Liver disease in dogs is a common finding in veterinary practice (Favier, 2009; Watson, 2004). Chronic liver disease is diagnosed more frequently than acute liver disease. In acute liver disease dogs may not be presented to the veterinarian because the signs are transient, and most dogs recover quickly following one or two days of vomiting, lethargy and anorexia. The liver is the largest and one of the most complex organs in the dog and has many vital functions. It is involved in carbohydrate, fat and protein metabolism. The production of protein and storage of glycogen, triglycerides, bile and the metabolism and storage of some vitamins and minerals also occurs in the liver. In addition, the liver is responsible for the metabolism and clearance of drugs, chemicals and the by-products of metabolism.

The liver also synthesis many important proteins, such as those involved in blood clotting.  The reasons for liver disease are many and include degenerative, autoimmune, metabolic, nutritional, inflammatory/infectious and traumatic causes. Liver disease can affect the functional tissue i.e. the liver parenchyma, the bile ducts and gall bladder or a combination of all of these. Prolonged inflammation and oxidative stress frequently result in liver disease in dogs (Au, Hasenwinkel, & Frondoza, 2013).  Irrespective of the cause of the liver disease and the part of the liver affected, a prolonged reaction by the liver to an insult results in chronic inflammation, fibrosis, cirrhosis and ultimately liver failure. The cause of liver disease is best obtained by liver biopsy.

Cholestasis (a reduction or cessation of the normal flow of bile) results when there is an obstruction to the biliary tract anywhere between the hepatocyte and the duodenum, where bile enters the small intestine. Cholestasis can occur as a result of intrahepatic or extrahepatic causes and distension of the bile ducts results in hepatocellular damage.

Oxidative stress in the liver

By virtue of the array of functions of the liver, it is subject to great oxidative stress. Oxidative stress has a major role in most forms of hepatobiliary injury. Oxidative stress is traditionally defined as an imbalance between pro-oxidant compounds and antioxidant defences (Webb & Twedt, 2008).

Clinical signs of liver disease

Given the extensive role of the liver, clinical signs associated with liver disease are diverse and varied.  Symptoms may not be observed until there is extensive liver damage because the liver has remarkable powers of regeneration. It is often said that symptoms of liver disease may not be apparent until there is loss of more than 80% of hepatocytes (liver cells). Clinical signs may include, but not be limited to

  • Anorexia
  • Vomiting
  • Weight loss
  • Jaundice
  • Lethargy
  • Diarrhoea
  • Weakness
  • In severe cases, coagulopathies, ascites and hepatic encephalopathy.

Clinical chemistry may show cyclical or persistent increases in ALT, AST, ALP, γGT. In advanced disease increased total serum bile acids, hyperbilirubinemia and an increase in blood ammonia leads to hepatic encephalopathy.  In the later stages of disease, portal hypertension causes acquired portal systemic shunts (PSS) to develop. PSS causes microcytosis, hypoalbuminemia, hypercholesterolemia and prolonged clotting times (APTT and/or PT). In the early stages of disease ultrasonography may be normal; however as the disease progresses ascites, cirrhosis, nodular hyperplasia may be observed (Sevelius, 1995; Watson, 2004).

The description of liver diseases is complex and the World Small Animal Veterinary Association has developed a guide to standardize the way in which liver disease is described (Center, 2009; Cullen, 2009; Favier, 2009). Furthermore, the liver disease can be described as intra hepatic, extrahepatic, acute and chronic. As primarily affecting the hepatocyte parenchyma, the biliary tree, the interstitial tissues or a combination of all. Irrespective of the cause of the liver disease, chronic liver disease of one sort or another is the most frequently observed in veterinary practice and the prolonged inflammation and injury result in cirrhosis that has a very poor prognosis. The aims of treatment therefore are to ameliorate progression of disease, where possible reverse disease and allow the liver opportunity to regenerate.

What causes Liver disease in dogs?

Factors that increase your dog’s likelihood of developing liver disease include:

Age: Several diseases, including liver dysfunction, are common in geriatric dogs.

Breed: Certain dog breeds, such as Dobermans, Rottweilers, Yorkshire terriers and Cocker Spaniels, are more likely to be born with or are prone to develop particular liver problems.

Some medications can damage the liver in dogs as well as other factors such as:

-Viral and bacterial infections

– Poisonous substances your dog has eaten

– Altered blood flow to the liver due to heart disease or other congenital abnormality

NSAIDs (non-steroidal anti-inflammatory drugs) :

Special care of the dogs liver needs to be taken where NSAIDs are used. NSAIDs are the go-to medications for pain in dogs. Hundreds of thousands of dogs and cats receive millions of doses of these medications every year for pain relief after surgery, following traumatic events, and to manage chronic pain. They are especially used in older dogs with problems such as arthritis, but as with any drugs your dog may be fed, there are side-effects. Liver and gastrointestinal issues are by far the most common unwanted findings found when dosing your pet with NSAID’s

Objectives of nutritional support in liver disease 

The objectives of treatment of liver disease are to decrease the metabolic burden and oxidative stress on the liver and whenever possible to remove the inciting cause. By doing this the aim is to slow the progression of fibrosis to end stage liver cirrhosis. Usually treatment is non-specific and empirical, except for copper storage diseases when low copper diets and copper binders are indicated.

The metabolic burden on the liver can be alleviated by reducing protein metabolism (and subsequent ammonia build up), reducing oxidative stress and promoting fat clearance. Cholestasis causing increase intrahepatic pressure can be relieved by promoting bile flow and relieving obstructions. Increasing the oxidative capacity of the liver can be achieved through the administration of antioxidants.

LIVERPAK 500 Paste for dogs

LIVERPAK 500 for dogs contains many of the nutritional supplements that have been demonstrated to support the liver during times of oxidative stress and to promote the clearance of fat from the liver. LiverPak500 Paste for dogs is suggested when dogs are experiencing metabolic stress or toxicity. For example, following toxicity (or during the administration of nonsteroidal anti-inflammatory drugs); during times of metabolic stress (e.g. Cushing’s disease, diabetes mellitus, severe anorexia and fasting).

LiverPak500 paste is veterinary formulated with key ingredients for your dogs liver including s-adenosyl methionine (SAMe), milk thistle, artichoke, carnitine, vitamin E and vitamin C. These antioxidants play an essential role by controlling the oxidation of sensitive membranes  and protect the cells from damage.

  • S-adenosylmethionine :

S-adenosylmethionine is a nucleotide-like molecule that is synthesised by all living cells. It is derived from methionine and ATP and initiates pathways, one of which is essential for glutathione production. S-adenosylmethionine :

– Increases hepartic glutathione concentrations

– Helps maintain plasma membrane fluidity and function

– Is involved in many biochemical pathways that can help maintain normal liver cell function.

  • Choline :

Choline plays an essential role in fat metabolism in the liver. It acts to prevent excess fat accumulations in the liver by converting excess fat into Lecithin or by increasing the utilisation of fatty acids in the liver.

  • Artichoke :

A member of the milk thistle family that helps control blood sugar levels, the artichoke is a fibrous, green vegetable containing cynarin. Cynarin is a phenolic acid compound that experts believe is important for cholagogue and choleretic properties; stimulating the production of bile in the liver and promoting the discharge of bile from the system.

  • Milk Thistle

Milk thistle has been used since the time of ancient physicians and herbalists to treat a range of liver and gallbladder disorders, including hepatitis, cirrhosis and jaundice, and to protect the liver against poisoning from chemical and environmental toxins, including snakebites, insect stings, mushroom poisoning, and alcohol (Ludvico, 2010). Several pharmacological studies have been carried out on the active components of Milk thistle, silymarin and silybinin. It has been found that these substances exert hepatoprotective, antioxidant, anti-inflammatory and anti-fibrotic properties. In addition, they stimulate protein biosynthesis and liver regeneration, increase lactation and possess immunomodulation activity.

  • Carnitine :

Carnitine is an amino acid derivative and nutrient involved in lipid (fat) metabolism in mammals. It is specifically required for the transport of fatty acids from the intermembraneous space in the mitochondria into the mitochondrial matrix during the catabolism of lipids.

To see LiverPak500 and learn more click here


Au, A. Y., Hasenwinkel, J. M., & Frondoza, C. G. (2013). Hepatoprotective effects of Sadenosylmethionine and silybin on canine hepatocytes in vitro. J Anim Physiol Anim Nutr (Berl), 97(2), 331-341. doi:10.1111/j.1439-0396.2012.01275.x

Center, Sharon A. (2009). Diseases of the Gallbladder and Biliary Tree. Veterinary Clinics of North America: Small Animal Practice, 39(3), 543-598 . doi:

Favier, Robert P. (2009). Idiopathic Hepatitis and Cirrhosis in Dogs. Veterinary Clinics of North America: Small Animal Practice, 39(3), 481-488. doi:

Sevelius, E. (1995). Diagnosis and prognosis of chronic hepatitis and cirrhosis in dogs. Journal of Small Animal Practice (United Kingdom)(12), 521.

Webb, C., & Twedt, D. (2008). Oxidative stress and liver disease. Vet Clin North Am Small Anim Pract, 38(1), 125-135, v. doi:10.1016/j.cvsm.2007.10.001


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