Medical expert of the article

Hematologist, oncohematologist

New publications

Indirect bilirubin in the blood

Alexey Kryvenko, medical expert
Last reviewed: 06.07.2025

All iLive content is medically reviewed or fact checked to ensure as much factual accuracy as possible.

We have strict sourcing guidelines and only link to reputable media sites, academic research institutions and, whenever possible, medically peer reviewed studies. Note that the numbers in parentheses ([1], [2], etc.) are clickable links to these studies.

If you feel that any of our content is inaccurate, out-of-date, or otherwise questionable, please select it and press Ctrl + Enter.

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

The study of indirect bilirubin plays a key role in the diagnosis of hemolytic anemia. Normally, 75% of the total bilirubin in the blood is indirect (free) bilirubin and 25% is direct (bound) bilirubin.

The content of indirect bilirubin increases in hemolytic anemia, pernicious anemia, neonatal jaundice, Gilbert's, Crigler-Najjar, and Rotor syndromes. The increase in the concentration of indirect bilirubin in hemolytic anemia is due to its intensive formation as a result of hemolysis of erythrocytes, and the liver is unable to form such a large amount of bilirubin glucuronides. In the above syndromes, conjugation of indirect bilirubin with glucuronic acid is impaired.

Pathogenetic classification of jaundice

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

Mainlyindirecthyperbilirubinemia

I. Excessive formation of bilirubin.
- A. Hemolysis (intra- and extravascular).
- B. Ineffective erythropoiesis.
II. Decreased uptake of bilirubin in the liver.
- A. Long-term fasting.
- B. Sepsis.
III. Impaired conjugation of bilirubin.
- A. Hereditary glucuronyl transferase deficiency
  - Gilbert's syndrome (mild glucuronyl transferase deficiency).
  - Crigler-Najjar syndrome type II (moderate glucuronyl transferase deficiency).
  - Crigler-Najjar syndrome type I (absence of glucuronyl transferase activity)
- B. Physiological jaundice of newborns (transient glucuronyl transferase deficiency; increased formation of indirect bilirubin).
- B. Acquired glucuronyl transferase deficiency.
  - Taking certain medications (eg, chloramphenicol).
  - Jaundice from breast milk (inhibition of glucuronyl transferase activity by pregnanediol and fatty acids contained in breast milk).
  - Damage to the liver parenchyma (hepatitis, cirrhosis).

Mainlystraighthyperbilirubinemia

I. Violation of the excretion of bilirubin into bile.
- A. Hereditary disorders.
  - Dubin-Johnson syndrome.
  - Rotor syndrome.
  - Benign recurrent intrahepatic cholestasis.
  - Cholestasis of pregnancy.
- B. Acquired disorders.
  - Damage to the liver parenchyma (for example, in viral or drug-induced hepatitis, liver cirrhosis).
  - Taking certain medications (oral contraceptives, androgens, chlorpromazine).
  - Alcoholic liver disease.
  - 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 bile ducts (strictures, atresia, bile duct cysts).
  - Helminthiasis (clonorchiasis and other liver trematodes, ascariasis).
  - Malignant neoplasms (cholangiocarcinoma, carcinoma of the ampulla of Vater).
  - Hemobilia (trauma, tumors).
  - Primary sclerosing cholangitis.
- B. Compression.
  - Malignant neoplasms (pancreatic cancer, lymphomas, lymphogranulomatosis, metastases to the lymph nodes of the liver porta).
  - Inflammation (pancreatitis).

trusted-source [ 1 ], [ 2 ], [ 3 ]