How to Read a Hepatic Function Panel

Introduction

Liver part tests (LFTs) are among the most commonly ordered blood tests in both primary and secondary intendance. The ability to translate LFTs is, therefore, an of import skill to develop. This guide provides a structured approach to the interpretation of LFTs which you should be able to utilize in well-nigh circumstances.

Why check LFTs?

LFTs are requested for ii primary reasons:

To ostend a clinical suspicion of potential liver injury or disease.
To distinguish between hepatocellular injury (hepatic jaundice) and cholestasis (mail-hepatic or obstructive jaundice).

What blood tests are used to assess liver part?

Alanine transaminase (ALT)
Aspartate aminotransferase (AST)
Alkaline phosphatase (ALP)
Gamma-glutamyltransferase (GGT)
Bilirubin
Albumin
Prothrombin time (PT)

Hint:ALT, AST, ALP and GGT are used to distinguish between hepatocellular damage and cholestasis. Bilirubin, albumin and PT are used to assess the liver'south synthetic function.

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Reference ranges

Beneath is a summary of the reference ranges for LFTs, however, these often vary between laboratories, then make certain to check your local guidelines.

ALT	3-xl iu/l
AST	3-30 iu/l
ALP	30-100 umol/fifty
GGT	8-sixty u/l
Bilirubin	3-17 umol/50
Albumin	35-l grand/l
PT	ten-fourteen seconds

Appraise ALT and ALP

Assess if ALT and/or ALP is raised:

If the ALT is raised, decide if this is a more than a ten-fold ascension (↑↑) or less than a ten-fold rising (↑).
If the ALP is raised, decide if this is a more than than a iii-fold ascension (↑↑) or less than a 3-fold rise (↑).

Compare ALT and ALP levels

Key facts about ALT and ALP

ALT is plant in loftier concentrations inside hepatocytes and enters the blood following hepatocellular injury. Information technology is, therefore, a useful marker of hepatocellular injury.

ALP is particularly concentrated in the liver, bile duct and os tissues. ALP is often raised in liver pathology due to increased synthesis in response to cholestasis. Equally a result, ALP is a useful indirect marker of cholestasis.

How do we compare the rising in ALT and ALP?

A greater than x-fold increment in ALT and a less than 3-fold increment in ALP suggests a predominantly hepatocellular injury.
A less than x-fold increment in ALT and a more than 3-fold increase in ALP suggests cholestasis.
It is possible to have a mixed picture involving both hepatocellular injury and cholestasis.

What almost Gamma-glutamyl transferase ?

If in that location is a rising in ALP, information technology important to review the level of gamma-glutamyl transferase (GGT). A raised GGT tin exist suggestive of biliary epithelial damage and bile menstruation obstacle. It can also exist raised in response to alcohol and drugs such as phenytoin. A markedly raised ALP with a raised GGT is highly suggestive of cholestasis.

Isolated rise of ALP

A raised ALP in the absence of a raised GGT should raise your suspicion of non-hepatobiliary pathology. Alkaline phosphatase is also present in bone and therefore anything that leads to increased bone breakup can elevate ALP.

Causes of an isolated rise in ALP include:

Bony metastases or primary os tumours (e.g. sarcoma)
Vitamin D deficiency
Contempo os fractures
Renal osteodystrophy

Hint:Compare to what degree the ALT and ALP are raised. If ALT is raised markedly compared to the ALP, this is primarily a hepatocellular pattern of injury. If ALP is raised markedly compared to ALT, this is primarily a cholestatic pattern of injury.

What if the patient is jaundiced simply ALT and ALP levels are normal?

An isolated rise in bilirubin is suggestive of a pre-hepatic cause of jaundice.

Causes of an isolated rise in bilirubin include:

Gilbert's syndrome: the most mutual crusade.
Haemolysis: check a claret film, full blood count, reticulocyte count, haptoglobin and LDH levels to confirm.

Assess hepatic part

The liver's main synthetic functions include:

Conjugation and elimination of bilirubin
Synthesis of albumin
Synthesis of clotting factors
Gluconeogenesis

Investigations that can be used to assess constructed liver function include:

Serum bilirubin
Serum albumin
Prothrombin time (PT)
Serum blood glucose

Bilirubin

Bilirubin is a breakdown product of haemoglobin. Unconjugated bilirubin is taken up by the liver then conjugated. Hyperbilirubinaemia may not always crusade clinically apparent jaundice (usually visible >60 umol/l). The patient'south symptoms and clinical signs tin can help differentiate between conjugated and unconjugated hyperbilirubinaemia. Unconjugated bilirubin is not water-soluble and, therefore, doesn't touch the color of the patient's urine. Conjugated bilirubin, however, tin laissez passer into the urine as urobilinogen, causing the urine to become darker. ¹

In a similar fashion, the colour of the stools can be used to differentiate the causes of jaundice. If bile and pancreatic lipases are unable to reach the bowel because of a blockage (e.g. in obstructive mail-hepatic pathology), fatty is not able to be absorbed, resulting in stools actualization stake, bulky and more difficult to flush.

The combination of the colour of urine and stools tin can give an indication as to the crusade of jaundice:

Normal urine + normal stools = pre-hepatic cause
Dark urine + normal stools = hepatic cause
Nighttime urine + pale stools = post-hepatic cause (obstructive)

Causes of unconjugated hyperbilirubinaemia include:

Haemolysis (eastward.g. haemolytic anaemia)
Impaired hepatic uptake (due east.g. drugs, congestive cardiac failure)
Impaired conjugation (east.g. Gilbert'due south syndrome)

Causes of conjugated hyperbilirubinaemia include:

Hepatocellular injury
Cholestasis

Albumin

Albumin is synthesised in the liver and helps to bind water, cations, fatty acids and bilirubin. Information technology likewise plays a key office in maintaining the oncotic pressure of blood.

Albumin levels can autumn due to:

Liver disease resulting in a decreased product of albumin (e.g. cirrhosis).
Inflammation triggering an acute phase response which temporarily decreases the liver's production of albumin.
Excessive loss of albumin due to poly peptide-losing enteropathies or nephrotic syndrome.

Prothrombin time

Prothrombin time (PT)is a measure of the claret'southward coagulation tendency, specifically assessing the extrinsic pathway. In the absence of other secondary causes such as anticoagulant drug use and vitamin M deficiency, an increased PT tin point liver illness and dysfunction. The liver is responsible for the synthesis of clotting factors, therefore hepatic pathology can impair this process resulting in increased prothrombin time.

AST/ALT ratio

The AST/ALT ratio can exist used to make up one's mind the likely cause of LFT derangement:

ALT > AST is associated with chronic liver disease
AST > ALT is associated with cirrhosis and acute alcoholic hepatitis

Gluconeogenesis

Gluconeogenesis is a metabolic pathway that results in the generation of glucose from certain non-carbohydrate carbon substrates. The liver plays a pregnant function in gluconeogenesis and, therefore, assessment of serum claret glucose can provide an indirect cess of the liver'southward synthetic role. Gluconeogenesis tends to be one of the last functions to go dumb in the context of liver failure.

Common patterns of LFT derangement

The table below demonstrates the typical LFT patterns associated with acute hepatocellular damage, chronic hepatocellular damage and cholestasis. A single arrow (↑) refers to a mild impairment and a double pointer (↑↑) refers to astringent harm.

	Astute hepatocellular damage	Chronic hepatocellular harm	Cholestasis
ALT	↑↑	Normal or ↑	Normal or ↑
ALP	Normal or ↑	Normal or ↑	↑↑
GGT	Normal or ↑	Normal or ↑	↑↑
Bilirubin	↑ or ↑↑	Normal or ↑	↑↑

What to do next

Once the pattern of LFT derangement has been established, information technology is crucial to determine the cause.

Common causes of astute hepatocellular injury include:

Poisoning (paracetamol overdose)
Infection (Hepatitis A and B)
Liver ischaemia

Mutual causes of chronic hepatocellular injury include:

Alcoholic fatty liver affliction
Non-alcoholic fatty liver illness
Chronic infection (Hepatitis B or C)
Principal biliary cirrhosis

Less common causes of chronic hepatocellular injury include:

Alpha-1 antitrypsin deficiency
Wilson's affliction
Haemochromatosis

The liver screen

A 'liver screen' is a batch of investigations focused on ruling underlying causes of liver disease in or out.

A typical liver screen includes:

LFTs
Coagulation screen
Hepatitis serology (A/B/C)
Epstein-Barr Virus (EBV)
Cytomegalovirus (CMV)
Anti-mitochondrial antibody (AMA)
Anti-polish muscle antibody (ASMA)
Anti-liver/kidney microsomal antibodies (Anti-LKM)
Anti-nuclear antibody (ANA)
p-ANCA
Immunoglobulins – IgM/IgG
Alpha-i Antitrypsin (to rule out blastoff-1 antitrypsin deficiency)
Serum Copper (to rule out Wilson's disease)
Ceruloplasmin (to rule out Wilson's disease)
Ferritin (to rule out haemochromatosis)

References

Roxe DM. Urinalysis. In: Walker HK, Hall WD, Hurst JW, editors. Clinical Methods: The History, Concrete, and Laboratory Examinations. tertiary edition. Boston: Butterworths; 1990. Chapter 191. Available from: [LINK].

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