Abstract Biluribin is a degradation product of haemoglobin that reaches the liver in its unconjugated form tightly bound to albumin and so is not excreted into urine. In the liver, it is taken up by active transport and conjugated within the hepatocytes to form bilirubin monoglucuronides and diglucuronides. These are water soluble, are excreted into bile and are further metabolized by gut bacteria into urobilinogen (partly reabsorbed into an enterohepatic circulation) and the various stercobilins that produce the brown pigmentation of stool. An understanding of bilirubin metabolism is central to the approach to jaundice. Jaundice is best subdivided into unconjugated and conjugated types. Routine chemical methods of differentiating unconjugated (indirect) bilirubin from conjugated (direct) bilirubin are unreliable; it is preferable to depend on the presence of bile in urine as evidence of conjugated jaundice. The disappearance of urobilinogen from urine in conjugated jaundice (e.g. extrahepatic obstruction) or its appearance in excess in unconjugated jaundice demonstrates the pathophysiology but is seldom of value in clinical practice. Dipsticks for urinary urobilinogen are unreliable. Jaundice becomes clinically apparent when plasma concentrations are 2–3 times normal. In unconjugated jaundice in adults, plasma bilirubin of more than 100 μmol/litre is uncommon (normal