Gilbert syndrome

Gilbert syndrome is a benign inherited condition in which the liver enzyme UGT1A1 — responsible for conjugating bilirubin so it can be excreted in bile — works at roughly 30% of normal capacity. The result is mildly elevated unconjugated (indirect) bilirubin in blood, especially during fasting, illness, dehydration, intense exercise or after alcohol. About 5–10% of the population have it, often discovered incidentally on routine lab work; many never have any symptoms. It is not a liver disease, requires no treatment, and does not progress to anything serious. Importantly, it changes the metabolism of certain drugs (especially irinotecan, indinavir, some statins) and is worth flagging to anesthesiologists and oncologists.

• Total bilirubin — typically 17–60 µmol/L (1–3.5 mg/dL); rarely above 5 mg/dL.
• Direct (conjugated) bilirubin — normal; the elevation is entirely in the indirect fraction.
• ALT, AST, GGT, alkaline phosphatase — all normal (this is the key distinction from real liver disease).
• Complete blood count, reticulocytes, haptoglobin, LDH — normal (excludes haemolysis as a cause of indirect bilirubin rise).

Most people have NO symptoms. When present:

• Mild yellowing of the whites of the eyes during illness, fasting, or stress
• Vague fatigue (often disputed — many studies find no difference vs general population)
• Mild abdominal discomfort