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Liver (parenchymatous) jaundice
Last reviewed: 04.07.2025
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Hepatic jaundice is caused by damage to hepatocytes, bile capillaries, impaired capture, conjugation and excretion of bilirubin by liver cells, as well as its regurgitation (return to the blood). Currently, depending on the level at which the metabolism and transport of bilirubin are impaired, hepatic jaundice is divided into hepatocellular and posthepatocellular, and hepatocellular is additionally divided into premicrosomal, microsomal and postmicrosomal.
Premicrosomal jaundice is based on a violation of the uptake of bilirubin by the hepatocyte, difficult cleavage of it from albumin and a violation of the connection with cytoplasmic proteinases.
In the pathogenesis of microsomal jaundice, the leading role is played by a violation of the conjugation of bilirubin with glucuronic acid in the smooth cytoplasmic reticulum, as a result of which the level of free (indirect, unconjugated) bilirubin in the blood increases.
Postmicrosomal hepatocellular jaundice occurs most frequently. Its primary pathogenetic link is the disruption of the excretion of bound bilirubin into bile and its entry from the hepatocyte into the blood, as a result of which the fraction of bound (direct, conjugated) bilirubin increases in the blood. At the same time, the capture of bilirubin and its transport can be suppressed, therefore, a simultaneous increase in unconjugated bilirubin is possible.
Posthepatocellular hepatic jaundice is observed in intrahepatic cholestasis. Its primary pathogenetic link is the return of conjugated bilirubin into the blood from the intrahepatic bile ducts.
The main features of hepatic (parenchymatous) jaundice:
- jaundice has a reddish tint (rubinictenis);
- often (in chronic hepatitis and liver cirrhosis) there are minor liver signs (palmar erythema, gynecomastia, testicular atrophy, spider veins, carmine-red lips);
- skin itching and traces of scratching may be observed on the skin;
- signs of portal hypertension (ascites, “caput medusae”) in liver cirrhosis in its severe stage;
- enlarged liver;
- enlarged spleen (not always); there may be moderate anemia;
- there are no signs of hemolysis, the osmotic stability of erythrocytes is normal;
- the bilirubin content in the blood is increased, mainly due to conjugated (direct) bilirubin;
- cytolysis syndrome is expressed (the content of aminotransferases, organ-specific liver enzymes fructose-1-phosphate aldolase, arginase, ornithine carbamoyltransferase in the blood is sharply increased);
- bilirubin can be detected in urine at the height of jaundice, then it disappears;
- urobilin in urine is not detected at the height of jaundice, then it appears and disappears again;
- Liver biopsy and laparoscopy reveal signs of hepatitis or cirrhosis.
Features of posthepatocellular hepatic jaundice (intrahepatic cholestasis):
- severe jaundice;
- persistent itching of the skin;
- xanthelasmas and xanthomas are often present;
- characterized by high levels of biochemical markers of cholestasis in the blood: alkaline phosphatase, gamma-GTP, 5-nucleotidase, cholesterol, beta-lipoproteins, bile acids, copper;
- high degree of hyperbilirubinemia mainly due to direct (conjugated) bilirubin;
- absence of urobilin in urine;
- acholia feces;
- Bile stasis in the intrahepatic bile ducts according to puncture biopsy data.
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