Liver function tests

Amylase

Rises with hours after onset of pancreatitis symptoms, peaks within 48 hours and normalises within 3-5 days
20% of patients with pancreatitis, mostly with alcohol and hypertriglyceridaemia-related disease, will have a normal amylase
Sensitivity of only 70%, PPV 15-72%
Low specificity
- Can be elevated in acute appendicitis, cholecystitis, intestinal obstruction or ischaemia, gynaecological disorders

Lipase

More specific
Remains elevated for longer after symptom onset
May be elevated in diabetics at baseline
May also be elevated in renal disease, appendicitis and cholecystitis, but is less associated with non-pancreatic disease than amylase
More sensitive in delayed presentation and alcohol or hypertriglyceridaemia-related cases
No evidence that adding amylase to lipase testing improves diagnostic accuracy over lipase alone
ALT >150 within first 48 hours of symptoms predicts gallstone pancreatitis with >85% PPV

Biliary colic

Lab tests usually normal
Leukocytosis in acute cholecystitis but absence does not exclude the diagnosis
- Leukocyte >10 has 63% sensitivity, 57% specificity, +LR 1.5 and -LR 0.6
- Mean WCC in cholecystitis is 12.6
Elevation of CRP is associated with acute cholecystitis but not specific
LFT’s often normal in acute cholecystitis
More likely elevated in choledocholithiasis or other cause of bile duct obstruction
GGT is the most sensitive and specific serum marker for choledocholithiasis
ALT or AST >1000 can occur in choledocholithiasis but are more suggestive of a hepatocellular necrotic process

LFT

Bilirubin

Increased total and indirect (unconjugated) bilirubin signifies overwhelming supply of unconjugated bilirubin e.g. haemolytic anaemia or an injury limiting hepatocyte capacity to conjugate a normal supply of unconjugated bilirubin e.g. acute or chronic viral hepatitis
Total and direct (conjugated) bilirubin is increased in obstruction e.g. obstructing gallstone, pancreatic mass or biliary atresia

Bilirubin

Transaminases

Released in hepatocyte injury
Elevation in the hundreds suggests mild injury or smoldering inflammation
Elevation in the thousands suggests extensive hepatocyte necrosis
Elevations <5x ULN suggest alcoholic liver disease or NASH
May be near normal in end-stage liver failure (burnt out)
AST = ALT suggests more acute or severe hepatitis as AST has significantly shorter half-life
Reduction in AST:ALT ratio <0.4 is often first sign of recovery
AST:ALT >2 suggests alcoholic hepatitis as alcohol stimulates AST production
Incidental elevations 3-5x ULN and ALP up to 2x ULN suggests NASH in diabetic or obese patients
ALT is more specific than AST
- AST also found in heart, smooth muscle, kidney and brain
- AST raised due to paracetaol, NSAID’s, ACEi, nicotinic acid, sulfonamides, erythromycin, griseofulvin and fluconazole

Transaminases

Mild <5x normal
Moderate 5-10x normal
Severe >10x normal
AST >200
- 90% sensitive and 95% specific for acute hepatic disease
ALT >300
- 95% sensitive and 95% specific for acute hepatic disease
>1000
- Toxins, ischaemia, viral hepatitis (A or E usually)
300-500
- Autoimmune, alcoholic, cholestasis
<300
- Fatty liver, haemochromatosis, Wilson’s, HCC, metastases, cirrhosis
Transaminase + ALP rise
- Often due to medication effect causing cholestasis or enzyme induction
  - Allopurinol, augmentin, captopril, carbamazepine, erythromycin, flucloxxacillin, oestrogens, phenytoin, bactrim

Gamma-GT

Production stimulated by alcohol consumption
Elevated by drugs inducing hepatic microsomal enzyme activity, including phenobarbital and warfarin
May rise in acute and chronic pancreatitis, acute MI, uraemia, COPD, RA and diabetes
In the setting of hepatitis, this suggests an alcoholic cause
Sensitive but not specific for hepatic disease
>10x ULN = 95% sensitive for obstructive liver disease

Alkaline phosphatase

Lactate dehydrogenase

Non-specific marker
Moderately elevated in all hepatocellular disorders and cirrhosis
Minimally elevated in purely cholestatic conditions
Haemolysis can cause raised LDH and unconjugated bilirubin
Also elevated by pulmonary disease (oedema, PE, PCP pneumonia), acute MI, muscle injury, heat stroke
Especially elevated in hepatic metastases, EBV and obstructive jaundice

Ammonia

Generated by hepatic metabolism of nitrogen-containing compounds
Very high levels indicate poor prognosis and overall toxicity in both acute and chronic liver failure

Prothrombin time

Prolonged in liver disease reflecting reduced synthesis of Vitamin-K dependent coagulation factors II, VII, IX, X, Protein C and Protein S
Occurs in cirrhosis, acute hepatitis and exacerbations of chronic liver disease
If present in acute viral hepatitis, signifies widespread hepatocellular necrosis
Correlated with clinical outcome in fulminant liver disease
Can occur from Vitamin K deficiency of other cause
- If deliver Vit K 10mg IM, a 30% reduction in prothrombin time suggests vitamin deficiency rather than hepatocellular failure

Albumin

May be reduced in advancing cirrhosis or severe acute hepatitis and suggests a poor short-term prognosis
Half-life of 3 weeks
Also low in malnutrition and in the chronically ill patient may not correlate with degree of hepatocellular dysfunction
Not as closely related to hepatocellular function as prothrombin time

Viral hepatitis

Alcohol abuse

Ischaemic/toxic injury

Acute viral hepatitis

Aminotransferases peak before bilirubin
ALT usually < AST
Causes greater rise in bilirubin than other hepatitic causes
- 5-10x normal
- Peaks after transaminases (1-2 weeks)
Jaundice occurs in >70% HepA, 33-50% HepB and 20-33% HepC

Drug-induced hepatitis

Last Updated on October 2, 2020 by Andrew Crofton

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