In the diagnosis of liver diseases, an important role is played by the determination of bilirubin metabolism. Normally, this pigment should be completely processed and neutralized by hepatocytes (liver cells). To identify metabolic disorders of this substance, doctors prescribe a blood test for bile pigments. This study can say a lot about the condition of the liver, and also allows you to determine the cause of jaundice. Next, we consider the features of normal bilirubin metabolism and liver pathophysiology.
What is bilirubin?
Bilirubin is a bile pigment. It has a yellow color. This is due to the fact that its molecules absorb light waves of the yellow spectrum. The color of bile is associated with the presence of this pigment in it.
Pure (indirect) bilirubin is a solid compound. It is poorly soluble in liquids and toxic to the body. Bilirubin metabolism normally occurs in the liver cells. There he neutralizes and becomes soluble. With impaired liver function, the metabolism of this pigment is disturbed, which leads to yellowing of the skin.
Bilirubin Exchange Scheme
Consider the features of normal bilirubin metabolism. This substance is formed from red blood cells. Cells of the reticular-epithelial system (macrophages) absorb old red blood cells, and then process them. Hemoglobin breaks down into heme and amino acids. They are affected by special compounds: hydrolases and oxidases.
Amino acids are quickly eliminated from the body. And heme is converted to pure (indirect) bilirubin. This pigment exits macrophages and binds to blood proteins. They deliver it to the liver, where the metabolic process begins. The exchange of bilirubin normally consists of several stages:
- Pure bilirubin enters the hepatocytes and enters into a binding reaction with glucuronic acid. The pigment becomes water soluble and loses its toxicity.
- Then one part of the bilirubin enters the bile, and the other into the bloodstream. The part of the bile pigment that circulates in the blood is called indirect bilirubin.
- Further it appears in the intestines. Here bilirubin is involved in the breakdown of fats. The pigment also reacts with pancreatic enzymes. Under their influence, bilirubin turns into urobilinogen. Part of this compound enters the liver with blood flow. There it is again metabolized. The other part is converted to urobilin and stercobilin. Urobilin is excreted by the kidneys and gives urine a yellow color. Sterkobilin leaves the body through the intestines. This is a pigment that stains feces in brown.
Normal bilirubin level
The exchange of bilirubin normally occurs quite quickly. In the liver, it is constantly being transformed from an indirect form to a direct one. As we have already mentioned, pure (indirect) bilirubin is formed immediately from red blood cells and enters the bloodstream to reach the liver. Its level in the blood should not exceed 17 μmol / l.
As for soluble (direct) bilirubin, the norms of analysis allow its content in the blood to be no more than 2.5 μmol / l.
Also, in a blood test for bile pigments, total bilirubin is determined. Its normal content should be about 20 μmol / L.
The exchange of bilirubin is normal and with pathology is very different. Various diseases lead to a deterioration in the metabolism of this substance and an increase in its content in the blood. This is called hyperbilirubinemia. This condition is always accompanied by staining of the skin yellow.
However, the yellowish color of the skin is not always associated with an increase in the level of bile pigments. This color of the epidermis can be caused by hypervitaminosis A, diseases of the thyroid or pancreas. However, with violations of pigment metabolism, not only the skin, but also the whites of the eyes turn yellow in color, which is a hallmark of such pathologies.
Possible causes of deviations
The following types of pathologies can adversely affect bilirubin metabolism:
- Hemolytic diseases. With such violations, a very rapid breakdown of red blood cells (hemolysis) occurs. As a result, an excessive amount of indirect bilirubin is formed, which the liver does not have time to process. Increased hemolysis is noted with anemia, infectious diseases, poisoning. Hereditary diseases can lead to accelerated decay of red blood cells: Rotor, Gilbert, Kriegler-Nayyar, Dabin-Jones syndrome, as well as hormonal and antibacterial drugs. The exchange of bilirubin in norm and in jaundices of hemolytic origin is sharply different. Therefore, the level of hepatic pigments in the blood can be many times higher than the reference values.
- Damage to liver cells due to hepatitis or cirrhosis. In this case, hepatocytes cannot fully process indirect bilirubin. The person has yellowing of the skin and sclera, feces acquire a light shade due to a deficiency of stercobilin. In the blood, the level of total bilirubin increases due to its indirect fraction.
- Stagnation of bile. Such a violation occurs when the bile duct is blocked with stones or tumors, as well as due to edema in inflammatory processes. Direct bilirubin seeps into the bloodstream. This pathology is called obstructive jaundice.
- Vitamin B12. Cyanocobalamin (vitamin B12) is necessary for the normal functioning of the hematopoiesis system. With its deficiency, anemia occurs, which is accompanied by the breakdown of red blood cells and an increase in the level of indirect bilirubin in the blood.
Features of pigment metabolism in children
Normally, the exchange of bilirubin in children is slightly different from the metabolism in an adult. In infants, the hepatic enzyme glucuronyl transferase is still weakly formed, therefore, an increase in bilirubin is noted in 80% of newborns. Such jaundice is called physiological. It is more commonly seen in premature babies. The level of bilirubin can reach 140-240 μmol / L. In the first days of life, this is not a pathology. Normally, the content of liver pigments normalizes during the first 2 weeks of life.
However, it should be remembered that jaundice in newborns can be associated with hereditary hemolytic diseases. In this case, the bilirubin level does not decrease and continues to remain high.
In older children, a high level of pigment is most often associated with infectious diseases, as well as with the use of hormones, antibiotics and sulfonamides.
How to reduce performance
If a person has increased bilirubin, then it is impossible to reduce it by folk methods. A sign of an increase in the content of liver pigments is the color of the skin and eye proteins in yellow. In this case, you should immediately consult a doctor, since it is impossible to cure hyperbilirubinemia at home.
The choice of treatment depends on the cause of the increase in bilirubin. If deviations in the analysis are associated with impaired liver function, then hospitalization of the patient is often required. With cirrhosis and hepatitis, the patient is given detoxification droppers, hepatoprotectors and a strict diet are prescribed. With obstructive jaundice, surgical treatment is indicated, since it is necessary to eliminate the cause of blockage of the bile ducts.
With a deficiency of vitamin B12, a course of injections of drugs with cyanocobalamin is carried out. Treating hemolytic jaundice is a challenge. Many diseases accompanied by increased hemolysis are hereditary and are not completely cured. Red blood cell transfusion is given to patients; in severe cases, an operation to remove the spleen is indicated.