Bilirubin is the end product of hemoglobin, which is broken down to produce free form bilirubin. Free bilirubin is insoluble in water and is carried to the liver by albumin in the blood. Free bilirubin is metabolized in hepatocytes to conjugated bilirubin, which is soluble in water and can be excreted from the bile. A slight increase in bilirubin can only be detected during a liver function test, while a significant increase will result in jaundice. To detect bilirubin, a reaction with a reagent is required. Conjugated bilirubin can react directly with bilirubin, which is called direct bilirubin; free bilirubin can only react indirectly with the reagent, which is called indirect bilirubin. These two types of bilirubin together are the total bilirubin in the laboratory test. In normal people, the destruction of aging red blood cells and the breakdown of hemoglobin produce a small amount of indirect bilirubin. Hemolytic disease produces large amounts of indirect bilirubin, which exceeds the ability of the liver cells to bind and metabolize it, and the indirect bilirubin in the blood rises, evident as hemolytic jaundice. Jaundice occurs after birth in infants because there is not enough oxygen in the womb and a very large number of red blood cells are needed to supply enough oxygen. After birth, not so many red blood cells are needed and the excess is dissolved, which is called physiological hemolytic jaundice. Indirect bilirubin is combined and metabolized in the liver cells into direct bilirubin, which is dissolved in water before it can be secreted into the bile. If bile is blocked by gallstones in the bile ducts, the bile will not be secreted properly and will flow back into the blood, raising the direct bilirubin in the blood, which is clearly called obstructive jaundice. The liver is the largest chemical plant in the body, and its function is to metabolize substances. It synthesizes many substances that are essential to the body and breaks down substances that the body does not need. Elevated serum aminotransferases indicate inflammation of the liver cells. In fact, aminotransferases do not reflect the function of the liver cells, but are only a sign of liver cell damage. Albumin and prothrombin can only be synthesized by hepatocytes, which is the true function of the liver. Excluding the causes of nutritional deficiencies, a decrease in albumin and coagulation factors both indicate a decrease in hepatocyte synthesis. The causes of elevated serum bilirubin in hepatitis are much more complex: they can reflect both hepatocyte destruction and inadequate hepatocyte catabolism. The inflammation and necrosis of hepatocytes increase bilirubin, and the transaminase also increases at the same time, which reflects the destruction of hepatocytes; if the transaminase is normal but bilirubin is elevated, it may not be due to the destruction of hepatocytes, but to the insufficient catabolism of hepatocytes. Therefore, elevated bilirubin can be both a sign of hepatocyte destruction and a real decrease in liver function. Elevated serum aminotransferases are a characteristic feature of hepatitis, and elevated aminotransferases mark inflammatory destruction of hepatocytes. When liver cells are damaged, of course, the uptake and binding of indirect bilirubin and the secretion of direct bilirubin will be affected, which means that the function of each link from indirect bilirubin uptake into liver cells, to direct bilirubin, and then to direct bilirubin excretion from liver cells will be reduced. When both indirect and direct bilirubin are elevated in the blood, if jaundice develops, it is called hepatocellular jaundice. Hepatocellular jaundice occurs during the active phase of hepatitis. After recovery from acute hepatitis or after treatment of chronic hepatitis, serum transaminases are normal, but indirect bilirubin is still abnormal in a number of patients. After a blow to the liver, some hepatocytes have just recovered from the injury, some hepatocytes are newly replenished, and the metabolic function is not completely normal, and indirect bilirubin cannot all combine into direct bilirubin, and this indirect elevation in the recovery period may last longer in chronic hepatitis. The above-mentioned changes are disease-related, but if none of them are, they are “constitutional”. Most of the constitutional bilirubin elevations are indirect bilirubin, which is mild and can be reduced by rest, but becomes more pronounced with exertion. There are many such cases, and Western Europeans account for 7% of the population, but there is no survey data in China, so it is not rare. Another rare condition is elevated direct bilirubin, which can lead to jaundice. The effect of other factors should also be considered: fasting before liver function tests, because diet may cause an increase in bilirubin and transaminases; drugs, alcohol, and exertion may cause an increase in bilirubin, all of which are transient and will be normal when the triggering factors are removed.