Bilirubin fractions (total, direct, indirtect)
Why this test?
- For differential diagnosis of conditions accompanied by yellowing of the skin and sclera.
- To assess the degree of hyperbilirubinemia.
- For the differential diagnosis of jaundice in newborns and to identify the risk of developing bilirubin encephalopathy.
- For the diagnosis of hemolytic anemia.
- To study the functional state of the liver.
- For the diagnosis of bile outflow disorders.
- To monitor the patient who takes drugs with hepatotoxic and / or hemolytic properties.
- For dynamic monitoring of patients with hemolytic anemia or liver pathology and biliary tract.
In what cases is it prescribed?
- With clinical signs of pathology of the liver and biliary tract (jaundice, darkening of the urine, discoloration of the stool, itching of the skin, heaviness and pain in the right hypochondrium).
- When examining newborns with severe and prolonged jaundice.
- If hemolytic anemia is suspected.
- When examining patients who regularly drink alcohol.
- When using drugs with possible hepatotoxic and/or hemolytic side effects.
- When infected with hepatitis viruses.
- In the presence of chronic liver diseases (cirrhosis, hepatitis, cholecystitis, gallstone disease).
- During a comprehensive preventive examination of the patient.
Bilirubin is a yellow pigment that is a component of bile and is formed in the spleen and bone marrow during the breakdown of erythrocytes. Normally, erythrocytes are destroyed 110-120 days after leaving the bone marrow.
At the same time, the metalloprotein hemoglobin is released from the dead cells, consisting of the iron-containing part - heme and the protein component - globin. Iron is cleaved from heme, which is reused as a necessary component of enzymes and other protein structures, and heme proteins are converted into bilirubin.
Indirect (unconjugated) bilirubin is delivered by blood to the liver with the help of albumins, where, thanks to the enzyme glucuronyltransferase, it combines with glucuronic acid and forms direct (conjugated) bilirubin.
The process of converting water-insoluble bilirubin into water-soluble is called conjugation. The associated pigment fraction practically does not enter the blood and is normally excreted with bile. Bilirubin in the intestinal lumen is metabolized by intestinal bacteria and excreted with feces, giving it a dark color.
Direct bilirubin is named so in connection with the method of laboratory research. This water-soluble pigment directly interacts with reagents (Ehrlich's diazo reagent) added to the blood sample. Unconjugated (indirect) bilirubin dissolves in water, and additional reagents are required for its determination.
Normally, the human body produces 250-350 mg of bilirubin per day. The production of more than 30-35 μmol / l is manifested by jaundice of the skin and sclera. According to the mechanism of development of jaundice and the predominance of bilirubin fractions in the blood, suprahepatic (hemolytic), hepatic (parenchymal) or subhepatic (mechanical, obturation) jaundice is distinguished. With increased destruction of erythrocytes (hemolysis) or impaired absorption of bile pigment by the liver, the content of bilirubin increases due to the unconjugated fraction without increasing the level of the associated pigment (suprahepatic jaundice).
This clinical situation is observed in some congenital conditions associated with a violation of bilirubin conjugation, for example, in Gilbert's syndrome. In the presence of an obstruction in the way of the exit of bile into the duodenum or violations of bile secretion, direct bilirubin in the blood increases, this is often a sign of obstructive (mechanical) jaundice.
When the biliary tract is obstructed, direct bilirubin enters the blood and then into the urine. It is the only fraction of bilirubin capable of being excreted by the kidneys and coloring urine in a dark color. An increase in bilirubin due to the direct and indirect fraction indicates a liver disease with a violation of the capture and release of bile pigments. An increase in indirect bilirubin is often observed in newborns in the first 3 days of life.
Physiological jaundice is associated with increased breakdown of erythrocytes from fetal hemoglobin and insufficient maturity of liver enzyme systems. With prolonged jaundice in newborns, it is necessary to exclude hemolytic disease and congenital pathology of the liver and biliary tract. When there is a conflict between the blood groups of the mother and the child, there is an increased breakdown of the baby's erythrocytes, which leads to an increase in indirect bilirubin.
Unconjugated bilirubin has a toxic effect on cells of the nervous system and can cause damage to the brain of a newborn. Hemolytic disease of newborns requires immediate treatment. Biliary atresia is found in 1 in 10,000 babies.
This pathology threatens the life of the child and is accompanied by an increase in bilirubin due to the direct fraction and requires urgent surgical intervention and in some cases liver transplantation. In newborns, there is also a possibility of hepatitis with an increase in both direct and indirect bilirubin. Changes in the level of bilirubin fractions in the blood, taking into account the clinical picture, make it possible to assess the possible causes of jaundice and determine the further tactics of examination and treatment.