Liver function

Last updated: Sunday, July 12, 2015


There is no single test that gives a good measure of liver dysfunction. Assessments are made according to the whole clinical picture, which includes:

  1. Signs and symptoms (e.g. jaundice, encephalopathy, varices).

  2. Blood tests – such as liver function tests (see below), clotting screen, virological markers (e.g. hepatitis B or C).

  3. Biopsy and imaging techniques.

Viral disease Hepatitis A manifested here as jaundice       
Courtesy of CDC/ Dr. Thomas F. Sellers; Emory University

Liver Function Tests (LFTs)

Not all elements of LFTs are specific to the liver, and they do not in themselves provide a diagnosis, although they can help to confirm or exclude liver disease. Symptomatology and other test results should always be considered together with LFTs.

LFTs can be useful for monitoring disease progression and response to therapy. But LFTs alone are not necessarily a good indicator of severity of liver disease or extent of liver dysfunction.

A significant change in any particular enzyme is difficult to quantify, but greater than double the upper limit of normal (or baseline) is a useful guide. A particular enzyme should not, however, be considered in isolation. The ‘battery’ of liver function tests should be considered as a whole in order to identify the ‘picture’ generated.

Note that drugs which induce cytochrome p450 enzymes may elevate some LFT values.

The individual elements of LFTs are discussed briefly below:

  1. Bilirubin. This is a product of haemoglobin breakdown and is normally excreted in the bile. It is particularly raised in cholestasis, but can also be raised in hepatocellular disease.

  2. Alkaline Phosphatase (ALP). Is raised in cholestasis since it is secreted into bile ducts. It is slightly raised in hepatocellular disease. Reference values vary markedly between hospitals according to assay technique so make sure you know your own local ones!

    1.  © Crown copyright 2017

  3. Transaminases. These are markers of hepatocellular injury. Alanine aminotransferase (also known as alanine transaminase – ALT) is more specific to the liver than aspartate aminotransferase (also known as aspartate transaminase – AST). Note in the US, ALT is known as SGPT (serum glutamic pyruvate transaminase) and AST is known as SGOT (serum glutamic oxaloacetic transaminase).

  4. Gamma Glutamyl Transferase (GGT). Levels rise in almost all kinds of liver disease and are therefore of little value in differentiating between them. Levels may also rise in patients taking enzyme-inducing drugs and in alcohol dependency.

  5. Albumin. This is synthesised in the liver but has a long half-life (20 days). Although not a very specific indicator, a low albumin in association with deranged LFTs may suggest chronic liver disease.

  6. Prothrombin Time. Clotting factors are made in the liver, and an elevation of PT by more than 3 seconds is significant. It is a useful indicator of the synthetic ability of the liver and can increase in both acute and chronic liver disease. Changes can occur rapidly due to the relatively short half-life of clotting factors.
Note that some patients will have a combined cholestatic/hepatocellular picture.

Make sure you are familiar with the local LFT reference ranges that are appropriate for the age of your patient. Usual paediatric ranges may be different to those used for adults.