Page 715 - Clinical Small Animal Internal Medicine

62 Metabolic, Toxic, and Neoplastic Diseases of the Liver 683

breed is also 4–7 years. The copper concentrations in development of canalicular cholestasis, and therefore the
VetBooks.ir Labrador retrievers remain much lower than in Bedlington cholestatic enzymes ALP, GGT, and bile acids are the most
important markers. In many primary liver diseases, the
terriers (by a factor of 10), and liver samples from Labrador
retrievers usually do not exceed 2000 μg/g dry weight,
nant markers, with cholestatic markers less affected.
whereas Bedlington terriers may have concentrations hepatocellular enzymes ALT and AST are the predomi-
exceeding 15 000 μg/g dry weight. Another difference is However, there are many exceptions to this general rule.
that Labrador retrievers do not develop a hemolytic crisis The circulating toxins, inflammatory mediators, and
as easily as Bedlington terriers. The hepatitis may remain microbes cause reticuloendothelial proliferation and
“hidden” for a long period since the most sensitive marker, infiltration of neutrophils into the liver. There can also
ALT, may stay within normal limits for years, even when be focal liver necrosis. In chronic cases, there is also lym-
copper accumulation and hepatitis are already present. In phocytic and plasmacytic inflammation. There can be
more advanced cases, fibrosis and cirrhosis may develop, mild to severe cholestasis in the canaliculi. In some cases
similar to other breeds with copper storage disease. associated with sepsis, there are diffuse foci of necrosis,
The diagnosis is made in the same way as the microabscesses, or granulomas (e.g., infection with
Bedlington terrier, and prevention and therapy are also Herpes canis, toxoplasmosis, brucellosis, tuberculosis,
comparable. Commercial hepatic diet has proven very E. coli and migrating larvae of Toxocara canis).
effective in this breed. Although it is a proven genetic Hepatocellular functions usually remain intact in this
disease, it appears to be much more complex than in the group of secondary liver diseases. Therefore, hypoalbu-
Bedlington terrier, and as such a reliable genetic test is minemia, coagulopathies and hepatic encephalopathy are
not yet available. Due to the complexity of the disease, it not seen in animals with nonspecific reactive hepatitis.
is difficult to give good advice to breeders to aid in pre-
vention of the disease. History and Clinical Signs
The clinical signs are often determined by the primary
disorder. Hence, there is often vomiting and/or diarrhea,
Toxic Diseases and sometimes fever. When reactive hepatitis is severe,
there can be icterus, general lethargy, and sometimes
reduced exercise intolerance.
Nonspecific Reactive Hepatitis
Due to Endotoxins
Diagnosis
Etiology/Pathophysiology Differentiation between primary liver diseases and reac-
Nonspecific reactive hepatitis is a diffuse or focal liver tive hepatitis is only possible by histologic examination
disease with secondary inflammatory reaction resulting of a liver biopsy. The abnormalities described under
from toxemia or sepsis. Reactive hepatitis can occur with pathogenesis are characteristic. Once the diagnosis of
every toxemia, sepsis, inflammation, and necrotizing pro- reactive hepatitis is made, it can be very difficult to local-
cess (including necrosis in tumors). When the process is in ize the primary process. Further examination and inves-
tissues drained by the portal system, toxins are transported tigation of the gastrointestinal system are usually
exclusively to the liver. Toxins and bacteria from processes therefore indicated.
elsewhere are first diluted in the general circulation before
reaching the liver. It is therefore logical that reactive hepati- Therapy
tis is most often caused by processes within the abdomen. Therapy and prognosis depend on the primary disorder.
Reactive hepatitis develops in most cases of gastroen- Reactive hepatitis itself requires no treatment, since it
teritis and extensive gastric or intestinal tumours (e.g., resolves spontaneously after removal of the cause. The
lymphoma), as a result of increased endotoxin absorption. underlying, likely gastrointestinal disease should there-
It also develops in peritonitis, including local peritonitis fore be treated.
resulting from abdominal surgery, and in other inflamma-
tory processes in the organs drained by the portal vein. Drug Toxicity
Reactive hepatitis is thus most often caused by gastroin-
testinal disorders. On the other hand, vomiting and/or Many toxins and drugs are concentrated in the liver and
diarrhea often occur with primary liver disorders. Hence, may cause direct toxic damage (intrinsic toxicity), and
when a patient with gastrointestinal problems is found to rarely cause idiosyncratic (very acute and severe) toxicity.
have high liver enzyme levels, the classic chicken‐or‐egg Direct toxic damage may primarily involve the hepato-
situation is encountered, and this problem may only be cytes, causing necrosis and/or steatosis, or bile canaliculi,
solved with liver histopathology. However, the reaction causing intrahepatic canalicular cholestasis. In veterinary
pattern in the liver to endotoxins primarily involves the medicine, documented idiosyncratic liver toxicity is