How to Read a Liver Function Test

Introduction

Liver function tests (LFTs) are among the most commonly ordered blood tests in both primary and secondary care. The ability to interpret 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 apply in most circumstances.

Why check LFTs?

LFTs are requested for two master reasons:

To confirm a clinical suspicion of potential liver injury or affliction.
To distinguish between hepatocellular injury (hepatic jaundice) and cholestasis (post-hepatic or obstructive jaundice).

What claret tests are used to assess liver function?

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'due south synthetic function.

You might also be interested in our OSCE Flashcard Drove which contains over 2000 flashcards that cover clinical examination, procedures, communication skills and data estimation.

Reference ranges

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

ALT	3-40 iu/l
AST	3-30 iu/50
ALP	30-100 umol/l
GGT	8-60 u/l
Bilirubin	3-17 umol/l
Albumin	35-50 g/l
PT	x-fourteen seconds

Assess ALT and ALP

Assess if ALT and/or ALP is raised:

If the ALT is raised, decide if this is a more than a 10-fold rising (↑↑) or less than a 10-fold rise (↑).
If the ALP is raised, make up one's mind if this is a more than a 3-fold rising (↑↑) or less than a 3-fold rise (↑).

Compare ALT and ALP levels

Key facts about ALT and ALP

ALT is institute in high concentrations within hepatocytes and enters the claret post-obit hepatocellular injury. It is, therefore, a useful mark of hepatocellular injury.

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

How practise we compare the rise in ALT and ALP?

A greater than x-fold increase in ALT and a less than iii-fold increase in ALP suggests a predominantly hepatocellular injury.
A less than 10-fold increment in ALT and a more 3-fold increase in ALP suggests cholestasis.
It is possible to have a mixed flick involving both hepatocellular injury and cholestasis.

What about Gamma-glutamyl transferase ?

If there is a rise in ALP, it important to review the level of gamma-glutamyl transferase (GGT). A raised GGT can exist suggestive of biliary epithelial damage and bile catamenia obstacle. Information technology can besides 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 metal phosphatase is also present in os and therefore annihilation that leads to increased bone breakdown can drag ALP.

Causes of an isolated rise in ALP include:

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

Hint:Compare to what caste 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 but 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'south syndrome: the most common cause.
Haemolysis: bank check a blood moving-picture show, full blood count, reticulocyte count, haptoglobin and LDH levels to ostend.

Assess hepatic function

The liver's main synthetic functions include:

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

Investigations that tin can be used to appraise constructed liver role 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 and then conjugated. Hyperbilirubinaemia may not always cause clinically apparent jaundice (usually visible >60 umol/50). The patient's symptoms and clinical signs can assist differentiate betwixt conjugated and unconjugated hyperbilirubinaemia. Unconjugated bilirubin is not water-soluble and, therefore, doesn't affect the colour of the patient'south urine. Conjugated bilirubin, however, can pass into the urine as urobilinogen, causing the urine to become darker. ¹

In a like mode, the colour of the stools tin 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 post-hepatic pathology), fat is non able to be captivated, resulting in stools appearing stake, bulky and more than difficult to flush.

The combination of the color of urine and stools tin give an indication as to the cause of jaundice:

Normal urine + normal stools = pre-hepatic cause
Night urine + normal stools = hepatic crusade
Dark urine + stake stools = post-hepatic cause (obstructive)

Causes of unconjugated hyperbilirubinaemia include:

Haemolysis (e.one thousand. haemolytic anaemia)
Impaired hepatic uptake (e.g. drugs, congestive cardiac failure)
Impaired conjugation (due east.g. Gilbert's syndrome)

Causes of conjugated hyperbilirubinaemia include:

Hepatocellular injury
Cholestasis

Albumin

Albumin is synthesised in the liver and helps to demark water, cations, fat acids and bilirubin. It also plays a key function in maintaining the oncotic pressure of claret.

Albumin levels can fall due to:

Liver illness resulting in a decreased product of albumin (e.yard. cirrhosis).
Inflammation triggering an acute stage response which temporarily decreases the liver'south product of albumin.
Excessive loss of albumin due to protein-losing enteropathies or nephrotic syndrome.

Prothrombin time

Prothrombin time (PT)is a measure of the blood's coagulation trend, specifically assessing the extrinsic pathway. In the absence of other secondary causes such equally anticoagulant drug use and vitamin M deficiency, an increased PT can betoken liver disease 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 be used to determine the likely crusade 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 not-carbohydrate carbon substrates. The liver plays a significant role in gluconeogenesis and, therefore, assessment of serum claret glucose can provide an indirect assessment of the liver's constructed office. Gluconeogenesis tends to be 1 of the last functions to get dumb in the context of liver failure.

Common patterns of LFT derangement

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

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

What to exercise next

Once the design 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

Common causes of chronic hepatocellular injury include:

Alcoholic fatty liver disease
Not-alcoholic fatty liver disease
Chronic infection (Hepatitis B or C)
Chief biliary cirrhosis

Less mutual causes of chronic hepatocellular injury include:

Blastoff-one antitrypsin deficiency
Wilson's disease
Haemochromatosis

The liver screen

A 'liver screen' is a batch of investigations focused on ruling underlying causes of liver illness 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-shine muscle antibiotic (ASMA)
Anti-liver/kidney microsomal antibodies (Anti-LKM)
Anti-nuclear antibiotic (ANA)
p-ANCA
Immunoglobulins – IgM/IgG
Alpha-1 Antitrypsin (to rule out alpha-1 antitrypsin deficiency)
Serum Copper (to rule out Wilson's disease)
Ceruloplasmin (to rule out Wilson's affliction)
Ferritin (to rule out haemochromatosis)

References

Roxe DM. Urinalysis. In: Walker HK, Hall WD, Hurst JW, editors. Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd edition. Boston: Butterworths; 1990. Chapter 191. Available from: [LINK].

sansonefamak1948.blogspot.com

Source: https://geekymedics.com/interpretation-of-liver-function-tests-lfts/