The Role of the Liver and Why It Matters
The liver is one of the most metabolically active organs in the body. It performs hundreds of essential functions, including detoxifying waste products and drugs from the bloodstream, producing bile for fat digestion, synthesising proteins including clotting factors and albumin, storing glucose as glycogen, metabolising fats and proteins, and removing ammonia — a toxic by-product of protein metabolism — by converting it to urea for excretion by the kidneys.
The liver has an impressive capacity for regeneration: in healthy animals, up to 70 percent of liver tissue can be destroyed before clinical signs of failure become apparent. This resilience is a double-edged sword — it means liver disease is often well advanced before an owner notices anything is wrong. By the time overt signs appear, significant and sometimes irreversible damage may already have occurred.
Portosystemic Shunts
A portosystemic shunt (PSS) is an abnormal blood vessel that allows blood from the digestive tract to bypass the liver and flow directly into the systemic circulation. Normally, blood from the intestines is carried to the liver via the portal vein, where it is detoxified before entering the general circulation. When a shunt is present, this detoxification does not occur. Ammonia, gut-derived toxins, and other waste products accumulate in the bloodstream, eventually reaching the brain and causing hepatic encephalopathy — a neurological syndrome characterised by disorientation, circling, apparent blindness, seizures, drooling, and behavioural changes that often worsen after meals.
Congenital Shunts
Congenital portosystemic shunts are present from birth and are most common in small and toy breeds, particularly Yorkshire Terriers, Maltese, Shih Tzu, Miniature Schnauzers, and Pugs. They are usually single vessels and can be either intrahepatic (located within the liver) or extrahepatic (outside the liver). Intrahepatic shunts are more commonly seen in large breeds such as the Irish Wolfhound and Labrador Retriever. Puppies with congenital shunts are typically smaller than their littermates, grow slowly, and show neurological signs — particularly after eating — from a young age.
Acquired Shunts
Acquired shunts develop secondary to chronic liver disease and portal hypertension. As the liver becomes fibrotic and its architecture disrupted, blood pressure within the portal vein rises, and multiple small collateral vessels open up to bypass the resistance. These acquired shunts are a sign of advanced underlying liver disease rather than a primary problem in themselves.
Surgical attenuation of congenital shunts — gradually narrowing or closing the abnormal vessel — is the treatment of choice for extrahepatic congenital shunts and can be curative in many cases. Medical management using a low-protein diet, lactulose, and antibiotics to reduce ammonia production is used while awaiting surgery or in cases where surgery is not possible.
Copper Storage Hepatopathy
Copper is an essential trace mineral obtained through the diet. In healthy dogs, excess copper is excreted in the bile. In certain breeds, genetic mutations affect the proteins responsible for copper transport and excretion, causing copper to accumulate progressively within liver cells until it reaches toxic concentrations. This condition — copper storage hepatopathy — leads to oxidative damage, hepatocyte death, and eventually cirrhosis.
Bedlington Terriers and the COMMD1 Gene
The Bedlington Terrier is the breed most severely affected. A mutation in the COMMD1 gene (also known as MURR1) impairs biliary copper excretion, and affected dogs accumulate extreme quantities of copper within their liver cells. Without intervention, most affected Bedlingtons develop liver failure. DNA testing for the COMMD1 mutation is available and should be mandatory for all breeding Bedlingtons, as the condition follows an autosomal recessive pattern — a dog must inherit two copies of the mutated gene to be affected.
Other Affected Breeds
Copper storage hepatopathy is also well recognised in Labrador Retrievers, West Highland White Terriers, Dalmatians, and Dobermann Pinschers, though the genetic basis differs between breeds and is not always fully characterised. In Labradors in particular, copper accumulation has become an increasingly reported cause of hepatitis and cirrhosis.
Treatment involves a copper-restricted diet — avoiding ingredients such as liver, kidney, shellfish, and wholegrains that are naturally high in copper — alongside chelation therapy using d-penicillamine or trientine to bind copper in the bloodstream and promote its excretion. Zinc supplementation is also used to competitively block copper absorption from the gut. Treatment is lifelong in affected animals.
Chronic Hepatitis
Chronic hepatitis refers to persistent inflammatory liver disease that does not resolve and leads to progressive fibrosis and loss of function over time. In many dogs, no specific infectious, toxic, or metabolic cause can be identified, and the condition is presumed to be immune-mediated — the immune system inappropriately targeting liver tissue. Cocker Spaniels, Dobermanns, and Standard Poodles have a reported predisposition to immune-mediated chronic hepatitis, though any breed can be affected.
Signs are often non-specific: reduced appetite, weight loss, vomiting, increased thirst and urination, and a distended abdomen due to ascites (fluid accumulation caused by reduced albumin production and portal hypertension). Jaundice may appear in more advanced cases.
Liver Enzymes: ALT as a Marker
Alanine aminotransferase (ALT) is the primary liver enzyme measured on routine blood chemistry panels in dogs. It is highly liver-specific — elevated ALT signals damage to hepatocytes — and is a useful screening tool for liver disease. However, ALT elevation is not specific to any particular type of liver disease. A mildly elevated ALT can result from anything from a dietary indiscretion or drug reaction to severe hepatitis or a shunt. Furthermore, ALT can be normal even in dogs with significant chronic liver disease if the pace of cell death has slowed and fibrosis has replaced active inflammation. ALT is best interpreted as part of a broader clinical picture, including other liver enzymes (ALP, GGT), bilirubin, albumin, bile acids, and diagnostic imaging.
Liver Biopsy: The Definitive Diagnostic Tool
A liver biopsy remains the only way to definitively characterise the nature and severity of liver disease, identify copper accumulation, quantify fibrosis, and guide targeted treatment. Biopsies can be obtained via ultrasound-guided needle, laparoscopy, or laparotomy. The choice of technique depends on the clinical situation, the dog's clotting status, and the quality of tissue required. Histopathology by a specialist pathologist, combined with copper quantification using tissue analysis, provides the most actionable information for long-term management.
Hepatoprotectants: SAMe and Milk Thistle
Several nutraceuticals are commonly used as adjunctive support in dogs with liver disease, most notably S-adenosylmethionine (SAMe) and silymarin (the active compound derived from milk thistle, Silybum marianum). SAMe is a naturally occurring compound that plays a central role in methylation pathways and glutathione production. Glutathione is one of the liver's primary antioxidants, and its depletion is a key mechanism of hepatocyte damage. Supplementing SAMe helps replenish glutathione stores and reduce oxidative stress within liver cells. Silymarin from milk thistle has anti-inflammatory, antifibrotic, and antioxidant properties and may help reduce liver cell damage and slow the progression of fibrosis.
Both are considered safe for long-term use in dogs and are available as veterinary-specific formulations. They are not a substitute for treating the underlying cause of liver disease but can support liver function and recovery alongside primary treatment.
Dietary Management
Diet plays an important supporting role in managing canine liver disease. A moderately protein-restricted diet using high-quality, easily digestible protein sources helps reduce ammonia production without causing protein deficiency. Dogs with hepatic encephalopathy may require more significant protein restriction. Copper-restricted diets are essential in copper storage hepatopathy. Small, frequent meals are better tolerated than large meals as they reduce the ammonia load reaching the bloodstream at any one time. Many commercial veterinary liver diets are formulated with these principles in mind and provide a convenient option for owners.