Indirect bilirubin in the blood

The reference values (norm) of the indirect bilirubin content in serum are 0.2-0.8 mg / dl or 3.4-13.7 μmol / l.

The study of indirect bilirubin plays a crucial role in the diagnosis of hemolytic anemia. Normally, in the blood, 75% of the total bilirubin falls on the proportion of indirect (free) bilirubin and 25% on the share of direct (bound) bilirubin.

The content of indirect bilirubin increases with hemolytic anemia, pernicious anemia, with jaundice of newborns, Gilbert syndrome, Kriegler-Nayar syndrome, Rotor. An increase in the concentration of indirect bilirubin in hemolytic anemia is due to its intensive formation due to hemolysis of red blood cells, and the liver is incapable of forming such a large amount of bilirubin glucuronides. With these syndromes, the conjugation of indirect bilirubin with glucuronic acid is disrupted.

Pathogenetic classification of jaundice

Below is a pathogenetic classification of jaundice, which makes it easy to establish the etiology of hyperbilirubinemia.

Advantageously indirect hyperbilirubinemia

• I. Excessive formation of bilirubin.
  • A. Hemolysis (intra- and extravascular).
  • B. Ineffective erythropoiesis.
• II. Decreased seizure of bilirubin in the liver.
  • A. Long-term fasting.
  • B. Sepsis.
• III. Violation of conjugation of bilirubin.
  • A. Hereditary insufficiency of glucuronyltransferase
    • Gilbert's syndrome (mild glucuronyltransferase insufficiency).
    • Syndrome Kriegler-Nayyar type II (moderate insufficiency of glucuronyl transferase).
    • The Krigler-Nayar type I syndrome (lack of glucuronyl transferase activity)
  • B. Physiological jaundice of newborns (transient insufficiency of glucuronyltransferase, increased production of indirect bilirubin).
  • B. Acquired glucuronyl transferase deficiency.
    • Acceptance of some drugs (eg, chloramphenicol).
    • Jaundice from mother's milk (oppression of glucan-ronyltransferase activity by pregnanediol and fatty acids contained in breast milk).
    • The defeat of the liver parenchyma (hepatitis, cirrhosis).

Mainly direct hyperbilirubinemia

• I. Violation of excretion of bilirubin in bile.
  • A. Hereditary disorders.
    • Dabin-Johnson syndrome.
    • Rotor Syndrome.
    • Benign, recurrent intrahepatic cholestasis.
    • Cholestasis of pregnant women.
  • B. Acquired violations.
    • The defeat of the liver parenchyma (for example, with viral or drug-induced hepatitis, liver cirrhosis).
    • Acceptance of some drugs (oral contraceptives, androgens, chlorpromazine).
    • Alcoholic liver damage.
    • Sepsis.
    • Postoperative period.
    • Parenteral nutrition.
    • Biliary cirrhosis of the liver (primary or secondary).
• II. Obstruction of extrahepatic bile ducts.
  • A. Obturation.
    • Choledocholithiasis.
    • Malformations of the development of the biliary tract (strictures, atresia, bile duct cysts).
    • Helminthiases (clonorchiasis and other hepatic trematodes, ascariasis).
    • Malignant neoplasms (cholangiocarcinoma, cancer of the fater nipple).
    • Hemobiology (trauma, tumors).
    • Primary sclerosing cholangitis.
  • B. Compression.
    • Malignant neoplasms (pancreatic cancer, lymphomas, lymphogranulomatosis, metastases to the lymph nodes of the liver gates).
    • Inflammation (pancreatitis).

[1], [2], [3]