LIVER DISEASE 0195-5616/95 $0.00 + .

20

FELINE CHOLANGIOHEPATITIS
COMPLEX
Deborah G. Day, DVM, MS

The cholangitis/ cholangiohepatitis complex includes three charac-

teristic histopathologic lesions, each reflecting progressive stages of one
disease. Suppurative cholangitis/ cholangiohepatitis, long-term nonsup-
purative cholangitis/ cholangiohepatitis, and biliary cirrhosis comprise
this syndrome. Although the histologic appearance of the cholangiohep-
atitis complex is well characterized, the pathogenesis is incompletely
understood, and the etiology is undetermined. Cholangitis refers to
inflammation of the intrahepatic biliary system, cholangiohepatitis de-
notes inflammation of the biliary system that has spread to include the
adjacent hepatocytes, and biliary cirrhosis is the sequella to long-term
inflammation that results in portal fibrosis and bile duct hyperplasia. 17• 44
This syndrome is common in cats and included 24 of 80 (30%) cats in
one study/ and 29 of 185 (16%) in another study. 25 In the latter report,
cases of hepatitis with a known etiology were listed separately, which
may have resulted in a slightly lower estimation of cholangiohepatitis
than expected.
A disease that is similar to sclerosing cholangitis in humans has
been reported in the catY· 15• 30 Primary sclerosing cholangitis is a long-
term fibrosing inflammatory disease of intrahepatic and extrahepatic
bile ducts, characterized by interlobular bile duct hyperplasia, fibrosis,
and mild inflammation. 30 Whether this is a separate disease or a form of
suppurative or nonsuppurative feline cholangitis is unknown.

From the Animal Health Center, College of Veterinary Medicine, Mississippi State Univer-
sity, Mississippi State, Mississippi

VETERINARY CLINICS OF NORTH AMERICA: SMALL ANIMAL PRACTICE

VOLUME 25 • NUMBER 2 • MARCH 1995 375

376 DAY

SUPPURATIVE CHOLANGITIS/CHOLANGIOHEPATITIS

Neutrophilic infiltration of portal triads characterizes acute suppu-

rative cholangitis, a disease rarely diagnosed in cats, possibly because
this disease results in very early histologic change that occurs before the
onset of clinical signs?, 46 Suppurative cholangiohepatitis is often seen
and is characterized by periportal and hepatic parenchymal invasion of
neutrophils, Bile ductules may be filled with white blood cell debris,
and mild fibrosis and bile duct hyperplasia may be present 46 Enteric
organisms often are isolated from the bile of these cats, suggesting
that ascending intestinal bacterial infection is the underlying etiology.
Additionally, suppurative cholangiohepatitis has been associated with
long-term pancreatitis, cholelithiasis, hepatobiliary parasites, anatomic
abnormalities of the biliary tract, nephrotic syndrome, and periductal
biliary fibrosis. 20, 22, 23 , 26, 28 Additional infectious agents associated with
suppurative cholangiohepatitis include a coccidia-like organism, likely
from the protozoan family Eimeriidae,34 a protozoan parasite similar to
Hepatozoon canis/ 4 and toxoplasmosis. 42
Sex and breed predispositions for suppurative cholangitis/ cholangi-
ohepatitis have not been recognized. Although cats of any age may be
affected, middle-aged to old cats are most commonly affected?, zo, zz, 41
Weight loss, icterus, depression, anorexia, vomiting, and fever are com-
mon signs associated with this disorder. Signs are vague and often
intermittent, suggesting a long-term disease process in some cats. Hema-
tologic abnormalities may include neutrophilia with a left shift and
lymphopenia. Biochemical findings are variable, but ALT, AST, and ALP
enzyme activities are often mildly to moderately increased. Hyperbili-
rubinemia is the most consistent biochemical abnormality?, 8, 20, 41 Fasting
serum bile acid (FSBA) concentrations were normal in 6 of 12 (50%) 8
and three of eight (37.5%)7 cats with cholangiohepatitis, but postprandial
serum bile acid (PPSBA) concentrations are usually abnormal.
Hepatic biopsy is required for definitive diagnosis of this disease.
Suppurative cholangitis/ cholangiohepatitis is a diffuse cholestatic dis-
ease, thus collection of a liver sample by noninvasive methods may be
diagnostic. Fine-needle aspiration is the least invasive method of ob-
taining hepatic cells. for cytologic examination. This technique requires
minimal to no sedation and is easy to perform,Z9 but does not allow
examination of hepatic architecture, which is essential for diagnosing
suppurative cholangiohepatitis. Percutaneous blind or ultrasound-
guided needle biopsy is a fast, inexpensive, and relatively safe method
for obtaining hepatic tissue for histologic evaluation. The tissue speci-
men is small compared with wedge biopsies, but this method usually
provides an adequate specimen for diagnosis. The technique may be
performed using light to moderate sedation, depending on the tempera-
ment and clinical status of the cat. Rarely is general anesthesia required.
This technique and various needle types have been described. 18, 19 Possi-
ble complications include hemorrhage, hepatic laceration, biopsy of
adjacent organs, and perforation of the gallbladder, biliary structures, or
 FELINE CHOLANGIOHEPATITIS COMPLEX 377

other organs. 18• 21 Because of the possible association of this disease with
cholelithiasis and extrahepatic bile duct obstruction, open-wedge biopsy
has often been performed because the biliary system and pancreas may
be examined at the time of biopsy. This technique allows visualization
and exploration of the abdomen, palpation of the liver, expression of
the gallbladder, and immediate correction of certain problems. Surgical
biopsy does not require special equipment; however, this method is the
most invasive, most expensive, and requires general anesthesia, which
may be contraindicated in some cats with liver disease. Open-wedge
biopsy techniques have been described. 6 • 37• 40
Recently, a technique using biliary cholescintigraphy was described
as a noninvasive way to distinguish obstructive from nonobstructive
hepatobiliary disease. 5 Radiography or ultrasonography may be helpful
in identifying choleliths, cholecystitis, biliary neoplasia, and pancreatitis.
White bile syndrome may be seen in cats with cholangiohepatitis
and severe intrahepatic cholestasis, resulting in the absence of the nor-
mal green coloration of bile due to the absence of biliary pigment. 13• 46
Severe cholestasis or biliary obstruction blocks bile flow and secretion
of biliary pigment into bile. Instead of the normal biliary secretions, bile
is composed of fluid and mucus secreted by the gallbladder epithelium. 46
This condition is usually diagnosed during exploratory laparotomy or
necropsy and warrants a poor prognosis.
Aerobic and anaerobic culture of bile or hepatic tissue may be
helpful in confirming the diagnosis, and sensitivity results aid in anti-
biotic selection. Enteric organisms, usually Escherichia coli, are most
frequently cultured from the bile of cats with cholangitis/ cholangiohepa-
titis/0· 41 although an enterococcus, Bacteroides, Fusobacterium, and
alpha hemolytic streptococcus have also been isolated. 26
Antibiotics are the mainstay of therapy for suppurative cholangitis/
cholangiohepatitis and are preferably chosen based on culture and sensi-
tivity results of bile or hepatic tissue. In the absence of culture results,
choose a broad-spectrum antibiotic that reaches therapeutic concentra-
tions in bile, is not hepatotoxic, and does not require hepatic excretion.
Ampicillin, amoxicillin, and cephalexin fit these criteria in humans and
are frequently used in cats with hepatobiliary disease?· 11 Metronidazole
is a good choice for anaerobes resistent to the penicillins previously
listed, but the dosage may require reduction in cats with severe hepatic
failure?· 11 • 12 Table 1 lists the dosages of antibiotics commonly used in
treating feline liver disease.
Controversy surrounds the use of corticosteroids for treatment of
suppurative cholangiohepatitis. The addition of prednisolone or predni-
sone to the treatment regimen may be helpful for those cats that respond
poorly to antibiotics or for those cats suspected to have had a more
long-term course of disease. In such cases, an anti-inflammatory dosage
of prednisolone (Table 1) may be tried cautiously in addition to antibiotic
therapy.
Cats with cholangiohepatitis often have thickened inspissated bile
378 DAY

Table 1. DRUGS COMMONLY USED IN CATS FOR THE TREATMENT OF

LIVER DISEASE
Drug Dosage (mglkg) Frequency (hours) Routet

Amoxicillin 11-22 8-12 IM, SQ, PO

Ampicillin 10-25 8-12 IV, IM, SQ, PO
Cephalexin 11-22 8 PO
Cephalothin 22 6-8 IV, IM,SQ
Cefazolin 1Q-20 8 IV, IM,SQ
Dehydrocholic acid 1Q-15 8 PO
Enalapril* 0.125-0.25 12-24 PO
Furosemide 2.5-5/cat 24-48 PO
Metronidazole 7.5-10 8-12 PO
Prednisolone
(anti-inflammatory) 1.1 24-48 PO
(immunosuppressive) 2.2-4.4 24-48 PO
Ursodeoxycholic acid 1Q-15 24 PO
Vitamin K, 5 mg/cat 12-48 IM, PO

*See text for discussion.

tiV = intravenous; IM = intramuscular; SO = subcutaneous; PO = oral.

secretions, possibly associated with long-term cholestasis or bacterial

infection. Bile sludging may occur in the gallbladder, bile duct, or
intrahepatic bile ductules. Cholecystotomy, removal of the sludged bile
material, as well as irrigation of the common bile duct, may be required
in some cats. Bile sludging severe enough to require surgical interven-
tion is usually associated with a poor prognosis. 7' 46 Various choleretics
have been advocated empirically for use in this disease, but efficacy is
unproven. Because of its purported hydrocholeretic properties, dehydro-
cholic acid (Table 1) has been recommended to promote bile flow and
prevent bile sludging. The long-term safety of dehydrocholic acid in cats
has not been established. This drug should not be used in the presence
of extrahepatic bile duct obstruction.
Ursodeoxycholic acid (UDCA) is a dihydroxy bile acid used for
gallstone dissolution and for treatment of long-term cholestatic liver
disease in humans. The exact mechanism of action is unknown, but
UDCA is thought to ameliorate the toxic effects of hydrophobic bile
acids on hepatocellular membranes16 and to change the composition of
the bile acid pool.38 Several studies have documented a decrease in
serum hydrophobic bile acids/' 33 while others have not. 3 Also, UDCA
may modulate the immune-mediated hepatobiliary destruction that oc-
curs in humans with primary biliary cirrhosis. An in vitro study demon-
strated suppression of immunoglobulin G (IgG), IgM, IgA, 'Y-interferon,
interleukin-2 (IL-2), and IL-4 in cell cultures exposed to UDCA. 45 Addi-
tionally, serum IgG 2 and IgM2, 38 concentrations decreased in humans
with primary biliary cirrhosis treated with UDCA. Clinical signs, bio-
chemical parameters, and histologic changes improved significantly in
humans with primary biliary cirrhosis and primary sclerosing cholan-
gitis.3' 31, 38 Clinical improvement has been reported in a dog with long-
 FELINE CHOLANGIOHEPATIDS COMPLEX 379

term cholestatic liver disease using this drug. 43 No side effects were
observed when UbCA was administered to healthy cats for 3 months
(Table 1).1°Clinical studies evaluating the efficacy of this drug in cats
with long-term cholestatic liver disease are needed.
The prognosis for the suppurative form of cholangiohepatitis has
been considered poor, but information about long-term follow-up is
lacking. A single case report documents resolution of neutrophilic infil-
trates 11 months after diagnosis. Length of antibiotic administration was
not disclosed in that report, but the cat continued to be normal clinically
and biochemically 4 years after initial diagnosisY This disease has been
reported to undergo spontaneous remission in some cats or progress to
long-term nonsuppurative cholangiohepatitis. 17

NONSUPPUFlATIVE CHOLANGITIS/
CHOLANGIOHEPATITIS

The etiology of nonsuppurative cholangitis/ cholangiohepatitis is

unclear, but long-term inflammation associated with progression of sup-
purative cholangitis/ cholangiohepatitis, other inflammatory disease, and
immune-mediated disease have been proposed as pathogenic mecha-
nisms in this disease. Nonsuppurative cholangitis has been associated
with pancreatitis and liver flukes.u, 39 Histologically, this disease differs
from suppurative cholangitis/ cholangiohepatitis with lymphocytic and
plasmacytic periportal inflammation, bile ductule hyperplasia, and peri-
portal fibrosis being the predominant histologic findings (Fig. 1).32· 39
Some of the cases reported have had significant hepatic lymphoid aggre-
gates, which were compared with the lesions observed in humans with
primary biliary cirrhosis. 27· 39 Unlike suppurative cholangitis/ cholangio-
hepatitis complex, neutrophilic infiltrates are minimal.
Sex and breed predispositions have not been identified for nonsup-
purative cholangiohepatis, although Persian cats were overrepresented
in one study.7· 32· 39 As opposed to suppurative cholangitis/cholangiohep-
atitis, this disease primarily affects cats younger than 4 years of age
(range, 6 months to 10 years). 32· 39 Ascites and icterus were the most
common signs of illness associated with this disease in one report;
however, six of seven cats with ascites had histologic evidence of cirrho-
sis.32 Weight loss, anorexia, depression, and fever are uncommonly ob-
served with this disease. Most of these cats are bright and alert, with a
normal or increased appetite, but show intermittent evidence of systemic
illness. Hematologic abnormalities, such as mild anemia, reflect long-
term disease. Biochemical abnormalities are similar to those seen with
suppurative cholangiohepatitis, except hyperglobulinemia and hypoal-
buminemia are common findings. Hepatomegaly or lymphadenopathy
may be present.
Hepatic biopsy is required for definitive diagnosis of this disease.
Percutaneous needle biopsy is often diagnostic, but if patency of the
biliary system is in doubt, an exploratory laparotomy may be more
380 DAY

Figure 1. Low-power view of feline liver with mild portal fi brosis characteristic of long-term
cholangiohepatitis. Portal tracts are increased in prominence as a result of portal fibrosis
and proliferation of bile ducts. Bridging of portal tracts between lobules is observed at the
right, with incipient bridging evident at the center of the photograph. Inflammatory infiltrates
are minimal. The clear oval space at the lower left is a central vein. (Courtesy of Dr.
William Maslin)

helpful by allowing inspection of the biliary system . Noninvasive tech-

niques, such as ultrasonography or hepatobiliary scintigraphy, may be
helpful in determining biliary patency without the added risk of anesthe-
sia and surgery. Culture of bile or hepatic tissue should be performed
to rule out a bacterial etiology and need for specific antibiotic therapy.
Treatment of nonsuppurative cholangiohepatitis is largely empiri-
cal. Antibiotics were discussed with suppurative cholangiohepatitis and
should be used initially in the treatment of nonsuppurative ch olangitis /
cholangiohepatitis as previously discussed. Immunosuppressive dosages
of corticosteroids (see Table 1) should be added to the treatment plan
once nonsuppurative cholangitis / cholangiohepatitis is identified, taper-
ing the dose during a 30 to 60 day period. Therapeutic uses of UDCA
were discussed with treatment of suppurative cholangiohepatitis. This
drug may prove useful in the treatment of long-term nonsuppurative
cholangiohepatitis, esp ecially if immune modulation is one mechanism
of action of this drug.
Response of this disease to therapy is variable. Some cats respond
well initially, but relapse w hen therapy is discontinued. Others respond
poorly to therapy and die or are euthanatized as a result of progressive
signs of disease. A few cats seem to do well for prolonged periods
(months to years) after drug therap y is discontinued. 32• 39
 FELINE CHOLANGlOHEPATITIS COMPLEX 381

BILIARY CIRRHOSIS

Biliary cirrhosis seems to be the end-stage result of long-term cho-

langiohepatitis in some cats?· 32• 39 This disease is uncommon in cats,
possibly because most cats with severe cholangiohepatitis die before
reaching this stage of disease. Although biliary cirrhosis is presumed to
result from progressive cholangiohepatitis, feline biliary cirrhosis may
represent a distinct disease of unknown etiology. Common clinical find-
ings in cats with cirrhosis include icterus, hepatomegaly, cachexia, and
ascites. 46 Serum liver enzymes may be normal or increased. Additional
serum biochemical abnormalities include hypoalbuminemia, hyperglo-
bulinemia, and hyperbilirubinemia. Coagulopathy may be evident. Hy-
poalbuminemia, coupled with a coagulopathy that is unresponsive to
vitamin K1 therapy, indicates a poor prognosis.
Hepatomegaly is commonly present in cats with cirrhosis, and the
liver has a firm, nodular appearance. Histologically, severe portal fibro-
sis, bile duct hyperplasia, nodular hyperplasia, and a variable degree of
chronic inflammation characterizes feline biliary cirrhosis (Fig. 2).44
Hepatic biopsy is necessary for definitive diagnosis. Percutaneous
biopsy techniques should be performed using extreme caution. Open-
wedge biopsy may be safer because of the greater visualization obtained
from this procedure, which may be needed because of the possibility of

Figure 2. High-power view of a feline liver with long-term cholangiohepatitis or early

cirrhosis. There is marked thickening of the portal tract with fibrous connective tissue. A
microabscess is seen and is associated with the markedly enlarged and hyperplastic bile
duct located at the center. Several smaller bile ducts are noted at the upper and lower left
of the photograph . Heavy aggregates of lymphocytes and plasma cells are seen at the
periphery of the portal tract. The clear space at the left is a portion of a dilated portal vein.
(Courtesy of Dr. William Maslin)
382 DAY

severe hemostatic abnormalities. If a severe coagulopathy is presen1,

biopsy should be postponed, or fresh whole blood transfusion should
be administered prior to the biopsy procedure. Vitamin K1 therapy (see
Table 1) may be helpful in correcting the coagulopathy, if severe chole-
stasis rather than loss of functional hepatic mass is the underlying cause
of the hemostatic defect. With advanced cirrhosis, vitamin K1 therapy is
unlikely to be helpful.
Ascites is a rare clinical finding in cats with liver disease, but it may
be present in cats with cirrhosis. 46 Hepatic fibrosis may cause increased
intrahepatic vascular resistance with subsequent portal hypertension
and increased intravascular hydrostatic pressure. Consequently, blood
is sequestered in the portal vasculature, decreasing the effective plasma
volume. The renin-angiotensin-aldosterone system is activated, and so-
dium and water retention is promoted. Portal blood volume is also
expanded, and ascites formation is enhanced. Hypoalbuminemia may
also predispose to ascites formation by decreasing plasma oncotic pres-
sure. Usually, portal hypertension and hypoalbuminemia are present
when ascites develops in clinical cases. 24
Ascites may be controlled in cats with biliary cirrhosis but rarely
eliminated. Low salt diets may be beneficial in reducing ascites forma-
tion, but salt restriction must be severe to be effective in most casesP
Protein should not be restricted in cats, especially if hypoalbuminemia
is present, unless hepatic encephalopathy (HE) is present or develops.
Because of the resistance of cats in accepting new diets, dietary changes
should not be made when cats are ill, unless the cat likes the new diet
and eats readily.
Loop diuretics, such as furosemide (see Table 1), prevent renal
sodium reabsorption, promote diuresis, and may be helpful in reducing
ascites formation in mild cases. Cats are exquisitely sensitive to the
effects of furosemide, and dehydration, hypokalemia, and anorexia fre-
quently result. Azotemia, hypokalemia, and anorexia (through tissue
catabolism) predispose to HE. Thus, serum electrolytes, hydration status,
and appetite must be closely monitored. Loop diuretics may be less
effective than expected when hyperaldosteronism develops. 36 Aldoste-
rone promotes sodium reabsorption in the distal renal tubule, overriding
the sodium excretion promoted by the loop diuretic. If hyperaldosteron-
ism is suspected in cats with biliary cirrhosis, blockage of sodium reab-
sorption through use of an angiotensin converting enzyme inhibitor may
be appropriate. The author has successfully used enalapril (Vasotec) for
refractory ascites in dogs with liver disease. A suggested initial dosage
of enalapril in cats is listed in Table 1. The low end of the dosage range
should be used initially, especially if it is used in conjunction with
furosemide. Possible side effects include hypotension, azotemia, an-
orexia, vomiting, and diarrhea. Enalapril requires hepatic conversion to
the active form, enalaprilat, but whether this is of practical significance
is unknown. A kinetics study in humans with cirrhosis has documented
that the half-life of enaliprilat is prolonged compared to healthy controls,
but there were no differences in blood pressure or heart rate between
 FELINE CHOLANGIOHEPATITIS COMPLEX 383

groups in that study. 35 Studies evaluating this drug in cats with liver
disease have not been performed, and further studies are needed. Alter-
natively, spironolactone, an aldosterone antagonist, may be tried in
conjunction with furosemide administration. This drug competitively
inhibits aldosterone at the distal renal tubule, preventing sodium, and
water reabsorption. Hyperkalemia is a potential adverse effect, especially
when used concurrently with potassium supplementation.
Although corticosteroids are indicated for the treatment of nonsup-
purative cholangiohepatitis, continued use with cirrhosis may produce
unwanted side effects. Corticosteroids enhance sodium reabsorption,
which may worsen ascites. Additionally, corticosteroids are catabolic,
and the breakdown of body tissues may promote HE.
Early use of UDCA may slow progression of biliary cirrhosis, but
this drug is untested in cats with cirrhosis. UDCA therapy was discussed
with treatment of suppurative cholangiohepatitis.

SUMMARY

Feline cholangiohepatitis complex causes a diffuse intrahepatic cho-

lestasis of unknown etiology. Recognized histologic forms include acute
suppurative cholangitis/ cholangiohepatitis, long-term nonsuppurative
cholangitis/ cholangiohepatitis, and biliary cirrhosis. Treatment of cho-
langiohepatitis complex varies based on histologic type. Thus a liver
biopsy is necessary for definitive diagnosis and treatment. Because cho-
langiohepatitis complex causes diffuse hepatic change, percutaneous
needle biopsies are often sufficient for obtaining a diagnosis. Antibiotics
are used to treat all forms of feline cholangiohepatitis complex, but
steroids may be of equal or greater importance for use in the treatment
of long-term nonsuppurative cholangiohepatitis. Prognosis is guarded
for cats with any form of cholangiohepatitis complex due to the variable
response to treatment seen in many cats. Spontaneous remission occa-
sionally occurs.

ACKNOWLEDGMENT
The author thanks Dr. William Maslin for producing the photographs for this article.

References

1. Barriga 00, Caputo CA, Weisbrode SE: Liver flukes (Platynosomum concinnum) in an
Ohio cat. JAm Vet Med Assoc 179:901, 1981
2. Battezzati PM, Podda M, Bianchi FB, et a!: Ursodeoxycholic acid for symptomatic
primary biliary cirrhosis. J Hepatol 17:332, 1993
3. Beuers U, Spengler U, Kruis W, et a!: Ursodeoxycholic acid for treatment of primary
sclerosing cholangitis: A placebo-controlled trial. Hepatology 16:707, 1992
4. Bielsa LM, Greiner EC: Liver flukes (Playtnosomum concinnum) in cats. J Am Anim
Hosp Assoc 21:269, 1985
384 DAY

5. Boothe HW, Boothe DM, Komkov A, eta!: Use of hepatobiliary scintigraphy in the
diagnosis of extrahepatic biliary obstruction in dogs and cats: 25 cases (1982-1989). J
Am Vet Med Assoc 201:134, 1992
6. Breznock EM: Surgery of hepatic parenchyma and biliary tissues. In Bojrab MJ (ed):
Current Techniques in Small Animal Surgery, ed 2. Philadelphia, Lea & Febiger, 1983,
p. 212
7. Center SA: Feline liver disorders and their management. Compend Contin Educ Pract
Vet 8:889, 1986
8. Center SA, Baldwin BA, Erb H, et a!: Bile acid concentrations in the diagnosis of
hepatobiliary disease in the cat. JAm Vet Med Assoc 189:891, 1986
9. Cornelius LM, DeNovo RC: Icterus in cats. In Kirk RW (ed): Current Veterinary
Therapy VIII. Philadelphia, WB Saunders, 1983, p. 822
10. Day DG, Meyer DJ, Johnson SE, et a!: Evaluation of total serum bile acids and bile
acid profiles in healthy cats following exogenous administration of ursodeoxycholic
acid. Am J Vet Res 55:1474, 1994
11. Dooley JS, Hamilton-Miller JMT, Brumfitt W, et al: Antibiotics in the treatment of
biliary infection. Gut 25:988, 1984
12. Dow SW, Papich MG: An update on antimicrobials: New uses, modifications, and
developments. Vet Med 86:707, 1991
13. Edwards DF, McCracken MD, Richardson DC: Sclerosing cholangitis in a cat. J Am
Vet Med Assoc 182:710, 1983
14. Ewing GO: Granulomatous cholangiohepatitis in a cat due to a protozoan parasite
resembling Hepatozoon canis. Fe! Pract 7:37, 1977
15. Grijm R, Huibregtse K, Bartelsman J, et al: Therapeutic investigations in primary
sclerosing cholangitis. Dig Dis Sci 31:792, 1986
16. Guldutuna S, Zimmer G, Imhof M, et al: Molecular aspects of membrane stabilization
by ursodeoxycholate. Gastroenterology 104:1736, 1993
17. Hardy RM: Diseases of the liver and their treatment. In Ettinger SJ (ed): Textbook of
Veterinary Internal Medicine, ed 3. Philadelphia, WB Saunders, 1989, p. 1479
18. Hardy RM: Hepatic biopsy. In Kirk RW (ed): Current Veterinary Therapy VIII. Phila-
delphia, WB Saunders, 1983, p. 813
19. Hardy RM: Liver biopsy the percutaneous approach. Vet Med Report 2:192, 1990
20. Hirsch VM, Doige CE: Suppurative cholangitis in cats. J Am Vet Med Assoc
182:1223, 1983
21. Hitt ME, Hanna P, Singh A: Percutaneous transabdominal hepatic needle biopsies in
dogs. Am J Vet Res 53:785, 1992
22. Johnson ME, DiBartola SP, Gelberg HB: Nephrotic syndrome and pericholangiohepa-
titis in a cat. JAm Anim Hosp Assoc 19:191, 1983
23. Johnson SE: Cholelithiasis and cholangitis. In Kirk RW (ed): Current Veterinary Ther-
apy X. Philadelphia WB Saunders, 1989, p. 884
24. Johnson SE: Portal hypertension. Part I. Pathophysiology and clinical consequences.
Compend Contin Educ Pract Vet 9:741, 1987
25. Jones BR: Feline liver disease. Aust Vet Pract 19:28, 1989
26. Jorgensen LS, Pentlarge VW, Flanders JA, et a!: Recurrent cholelithiasis in a cat.
Compend Contin Educ Pract Vet 9:265, 1987
27. Kaplan MM: Primary biliary cirrhosis. N Eng! J Med 316:521, 1987
28. Kelly DF, Baggott DG, Gaskell CJ: Jaundice in the cat associated with inflammation of
the biliary tract and pancreas. JSmall Anim Pract 16:163, 1975
29. Kristensen AT, Weiss DJ, Klausner JS, et al: Liver cytology in cases of canine and
feline hepatic disease. Compend Contin Educ Pract Vet 12:797, 1990
30. LaRusso NF, Wiesner RH, Ludwig J, et a!: Primary sclerosing cholangitis. N Engl J
Med 310:899, 1984
31. Leuschner U, Fischer H, Kurtz W, et al: Ursodeoxycholic acid in primary biliary
cirrhosis: Results of a controlled double-blind trial. Gastroenterology 97:1268, 1989
32. Lucke VM, Davies JD: Progressive lymphocytic cholangitis in the cat. J Small Anim
Pract 25:249, 1984
33. Mazzella G, Parini P, Bazzoli F, et al: Ursodeoxycholic acid administration on bile acid
metabolism in patients with early stages of primary biliary cirrhosis. Dig Dis Sci
38:896, 1993
 FELINE CHOLANGIOHEPATITIS COMPLEX 385

34. Neufeld JL, Brandt RW: Cholangiohepatitis in a cat associated with a coccidia-like
organism. Can Vet J 15:156, 1974
35. Ohnishi A, Tsuboi Y, Ishizaki T, et a!: Kinetics and dynamics of enalapril in patients
with liver cirrhosis. Clin Pharmacal Ther 45:657, 1989
36. Perez-Ayuso RM, Arroyo V, Planas R, eta!: Randomized comparative study of efficacy
of furosemide versus spironolactone in nonazotemic cirrhosis with ascites. Gastroenter-
ology 84:961, 1983
37. Pope ER: Liver biopsy the surgical approach. Vet Med Report 2:197, 1990
38. Poupon RE, Balkau B, Eschwege E, et a!: A multicenter, controlled trial of ursodiol for
the treatment of primary biliary cirrhosis. N Eng! J Med 324:1548, 1991
39. Prasse KW, Mahaffey EA, DeNovo R, et a!: Chronic lymphocytic cholangitis in three
cats. Vet Pathol 19:99, 1982
40. Putnam CW, Starzl TE: Simplified biopsy of the liver in dogs. Surg Gynecol Obstet
144:759, 1977
41. Shaker EH, Zawie DA, Garvey MS, et a!: Suppurative cholangiohepatitis in a cat. J
Am Anim Hosp Assoc 27:148, 1991
42. Smart ME, Downey RS, Stockdale PHG: Toxoplasmosis in a cat associated with
cholangitis and progressive pancreatitis. Can Vet J14:313, 1973
43. Thompson MB, Meyer DJ, Senior DF: Effects of treatment with ursodeoxycholic acid
on bile acid profiles in a dog with chronic hepatic disease (abstract). In Ninth Forum
of the American College of Veterinary Internal Medicine, New Orleans, LA, 1991,
p. 886
44. Twedt DC: Cirrhosis: A consequence of chronic liver disease. Vet Clin North Am (Sm
Anim Pract) 15:151, 1985
45. Yoshikawa M, Tsujii T, Matsumura K, eta!: Immunomodulatory effects of ursodeoxy-
cholic acid on immune responses. Hepatology 16:358, 1992
46. Zawie DA, Garvey MS: Feline hepatic disease. Vet Clin North Am (Sm Anim Pract)
14:1201, 1984

Address reprint requests to

Deborah G. Day, DVM, MS
Animal Health Center
College of Veterinary Medicine
Mississippi State University
PO Box 9825
Mississippi State, MS 39762-9825