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Symptoms of jaundice
Last reviewed: 04.07.2025
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Suprahepatic jaundice. The main symptom of jaundice is an increase in the content of indirect bilirubin in the blood. This makes it easy to distinguish it from hepatic and subhepatic jaundice. Suprahepatic jaundice can be a consequence of:
- increased formation of bilirubin (hemolysis of red blood cells);
- disturbances in bilirubin transport (disruption of the process of binding to albumin);
- disturbances in the metabolism (conjugation) of bilirubin in hepatocytes.
During hemolysis of erythrocytes, a large amount of direct bilirubin is formed in the liver and enters the intestine. In the intestine, under the influence of microflora, bilirubin is restored to mesobilirubinogen, from which urobilinogen (urobilin) and stercobilinogen (stercobilin) are formed. Urobilinogen is excreted by the kidneys with urine, stercobilinogen - with feces.
Hepatic jaundice. Due to damage and necrosis of some hepatocytes, the concentration of total bilirubin in the blood serum increases mainly due to the direct bilirubin fraction. The resulting direct bilirubin partially enters the systemic circulation, which leads to jaundice. Bile excretion is also impaired, so less bilirubin enters the intestine than normal. The amount of urobilinogen formed decreases, the stool is less colored (hypocholic). Urine, on the contrary, has a more intense color due to the presence of not only urobilinogen, but also an excess of indirect bilirubin, which dissolves well in water and is excreted with urine. Hepatic jaundice is accompanied by hyperfermentemia and impaired synthetic function of the liver.
Subhepatic jaundice develops when bile secretion into the duodenum is impaired. It may be a consequence of a disease or caused by postoperative narrowing of the common bile duct. With this type of jaundice, hepatocytes produce conjugated bilirubin, but it does not enter the intestine as part of the bile. Since the normal pathways for bilirubin excretion are blocked, it is transported retrogradely into the blood. The concentration of direct bilirubin in the blood increases. Since bilirubin does not enter the intestine, its catabolism products are absent in the urine and feces. The feces become acholic, and the urine is colored orange-brown. The patient's condition is not significantly impaired, but in addition to the symptoms of the underlying disease, such symptoms of jaundice as skin itching may occur. As jaundice progresses, the activity of GGT, alkaline phosphatase, as well as the level of total cholesterol and conjugated bile acids, increase in the blood serum. Steatorrhea results in decreased body weight and impaired absorption of vitamins A, D, E, K and calcium.
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