How I treat liver disease (Proceedings)


How I treat liver disease (Proceedings)

Apr 01, 2009

The discussion below is directed at therapy for chronic hepatitis but much of what is presented can also be extrapolated to other types of liver disease in both the dog and cat. I have four general goals in therapy: 1) remove the etiology, 2) provide an adequate diet, 3) specific therapy and 4) providing general liver support. So first the therapy for chronic hepatitis and other liver diseases involves removing the primary etiology if it can be identified. Short of treating the primary etiology all other therapies suggested are unproven in the management of liver disease in dogs. Much of the therapy is directed at providing adequate liver support. This often involves the use of multiple therapies.


Adjusting diet therapy should be considered in all cases however only general guidelines should be given. First, palatability is important to assure adequate energy requirements are met. Next, there is a misconception about diet and liver disease that liver patients should be placed on a protein restricted diet. Protein restriction should only be instituted in the patient that has clinical evidence of protein intolerance (i.e. hepatic encephalopathy). The goal of dietary therapy is to adjust the quantities and types of nutrients to provide nutrient requirements but to avoid the production of excess nitrogen by-products associated with liver disease. As a general recommendation the dietary protein should represent 17 to 22% of digestible Kcal.

High carbohydrate and moderate fat content is important to supply caloric needs. Mineral supplementation containing high concentrations of both copper and iron should be avoided.

There is also evidence that fiber may have several beneficial actions in patients having liver disease. First, dietary fiber effectively binds bile acids in the intestinal tract and promotes their removal. Secondly soluble fiber appears to have some benefit in managing hepatic encephalopathy by generation of fermentation products (short chain fatty acids). These act by impairing the intestinal uptake of the surrogate marker of HE, ammonia. Soluble dietary fiber has a similar effect as lactulose and would provide a logical long-term nutritional approach in the management of some animals with hepatic encephalopathy. Psyllium, as a source of soluble fiber given at a dose of 1-3 tsp/day can be used as a dietary supplement.

Diets low in copper are recommended for the breeds known to accumulate copper or that have documented increased concentrations on biopsy. The restriction of dietary copper however probably does little to lower hepatic copper concentrations in diseased dogs having large amounts of hepatic copper. Diet will lessen further absorption of the metal. It is difficult to limit dietary copper because most commercial dog foods contain supplemental copper that meet, or more frequently exceed the minimal dietary requirements. Most formulated "liver diets" have lower copper concentrations. Homemade diets can also be prepared that do not to contain excess copper. These diets should exclude liver, shellfish, organ meats and cereals that are all high in copper content. Vitamins or mineral supplements should not contain copper or iron.

Antinflammatory Therapy

Decreasing inflammation as a specific therapy for chronic hepatitis in the dog and cholangitis in the cat is unproven although the author's clinical impression suggests anti-inflammatory therapy is beneficial in some cases. The treatment of chronic hepatitis is quite controversial and there are as yet no good controlled studies in animals to support corticosteroids use in every case.

In a study by Strombeck found that some dogs with chronic hepatitis tended to have a prolonged survival when treated with corticosteroids. This retrospective study is one with a wide diversity of diseases and concurrent therapies. But none-the-less, it appears that corticosteroids offer benefit in at least some cases (possibly around 25%). A suggested dose of 1 to 2 mg/kg/day using either prednisone or prednisolone should be instituted. When clinical improvement is suspected or after several weeks the dose is then gradually tapered eventually to a dose of 0.5 mg/kg/day or every other day. The only accurate way to evaluate a response to any therapy is to re-biopsy the patient in 6 months to 1 year because the patient will develop a concurrent steroid hepatopathy with increased liver enzymes making laboratory determination of any improvement impossible.