Increased urinary bilirubinogen excretion is a symptom of shunt hyperbilirubinemia syndrome. The shunt hyperbilirubinemia syndrome is known as Israel syndrome. It is caused by excessive bilirubin production by bone marrow erythrocytes or precursors, or directly by the destruction and production of subtilisin or tetrapyrrole precursors. How can we check for increased urobilinogen excretion? It can occur in both sexes, with jaundice and splenomegaly between the ages of 10 and 20. Blood tests show increased spherical erythrocytes and erythrocyte fragility, moderate increase in reticulocytes, indirect hyperbilirubinemia, increased urinary bilirubin excretion, normal free lysis and mechanical fragility, and normal liver function. The diagnosis can be made on the basis of clinical features and laboratory tests, but definitive diagnosis requires liver tissue biopsy to exclude other types of congenital jaundice. In case of jaundice, serum total bilirubin and direct bilirubin should be checked to distinguish the type of bilirubin elevation, and urinary bilirubin, urobilinogen and liver function are also essential. Ancillary tests include routine blood, urine, jaundice index, quantitative serum bilirubin test; urine bilirubin, urobilinogen, and urobilin tests; serum enzymatic tests; blood cholesterol and cholesteryl ester measurements; immunological tests; X-ray tests; B-mode ultrasonography; radionuclide tests; liver biopsy; and laparoscopy. The detection of bilirubinogen group can reflect hepatocyte function sensitively, and clinical experience shows that bilirubinogen group in urine is significantly increased in the early stage of viral hepatitis before jaundice appears. In combination with bilirubin it can provide a basis for diagnosing the type of jaundice. Jaundice can be broadly divided into three categories: (1) prehepatic jaundice, or hemolytic jaundice, (2) hepatogenic jaundice, or hepatocellular jaundice, which is caused by a large number of lesions of hepatocytes or intrahepatic capillary bile ducts in cases of infection (such as viral hepatitis), poisoning and cirrhosis, resulting in impaired uptake, binding, transport and excretion of bilirubin by hepatocytes; (3) posthepatic jaundice, or obstructive jaundice, due to stones, tumors or congenital (3) post-hepatic jaundice, or obstructive jaundice, due to stones, tumors or congenital atresia of the bile duct. The diagnosis should be differentiated from increased urobilinogen: urobilinogen is converted from conjugated bilirubin. Conjugated bilirubin is unconjugated in the lower part of the small intestine and colon by the action of intestinal bacteria, and the bilirubin undergoes several stages of reduction to become urobilinogen, which is then excreted in the feces. Part of the urobilinogen is absorbed from the intestine into the portal vein, most of which is taken up by hepatocytes and then excreted into the intestinal fluid (enterohepatic circulation), and part of it enters the body circulation from the portal vein and is excreted from the urine via the kidneys. A variety of factors can cause an increase in urobilinogen. The diagnosis can be made on the basis of clinical features and laboratory tests, but a liver tissue biopsy is required to confirm the diagnosis to exclude other types of congenital jaundice.