Hepatic (parenchymal) jaundice

At the heart of hepatic jaundice is damage to hepatocytes, bile capillaries, disruption of 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 metabolic and transport disorders occur, biliary jaundice is divided into hepatocellular and post-hepatocellular, and hepatocellular additionally to premicrosomal, microsomal and postmicrosomal.

At the heart of premicrosomal jaundice is a violation of the seizure of bilirubin by hepatocyte, its difficult elimination from albumin and disruption of the connection with cytoplasmic proteinases.

In the pathogenesis of microsomal jaundice, the leading role is played by the disruption of conjugation of bilirubin with glucuronic acid in the smooth cytoplasmic network, as a result of which the level of free (indirect, unconjugated) bilirubin increases in the blood.

Postmicrosomal hepatocellular jaundice occurs most often. Its primary pathogenetic link is a violation of the excretion of bound bilirubin in bile and its entry from the hepatocyte into the blood, as a consequence of which the fraction of bound (direct, conjugated) bilirubin grows in the blood. In this case, the capture of bilirubin and its transport can be suppressed, so simultaneous increase of unconjugated bilirubin is possible.

Posthepatic cellulosic hepatic jaundice is observed with intrahepatic cholestasis. Its primary pathogenetic link is the return of bound bilirubin to the blood from the intrahepatic bile ducts.

The main features of hepatic (parenchymal) jaundice:

• jaundice has a reddish hue (rubinictenis);
• often (with chronic hepatitis and cirrhosis) there are small liver signs (palmar erythema, gynecomastia, testicular atrophy, vascular sprouts, carmine-red lips);
• itching can occur and there are traces of scratching on the skin;
• signs of portal hypertension (ascites, "caput medusae") with cirrhosis of the liver in its expressed stage;
• enlargement of the liver;
• enlarged spleen (not always); there may be mild anemia;
• there are no signs of hemolysis, osmotic resistance of erythrocytes is normal;
• the content of bilirubin in the blood is increased, mainly due to konyogirovannogo (direct) bilirubin;
• the cytolysis syndrome is marked (the blood content of aminotransferases, organ-specific liver enzymes of fructose-1-phosphatalldolase, arginase, ornithine carbamoyltransferase) is sharply increased;
• in the urine at the height of jaundice can be determined bilirubin, then it disappears;
• urobilin in urine at the height of jaundice is not determined, then appears and again disappears;
• puncture liver biopsy and laparoscopy reveal signs of hepatitis or cirrhosis of the liver.

Features of posthepatocellular hepatic jaundice (intrahepatic cholestasis):

• intense jaundice;
• persistent itching;
• often there are xanthomas;
• a high level in the blood of biochemical markers of cholestasis: alkaline phosphatase, gamma-GTP, 5-nucleotidase, cholesterol, beta-lipoproteins, bile acids, copper;
• high degree of hyperbilirubinemia mainly due to direct (konyogirovannogo) bilirubin;
• absence of urobilin in urine;
• Acholia of the feces;
• stasis of bile in the intrahepatic bile ducts according to the puncture biopsy.

[1], [2], [3], [4], [5], [6], [7], [8], [9]