Buku Medicine


Patients have liver function tests checked for a variety of reasons both in the community and in hospital settings. Liver tests can be acutely or chronically deranged and can be abnormal for a number of reasons. A ‘liver screen’ is commonly requested to investigate abnormal liver functions tests. The screen can be modified depending on the age of the patient and whether acute or chronic liver disease is suspected.  

A careful history is vital. Salient points in the history should be: 

  • Personal or family history of liver disease 
  • Personal or family history of autoimmune disease 
  • Alcohol – pattern of consumption, including volume and duration 
  • Risk factors for viral hepatitis (injecting drug use, tattoos, blood transfusions and lived or had medical treatment in a country where Hepatitis C is common) 
  • Medication history for the past 6 months including antibiotics, over the counter and herbal remedies and recreational drugs 

A thorough examination should include 

  • Signs of chronic liver disease 
  • Evidence of decompensation (jaundice, ascites, hepatic encephalopathy) 

The following tests should be included in a non-invasive liver screen: 

  • Hepatitis B surface antigen and core antibody 
  • Hepatitis C antibody 
  • Liver autoantibodies – anti-mitochondrial antibody (AMA), anti-nuclear antibody  (ANA), anti-smooth muscle antibody (ASMA) 
  • Immunoglobulins 
  • Ferritin and transferrin saturations 
  • Alpha-1 antitrypsin 
  • An abdominal ultrasound scan should also form part of the initial liver screen 

In patients <40 years old – caeruloplasmin should be checked 

If an acute hepatitis is suspected then Hepatitis A IgM, Hepatitis E IgM, CMV IgM, EBV IgM and HSV IgM should also be checked. If the patient is immunosuppressed then Hepatitis E PCR should be checked rather than the IgM.

Hepatitis B

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Hepatitis C

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Liver autoantibodies

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Caeruloplasmin is a copper binding protein. It is requested as part of a liver disease to screen for Wilson’s disease. 

Levels can be reduced in: 

  • Wilson’s disease 
  • Severe liver disease of any aetiology 
  • Malnutrition 

Levels can be raised in: 

  • Any form of infection or inflammation as it is an acute phase reactant 
  • Pregnancy 
  • Oestrogen therapy 

Wilson’s disease is an autosomal recessive disorder. It is caused by various mutations in a gene (ATP7B) on chromosome 13. In Wilson’s disease there is a defect in hepatic copper metabolism which causes decreased hepatocellular excretion of copper into bile. This results in accumulation of copper within the liver which is toxic to hepatocytes. Copper is then released into the bloodstream and is deposited in the kidneys, brain and cornea.  

Wilson’s disease usually present in childhood or early adulthood. Most patients present with acute or chronic liver disease, neurological or psychiatric symptoms.  

Diagnostic features are: 

  • Low caeruloplasmin 
  • Low serum copper 
  • Increased 24 hour urinary copper 
  • Normal or low alkaline phosphatase 
  • Haemolytic anaemia 
  • Kayser-Fleischer rings 
  • Raised hepatic dry weight copper content 

Wilson’s disease can be very challenging to diagnose and patients with suspected Wilson’s disease should be discussed with and or referred to a hepatologist.  

Alpha-1 antitrypsin

Alpha-1 antitrypsin is an enzyme inhibitor which is produced by hepatocytes and transported to the lungs. It protects the lungs against the proteases released by inflammatory cells, particularly neutrophils.  

Alpha-1 antitrypsin deficiency is an inherited disorder which increases the risk of chronic obstructive pulmonary disorder (COPD) and chronic liver disease. It is characterised by low levels of alpha-1 antitrypsin. If low levels are detected then phenotyping studies should be done. There are a number of different phenotypes which are coded by the allele which has been inherited. The different phenotypes confer different risks of patients having lung or liver disease. Patients with liver disease are at risk of cirrhosis and hepatocellular carcinoma.  

Patients with suspected or confirmed alpha-1 antitrypsin deficiency should be discussed and or referred to a hepatologist for assessment.