Penny J. Watson,     Cambridge, Cambridgeshire, Great Britain

Etiology

The most effective treatment for CH is to treat the primary etiology. However, although canine CH is common, it is a frustrating disease in dogs because the cause is often unknown. One recent pathology study suggested as many as 12% of dogs from first opinion veterinary practices had histologic lesions in the liver consistent with CH by the time of death from any disease (Watson et al, 2010). Any breeds and crossbreeds can suffer from CH, but studies of CH from various countries in various decades have noted increased breed prevalence, some of which are consistent between countries and decades and some of which have changed. Although not definitively proving an inherited basis for CH in certain dog breeds, these findings certainly are suggestive of a genetic basis to the disease.

Potential and proven causes of canine CH are detailed in Table 142-1 and include copper storage disease, chronic drug toxicities, and a number of proven or suggested infectious agents. However, many cases remain idiopathic, and a number of these may have autoimmune hepatitis. This has not been proven conclusively in canine CH; however, it is suspected from recent work in Doberman pinschers in Scandinavia and also may occur in other breeds. Some of the other idiopathic cases may have a currently unknown canine chronic hepatitis virus. This has been suspected for a number of years, since the first description of a transmissible “acidophil cell hepatitis virus” in Glasgow in the 1980s (Jarrett and O’Neil, 1985). Some canine CH cases look clinically and histologically similar to chronic viral hepatitis in humans, but the putative virus has yet to be identified. Therefore currently it is difficult if not impossible for a clinician or pathologist to determine whether a particular non-copper-associated canine CH case is potentially viral or autoimmune, which obviously has profound implications for treatment, particularly with immunosuppressive drugs.

Treatment Goals

The approach to treatment of canine CH is outlined in Figure 142-1. The aims of treatment of any dog with CH are the following:

The underlying goal in all cases is to try to prevent the progression of disease to the end stage (i.e., cirrhosis). The WSAVA Liver Standardization Group defines cirrhosis as a diffuse process characterized by fibrosis of the liver and the conversion of normal liver architecture into structurally abnormal nodules. The liver has a high reserve capacity, but when loss of hepatocytes and fibrosis reduces liver function to less than 25% of normal, hepatic failure ensues, which is incompatible with life. Cirrhosis often is 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) (see Chapter 144). In humans, the development of portal hypertension in end-stage liver disease is a poor prognostic indicator. This has not been demonstrated specifically in dogs, although it is known that ascites is a negative prognostic indicator in canine CH (Raffan et al, 2009).

The overarching aim in treating canine CH is therefore to diagnose it early and prevent progression to end-stage cirrhosis because liver transplantation is not as yet an option. However, fibrosis of the liver is not inevitably progressive in one direction, and even early cirrhosis can be reversible if the underlying cause is removed, as has been demonstrated clearly in humans with alcoholic and viral hepatitis. The goal in treating canine CH therefore should be to identify and treat the cause wherever possible.