Turnaround times
The quoted turnaround time is from sample receipt in the laboratory, to results authorisation in the Laboratory Information Management system. The times do not include transport of specimen to the laboratory or the administrative process to print and post/email reports. Service users must allow for transport and reporting time when ordering tests.
Clinical background:
Bilirubin is a product of the breakdown of haemoglobin. In plasma it is present in three forms:
• albumin-bound (reversibly: ‘unconjugated bilirubin’), normally the major component
• conjugated
• delta bilirubin (conjugated bilirubin covalently bound to albumin).
The excess bilirubin in hepatobiliary disorders is mainly conjugated however an increase in serum bilirubin concentration is not specific to hepatobiliary disease; it can occur in haemolytic conditions or conditions of ineffective erythropoiesis. The excess bilirubin in these instances is unconjugated. Delta bilirubin becomes present in significant quantities only in prolonged cholestasis
Specimen container paediatric:
Serum (SST or plain tube)
Specimen container adult:
Serum (SST or plain tube)
Minimum volume paediatric:
0.5 mL blood
Minimum volume adult:
1 mL blood
Sample stability:
Unseparated: day of collectionSeparated: day of collection at room temperature, 7 days at 4ºC, 6 months at -20C
Availability:
24/7, analysed at RVI and Freeman
Interpretation:
1. Increased production of bilirubin may exceed the ability of the liver to conjugate and excrete the pigment, causing an increase in the plasma
[unconjugated bilirubin]. However, the capacity of the liver to process bilirubin exceeds the normal rate of production, so that increased production does not necessarily cause hyperbilirubinaemia. Specific causes include:
• haemolysis (autoimmune, congenital and other haemolytic anaemias)
• ineffective erythropoesis
• rhabdomyolysis (because of increased breakdown of myoglobin).
2. Decreased hepatic uptake can be caused by several drugs, e.g. rifampicin. Although bilirubin uptake may be decreased in hepatocellular disease, the excess bilirubin in the plasma is primarily conjugated, reflecting decreased secretion into the biliary system.
3. The conjugation of bilirubin may also be impaired in hepatocellular disease, but any excess bilirubin in the plasma is primarily conjugated. Two inherited conditions of impaired bilirubin conjugation can cause unconjugated hyperbilirubinaemia.These are:-
• Gilbert’s syndrome (common and benign) typically causing only mild hyperbilirubinaemia (≤100 µmol/L) and sporadic jaundice, typically
in young adults
• Crigler-Najjar syndromes types I and II, causing severe hyperbilirubinaemia and typically presenting in infancy.
4. Impaired secretion of bilirubin into the biliary system can occur in hepatocellular diseases. It can also be caused by drugs, including chlorpromazine, carbamazepine and erythromycin. Impaired secretion bilirubin into the biliary system is a feature of two rare inherited disorders, Rotor syndrome and Dubin-Johnson syndrome.
5. Biliary obstruction can cause diffusion of conjugated bilirubin from the biliary system into the bloodstream. Such obstruction can be intrahepatic
(e.g. cirrhosis) or extrahepatic (e.g. sclerosing cholangitis, carcinoma of the head of the pancreas, causing obstruction through external pressure on the common bile duct.
Reference ranges:
Up to and including 14 days: 0 – 150 umol/L
Over 14 days: 0 – 21 umol/L
Other info:
lithium heparin plasma sample also acceptable