1. Increased bilirubin synthesis: Hemolysis: If the liver is functioning normally, hemolysis generally causes only a mild increase in bilirubin (1-4 mg/dL) or briefly exceeds this limit. When the survival time of red blood cells is reduced by 50%, bilirubin can still be normal in most patients. This is also true for ineffective erythropoiesis or idiopathic transcellular dysplasia. Abnormal bilirubin uptake by the liver: The most common cause is pharmacological hepatitis viral hepatitis, and less common causes are congestive heart failure leading to stasis liver damage, portal venous shunt affecting liver blood flow, etc. Drugs, contrast agents such as: rifampicin, propofol, etc. Neonatal jaundice: physiological neonatal jaundice; jaundice may be slightly higher with breastfeeding than with formula. Pathological neonatal jaundice: Lucey-Driscoll syndrome (maternal serum jaundice) hemolysis, metabolic abnormalities or endocrine disorders (Metabolic/endocrine disorders); Galactosemia fructosemia (Galactosemia), hypoglycemia ( Fructosemia), hypoglycemia hypoproteinemia hypothyronemia, sepsis, hypoxia, pyloric loss hypertonic stenosis. 3. Bilirubin binding disorders: three congenital splicing disorders: Crigler-Najjar syndrome type I, type II and Gilbert syndrome. Gilbert syndrome, also called somatic hepatic dysfunction or familial nonhemolytic jaundice, is a relatively mild form of hereditary nonhemolytic hyperinfluential bilirubinemia. Crigler-Najjar type I: absence of hepatic bilirubin UGT activity; type II (also known as Arias syndrome): incomplete UGT enzyme activity. A small number of individuals can also have promoter variants in the UGT1A1 gene, and this variant results in reduced enzyme activity as the mechanism of Gilbert syndrome, where enzyme activity can be less than 30% of normal, more in males than females after puberty. Severity of the condition: Chronic excess indirect bilirubin in the blood may stimulate the stellate cells of the nervous system, leading to damage to the nucleus accumbens within the brain, such as areas affecting the basal ganglia, but most conditions are not so severe. Symptoms, such as poor erythropoiesis, are usually mild. Neonatal jaundice, such as breast milk jaundice and Lucey-Driscoll syndrome, persists for several weeks and subsides with a good prognosis. Among the disorders of bilirubin splicing, Crigler-Najjar syndrome type I, unless treated aggressively (liver transplantation), most die within the first 15 months of life, but fortunately, this type is rare. Gilbert’s syndrome is less severe and has a good prognosis.