Suprahepatic (hemolytic) jaundice

Suprahepatic jaundice is caused by excessive formation of bilirubin, exceeding the liver's ability to remove it. The liver is capable of metabolizing and excreting bilirubin into bile in quantities 3-4 times greater than its production under normal conditions. When the liver's ability to metabolize all bilirubin is exceeded, suprahepatic jaundice develops. In this case, despite the fact that the liver metabolizes more bilirubin than normal, all of its excess cannot be removed from the blood, and the level of free (unconjugated) bilirubin in the blood increases.

The main features of suprahepatic (hemolytic) jaundice:

• yellowness of the sclera and skin, as a rule, is moderate, has a lemon-yellow tint;
• at the same time there is paleness of the skin (due to anemia);
• there is no itching of the skin or scratching of the body;
• pain in the liver area occurs rarely, usually only with gallbladder calculus;
• liver enlargement is usually minor;
• significant enlargement of the spleen during the chronic course of the process;
• anemia of varying severity;
• pronounced reticulocytosis in the peripheral blood;
• decrease in osmotic stability of erythrocytes;
• liver function tests (blood levels of AST, ALT, alkaline phosphatase, prothrombin, cholesterol; thymol, sublimate tests) are normal;
• hyperbilirubinemia rarely exceeds 85.5 μmol/l, indirect (unbound, unconjugated) bilirubin predominates;
• the urine has a sharply increased urobilin content and no bilirubin;
• pleiochromia (sharp dark coloration) of feces is observed due to the large amount of stercobilin;
• With chronic hemolysis, calculosis of the bile ducts develops, which can manifest as biliary colic. Stones are detected on cholecystograms and during ultrasound examination of the bile ducts;
• puncture biopsy reveals secondary hemosiderosis of the liver;
• the life span of red blood cells is shortened (according to studies with 51Cr).

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