Total bilirubin in the blood

Bilirubin is a bile pigment formed by the breakdown of heme proteins. Indirect bilirubin dissolves in fats and is transported by blood plasma in an albumin-bound condition. Its conjugation occurs in the liver with the formation of water-soluble bound bilirubin. Associated bilirubin is secreted through the biliary tract into the duodenum, where it undergoes metabolism, transforming into unbound bilirubin, colorless urobilinogen and then into orange-colored urobilins that are mostly excreted with feces.

The reference values (norm) of the concentration of total bilirubin in the serum are less than 0.2-1.0 mg / dL (less than 3.4-17.1 μmol / L).

Hyperbilirubinemia occurs as a result of hypersecretion of bilirubin, inhibition of re-uptake and conjugation of bilirubin in the liver, and a decrease in biliary excretion. The content of the total, mostly unbound, bilirubin in the blood plasma does not exceed 1.2 mg / dL (<20 μmol / l). Fractionation can determine the content of bound bilirubin (or direct, ie, determined directly). Separation into fractions is necessary only for jaundice of newborns or if there is an increase in the level of bilirubin with normal indices of other liver tests, which indicates a different cause of jaundice.

An increase in the level of unbound bilirubin (indirect bilirubin fraction greater than 85%) reflects an increase in the formation of bilirubin (for example, in hemolysis), disruption of reuptake or conjugation of bilirubin in the liver (eg, Gilbert's syndrome ). In this case, unbound bilirubin increases no more than 5 times [<6 mg / dl (<100 μmol / l)] in the absence of concomitant liver disease.

Associated hyperbilirubinemia (fraction of direct bilirubin> 50%) develops as a result of decreased formation or excretion of bile (cholestasis). Serum bilirubin is not sensitive to violations of liver function and does not differentiate cholestasis from hepatocellular lesions. At the same time, severe hyperbilirubinemia may be a harbinger of an unfavorable outcome in liver cirrhosis, primary biliary cirrhosis, alcoholic hepatitis, and acute hepatic insufficiency.

Unbound bilirubin can not be excreted in the urine, since it is insoluble in water and is bound to albumin. Thus, bilirubinuria usually indicates a high serum content of bound bilirubin and hepatobiliary pathology. Bilirubinemia can be determined using test strips (urinalysis) in acute viral hepatitis or other hepatobiliary disorders before jaundice appears. However, the diagnostic value of such a urine test is limited, as long-term storage of a portion of urine, intake of vitamin C from food or in the presence of nitrates in urine (for example, with urinary tract infection) may result in a false negative result. Similarly, the diagnostic value of increasing the level of urobilinogen is limited; these analyzes are neither specific nor sensitive.

The increase in serum bilirubin concentration above 17.1 μmol / l is called hyperbilirubinemia. This condition can be a consequence of the formation of bilirubin in amounts exceeding the ability of a normal liver to excrete it; liver damage that disrupts the excretion of bilirubin in normal amounts, and also due to blockage of the bile ducts, which prevents the excretion of bilirubin. In all these cases, bilirubin accumulates in the blood and when it reaches certain concentrations diffuses into the tissues, staining them in a yellow color. This condition is called jaundice. There are a slight form of jaundice (bilirubin concentration in blood up to 86 μmol / l), medium-heavy (87-159 μmol / l) and heavy (above 160 μmol / l).

Depending on what type of bilirubin is present in the blood serum - unconjugated (indirect) or conjugated (direct) - hyperbilirubinemia is classified as post-hepatitis (unconjugated) and regurgitant (conjugated), respectively. In clinical practice, the most widespread was the division of jaundice into hemolytic, parenchymal and obturation. Hemolytic and parenchymal jaundices are unconjugated, and obturation ones are conjugated hyperbilirubinemia. In some cases, jaundice can be mixed by pathogenesis. Thus, with prolonged disturbance of the outflow of bile (mechanical jaundice) as a result of secondary damage to the liver parenchyma, excretion of direct bilirubin into the bile capillaries can be disturbed, and it directly enters the blood; In addition, the ability of the hepatic cells to synthesize glucuronides of bilirubin decreases, as a result, the amount of indirect bilirubin also increases.

In clinical practice, the determination of serum bilirubin concentration is used to solve the following problems.

• Identification of increased bilirubin in the blood in cases when the patient does not see jaundice when examined, or if the presence of it causes doubt. Jaundice coloration of the skin appears when the content of bilirubin in the blood exceeds 30-35 μmol / l.
• Objective assessment of the degree of bilirubinemia.
• Differential diagnosis of various types of jaundice.
• Assessment of the course of the disease through repeated studies.

The content of bilirubin in the blood can be lowered with low hemolysis, which is observed in posthemorrhagic anemia and alimentary dystrophy. Reduction of the bilirubin content has no diagnostic value.