Pigmentary exchange

The definition of violations pigmentary exchange, is a diagnostic interest from two points of view: the evaluation of the functional state of the liver cells and differentiation of different types of jaundice (liver, nadrecinoie and obstructive).
Research Talafant (1956) and Schmidt (1956) and work Billing, Lathe (1958) and Bollman (1959), who applied chromatographic method of research of bilirubin, revealed separate stages pigmentary exchange. The paper chromatography method defined in the blood 3 different forms of bilirubin: free bilirubin (not associated with glukuronova acid), bilirubinometry and bilirubinuria *. The terms "direct" and "indirect" bilirubin should be left as not reflecting the essence of the change process bilirubin. In the modern view, free bilirubin, formed in RES, connected with albumin and in the form of the albumin-bilirubin complex circulates in the blood and enters the liver. In coppersky cells of the complex falls apart, insoluble free bilirubin enter liver cells - hepatocytes. In hepatocytes with the participation transfertnykh systems, connection of bilirubin with glukuronova acid. The resulting water-soluble di - and monoglukuronida come from the cells of the liver in the bile capillaries. Increased bilirubinemia - jaundice - may be due to: 1) increase the formation of free bilirubin in reticuloendothelial (hemolytic or nadrechenskaya jaundice); 2) the obstruction of bile ducts (obstructive, mechanical jaundice); 3) lesion of liver cells with infringement of education bilirubinuria and highlight them in the lumen of the bile capillaries (hepatic jaundice); 4) congenital deficiency transferases system of liver cells with infringement of education bilirubinuria (congenital non-haemolytic jaundice).
In healthy individuals on chromatograms is only a fraction of free bilirubin. When parenchymal liver, along with the increased amount of free bilirubin, there are fractions of glukuronidov bilirubin. This indicates the presence of synthesis of glukuronidov in the liver and retrograde flow produced substances in the blood stream. Study 3. D. Shvartsman (1961) showed the existence of dependence between the degree of defeat of the liver parenchyma and change the content of separate fractions of bilirubin in the blood.
For hemolytic jaundice is characterized by increase of the total amount of bilirubin is basically free. Sometimes when hemolytic jaundice appears a small amount of bilirubin monoglukuronida that speaks about violation of the functions of the liver cells. Similar changes are in congenital non-haemolytic and some other types of jaundice associated with the violation education glukuronidov due to lack transfertnykh systems.
When mechanical jaundice chromatographic study finds increasing the number of all three factions bilirubin, but, unlike Botkin's disease, there is no typical for this disease recurrence in the appearance and disappearance of the faction di - and monoglukuronida. The emergence of these fractions for mechanical jaundice due to a violation of the outflow of bile in the ongoing synthesis of glukuronidov.
As a test, allowing to judge liver functions in the sphere of pigmentary exchange, along with the definition in the blood of the number of total bilirubin and its fractions, is the determination of bilirubin in the bile, urobilin in the urine and stercobilin in Calais.
In bile bilirubin is contained in the form of glukuronidov. The number in the duodenal contents varies widely in individual portions of bile, concentration decreases with increase of the amount of bile. The ratio of the number of mono - and diglucuronide in bile healthy persons is defined as 1 : 3. Chromatographic study of duodenal contents of patients with disease Hungary reveals a uniform reduction of both factions of bilirubin with preservation of their normal ratio; as the recovery increases the excretion and mono-, and diglucuronide (3. He Beskorovainy, 1964).
The next step changes bilirubin is education urobilinemia bodies, which are determined in the urine in the form of urobilinogen (Metoborudovanie), D-urobilinogen and L-urobilinogen (end product changes bilirubin). Urobilinogen fresh urine is rapidly oxidized in the relevant urobilin.
The question of the place and the mechanism of formation urobilinemia bodies of bilirubin there are currently two theories: classic intestinal and dualistic. According to the classical theory of transformation of bilirubinuria in metabolising and urobilinogen occurs in the colon under the influence of bacteria. A small amount is absorbed by the system of portal vein enters the liver and again excreted in the bile, and partially collapses. Not stimulate urobilinogen under the influence of microbes subject to further change and becomes a stercobilinogen. A small part of stercobilinogen absorbed in the upper sections of the colon and flows through the portal vein to the liver (and destroyed), of the distal colon stercobilinogen, sucking, goes on hemorrhoidal veins in the systemic circulation and excreted in the urine. The largest part of stercobilinogen excreted in the faeces, becoming stercobilin.
According to the dualistic theory Baumgartel the transformation of bilirubin in urobilinogen is happening in the intestines and bile ducts: the process of transformation begins in the lower sections of the biliary tract and gall bladder under the influence of cellular enzymes. Thus, in the small intestine and gets bilirubin and urobilinogen, last absorbed by the system of portal vein enters the liver, and there is disintegrating. Bilirubin under the influence of microflora of the large intestine becomes mutability, and then in the stercobilinogen. Most stercobilinogen excreted in faeces, a small - absorbed and hemorrhoidal veins enters the systemic circulation and excreted in the urine.
The definition urobilinemia bodies and stercobilinogen in the urine and feces is of great diagnostic value not only to detect lesions of the liver parenchyma, but also to clarify the nature of jaundice.
In the clinic are more common methods of determining the total number stercobilin, stercobilinogen, all forms of urobilinogen and urobilin. The term " urobilin" refers to substances contained in the urine, the term " stercobilin" - contained in Calais **.
With the defeat of the liver parenchyma one of the early symptoms of the disease is the increase in the number of urobilin in the urine.
When mechanical jaundice presence of a certain number of urobilin in urine if complete obstruction of the common bile duct is explained by the formation of his gall bladder and intrahepatic moves. This possibility is recognized in this situation and supporters of the classical theories that explain this fact by the appearance of microflora in the biliary tract stagnation of bile. After prolonged blockage of the bile ducts, urobilinemia may increase due developing damaging liver cells.
For differential diagnosis of the nature of jaundice public and valuable diagnostic method is the determination of the ratio of the number of urobilin in urine and stercobilin in Calais.
Normal daily allocation stercobilin with faeces varies between 100-300 mg, exceeding the number of urobilin in urine 10-30 times.
In hepatic jaundice due to the decrease excretion of bilirubin with bile number stercobilin in Cala decreased; at the same time increasing urobilinemia because of the violation of transformation urobilinemia bodies and stercobilinogen in hepatocytes. The ratio of the urobilin/stercobilin equal to the norm of 1 : 10-1 : 30 is changed to 1 : 5-1 : 1; the heavy defeat of the liver urobilinemia coefficient distorted, reaching up to 3 : 1, i.e. the daily allocation of urobilin with urine exceeds the number stercobilin in Calais.
Hemolytic jaundice due playography bile number stercobilin increases in some cases up to 10 000 mg of the ratio of the number of urobilin to stercobilin can reach up to 1 : 300-1 : 1000.
The definition urobilinogen coefficient is a valuable method in the diagnosis of hemolytic jaundice, but the characteristic changes of the coefficients are determined only during the onset of hemolytic crisis.

* Methodology see: 3. He Beskorovainy and 3. D. Schwarzmann. Proceedings of LSGE, so 79, 1964.
** Possible and separate definition factions urobilinemia bodies, see N. C. Mukhacheva - in the book: "Physical and chemical methods in experiment and clinic", Bitter, 1967.