Page 38 - WSAVA2018
P. 38

 25-28 September, 2018 | Singapore
P. Watson1
1Department of Veterinary Medicine, University of Cambridge, UK
What is canine chronic hepatitis?
· ‘Chronic hepatitis’ = hepatic mononuclear or mixed inflammatory infiltrate with piecemeal necrosis and varing degrees of fibrosis. Fibrosis tends to progress to cirrhosis, but not inevitably.
· Cirrhosis describes progressive bridging fibrosis, inflammation and nodular regeneration which has classically been considered end stage and irreversible.
What isn’t chronic hepatitis?
In addition, it is important to rule out secondary hepatopathies which are a much commoner cause of increased liver enzymes than primary liver disease. This differentiation is usually achieved through careful interpretation of clinical examination, history, clinicopathological tests and diagnostic imaging. Secondary hepatopathies are usually not clinically significant in their own right and resolve when the underlying cause is treated.
Causes of canine chronic hepatitis
Chronic hepatitis frustratingly usually remains a non- specific diagnosis in dogs and the cause is generally unknown. The potential causes of canine chronic hepatitis are reviewed in. They include copper storage disease and autoimmune disease in some dogs particularly English Springer Spaniels.
· Recognised in wide variety of dog breeds including cross breeds.
· Consistently increased incidences in certain specific breeds: middle aged dogs of a number of breeds including English Springer Spaniels; American
and English Cocker spaniels (males more than females), West Highland White terriers (no apparent sex predisposition), Dobermans (strong female predisposition) and Labrador retrievers (female bias). Skye terrier hepatitis is now believed to be a congenital ductal plate abnormality
· Suggests a genetic basis for the disease but so far studies in dogs failed to elucidate specific genetic mechanisms apart from DLA associations in English Springer Spaniels and Dobermans.
· SOME cases are associated with primary or secondary increases in copper
· SOME cases may be autoimmune, but not all. The most likely breeds to have autoimmune hepatitis on current evidence are cocker spaniels, English Springer spaniels and some Dobermans.
· Potential low grade infections such as atypical leptospira could also potentially be involved but, again, these causes are not well investigated in
dogs. Chronic bacterial infections are typically associated with more of a granulomatous inflammatory response (- neutrophils and macrophages) and eubacterial fluorescent-in-situ hybridisation should be considered in these cases.
  Potential Genetic reason for susceptibility to chronic hepatitis in dogs
 Susceptibility to infectious causes of CH and/or to chronicity of infection rather than recovery
  Susceptibility to autoimmune disease
 Mutation of gene coding for protein involved in metal transport/ storage/excretion *
 Gene mutations resulting in hepatic accumulation of glycoprotein protease inhibitor
 Increased susceptibility to chronic hepatic damage with toxic causes
  Treatment of canine chronic hepatitis
The aims of treatment of any dog with chronic hepatitis are:
· To treat the underlying cause, if this can be identified
· To try to slow progression of the disease even if the cause if not identified
· To support liver function as long as possible and support the dog in positive calorie and nitrogen balance
· To treat the complications of liver disease which affect quality and length of life
The aim in all cases is to try to prevent the progression of disease to the end stage ie cirrhosis. Cirrhosis is often accompanied by the development of portal hypertension, where increased resistance to flow through the hepatic vasculature raises portal pressure resulting in splanchnic congestion, development
of ascites and often acquired portosystemic shunts
and hepatic encephalopathy (HE). It is, however, very important to remember that fibrosis of the liver is not inevitably progressive in one direction and that even early cirrhosis can be reversible if the underlying cause is removed, as has been clearly demonstrated in humans with alcoholic and viral hepatitis. The aim in treating canine CH should therefore be to identify and treat the cause wherever possible.
The clinician should use all the information available to them to optimise treatment for an individual case. On the clinical examination, blood results and imaging, the clinician needs to assess the degree of loss of liver function and identify signs of biliary stasis, portal hypertension, acquired portosystemic shunts, ascites, gastrointestinal oedema or ulceration or protein- calorie malnutrition. On the liver biopsy if available, the clinician should assess the amount and distribution
of inflammation and the types of inflammatory cells involved, the degree and distribution of fibrosis and the presence of any obvious cause including build up of

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