Congenital non-hemolytic jaundice (Gilbert’s syndrome), a comprehensive group of disorders, was first reported by the French physician Gilbert in 1092 as jaundice due to non-hemolytic, non-conjugated bilirubinemia. It is an autosomal dominant disorder that occurs in approximately 25% to 50% of families of congenital patients. Strictly speaking, it is characterized by non-hemolytic, non-conjugated hyperbilirubinemia with normal serum bile acids and normal liver function. The main manifestation is chronic intermittent jaundice from early childhood, which may be recessive; jaundice may persist into old age, but tends to gradually diminish with age. Serum bilirubin is less than 102.6 μmol/L, usually less than 51.3 μmol/L, with diurnal or seasonal fluctuations, and normal in about 1/3 of cases at routine examination. Jaundice can be triggered or aggravated by fatigue, mood swings, hunger, infection, fever, surgery, alcoholism, and pregnancy. The cause of jaundice is believed to be due to a genetic or acquired deficiency of bilirubin glucuronosyltransferase activity in the microsomal apparatus of hepatocytes, which affects the normal conduct of the binding reaction of unconjugated bilirubin in hepatocytes, so that the uptake of bilirubin by hepatocytes is also impaired, thus causing a double defect in the uptake and binding function of unconjugated bilirubin by hepatocytes. Complications Mild hemolytic anemia may occur. Treatment 1. Treatment No special treatment is usually required, but care should be taken to avoid triggers that lead to increased jaundice. 2. Prognosis Gilbert syndrome is a benign disease with a good prognosis.