Bilirubin is a bile pigment that is formed by the breakdown of erythrocytes. Under physiological conditions, 800 billion(!) blood cells are broken down every hour and the same amount is formed. The result is 2 components: haeme and globin. Haeme further transforms into indirect (unconjugated, indirect) bilirubin, binds to albumin and is transported to the liver. There it is conjugated ("straightened"). The bilirubin now becomes direct (conjugated, direct) bilirubin. Hence the following three laboratory values: Bilirubin direct + bilirubin indirect = bilirubin total.

Bilirubin gives color to physiological secretions : urine - yellow color, feces - dark brown (respectively, the more pigment - the more intense the color) If there is an increase in pigment over 30 nmol/l, the sclera of the eyes turns yellow, at 40 nmol/l - the skin turns yellow. This clinical picture is most often observed in hepatitis (inflammation of the liver).

Doctors need this analysis to determine the cause of yellowing of the skin and to monitor the dynamics of liver disease. Elevated indirect bilirubin occurs with excessive erythrocytoschisis (hemolytic anemia), as a huge amount of it is formed from dead blood cells. Skin color will be lemon (skin pallor due to anemia + yellowness due to bilirubin)

Increase in the direct fraction is observed in hepatitis and biliary engorgement - violates the outflow into the intestine and there is an abundant entry into the bloodstream. The feces are discolored, and the urine becomes the color of beer. There are innate diseases (Crigler-Najjar, Gilbert, Dubin-Johnson) in which the metabolism of bilirubin is disturbed.