LIVER FUNCTION TESTS GROUP TWO

[LFTs]
INTRODUCTION
Used to:
 Confirm clinical suspicion of potential liver injury or disease,
 Distinguish between hepatocellular injury (hepatic jaundice) and cholestasis (post-hepatic or
obstructive jaundice)

Include:
 Alanine transaminase (ALT)
 Aspartate aminotransferase (AST) Distinguish between hepatocellular
 Alkaline phosphatase (ALP) damage and cholestasis
 Gamma-glutamyl transferase (GGT)

 Bilirubin
 Albumin Assess the liver’s synthetic function
 Prothrombin Time (PT)
GROUP MEMBERS
1. Karuga Stanley- HB101/G/5491/18

2. David Mwangi- HB101/G/5489/18

3. Teresiah Mwangi- HB101/G/5488/18

4. Brian Gakobo- HB101/G/5486/18

5. Belinda Ngugi- HB101/G/5492/18

6. Leah Nd’ung’u- HB101/G/5490/18

7. Steven Ngatia- HB101/G/

8. Emma Njeri- HB101/G/

9. Mohammed Juma- HB101/G/

10. Enoch Osuri- HB101/G/

 LFT REFERENCE RANGES
TEST RANGE
ALT (Alanine transaminase) 3 – 40 iu/l

AST (Aspartate aminotransferase) 3 – 30 iu/l

ALP (Alkaline phosphatase) 30 – 100 umol/l

GGT (Gamma-glutamyl transferase) 8 – 60 u/l

BILIRUBIN 3 – 17 umol/l

ALBUMIN 35 – 50 g/l

PT (Prothrombin Time) 10 – 14 seconds

Alanine transaminase (ALT) and Alkaline
phosphatase (ALP)
Assess if ALT and/or ALP is raised and: Isolated rise of ALP (without rise in GGT)
 If ALT is >10-fold or <10-fold may be caused by:
 If ALP is >3-fold or < 3-fold  Bony metastases or primary bone tumours
 Vitamin D deficiency
Elevated ALT is a useful marker of  Recent bone fractures
hepatocellular injury.  Renal osteodytrophy
Elevated ALP is a useful indirect marker of
cholestasis.
If the patient is jaundiced but ALT and
>10-fold increase in ALT and < 3-fold ALP levels are normal, it may be due to:
increase in ALP suggests a predominantly  Gilbert’s syndrome: most common cause.
hepatocellular injury.  Haemolysis
<10-fold increase in ALT and > 3-fold
increase in ALP suggests cholestasis.
It is possible to have both.
Alanine Transaminase (AST)/Alkaline
Phosphatase (ALT) Ratio

The AST/ALT ratio can be used to determine the likely cause of

LFT derangement.

ALT > AST is associated with chronic liver disease

AST > ALT IS associated with cirrhosis and acute alcoholic

hepatitis
Gamma-glutamyl transferase
(GGT)
If there’s a rise in ALP, it is important to review the level of gamma-glutamyl
transferase (GGT).
A raised GGT can be suggestive of biliary epithelial damage and bile flow
obstruction.
It can also be raised in response to alcohol and drugs such as phenytoin.
A markedly raised ALP with a raised GGT is highly suggestive of cholestasis.
 BILIRUBIN
Hyperbilirubinaemia may not always Causes of unconjugated
cause clinically apparent jaundice (usually hyperbilirubinaemia include:
visible >60 umol/l). Haemolysis (e.g. haemolytic anaemia)
The combination of the colour of urine Impaired hepatic uptake (e.g. drugs,
and stools can give an indication as to the congestive cardiac failure)
cause of jaundice: Impaired conjugation (e.g. Gilbert’s
 Normal urine + normal stools = pre-hepatic cause
syndrome)
 Dark urine + normal stools = hepatic cause
 Dark urine + pale stools = post-hepatic cause Causes of conjugated
(obstructive) hyperbilirubinaemia include:
Hepatocellular injury
Cholestasis
ALBUMIN
Albumin levels can fall due to:
Liver disease resulting in a decreased production 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 protein-losing enteropathies or
nephrotic syndrome.
Prothrombin Time (PT)
Prothrombin Time (PT) is a measure of the blood’s coagulation
tendency, specifically assessing the extrinsic pathway.
In the absence of other secondary causes such as anticoagulant drug
use and vitamin K deficiency, an increased PT can indicate 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.
CAUSES OF LFT
DERANGEMENT
Common causes of acute hepatocellular injury include:
 Poisoning (e.g. paracetamol overdose)
 Infection (Hepatitis A and B)
 Liver ischaemia

Common causes of chronic hepatocellular injury include:

 Alcoholic fatty liver disease
 Non-alcoholic fatty liver disease
 Chronic infection (Hepatitis B or C)
 Primary biliary cirrhosis

Less common causes of chronic hepatocellular injury include:

 Alpha-1 antitrypsin deficiency
 Wilson’s disease
 Haemochromatosis
REFERENCES
1. RoxeDM. Urinalysis. In: Walker HK, Hall WD,
Hurst JW, editor. Clinical Methods: The History,
Physical, and Laboratory Examinations. 3rd edition.
Boston: Butterworths; 1990. Chapter 191.