Common bilirubin is the product of the decomposition of substances of hemoglobin and myoglobin, as well as, cytochromes. By itself, bilirubin is a yellow pigment, a hemochromic species. A cell of myoglobin and hemoglobin, together with cytochromes, decays in the cells of the liver and spleen, and also in the reticuloendothelial system. Bilirubin is the main component in bile. In the blood serum it is contained in the form of original fractions, which is a direct bilirubin, which can be bound and conjugated, and also, indirect bilirubin - free / disconnected. All these substances together form a common bilirubin. In laboratory diagnosis, usually determine the parameters of total and direct bilirubin, in particular. The difference that is formed between these indicators is the magnitude of indirect or free bilirubin. Decaying, hemoglobin begins the formation of free bilirubin. If we talk about bilirubin properties, we can say that in water this substance does not dissolve, lipophilic in its characteristics and can easily dissolve only in membrane lipids, penetrating the mitochondrial membranes, violating metabolic processes in them. Itself is quite toxic. Bilirubin is transported to the liver directly from the spleen together with albumin. Already in the liver, free-form bilirubin is combined with glucuronic acid. So, a direct, soluble in ordinary water, not such a toxic, other bilirubin is formed. It can be excreted in the bile ducts, and along with the bile, it is excreted.
When the level of bilirubin in human blood rises to a level of 27 to 34 μmol per liter, then jaundice can occur. With a mild jaundice, the level of bilirubin can reach 85 μmol per liter, with an average form of 86 to 169 μmol, but the severe form of jaundice in the analyzes is shown in the values from 170 μmol per liter. Increase the level of bilirubin in the blood can, with a reduced ability to metabolize and transport bilirubin to the bile due to hepatocytes. Here there are parenchymal jaundices, which are associated with infectious and toxic hepatitis.
Also, the level of bilirubin may increase due to mechanical difficulties in biliary excretion, which could manifest themselves due to tumor processes and the formation of cholestatic and obturation stones. It increases the level of bilirubin and mechanical jaundice, when the total bilirubin increases due to the direct and indirect type of bilirubin. A sharp jump in bilirubin may indicate hemolysis of erythrocytes, which is otherwise called hemolytic jaundice, when the total bilirubin can be increased only by bilirubin indirect.
If we talk about children, then newborns can be observed physiological jaundice, which can manifest itself in the first weeks of his life. Here, the increase in total bilirubin occurs in connection with the fractions of indirect bilirubin. At this stage the erythrocytes are rapidly destroyed, and the bilirubin-conjugating system is not completely perfect. Newborns can be ill with hemolytic diseases because their blood is incompatible with the blood of the mother according to Rh-accessory.
In practice, more significant meaning has become the division of jaundice into the following categories:
- Hemolytic jaundice
- Parenchymal jaundice
- Obstructive jaundice
Thus, the first two species are jaundices unconjugated, while the obturative type of jaundice is conjugated. Sometimes, jaundice is mixed in so-called pathogenesis. When the outflow of bile is disrupted, and this process continues for a long time due to secondary lesions of the liver parenchyma, excretion of bilirubin of a direct species into the bile capillaries can be significantly impaired. Then, it immediately enters the blood, reducing the ability of liver cells to carry out the synthesis of bilirubins and glucuronides, thereby increasing the amount of indirect bilirubin.
What causes the increase in bilirubin in the blood of adults and children?
The main reasons are the presence of the following factors:
- Intensification of the intensity of the hemolysis process
- Disturbances in the activity of the liver parenchyma, in particular, a violation of the function of bilirubin release
- Essential problems with the outflow of bile to the intestine from the bile ducts
- The loss of the so-called enzymatic link that provides the biosynthesis of bilirubin, in particular, its glucuronides
- Violation of activityhepatic secretion of a direct form of bilirubin directly into the blood
- An increased intensity of hemolysis can be observed during hemolytic anemia.
Hemolysis can increase with anemia with B12 deficiency, and also, with malaria and significant hemorrhages and pulmonary infarctions, with a crushing disorder. Because of the process of hemolysis, free bilirubin begins to form intensively in the reticuloendothelial cells from hemoglobin. At the same time, the liver begins to show an inability to form a necessary, significant number of bilirubin-glucuronides, which can grow into an accumulation of indirect bilirubin in tissues and blood. But even with sufficient hemolysis, the index of unconjugated hyperbilirubinemia remains insignificant, being less than 68.4 μmol per liter because of the ability of the liver to conjugate bilirubin. In addition, that the overall level of bilirubin increases, and the excretion of urobilinogen together with feces and urine may also increase, because it is formed in the intestine in significant quantities.
In newborns, physiological jaundice, a form of unconjugated hyperbilirubinemia, can often be found. Its causes are the overestimated rate of hemolysis of erythrocytes and the undeveloped liver function of the absorption and secretion of bilirubin, as well as its conjugation. When the blood saturation with bilirubin exceeds the saturation of the blood with albumin( from 34.2 to 42, 75 μmol per liter), it is quite capable of overcoming the blood-brain barrier. It can develop hyperbilirubinemic toxic encephalopathy. To cure this kind of jaundice, it is necessary to effectively stimulate bilirubin conjugation systems due to phenobarbital.
When there is parenchymal jaundice, then the destruction of the hepatocyte may occur, as well as impairment of excretion of bilirubin of a direct species into bile capillaries. So, he gets into the blood immediately. Here, its level begins to increase, and the ability of liver cells to synthesize bilirubin-glucuronides, on the contrary, decreases. Because of this, indirect bilirubin also increases. However, despite the fact that the concentration of bilirubin is increased, its entry into the urine is impossible.
All changes in the body must be treated with utmost care, because any deviation of the urine and blood values from the norm, can be a signal about possible processes in the body, both acute and inflammatory. Therefore, it is necessary to visit doctors often at any suspicion or bad health, and also, at least periodically, take tests to confirm that everything is in order in the body.