinical sign. Other less frequently 

observed clinical signs include weight loss, depression, 

vomiting, diarrhea, and fever. Cats with acute cholangiohepatitis 

tend to be younger (median age, 3.3 years) 

than cats with chronic cholangiohepatitis (median age, 

9 years), lymphocytic portal hepatitis (median age, 8.2 

years), or hepatic lipidosis (median age, 6.2 years). 10 

Male cats are more frequently affected with acute 

cholangiohepatitis than are female cats. 10 Cats with 

acute cholangiohepatitis are more acutely and severely 

ill than cats with most other types of liver disease. 10 

Prominent clinical signs in acute cholangiohepatitis include 

fever, depression, and dehydration. 

Jaundice and altered liver size are frequently the only 

findings that direct attention to liver disease (Table 

1). 3,10 Jaundice is most easily observed in the sclera but 

TABLE 1 

Signalment and Clinical Signs Associated with Inflammatory Liver Diseases and Hepatic Lipidosis in Cats 

Acute Chronic Lymphocytic Hepatic 

Observation Cholangiohepatitis Cholangiohepatitis Portal Hepatitis Lipidosis 

Age Young Middle age Middle age Middle age 

Gender bias Males Males None None 

Onset of signs Days Weeks Weeks Days to weeks 

Severity of illness Severe Mild to moderate Mild Mild to severe 

Anorexia Frequent Frequent Frequent All cases 

Weight loss Frequent Frequent Frequent All cases 

Fever Frequent Infrequent Rare Rare 

Jaundice Frequent Frequent Frequent Frequent 

Hepatomegaly Frequent Frequent Frequent Frequent 

Ascites Rare Rare Rare Rare


TABLE 2 

Clinical Laboratory Alterations in Inflammatory Liver Diseases, Hepatic Lipidosis, and Hepatic Lymphoma 

Acute Chronic Lymphocytic Hepatic Hepatic 

Parameter Cholangiohepatitis Cholangiohepatitis Portal Hepatitis Lipidosis Lymphoma 

Neutrophilia Frequent Infrequent Rare Rare Frequent 

Left shift Frequent Infrequent Rare Rare Infrequent 

Serum bilirubin Mild increase Moderate increase Mild increase Marked increase Mild increase 

Alanine Moderate increase Moderate increase Mild to moderate Marked increase Moderate to 

aminotransferase increase marked increase 

Serum alkaline Frequently normal Mild to moderate Normal to mild Moderate to Moderate to 

phosphatase increase increase marked increase marked increase 

Fasting bile acids Increased Increased Increased Increased Increased 

may also be observed in the soft palate or under the 

tongue. Ecchymotic hemorrhages and/or prolonged 

bleeding from venipuncture sites may occur. When liver 

size is evaluated radiographically, approximately half 

of cats with acute or chronic cholangiohepatitis, lymphocytic 

portal hepatitis, or hepatic lipidosis have hepatomegaly 

and the remaining cats have normal-sized 

livers. 10 Therefore, hepatomegaly is a frequent finding 

in feline inflammatory liver diseases but cannot be used 

to differentiate the various causes. 

Laboratory Evaluation 

Hematologic and biochemical testing are essential to 

establish a diagnosis of liver disease (Table 2). Fasting 

bile acid determination is the test that is most consistently 

abnormal in all types of inflammatory liver disease. 10 

Laboratory changes typically seen with acute cholangiohepatitis 

include mild neutrophilia and left shift, 

normal or slightly increased serum bilirubin and serum 

alkaline phosphatase (SAP) levels, and substantially increased 

alanine aminotransferase (ALT) level. 10 This 

profile tends to differentiate acute cholangiohepatitis 

from chronic cholangiohepatitis, hepatic lipidosis, and 

hepatic neoplasia. 

Laboratory changes typical of chronic cholangiohepatitis 

include substantial increases in serum bilirubin, 

SAP, and ALT levels. 10 Other associated changes may 

include mild nonregenerative anemia, hyperglobulinemia, 

lymphocytosis, and hyperglycemia. 3,10 

Laboratory alterations associated with lymphocytic 

portal hepatitis include normal to variably increased 

serum bilirubin, ALT, and SAP levels. When all inflammatory 

liver diseases are compared with hepatic lipidosis, 

patients with hepatic lipidosis tend to have higher 

total bilirubin concentrations and higher ALT and SAP 

levels. 10 The hallmarks of hepatic lipidosis include jaundice 

and tenfold or greater increases in ALT and SAP 

levels without a corresponding increase in γ-glutamyl 

transferase (GGT). 12 In other forms of liver disease in 

cats, increases in GGT tend to parallel increases in SAP. 

When the clinical chemistry profile reveals evidence 

of liver disease, hyperthyroidism should be ruled out. 

Hyperthyroid cats frequently have changes in ALT and 

SAP levels that may be indistinguishable from those associated 

with inflammatory liver diseases. 13 The increased 

enzyme concentrations normalize with treatment 

of hyperthyroidism. Pathologic changes in the 

liver associated with hyperthyroidism have not been 

well characterized. 

Liver Imaging 

Abdominal ultrasonography is often helpful in evaluating 

extrahepatic disorders associated with cholangiohepatitis. 

14,15 Most cats with acute or chronic cholangiohepatitis 

or lymphocytic portal hepatitis have 

variable or no detectable alterations in the echogenicity 

of the hepatic parenchyma. Conversely, most cats with 

hepatic lipidosis have hyperechoic hepatic parenchyma. 

Bile duct abnormalities may be observed in cholangiohepatitis. 

These abnormalities include gallbladder 

and/or common bile duct distention, cholelithiasis, 

cholecystitis, and bile sludging (Figure 4). 2 The normal 

gallbladder is anechoic and appears round in the transverse 

scan and pear-shaped in the longitudinal scan. 14 It 

is important to remember that gallbladder filling occurs 

normally with fasting; therefore, caution must be exercised 

when interpreting gallbladder enlargement in an 

anorectic or fasting cat. 14 The common bile duct can 

usually be seen as an anechoic, tortuous, tubular structure 

2 to 4 mm in diameter with an echogenic wall. 14 

Distention of the gallbladder and common bile duct 

(i.e., greater than 5 mm in diameter) occurs as a result 

of cholecystitis or biliary obstruction. 14 The gallbladder 

wall may become thickened as a result of inflammation


Figure 4—Sonogram of a cat with complete bile duct obstruction. 

Note the enlarged common bile duct (large arrow) and 

dilated intrahepatic bile ducts (small arrows). Bile sludge 

within the common bile duct is echogenic. 

or edema. The thickened gallbladder wall has a layered 

or double-walled appearance. Bile sludge within the 

gallbladder or common bile duct appears echogenic. 14 

Liver Cytology/Histopathology 

Evaluation of pathologic changes in the liver is essential 

in differentiating inflammatory liver diseases from 

hepatic lipidosis and neoplasia. 16–20 Percutaneous fineneedle 

aspiration; percutaneous tissue biopsy; and keyhole, 

laparoscopic, and intraoperative wedge biopsy 

procedures have been described. 16,17 Fine-needle aspirates 

can usually be performed without anesthesia. 

When a 22-gauge needle is used for collection of aspiration 

specimens, the risk of hemorrhage is minimal; 

however, the risk is greater if large tissue biopsy needles 

are used. Therefore, coagulation testing is recommended 

before a tissue biopsy specimen is collected. Collection 

of bile from the gallbladder for cytologic evaluation 

and bacterial culture has the potential to result in 

rupture with resultant bile peritonitis. Therefore, aspiration 

of the gallbladder should be attempted only with 

ultrasonographic guidance or exploratory laparotomy. 

The diagnostic utility of liver cytology is controversial. 

Several reports indicate that cytologic evaluation is 

highly efficient in identifying hepatic lipidosis and hepatic 

lymphoma; however, inflammatory liver diseases are 

more difficult to identify cytologically. 17–19 Results of another 

retrospective study, however, indicate poor correlation 

between liver cytology and histopathology. 20 Hepatic 

lipidosis is cytologically characterized by clusters of 

hepatocytes in which the cytoplasm is distended with 

lipid-filled droplets (Figure 5). Malignant lymphoma 

cells readily exfoliate and can be diagnosed by cytologic 

Figure 5—Cytologic specimen from a cat with hepatic lipidosis. 

Note a cluster of hepatocytes in which the cytoplasm is 

distended with clear lipid droplets (Wright’s stain). 

Figure 6—Cytologic specimen from a cat with malignant 

lymphoma. Note many large lymphoblasts and normal-appearing 

hepatocytes (Wright’s stain). 

evaluation (Figure 6). Cytologic diagnosis of inflammatory 

liver diseases is hampered by blood contamination, 

which introduces variable numbers of blood leukocytes 

into the samples. Therefore, the cytologist is left to determine 

whether leukocytes are of blood origin or represent 

inflammatory lesions within the liver (Figure 7). 

Cytologic techniques in which samples are collected 

without aspirating minimize blood contamination and 

improve the chances that inflammatory lesions can be 

identified. 17 Use of a 22-gauge needle connected to a 

12-ml syringe via an 84-cm flexible extension set (i.e., 

used for intravenous infusion lines) has been recommended. 

17 The needle is inserted into the liver and 

moved back and forth 8 to 10 times without aspiration. 

Ultrasound-guided aspiration and biopsy techniques 

more consistently produce diagnostic specimens than 

do blind techniques. 21 Ultrasound-guided fine-needle 

aspiration can be used to sample bile as well as hepatic


Figure 7—Cytologic specimen from a cat with acute cholangiohepatitis. 

Note clusters of normal-appearing hepatocytes 

and large numbers of neutrophils (Wright’s stain). 

parenchyma. Such samples can be examined cytologically 

to look for inflammatory cells and bacteria and 

can be cultured to confirm bacterial infections. 

TREATMENT 

Cholangiohepatitis 

The major specific therapy for acute and chronic 

cholangiohepatitis is antibiotics. 2,4 Surgical intervention 

has been recommended if discrete choleliths or complete 

biliary obstruction is identified. When complete 

extrahepatic bile duct obstruction is identified, surgical 

decompression and biliary-to-intestinal diversion (i.e., 

cholecystoduodenostomy or cholecystojejunostomy) are 

recommended. 2 However, surgery is not indicated for 

bile duct enlargement or obstruction due to fluke infestation. 

Bacterial culture and sensitivity testing of liver 

tissue, bile, choleliths, or gallbladder specimens should 

be used to select appropriate antimicrobial agents whenever 

possible. Antibiotics chosen for treatment of 

cholangiohepatitis should be excreted in the bile in active 

form and should be active against aerobic and 

anaerobic intestinal coliforms. Tetracycline, ampicillin, 

amoxicillin, erythromycin, chloramphenicol, and 

metronidazole are excreted in the bile in active form; 

however, several of these agents have significant adverse 

side effects. 5 Erythromycin is not effective against gramnegative 

bacteria, tetracycline is hepatotoxic, and chloramphenicol 

may cause anorexia. As a result, ampicillin 

or amoxicillin combined with clavulanic acid is frequently 

used. All are broad-spectrum antibiotics, effective 

against both gram-negative and gram-positive organisms, 

and are well tolerated by cats. These drugs may 

be combined with metronidazole to extend the spectrum 

to anaerobes and more coliforms. Treatment with 

antibiotics for 2 months or longer is recommended. 

When cats with chronic cholangiohepatitis fail to respond 

to antibiotic therapy alone within 2 to 3 weeks, 

prednisolone is usually added as an empiric treatment. 5 

The antiinflammatory and immunosuppressive properties 

of prednisolone may be beneficial in limiting hepatocellular 

injury. Additionally, prednisolone may enhance 

appetite. An immunosuppressive dose of prednisolone 

(2.2 to 4 mg/kg q24h) should be used initially. The 

dosage is slowly tapered to an alternate-day regimen (1 to 

2 mg/kg q48h) for long-term maintenance. A schedule 

commonly used is to start therapy at 2 mg/kg bid for 2 

weeks, then progressively reduce the dosage as follows: 2 

mg/kg sid for 2 weeks; 1 mg/kg sid for 2 weeks; and 1 

mg/kg q48h for 4 weeks. Biochemical values should be 

monitored prior to each reduction in dosage, and the 

dosage should be reduced only if substantial improvement 

in clinical signs and substantial reductions in ALT 

and SAP levels are observed. Doses as low as 0.5 mg/kg 

q48h may be sufficient for long-term maintenance. 

Long-term corticosteroid treatment is well tolerated by 

most cats, and side effects are usually minimal.


Methotrexate in combination with prednisolone has 

been recommended for cats that fail to respond to 

prednisolone therapy. 2 A suggested dose is 0.4 mg per 

cat divided into three doses and given over 24 hours. 

The dose is repeated every 7 to 10 days. Because 

methotrexate has moderate myelosuppressive potential, 

total leukocyte count should be monitored and treatment 

should be discontinued if total leukocyte count 

drops below 3000/µl. 22 

Ursodeoxycholic acid is recommended for cats with 

all types of inflammatory liver disease. It has antiinflammatory, 

immunomodulatory, and antifibrotic properties 

as well as the ability to increase fluidity of biliary secretions. 

Ursodeoxycholic acid has been safely administered 

to cats at a dose of 10 to 15 mg/kg PO q24h. 3 However, 

ursodeoxycholic acid should not be given to cats with 

complete bile duct obstruction. Efficacy has not been 

established for any type of feline liver disease, but clinical 

trials in human patients with hepatitis support improved 

quality of life. 2 Adverse effects in cats are uncommon 

and usually limited to mild diarrhea. 

Cats with acute cholangiohepatitis require aggressive 

supportive care. These cats are frequently acutely ill 

and have fluid and electrolyte derangements that should 

be corrected. Treatment with injectable vitamin K 1 (5 

mg SC q24–48h) can be given if bleeding diatheses develop. 

2,5 Hepatic encephalopathy appears to be uncommon 

in cats with acquired liver disease and is manifest 

most frequently by excessive salivation. Hepatic encephalopathy 

can be managed by giving lactulose (0.5 

to 1.0 ml/kg PO q8h) with or without enteric antibiotics 

(neomycin [20 mg/kg PO q8–12h]). 5,23 Anorexia 

must be managed promptly to prevent further deterioration 

in clinical condition and possible development of 

concurrent hepatic lipidosis. Assisted oral feeding 

should be tried for up to 12 hours after which a nasoesophageal 

tube should be placed. Ensuring adequate 

intake of a high-energy, high-protein diet is a high priority 

throughout treatment. Protein is an important nutrient 

for liver repair and regeneration and should not 

be restricted unless hepatic encephalopathy occurs. 

The response of cats with cholangiohepatitis to therapy 

should be monitored though use of serial complete 

blood counts and chemistry profiles. Persistent increases 

in ALT activity and serum total bilirubin concentration 

and/or increasing SAP activity suggest that treatment 

has been inadequate. 

Lymphocytic Portal Hepatitis 

The approach to treatment of lymphocytic portal 

hepatitis is based on the hypothesis that the liver injury 

is immune mediated. Immunosuppressive doses of corticosteroids 

are used as described above for chronic 

cholangiohepatitis. Anecdotal reports indicate prolonged 

improvement in clinical signs with prednisolone 

treatment. Others, however, report poor control of disease 

progression with corticosteroid treatment. 2 Azathioprine 

(0.3 mg/kg PO q48–72h) has been tried, but 

side effects, including inappetence and leukopenia, limit 

its use. Low-dose weekly methotrexate therapy has 

been used in a few affected cats. 2 

Response to treatment for lymphocytic portal hepatitis 

is difficult to assess because the disease progresses 

very slowly. A persistent increase in ALT and/or increasing 

total serum bilirubin concentration during 

corticosteroid treatment indicates that the disease is inadequately 

controlled. 

PROGNOSIS 

Limited studies of the response of cats with cholangiohepatitis 

to antibiotic treatment suggest that survival 

of cats with acute and chronic forms of the disease is 

similar. Approximately half of the cats die or are euthanized 

within 90 days after diagnosis. The other half 

have prolonged survival. 10 Better understanding of the 

pathogenesis of these diseases and initiation of standard 

treatment protocols combined, when needed, with surgical 

correction of bile duct obstruction should increase 

the number of cats that survive long-term. 

Lymphocytic portal hepatitis appears to be a very 

slowly progressive condition. Mean survival for cats 

with this condition was reported to be 36.9 months. 10 

In three cats with an initial diagnosis of mild lymphocytic 

portal hepatitis with minimal fibrosis and no bile 

duct proliferation, necropsies were performed 4 to 7 

years after initial diagnosis. Liver sections at necropsy 

showed marked progression in the severity of lesions, 

which were characterized by marked lymphocytic infiltrates, 

severe fibrosis, and severe bile duct hyperplasia. 

Therefore, the prognosis for cats with lymphocytic portal 

hepatitis appears to be primarily dependent on the 

severity of lesions at the time of diagnosis. 

REFERENCES 

1. Gagne J, Weiss DJ, Armstrong PJ: Histopathologic evaluation 

of feline inflammatory liver diseases. Vet Pathol 

33:521–526, 1996. 

2. Center SA, Rowland PH: The cholangitis/cholangiohepatitis 

complex in the cat. Proc 12th Annu Vet Med Forum. Orlando, 

FL, American College of Veterinary Internal Medicine, 

1994, pp 771–776. 

3. Johnson S: Chronic hepatic disorders, in Ettinger S (ed): 

Textbook of Veterinary Internal Medicine, ed 4. Philadelphia, 

WB Saunders Co, 2000, pp 1308–1310. 

4. Jones BR: Feline liver disease. Aust Vet Pract 19:28–36, 1989. 

5. Zawie DA, Garvey MS: Feline hepatic disease. Vet Clin 

North Am Small Anim 2:1201–1230, 1984. 

6. Lucke VM, Davis JD: Progressive lymphocytic cholangitis in


the cat. J Small Anim Pract 25:249–260, 1984. 

7. Day MJ: Immunohistochemical characterization of the lesions 

of feline progressive lymphocytic cholangitis/cholangiohepatitis. 

J Comp Pathol 119:135–147, 1998. 

8. Bielsa LM, Greiner EC: Liver flukes (Pltynosomum concinnum) 

in cats. JAAHA 21:269–274, 1985. 

9. Weiss DJ, Gagne JM, Armstrong PJ: Relationship between 

inflammatory hepatic disease and inflammatory bowel disease, 

pancreatitis, and nephritis. JAVMA 209:1114–1116, 

1996. 

10. Gagne JM, Armstrong PJ, Weiss DJ, et al: Clinical features 

of inflammatory liver disease in cats: 41 cases (1983–1993). 

JAVMA 214:513–516, 1999. 

11. Weiss DJ, Gagne JM, Armstrong PJ: Characterization of 

portal lymphocytic infiltrates in feline liver. Vet Clin Pathol 

24:91–95, 1995. 

12. Biourge VB: Sequential findings in cats with hepatic lipidosis. 

Fel Pract 21:25–28, 1993. 

13. Peterson ME, Turrel JM: Feline hyperthyroidism, in Kirk 

RW (ed): Current Veterinary Therapy IX. Philadelphia, WB 

Saunders Co, 1986, pp 1026–1033. 

14. Leveille R, Biller DS, Shiroma JT: Sonographic evaluation of 

the common bile duct in cats. J Vet Intern Med 10:296–299, 

1996. 

15. Penninck D, Berry C: Liver imaging in the cat. Semin Vet 

Med Surg 12:10–21, 1997. 

16. Kristensen AT, Weiss DJ, Klausner JS, Hardy R: Evaluation 

of hepatic cytology as a diagnostic tool in canine and feline 

hepatic disease. Compend Contin Educ Pract Vet 12:797– 

809, 1990. 

17. Menard M, Papageorges M: Fine-needle biopsies: How to 

increase diagnostic yield. Compend Contin Educ Pract Vet 19: 

738–740, 1997. 

18. Stockhaus C, Teske E: Clinical usefulness of liver cytology in 

the dog and cat. Kleintierpraxis 42:687, 1997. 

19. Roth L: Comparison of liver cytology interpretation and 

biopsy diagnosis. Vet Pathol 36:487, 1999. 

20. Fondacaro JV, Guilpin VO, Powers BE, Twedt DC: Diagnostic 

correlation of liver aspiration cytology with histopathology 

in dogs and cats with liver disease. Proc 17th Am 

Vet Intern Med Forum. Chicago, IL, 1999, p 719. 

21. de Rycke LMJH, van Bree HJJ, Simoens PJM: Ultrasoundguided 

tissue-core biopsy of liver, spleen, and kidney in normal 

dogs. Vet Rad Ultrasound 40:294–299, 1999. 

22. Couto CG: Toxicity of anticancer chemotherapy. Proc 10th 

Kal Kan Symp:37–46, 1986. 

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pp 860–873. 

About the Authors 

Drs. Weiss and Gagne are affiliated with the Department 

of Veterinary Pathobiology, and Dr. Armstrong with the 

Department of Small Animal Clinical Sciences, University 

of Minnesota, St. Paul. Dr. Weiss is a Diplomate of the 

American College of Veterinary Pathologists. Dr. Armstrong 

is a Diplomate of the American College of Veterinary 

Internal Medicine. 

ARTICLE 

CE 

#5 CE TEST 

The article you have read qualifies for 1.5 contact 

hours of Continuing Education Credit from 

the Auburn University College of Veterinary 

Medicine. Choose the one best answer to each of the 

following questions; then mark your answers on 

the test form inserted in Compendium. 

1. Dilation of the gallbladder and/or common bile duct 

is most frequently seen in which of the following feline 

liver diseases? 

a. cholangiohepatitis c. lymphocytic portal hepatitis 

b. hepatic lipidosis d. toxic hepatopathy 

2. Histopathologic lesions consisting of infiltration of 

large numbers of neutrophils into portal areas and bile 

duct best describes which of the following types of feline 

liver disease? 

a. acute cholangiohepatitis 

b. hepatic lipidosis 

c. lymphocytic portal hepatitis 

d. hepatic cysts 

3. A serum chemistry profile characterized by marked increases 

in SAP, ALT, and bilirubin levels and normal 

or slight increases in GGT is most consistent with 

which of the following feline liver diseases? 





4. A cat presented with a history of acute onset of severe 

lethargy, dehydration, fever, and anorexia of 3 days’ 

duration is most consistent with which of the following 

types of feline liver disease? 





5. Finding clusters of hepatocytes in which the cytoplasm 

contains large, clear vacuoles in a cytologic specimen 

of feline liver is most consistent with which of the following 

types of liver disease? 




d. hepatic lymphoma 

6. Which of the following is the most definitive test(s) 

for differentiating cholangiohepatitis from lymphocytic 

portal hepatitis and hepatic lipidosis? 

a. SAP and ALT c. ultrasonography 

b. fasting bile acids d. liver biopsy 

7. Which of the following is the most appropriate antibiotic 

to use in treating acute or chronic cholangiohepatitis?


a. tetracycline c. sulfadiazine 

b. penicillin d. ampicillin 

8. Which of the following treatment protocols is most 

appropriate for a cat with chronic cholangiohepatitis 

and complete bile duct obstruction? 

a. Treat with ampicillin for 3 to 4 months and then 

reevaluate to see whether bile duct obstruction has 

resolved. 

b. Surgically correct bile duct obstruction before initiating 

medical treatment. 

c. Treat with ursodeoxycholic acid to dissolve inspissated 

bile in the common bile duct. 

d. Treat with a combination of antibiotics and ursodeoxycholic 

acid and reevaluate bile duct obstruction 

in 3 to 4 months. 

9. The presence of large immature lymphoid cells in portal 

areas is consistent with which of the following diseases? 

a. chronic cholangiohepatitis 



d. malignant lymphoma 

10. Mild neutrophilia and left shift are most frequently associated 

with which of the following feline liver diseases? 




d. chronic cholangiohepatitis

WEISS-April PV-SA Review - VetLearn.com

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