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Elevated liver enzymes: ALT, ALP, AST, GGT and bilirubin

ALT, ALP, AST, GGT and bilirubin each report a different kind of liver or biliary change in dogs and cats, so a high result is read by which value moved, how far it sits from the lab's own interval, and what else on the panel moved with it.

Reviewed by Brian Toncray, DVM ยท October 22, 2026

A liver value measured once is a snapshot. The standard review of canine and feline liver enzyme interpretation stresses that a single measurement is less reliable than a series, and that each enzyme has to be read in light of its tissue of origin, its half-life and the possibility of induction1. None of these enzymes measures how well the liver works. They report injury, cholestasis or induction, and a function question needs a function test.

ALT (alanine aminotransferase)

High can mean
Leakage from injured hepatocytes. ALT sits in the hepatocyte cytosol, so a rise points to hepatocellular injury or altered membrane permeability rather than to lost function1. In dogs, a persistent and unexplained ALT increase is a common route to the diagnosis of chronic hepatitis, which the ACVIM consensus says is confirmed only by liver biopsy and histopathology2. Dogs receiving phenobarbital often carry raised ALT and ALP without clinical signs of liver disease; a biopsy study found the serum rise was not explained by enzyme induction in the liver, which is why these dogs are monitored rather than reassured3. In cats, hyperthyroidism commonly raises liver enzymes, and in one study the increases were not tied to abnormal hepatic parenchyma or function and returned to normal once the thyroid disease was controlled4.
Low can mean
Little on its own. A falling ALT across serial panels is more informative than one low reading, because the trend shows whether injury is still going on1.
Can shift it artificially
Tissue of origin. ALT is not perfectly liver specific, so severe muscle injury belongs on the list when the rest of the panel does not fit a hepatic pattern1.
Next test
Repeat to document persistence; a pre and post meal bile acid test when function is the question; abdominal ultrasound; in a dog with a persistent unexplained rise, liver biopsy for histopathology and copper assessment as the consensus describes2.

ALP (alkaline phosphatase)

High can mean
Cholestasis, induction or bone. Dogs produce a corticosteroid-induced ALP isoenzyme, and its messenger RNA appears in the liver only after glucocorticoid treatment, so steroid exposure alone can push ALP well above the interval5. That is also why ALP is a frequent finding in canine hyperadrenocorticism, although the ACVIM panel warns that no screening test is perfect and that endocrine testing belongs only in dogs with compatible clinical signs6. Phenobarbital-treated dogs show increases in both the corticosteroid-induced and the liver isoenzymes3. Growing animals carry bone-derived ALP1. In cats, ALP has a short half-life and modest hepatic stores, so even a modest rise deserves attention, and feline hepatic lipidosis is a classic cause1,7. Hyperthyroid cats are another common source4.
Low can mean
No clinical meaning is attached to a low ALP in the sources cited on this page.
Can shift it artificially
Recent glucocorticoid treatment by any route that reaches the circulation5, and anticonvulsant therapy with phenobarbital3, change the reading before any hepatobiliary disease does.
Next test
Take a full drug history first. If the dog has signs that fit hyperadrenocorticism, follow the consensus testing pathway rather than testing on ALP alone6. In an older cat, measure total T4 before an extensive hepatobiliary work-up, since most hyperthyroid cats with high enzymes need none4. Imaging of the liver and biliary tree follows.

AST (aspartate aminotransferase)

High can mean
Hepatocellular or muscle injury. AST is found in both liver and muscle and has a mitochondrial fraction, so it rises with more severe hepatocyte damage and with myopathy1. Read it beside ALT and creatine kinase.
Low can mean
Not clinically meaningful in the sources used here.
Can shift it artificially
Muscle damage from trauma, seizures or intramuscular injections can raise AST without any hepatic process1.
Next test
Creatine kinase to separate muscle from liver; the same hepatic work-up as ALT when CK is unremarkable.

GGT (gamma-glutamyl transferase)

High can mean
Biliary epithelial change and cholestasis. In dogs, GGT also responds to glucocorticoids. In cats, GGT usually rises at least as much as ALP in inflammatory biliary disease, while hepatic lipidosis tends to raise ALP out of proportion to GGT, a contrast that helps rank the two conditions1,7.
Low can mean
No cited clinical meaning.
Can shift it artificially
Glucocorticoid exposure in dogs1.
Next test
Ultrasound of the gallbladder and bile ducts; fine needle aspirate or biopsy where the pattern and imaging justify it.

Total bilirubin

High can mean
Three routes: increased red cell destruction (prehepatic), reduced hepatic uptake or conjugation (hepatic), and obstructed bile flow (posthepatic). Hemolytic disease such as immune-mediated hemolytic anemia raises bilirubin through destruction, and the ACVIM diagnostic consensus lists hyperbilirubinemia among the supporting findings8. Hepatic and cholestatic causes are read with the enzyme pattern above1.
Low can mean
Not meaningful.
Can shift it artificially
Visible icterus in the serum tube is itself a result; hemolysis in the tube from a difficult draw is a different thing, and the PCV separates them.
Next test
PCV and a blood smear first, because a low PCV with spherocytes or agglutination points away from the liver8; imaging of the biliary tree if the PCV is unremarkable.

Reading these values together

Pattern matters more than any single number. A dominant ALT rise with smaller ALP and GGT changes reads as hepatocellular injury, while ALP and GGT leading with modest ALT reads as cholestasis or induction1. In a dog, an isolated and marked ALP increase with no bilirubin change should send you to the medication list and the endocrine history before the liver5,6. In a cat, a high ALP with a relatively normal GGT in an anorexic, overweight patient fits hepatic lipidosis, and a mild rise in ALT and ALP in an older cat losing weight with a good appetite fits hyperthyroidism7,4. When bilirubin climbs with a falling PCV, think destruction before obstruction8.

Time is the other axis. Enzymes with short half-lives fall quickly once injury stops, so a repeat panel a week or two later often says more than the first1. In dogs, the consensus on chronic hepatitis is built around persistence: values that stay up despite removal of drugs and treatment of other disease justify sampling the liver2.

Example: a panel worked through

Example. An 11-year-old spayed female Labrador retriever presents for drinking more, panting and a pot-bellied look. ALP is well above the lab's interval, ALT and GGT are mildly above, bilirubin is within the interval and cholesterol is above.

The owner reports no steroid tablets, ear drops or skin creams. The pattern is cholestatic or induced rather than hepatocellular, and the signs are the kind the ACVIM panel lists as a reason to test for hyperadrenocorticism6. The plan is urinalysis, endocrine testing per the consensus pathway, and abdominal ultrasound for the adrenal glands and liver. Had she been on prednisone for allergies, the same ALP result would have been expected and the endocrine question would wait5.

Frequently asked questions

What does elevated ALT and ALP mean in a dog?

Together they point to liver injury with a cholestatic or induced component. ALT reports hepatocyte leakage and ALP reports cholestasis or induction, often by glucocorticoids or phenobarbital, so the drug history comes before the liver work-up1,5,3.

Why can ALP be high in a dog without liver disease?

Dogs make a corticosteroid-induced ALP isoenzyme in the liver after glucocorticoid exposure, and young dogs carry bone ALP, so the enzyme can rise without hepatobiliary disease5,1.

Is a high ALP more significant in a cat than in a dog?

Usually yes. Feline ALP has a short half-life and smaller hepatic stores, so a rise is less likely to be induction and conditions such as hepatic lipidosis and hyperthyroidism head the list1,7,4.

Do high liver enzymes mean the liver is failing?

No. Enzymes report injury, cholestasis or induction. Liver function is assessed with tests such as bile acids, and in dogs a persistent unexplained rise is confirmed by biopsy1,2.

Sources

  1. Center SA. Interpretation of liver enzymes. Vet Clin North Am Small Anim Pract. 2007; 37(2):297-333, vii. PMID: 17336677. DOI: 10.1016/j.cvsm.2006.11.009.
  2. Webster CRL, Center SA, Cullen JM, et al. ACVIM consensus statement on the diagnosis and treatment of chronic hepatitis in dogs. J Vet Intern Med. 2019; 33(3):1173-1200. PMID: 30844094. DOI: 10.1111/jvim.15467.
  3. Gaskill CL, Miller LM, Mattoon JS, et al. Liver histopathology and liver and serum alanine aminotransferase and alkaline phosphatase activities in epileptic dogs receiving phenobarbital. Vet Pathol. 2005; 42(2):147-60. PMID: 15753468. DOI: 10.1354/vp.42-2-147.
  4. Berent AC, Drobatz KJ, Ziemer L, et al. Liver function in cats with hyperthyroidism before and after 131I therapy. J Vet Intern Med. 2007; 21(6):1217-23. PMID: 18196729. DOI: 10.1892/07-022.1.
  5. Wiedmeyer CE, Solter PE, Hoffmann WE. Kinetics of mRNA expression of alkaline phosphatase isoenzymes in hepatic tissues from glucocorticoid-treated dogs. Am J Vet Res. 2002; 63(8):1089-95. PMID: 12171159. DOI: 10.2460/ajvr.2002.63.1089.
  6. Behrend EN, Kooistra HS, Nelson R, et al. Diagnosis of spontaneous canine hyperadrenocorticism: 2012 ACVIM consensus statement (small animal). J Vet Intern Med. 2013; 27(6):1292-304. PMID: 24112317. DOI: 10.1111/jvim.12192.
  7. Center SA. Feline hepatic lipidosis. Vet Clin North Am Small Anim Pract. 2005; 35(1):225-69. PMID: 15627635. DOI: 10.1016/j.cvsm.2004.10.002.
  8. Garden OA, Kidd L, Mexas AM, et al. ACVIM consensus statement on the diagnosis of immune-mediated hemolytic anemia in dogs and cats. J Vet Intern Med. 2019; 33(2):313-334. PMID: 30806491. DOI: 10.1111/jvim.15441.