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Tests in Liver Disease: Usefulness and Interpretation

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These are not tests of liver function but liver damage or cholestasis. Normal LFTs does not mean a normal liver. The three main causes of an acute and severe derangement of all liver enzymes are hepatic ischaemia, viruses or drugs/toxins

Test	Usefulness
Aspartate Aminotransferase (AST)	Elevation often indicates liver damage, especially in alcoholic liver disease. AST is less specific than ALT for liver injury and can be elevated in conditions affecting other organs, like muscle or heart.
Alanine Aminotransferase (ALT)	ALT is more specific to the liver than AST. Elevated levels suggest hepatocellular injury, such as viral hepatitis or non-alcoholic fatty liver disease.
Alkaline Phosphatase (ALP)	ALP elevation suggests cholestasis or bile duct obstruction. It can also be elevated in bone disease, so liver-specific isoenzymes or GGT may be used to confirm liver origin.
Gamma-Glutamyl Transferase (GGT)	GGT is often elevated in cholestasis and can confirm that elevated ALP is of hepatic origin. It is also sensitive to alcohol intake and can be elevated in alcoholic liver disease.
Bilirubin (Total and Direct)	Total bilirubin includes both direct (conjugated) and indirect (unconjugated) bilirubin. Elevated bilirubin causes jaundice and can indicate hepatocellular injury, cholestasis, or haemolysis. Direct bilirubin elevation suggests hepatobiliary disease.
Albumin	Albumin is a protein produced by the liver. Low levels can indicate chronic liver disease, especially cirrhosis, and can contribute to edema and ascites. However, albumin levels can also be low in other conditions, such as nephrotic syndrome.
Prothrombin Time (PT) and INR	These tests measure the time it takes for blood to clot and can be prolonged in liver disease due to impaired production of clotting factors. They are useful in assessing the severity of liver dysfunction and in monitoring anticoagulation therapy.
Platelet Count	Thrombocytopenia (low platelet count) can be a sign of portal hypertension and splenomegaly in cirrhosis. It can also result from bone marrow suppression in chronic liver disease.
Alpha-Fetoprotein (AFP)	AFP is a tumour marker that can be elevated in hepatocellular carcinoma (HCC) and is often used to monitor patients with chronic liver disease at risk of developing HCC.
Ammonia	Elevated ammonia levels can occur in hepatic encephalopathy, a serious complication of advanced liver disease, due to the liver's inability to detoxify ammonia from the blood.
Liver Biopsy	Histological examination of liver tissue can provide definitive information about the type and extent of liver disease, including staging of fibrosis in chronic liver diseases.
FibroScan (Transient Elastography)	A non-invasive test that measures liver stiffness to assess the degree of fibrosis and cirrhosis. It is useful in monitoring chronic liver diseases and avoiding the need for liver biopsy.
Imaging Studies (Ultrasound, CT, MRI)	Imaging is used to assess liver size, shape, and structure, detect masses, assess bile ducts, and identify complications such as ascites, portal hypertension, and hepatic vein thrombosis.

History

Medication and Recent antibiotics

All recent medication including herbal

Travel: where, town or countryside

Water sports, lakes, canoeing (leptospirosis)

Intravenous or recreational drug use (hepatitis B/C)

Alcohol: amount CAGE and any DTs

Sexual history and Blood transfusions prior to 1990 (HIV)

Associated symptoms, Fevers, rigors, vomiting, pale stools, dark urine, pruritis, weight loss, abdominal pain

Signs of underlying chronic liver disease or malignancy

Any sepsis, acute liver failure, Coagulopathy, encephalopathy, jaundice

Causes of Liver damage

Viral hepatitis B and C
Alcoholic liver disease
Drug induced hepatotoxicity
Ischemia and liver congestion
Obstructive jaundice
NAFLD with T2DM (raised AST > ALT)

Prothrombin time (PT)

The liver produces clotting factors I,II,V,VII and X
Prognostic significance in Paracetamol overdose and liver failure
Prolonged PT may also be due to Vitamin K deficiency so give Vitamin K and any residual issue is impaired Liver function
Give oral or Vitamin K 5-10 mg slow IV
Raised PT seen with Warfarin therapy reversible with Vit K

Albumin

Produced at a rate of about 120 mg/kg/day
Production rate is reduced by cytokines as well as liver disease and cirrhosis
Low albumin leads to ascites and oedema
Low with non-liver causes - sepsis, malnutrition, nephrotic syndrome
Half-life is about 21 days

Urea

Low in liver disease perhaps due to impaired liver metabolism
High in an acute GI bleed /high GI protein load

Ammonia

May be high in acute Fulminant liver failure
Correlated with encephalopathy

Bilirubin

Breakdown product of Haem metabolism
Elevated conjugated Bilirubin identifies cholestasis - pancreatic carcinoma, gallstones, PBC
Elevated unconjugated Bilirubin suggests Haemolysis, Gilbert's syndrome

Alkaline Phosphatase (ALP)

Released by Bile canaliculi
This are markers of obstruction
Also produced by bone and placenta

Gamma Glutamyl transferase (GGT)

Microsomal enzyme and inducible by drugs and alcohol
Tends to rise in parallel with ALP
Hepatobiliary disease, Alcohol, Phenytoin, Barbiturates

AST and ALT

Transaminases - AST to ALT ratio is greater than 2:1 strongly suggests alcohol)
ALT is more liver specific
Normal - seen in end stage liver failure with massive loss of hepatocytes
Mildly elevated AST and ALT (<100 iu/L)
- Chronic Viral Hepatitis (B/C)
- Fatty liver disease
- Haemochromatosis, Cholelithiasis
Moderate elevated transaminases (100-300 iu/L)
- Above causes, Alcoholic hepatitis (AST >> ALT)
- Non-Alcoholic Steatohepatitis
- Autoimmune hepatitis, Wilson's disease
Major elevated (>300 iu/L)
- Drug toxicity, Paracetamol (Acetaminophen) overdose
- Acute viral hepatitis
- Autoimmune liver disease
- Ischaemic liver insult
- Toxins e.g. amanita phalloides
- Flare of Hepatitis B

Liver Disease	Abnormal test	Diagnostic test
Autoimmune hepatitis	Elevated AST and ALT	ANA anti-smooth muscle ab
Primary biliary cirrhosis	Elevated ALP	Antimitochondrial antibody
Alcoholic liver disease	AST/ALT >2	Improves with abstention
Primary sclerosing cholangitis	Raised ALP	MRCP pANCA
Haemochromatosis	Elevated AST and ALT	Ferritin, Genetic Analysis
Alpha-2 antitrypsin	Elevated AST and ALT	Phenotype analysis
Wilson's disease	Elevated AST and ALT	ALP low, Ceruloplasmin low, High urine copper, High liver copper
Hepatitis A	Elevated AST and ALT	Anti HAV IgM
Hepatitis B	Elevated AST and ALT	HbSAg, Anti HBc IgM, HbeAg, HBVDNA
Hepatitis C	Elevated AST and ALT	Anti HCV, HCV RNA

Investigations

Routine bloods including coagulation and glucose
Send a full non invasive liver screen
- Viral serology: HbSAg, hepatitis C antibody, hepatitis A IgM, herpes simplex virus, CMV, HIV. If hepatitis B virus serology is positive, send hepatitis D IgM
- Immunology: Check Anti-mitochondrial antibodies, anti-smooth muscle antibodies, anti-nuclear antibodies, Serum immunoglobulins
- Glucose, Cholesterol
- Metabolic and genetic
  - Caeruloplasmin, serum free copper levels if < 55 yo
  - Serum ferritin, transferrin saturation
  - A1 antitrypsin phenotype
  - Paracetamol and salicylate levels
  - Alpha fetoprotein - hepatocellular carcinoma
- Send ABG and consider arterial ammonia
- Contact your lab before sending. The sample will need to be sent on ice.
- Be vigilant for signs of sepsis.
- Blood cultures: consider low threshold for broad spectrum antibiotics, especially if there is evidence of evolving acute liver failure
- Have a low threshold for starting N-acetylcysteine and commence NAC if any suspicion of paracetamol overdose
- Request US abdomen: Liver echotexture, focal liver lesion, biliary obstruction, gallstones, portal vein patency
- If obstructive jaundice then MRCP or ERCP. ERCP is an invasive procedure. The patient will need to be fasted, and anticoagulants stopped. Check FBC and clotting screen the day before the procedure
Dilated bile ducts: consider ERCP or MRCP
Liver biopsy (can be via jugular if coagulopathy)

PLEASE NOTE LEGAL ADVICE: The contents are under continuing development and improvements and may contain errors of omission or fact. Feedback vital and always welcome at drokane at gmail.com. This is not to be used for the assessment, diagnosis or management of patients. It should not be regarded as medical advice. It is only for educational purposes. Please adhere to your local protocols. If you are unwell please seek healthcare advice from your doctor. This does not replace senior or specialist advice. If you do not accept this then please do not use the website. If you need medical advice, please consult a doctor or other appropriate medical professional. If you are a medical professional and you need advice then speak to your senior or colleagues.

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