The top 5 liver diseases in dogs Craig B Webb PhD, DVM, DACVIM (Small Animal) Colorado State University

TOP 5 Liver Conditions in Dogs
1. Hepatitis or hepatic insult
2. Hepatic fibrosis or cirrhosis
3. Copper-associated hepatitis
4. Congenital portosystemic vascular anomalies (PSVA)
5. “Nonhepatic” hepatic disease

The liver serves as the control-and-command center
for virtually all metabolic processes: production, packaging,
and distribution of proteins, lipids, and carbohydrates;
hormonal and enzymatic control of metabolic
pathways; metabolism of biologics; transformation of
xenobiotics; decontamination and removal of toxins;
and recirculation, recycling, and refilling of gallbladder
contents.
When the liver does not function at full capacity, clinical
manifestations are often ubiquitous and possibly
devastating.
1 Hepatitis or hepatic insult
Acute
The liver can be exposed to ingested toxins, bloodborne
pathogens, and drugs and their metabolites,
providing numerous causes for acute insult. Signs
can include anorexia, fever, vomiting, and abnormal
mentation. Jaundice is the classic sign of hepatic failure,
with RBC haemolysis as another important differential
for hyperbilirubinaemia.
Leptospirosis appears to be increasingly prevalent
and usually involves both the liver and kidneys. Other
possible infectious agents include infectious canine
hepatitis (canine adenovirus-1), Clostridium piliformis,
bacteria (especially Escherichia coli), and Toxoplasma
gondii. Ingestion of Amanitum spp mushrooms,
blue–green algae, and some drugs (eg, sulfonamides,
carprofen, amiodarone) can result in acute and significant
liver disease. Consequences of insult may be
idiosyncratic and unpredictable, and signs may vary.
ALT and bilirubin are the most pertinent biochemical
indicators of hepatic insult, although low BUN, albu-
The liver can be exposed to ingested toxins, blood-borne pathogens, and drugs and their
metabolites, providing numerous causes for acute insult.
min, cholesterol, and glucose levels along with
prolonged clotting times are indicative of fulminant
hepatic failure. Supportive care is essential.
Glucocorticoids may be contraindicated (infection) or
of minimal benefit in the acute setting. Acetylcysteine
has been used in critical patients with a loading dose
of 140 mg/kg IV, followed by additional treatments at
70 mg/kg.

Chronic
Signs of chronic canine hepatitis, often nonspecific
and systemic, include vomiting, lethargy, decreased
appetite, polyuria/polydipsia (PU/PD), and weight loss.
Increased ALT enzyme activity, usually the most telling
biochemical abnormality, is frequently monitored as a
quantifiable indicator of treatment response.
Although the primary disease cause may be undetermined,
several treatable causes warrant diagnostic
examination with histopathology, metal analysis,
and bacterial culture. Chronic hepatitis may present
as a slow progression of changes started by acute insult.
Culturing bile, not liver tissue, may yield better
growth.1
There is often an immune-mediated component to
chronic hepatitis progression, warranting immunomodulatory
therapy. Prednisone has been the preferred
drug, but Colorado State University has recently had success using
cyclosporine at a starting
dose of 5 mg/kg q24h.2 Unlike prednisone,
cyclosporine does not induce canine liver enzyme
elevation.
Hepatitis cases (acute and chronic) can be treated
with ursodeoxycholic acid at 7.5 mg/kg q12h to enhance
bile flow, dilute toxic bile acids, and provide
both immunomodulatory and antioxidant effects.
Antioxidants may benefit cases of canine hepatitis:
S-adenosylmethionine (SAMe; 10 mg/kg q12h), silymarin
(100–200 mg/dog q24h), and vitamin E (100–
400 IU/day).
2 Hepatic fibrosis or cirrhosis
Chronic hepatitis may progress to a cirrhotic liver as
fibrin replaces liver parenchyma, causing permanent
changes in hepatic architecture. This is a morphologic
diagnosis of prognostic significance.
The presentation, often severe, can include weight
loss, ascites, and jaundice. A PCV/TP can quickly rule
out haemolytic anaemia as the cause of jaundice, and
a serum bile acids test is redundant if the total bilirubin
is significantly elevated. Ascites may be a result of
portal hypertension from the cirrhotic liver, hypoalbuminaemia
from loss of liver function, retention of sodium
or water via stimulation of the renin–angiotensin–
aldosterone system, or a combination thereof.
Although the diagnostic work-up (eg, histopathology,
metal analysis, culture) is similar to that of less marked
cases of chronic hepatitis, it is often too late for specific
beneficial treatment, even if a primary cause is
identified (eg, copperassociated hepatitis). Supportive
care may include palliative abdominocentesis if the
ascites compromises respiration, but the newly emptied
space will likely refill. Spironolactone (1–2 mg/kg
q24h) combined with furosemide may be used when
fluid removal is less critical; however, it may increase
risk for hepatic encephalopathy from alkalosis or hypokalemia
effects.
Cirrhosis and ascites are negative prognostic indicators
against which colchicine at 0.025 mg/kg q24h
may be tried; however it lacks proven benefit. Prednisone
and nonspecific liver protectants are indicated,
but the prognosis can be grave.
*Editor’s Note: These cases with hypertension will/
may eventually develop acquired shunts, managing
the ascites clinical sign.
3. Copper-associated hepatitis
As a form of chronic hepatitis, copper-associated hepatitis
is thought to result from an inherited enzymatic
defect in several breeds, especially Bedlington terriers
but also Dalmatians, Labrador Retrievers, and West
Highland white and Skye terriers. Excessive hepatic
copper is a treatable component of chronic hepatitis
cases (common in Doberman Pinschers, Cocker
Spaniels, mixed breeds) in which copper accumulation
may be secondary to the disease.
The copper chelator D-penicillamine at 10 to 15 mg/
kg q12h is preferred for removing excess copper, and
elemental zinc at 10 mg/kg q12h can decrease GI
copper absorption; however, the two should not be
used simultaneously.
Most commonly seen as a chronic hepatopathy, copper-
associated liver disease can present as an acute
illness or acute hemolytic crisis (rare), so qualitative
or quantitative assessment of hepatic copper content
should be a standard diagnostic of liver biopsy.
4 Copper-associated hepatitis
The liver is normally the first stop for blood carrying digestive
and absorptive efforts of the GI tract to the rest
of the body. Various congenital vascular anomalies
can result in blood bypassing the liver, causing release
of digestive content systemically without screening or preparation and resulting in decreased liver function.
The nomenclature has recently been clarified by
WSAVA Standards.
The most common presentation is in young dogs
with stunted growth and/or abnormal mentation, but
more subtle signs of PSVA (eg, GI, PU/PD, weight loss,
lethargy, poor hair coat) in older pets are increasingly
appreciated; other signs are generally related to the
nervous or urinary system.
Serum biochemistry profile and urinalysis may reflect
the dysfunction (ie, low or low-normal glucose, cholesterol,
albumin, BUN, microcytic anemia or target
cells, ammonium biurate crystalluria); however, preand
postprandial serum bile acids testing (not liver
enzyme elevation) may best establish decreased liver
function, although it is not specific to PSVA.
When the clinical presentation and serum bile acids
test are consistent with decreased liver function, PSVA
can be confirmed and characterized by abdominal ultrasonography.
A single extrahepatic (small breed) or intrahepatic
(large breed) shunt is frequently visualised. Advanced
imaging or histopathology can be used if ultrasonography
is equivocal or if primary portal vein hypoplasia
(formerly microvascular dysplasia or noncirrhotic
portal hypertension) is suspected. It is necessary to
determine whether the PSVA patient requires surgical
(most single shunts) or nonsurgical (primary hypoplasia,
multiple acquired shunts) treatment.
Medical management includes dietary intervention
(low-quantity, high-quality protein) and pharmaceutical
manipulation of gut ammonia production (lactulose,
0.5 mL/kg q8–12h; neomycin, 22 mg/kg q8h).
5 “Nonhepatic” hepatic disease
Nonhepatic liver disease includes the following reactive
hepatopathies: vacuolar hepatopathy, steroid
hepatopathy, and benign nodular hyperplasia. Elevations
in liver enzyme activities do not necessarily indicate
primary liver disease.
The liver senses various conditions or diseases and reacts
with enzyme elevations; hence the term reactive
hepatopathy. Overlooking these differentials may lead
to unproductive diagnostic efforts. Steroids and anticonvulsants
can induce elevated canine liver enzyme
activities. Benign nodular hyperplasia in older dogs
can mimic enzymatic and ultrasonographic changes
similar to those seen in neoplastic disease.
Growth in young dogs, bone cancer in older dogs,
and endocrinopathies (eg, Cushing’s disease, diabetes
mellitus) can result in elevated liver enzymes. (ALP)
Idiopathic vacuolar hepatopathy is a histopathologic
diagnosis consistent with exogenous steroid administration,
Cushing’s disease, or other systemic illness.
After identifying and treating the primary disease, nonspecific
therapy (eg, antioxidants) aimed at the liver
may be administered. Elevated liver enzymes in a
dog without clinical signs may be reevaluated in 4 to
6 weeks before pursuing a more extensive diagnostic
work-up.
Closing thoughts
The liver is involved in most every aspect of life. Therefore,
primary liver disease makes the list of differentials
for most presentations, while secondary liver involvement
must be considered in most nonliver diseases.

References available on www.vet360.vetlink.co.za

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