Increased bilirubin due to the indirect fraction. Bilirubin tests detect severe liver disease. Impaired patency of the extrahepatic bile ducts

Bilirubin is a substance involved in pigment metabolism in the body. It is formed from the breakdown products of red blood cells. An increase in the level of bilirubin in the blood is called hyperbilirubinemia and occurs in certain types of diseases associated with liver dysfunction. Externally, in a patient, an increase in the content of this pigment is manifested by jaundice.

Where does bilirubin come from in the blood?

Erythrocytes and red blood cells live on average for about 4 months, after which they are destroyed in the organs of the reticuloendothelial system (mostly in the spleen, less in the liver and bone marrow). Approximately 1% of red blood cells undergo decay per day. During the decomposition process, hemoglobin is released, a protein pigment in the blood, which undergoes further breakdown to form verdoglobin. Protein is split off from it - globin and iron, resulting in biliverdin, which is reduced into bilirubin - an orange pigment, which enters the blood. The decomposition reactions of red blood cells release approximately 300 mg of bilirubin. Thus, about 85% of bilirubin appears in the blood, 15% is formed during the breakdown of other substances containing hemes (organic compounds in iron) - myoglobins, cytochromes.

Stages of bilirubin formation

After the breakdown of the red blood cell, bilirubin goes through the following stages of change:

At first it is in a free state (free bilirubin) and practically insoluble in water (hence the name - insoluble), forms a complex with proteins and circulates in the blood. Its second name - “indirect bilirubin”, because it is not capable of giving the so-called direct Van den Bergh reaction. This type of bilirubin is highly toxic to the body and cannot be excreted by the kidneys.
Indirect bilirubin is neutralized in liver cells by binding to glucuronic acid (conjugation) and forming a new form called bilirubin glucuronide. This type of bilirubin is already able to dissolve well ( soluble), does not have toxic properties and is able to be excreted with bile into the intestinal lumen. Gives a direct Van den Bergh reaction, which is why it is called "straight" bilirubin.
With bile (excretion), bilirubin enters the intestinal lumen, where it is reduced to stercobilinogen. Part of it is transformed into stercobelin and excreted in feces (from 50 to 300 mg). It is this pigment that colors stool dark. The main part of stercobilinogen is absorbed into the bloodstream and enters the kidneys, where it turns into urobilinogen, which changes into urobilin and is excreted in the urine, coloring it a specific straw color. The amount of urobilin excreted by the kidneys is approximately 4 mg per day.

Indirect bilirubin is constantly converted into direct form.

There are two types of bilirubin in the blood:

indirect (free, unconjugated, insoluble) – toxic. Appears immediately after the breakdown of red blood cells. Normally, its content does not exceed 17 µmol/l;
direct (bound, conjugated, soluble). It is formed in the liver after combining with glucuronic acid. It is no longer toxic and harmless to the body. Normally it contains up to 2.5 µmol/l;

Total bilirubin is also isolated. The normal level in the blood is about 20 µmol/l.

Various pathological conditions can cause an increase in the total bilirubin content - hyperbilirubinemia, which is accompanied by jaundice. Depending on the cause of the disease process, the increase in bilirubin occurs due to its direct or indirect fractions.

Important:in severe cases, bilirubin levels are several tens of times higher than normal, which indicates the need for immediate assistance to such patients.

The doctor talks about the problem of increased bilirubin in infants:

What are pigment metabolism disorders associated with?

Pigment metabolism may be disrupted for the following reasons:

the inability of the free fraction of bilirubin to enter the liver cells from the blood;
decreased transition (conjugation) of free bilirubin into bilirubin glucuronide;
decreased release of direct bilirubin from liver cells into bile.

Any type of metabolic disorder leads to an increase in bilirubin in the blood. Patients with this problem develop a icteric discoloration of the skin and sclera of the eye. At first, the face turns yellow, then the palms of the hands, soles and the rest of the skin surface. The intensity of jaundice may depend on the appearance of patients. In overweight people it is less noticeable, but in people of thin build it appears more clearly.

But you should not call any change in skin color jaundice, since there are different reasons for skin color change, for example, when eating foods high in carotene (carrots). Also, skin color may change due to diseases not related to problems of pigment metabolism (pathology of the thyroid and pancreas). A distinctive feature in this case is the normal color of the sclera.

Please note: bilirubin can accumulate in the nervous system and cause poisoning (intoxication). Also in this case, the balance of the ratio of direct and indirect bilirubin is disrupted.

What does “increased bilirubin” mean and what causes this condition?

What processes occur in the body, why does normal metabolism suddenly change?

High bilirubin occurs when:

Pathological processes leading to increased breakdown of red blood cells (hemolysis). Arises suprahepatic jaundice, or hemolytic. This type of disorder can be caused by different types of anemia (anemia), infectious diseases, toxic lesions, a group of hereditary jaundices (Dabin-Jones, Crigler-Nayar, Rotor), taking antibiotics, hormones, anti-inflammatory drugs.

The liver does not have time to “utilize” large amounts of indirect bilirubin and convert it into direct bilirubin. Excessive amounts of indirect bilirubin accumulate in the blood. The content of urobilin in urine and stercobilin in feces increases.

Infectious inflammation of the liver (hepatitis), cirrhotic processes causing damage to liver cells (hepatocytes). In these cases, it develops hepatocellular jaundice. In damaged liver cells, indirect bilirubin does not transform into direct bilirubin. Increased membrane permeability of hepatocytes promotes the release of indirect and direct bilirubin into the blood. Stercobilin in feces decreases, so the color of stool becomes light. Also, as a result of deficiency of the enzyme that converts indirect bilirubin into direct bilirubin, an increase in total bilirubin in the blood is observed due to the indirect fraction. The content of bilirubin and urobilin increases in the urine.

Congestion in the bile ducts, when normal outflow is disrupted due to blockage of the duct with stones, tumor, due to swelling due to inflammation. At the same time, the bile vessels swell, their permeability increases, and direct bilirubin goes directly into the blood, causing obstructive jaundice.
Insufficient intake of cyanocobalamin into the body(vitamin B12);

	Prehepatic jaundice	Hepatocellular jaundice	Obstructive jaundice
Total bilirubin	Normal / Increased	Increased	Increased
Unconjugated bilirubin	Increased	Normal / Increased	Norm
Conjugated bilirubin	Norm	Increased	Increased
Urobilinogen	Increased	Normal / Increased	Decreased / Negative
Urine color	Orange-yellow	Weakly colored	Dark (foamy, beer color)
Chair color	Dark	Bleached	Bleached
Alkaline phosphatase	Norm	Increased	Increased
ALT and AST	Norm	Increased	Norm

A detailed classification of jaundice is given in the video review:

Features of increased bilirubin in children

In childhood, jaundice appears more often. This is due to the fact that the baby has a large number of red blood cells. After childbirth, hemolysis occurs much faster than before childbirth. The neutralizing function of the liver is still imperfect. The child has high bilirubin with external manifestations of icteric skin color.

Children have some features of bilirubin metabolism. The occurrence of conjugation jaundice, caused by inadequate binding of the free fraction of bilirubin, leads to its accumulation in the blood. This condition occurs in 80% of newborns and is called physiological jaundice. It appears after 3 days from birth and lasts about 2 weeks. Jaundice gradually spreads to the face, torso, arms, legs, mucous membranes of the mouth, nasopharynx and conjunctiva of the eyes.

Bilirubin levels peak at the end of the first week and reach values from 140 µmol/L to 240 µmol/L. Jaundice occurs more often in babies born prematurely. Its duration in this case can last up to 4-5 weeks.

If from birth there is a deficiency of the glucuronyl transferase enzyme, then children develop a rare disease called congenital non-hemolytic hyperbilirubinemia with kernicterus. Bilirubin levels in the blood can reach 200-800 µmol/l. The normal level of bilirubin in a newborn is 51-60 µmol/l.

In some cases, there is a genetic link to glucuronyl transferase deficiency. The uptake of free bilirubin by liver cells is impaired. Indirect bilirubin remains at the level of 80-140 µmol/l.

In older children, bilirubin values increase when taking antibiotics, hormonal drugs, sulfonamide drugs, nonspecific infections that cause other diseases.

What to do to reduce bilirubin

In any case, if signs of icteric discoloration of the skin and sclera appear, you should immediately consult a doctor.

Important:You should not self-medicate and use drugs and traditional medicine until the cause of jaundice and increased bilirubin is established, especially in young children.

If infectious hepatitis or toxic liver damage is detected, hospitalization and treatment with detoxification solutions will be required.

The patient needs to create a sufficient drinking regime, use dietary nutrition, and limit physical activity.

Stepanenko Vladimir, surgeon

General information about the study

Bilirubin is a yellow pigment that is a component of bile and is formed in the spleen and bone marrow during the breakdown of red blood cells. Normally, red blood cells are destroyed 110-120 days after leaving the bone marrow. In this case, the metalloprotein hemoglobin is released from the dead cells, consisting of an iron-containing part - heme and a protein component - globin. Iron is cleaved from heme, which is reused as a necessary component of enzymes and other protein structures, and heme proteins are converted into bilirubin. Indirect (unconjugated) bilirubin is transported by blood to the liver with the help of albumins, where, thanks to the enzyme glucuronyltransferase, it combines with glucuronic acid and forms direct (conjugated) bilirubin. The process of converting water-insoluble bilirubin into water-soluble bilirubin is called conjugation. The bound fraction of the pigment practically does not enter the blood and is normally excreted in the bile. Bilirubin in the intestinal lumen is metabolized by intestinal bacteria and excreted in feces, giving it a dark color.

Direct bilirubin is so named in connection with the laboratory test technique. This water-soluble pigment directly interacts with reagents (Ehrlich's diazoreagent) added to the blood sample. Unconjugated (indirect, free) bilirubin is insoluble in water, and additional reagents are required for its determination.

Normally, the human body produces 250-350 mg of bilirubin per day. Production of more than 30-35 µmol/l is manifested by yellowness of the skin and sclera. According to the mechanism of development of jaundice and the predominance of bilirubin fractions in the blood, suprahepatic (hemolytic), hepatic (parenchymal) or subhepatic (mechanical, obstructive) jaundice is distinguished.

With increased destruction of red blood cells (hemolysis) or impaired uptake of bile pigment by the liver, the bilirubin content increases due to the unconjugated fraction without increasing the level of bound pigment (prehepatic jaundice). This clinical situation is observed in some congenital conditions associated with impaired bilirubin conjugation, such as Gilbert's syndrome.

If there is an obstruction to the exit of bile into the duodenum or bile secretion disorders, direct bilirubin in the blood increases, which is often a sign of obstructive (obstructive) jaundice. With obstruction of the biliary tract, direct bilirubin enters the blood and then into the urine. It is the only fraction of bilirubin that can be excreted by the kidneys and color the urine dark.

An increase in bilirubin due to direct and indirect fractions indicates liver disease with impaired uptake and release of bile pigments.

An increase in indirect bilirubin is often observed in newborns in the first 3 days of life. Physiological jaundice is associated with increased breakdown of red blood cells with fetal hemoglobin and insufficient maturity of liver enzyme systems. With prolonged jaundice in newborns, it is necessary to exclude hemolytic disease and congenital pathology of the liver and biliary tract. When there is a conflict between the blood groups of mother and child, increased breakdown of the baby’s red blood cells occurs, which leads to an increase in indirect bilirubin. Unconjugated bilirubin has a toxic effect on cells of the nervous system and can lead to brain damage in the newborn. Hemolytic disease of the newborn requires immediate treatment.

Biliary atresia is detected in 1 in 10 thousand infants. This life-threatening pathology of the child is accompanied by an increase in bilirubin due to the direct fraction and requires urgent surgical intervention and, in some cases, liver transplantation. Newborns are also likely to have hepatitis with an increase in both direct and indirect bilirubin.

Changes in the level of bilirubin fractions in the blood, taking into account the clinical picture, make it possible to assess the possible causes of jaundice and determine further tactics of examination and treatment.

What is the research used for?

For differential diagnosis of conditions accompanied by jaundice of the skin and sclera.
To assess the degree of hyperbilirubinemia.
For the differential diagnosis of jaundice in newborns and to identify the risk of developing bilirubin encephalopathy.
For the diagnosis of hemolytic anemia.
To study the functional state of the liver.
To diagnose bile outflow disorders.
To monitor a patient taking drugs with hepatotoxic and/or hemolytic properties.
For dynamic monitoring of patients with hemolytic anemia or pathology of the liver and biliary tract.

Whenappointedanalysis?

With clinical signs of pathology of the liver and biliary tract (jaundice, darkening of urine, discoloration of stools, itching of the skin, heaviness and pain in the right hypochondrium).
When examining newborns with severe and prolonged jaundice.
If hemolytic anemia is suspected.
When examining patients who regularly drink alcohol.
When using medications with possible hepatotoxic and/or hemolytic side effects.
When infected with hepatitis viruses.
In the presence of chronic liver diseases (cirrhosis, hepatitis, cholecystitis, cholelithiasis).
During a comprehensive preventive examination of the patient.

To study total bilirubin and its fractions, the following are used:

1. Straight spectrophotometric methods are based on measuring the absorption of bilirubin at 440-460 nm, the source of error here is the interference of yellow non-bilirubin pigments;

2. Enzymatic methods are based on the oxidation of the pigment with the copper-containing enzyme bilirubin oxidase (EC 1.3.3.5.), with the formation of biliverdin and the disappearance of absorption at 460 nm. The methods of this group are accurate and have high specificity and sensitivity;

3. Colorimetric diazo methods, are based on the interaction of bilirubin with diazotized sulfanilic acid with the formation of azopigments. Under the influence of acid, the tetrapyrrole structure of bilirubin breaks down to form two dipyrroles, the carbon atoms of the methylene groups react directly with diazotized sulfonic acid (diazo mixture) to form pink-violet isomers of azodipyrrole with an absorption maximum at 530 nm. Bound bilirubin reacts quickly, unbound bilirubin reacts only after adding an accelerator (caffeine, methanol, urea, benzoate or sodium hydroxide, acetic acid and others). The latter releases bilirubin from the complex with proteins and thereby accelerates the azo coupling reaction. The resulting azo dye behaves as an acid-base indicator with several color transitions: in a strongly acidic environment it is colored violet, in a weakly alkaline and slightly acidic environment it is colored pink, in a strongly alkaline environment it is colored blue or green.

4. Electrochemical methods using platinum and mercury electrodes;

5. Chromatographic separation of individual bilirubin fractions;

6. Fluorometric methods, the property of free bilirubin after absorption at 430 nm to emit light with a length of 520 nm is used. They allow you to determine the concentration of unconjugated bilirubin and, after treatment with a detergent, total bilirubin. The main advantage of the method is the ability to use micro amounts of serum.

Unified The method for determining the amount of bilirubin in serum is the Jendraszik-Cleghorn-Grof method using the diazoreaction in an alkaline or slightly acidic environment in the presence of an accelerator.

Determination of the concentration of bilirubin and its fractions
in blood serum according to diazoreaction

Principle

Bilirubin reacts with diazotized sulfonic acid in the presence of caffeine to form colored azo pigments.

Normal values

Serum (diazoreaction)	Direct bilirubin
Adults			2.2‑5.1 µmol/l
	Total bilirubin
Children		Full term	Premature
	umbilical cord blood	< 34,2 мкмоль/л	< 34,2 мкмоль/л
	age up to 2 days	< 136,8 мкмоль/л	< 205,2 мкмоль/л
	age up to 5 days	< 205,2 мкмоль/л	< 273,6 мкмоль/л
	subsequently	3.4‑17.1 µmol/l
Adults			8.5‑20.5 µmol/l
Urine (diazoreaction on diagnostic strips or tablets)			absence of bilirubin
Amniotic fluid (oxidation method)		28 weeks	<1,28 мкмоль/л
		40 weeks	<0,43 мкмоль/л
Feces			absent
Bile	hepatic		513.1‑1026.2 µmol/l
	cystic		on average 2394.6 µmol/l

Influencing factors

Inflated results are caused by hemolysis, taking steroid drugs, erythromycin, phenobarbital, and eating foods containing carotenoids (carrots, apricots). Prolonged exposure of serum to light causes oxidation of bilirubin and underestimates the values.

Clinical and diagnostic value

Serum

The accumulation of bilirubin in the blood above 43 µmol/l leads to its binding by elastic fibers of the skin and conjunctiva, which manifests itself in the form of jaundice. For the differential diagnosis of jaundice, it is necessary to determine which fraction causes bilirubinemia:

1. Hemolytic or suprahepatic jaundice - accelerated formation of bilirubin as a result of intravascular hemolysis. These are hemolytic anemias of various origins: sulfonamide poisoning, thalassemia, sepsis, radiation sickness, blood incompatibility, congenital spherocytosis, sickle cell anemia, glucose-6-phosphate dehydrogenase deficiency.

In this case hyperbilirubinemia develops at the expense of the faction indirect bilirubin. Hepatocytes intensively convert indirect bilirubin into a bound form, secrete it into bile, as a result, the content in feces increases stercobilin, coloring it intensely. The content in urine increases sharply urobilin, bilirubin is absent.

In newborns, hemolytic jaundice may develop as a symptom of hemolytic disease of the newborn.

2. Parenchymatous(hepatocellular) jaundice - the cause may be a violation at all stages of the conversion of bilirubin in the liver: the extraction of bilirubin from the blood by liver cells, its conjugation and secretion into bile. It is observed in viral and other forms of hepatitis, cirrhosis and liver tumors, fatty degeneration, in case of poisoning with toxic hepatotropic substances, and in congenital pathologies.

Since all bilirubin conversion reactions are not sufficiently carried out in the liver, hyperbilirubinemia develops due to both factions, predominantly direct bilirubin fractions. Quantity indirect bilirubin increases due to functional failure of hepatocytes and/or a decrease in their number, and direct- due to increased permeability of liver cell membranes, also due to impaired secretion into bile.

Determined in urine bilirubin(strong black tea color), moderately increased concentration urobilin, level stercobilin stool is normal or reduced.

In infants, the variants of parenchymal jaundice are jaundice of newborns and premature babies: physiological jaundice, jaundice caused by mother's milk, etc. Hereditary jaundice of hepatic origin are syndromes Gilbert-Meulengracht, Dubin-Johnson, Crigler-Nayyar.

3. Mechanical or subhepatic jaundice develops as a result of a violation of the outflow of bile due to blockage of the bile duct - gallstones, pancreatic neoplasms, helminthiasis. Also, subhepatic jaundice is detected with neoplasms of the pancreas and helminthiases.

As a result of bile stagnation, bile capillaries stretch, and the permeability of their walls increases. Having no outflow into bile direct bilirubin enters the blood and develops hyperbilirubinemia by increasing the concentration direct bilirubin. The level in urine is sharply increased bilirubin(dark beer color) and reduced amount of urobilin, practically absent in feces stercobilin(grayish-white color).

In severe cases, due to the overflow of hepatocytes with direct bilirubin, its conjugation with glucuronic acid may be disrupted and the amount of unconjugated bilirubin in the blood will increase, i.e. joins hepatocellular jaundice.

Urine

Extrahepatic bile duct obstruction is the classic cause of bilirubinuria. The indicator is useful in the differential diagnosis of jaundice, since bilirubinuria is characteristic of obstructive and parenchymal jaundice (an increase in the level of conjugated bilirubin in the serum), but is absent in hemolytic jaundice. With hepatitis, bilirubin can be detected in the urine before the appearance of jaundice.

Amniotic fluid

Bilirubin is found almost exclusively in non-esterified form in complex with albumin and accumulates in erythroblastosis, infectious hepatitis and sickle cell crisis in the mother.

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Bilirubin is a red-brown bile pigment. It is a product of hemoglobin catabolism, formed in the liver. Bilirubin tests are the best way to detect severe liver disease.

The price of a comprehensive analysis for bilirubin is 350 rubles. The price includes determination of fraction values: total bilirubin, direct bilirubin, indirect bilirubin. Taking venous blood - 170 rubles.

What is bilirubin, meaning

The bilirubin molecule consists of 4 pyrrole rings connected to each other. The molecular weight of the molecule is 548.68. Pure bilirubin is a sparingly soluble crystalline substance.

Being a breakdown product of red blood cells, bilirubin is toxic. Its indirect form is constantly formed in tissues and blood and is not excreted from the body. The liver processes the toxic substance and converts it into a direct form that is soluble in water. The direct form is excreted in feces or urine, turning them brown.

Of great importance in diagnosis is the study of the relationship between bilirubin levels in the blood, urine and feces. Even if a blood test shows total bilirubin is normal, but the absolute values and the ratio of pigment fractions have deviations, a differential diagnosis of the disease should be made.

The sum of the fractions can give an overall normal value of total bilirubin, but it often happens that primary bilirubin is elevated and conjugated bilirubin is below normal. This fractional ratio is observed in initial forms of liver enzyme deficiency and the threat of excessive accumulation of toxic indirect bilirubin in tissues.

Bilirubin norms by age

Type of bilirubin	Children: first 3 days after birth, µmol/l	Children: from 3 to 6 days of life, µmol/l	Children: over 1 month, µmol/l	Adults, µmol/l
General	24 - 190	28 - 210	3,5 - 20,4	8 - 20,5
Direct	0,5 - 10,2	1 - 12,4	0 - 5,1	0 - 5,1
Indirect	23,5 - 179,8	27 - 197,6	Up to 16.5	Up to 16.5

Blood test for bilirubin

The outcome of treatment for any disease largely depends on the accuracy of the diagnosis. Quite often, the doctor has to carry out differentiated diagnostics, analyzing the indicators of laboratory, instrumental and instrumental studies, since different diseases can have similar symptoms.

First of all, the doctor focuses on the universality of the characteristics of this complex test. Among the basic indicators, one of the most important is the content of bilirubin in the blood, which assesses the functioning of the liver, pancreas and gall bladder. The special significance of the “bilirubin” indicator and its relationship with other blood characteristics will be confirmed by any medical forum with numerous questions on this topic.

Increased bilirubin in the blood - what does it mean?

If the test results indicate an increase in bilirubin in the blood, this may indicate the presence of serious diseases and pathological conditions:

hereditary or caused by other diseases liver enzyme deficiency;
liver cirrhosis and hepatitis;
diseases of the biliary tract and gallbladder;
hemolytic anemia;
cancer or metastases to the liver from other organs;
vitamin deficiency B12;
injuries with multiple hematomas.

An exception is infant physiological jaundice, which occurs due to the restructuring of the newborn’s body after intrauterine development. In all other cases, it is necessary to determine the exact cause of high bilirubin levels.

It is not always possible to identify the true disease based on one indicator, so the doctor compares the values of different indicators, obtaining more detailed information about the pathological process.

How is bilirubin related to other blood parameters?

Bilirubin and hemoglobin. Hemoglobin and bilirubin are substances connected by a single chain of chemical reactions, which increases interest in comparing their values in blood tests and serves as additional information in diagnosing diseases. Hemoglobin breaks down during the process of red blood cell renewal into globin chains and heme, which is converted by enzymes into toxic indirect bilirubin.

Therefore, high levels of hemoglobin and bilirubin indicate hemolytic anemia or injuries with contusions and bruises with a large number of destroyed red blood cells. If low hemoglobin and high unconjugated bilirubin are observed, then the pathology may be associated with a lack of albumin, which is responsible for moving the yellow pigment to the liver.

Bilirubin and cholesterol. Increased cholesterol and bilirubin may indicate an incorrect dietary pattern, as a result of which the biliary system suffers, and fatty liver hepatosis is possible. As a rule, such a diagnosis is clarified after considering bile pigment fractions, other indicators from a detailed biochemical blood test, and ultrasound of the abdominal organs.

Urine tests for bilirubin: bilirubinuria

In healthy people, the urine of the bile pigment bilirubin may be contained in small quantities and is not determined by standard laboratory methods. That's whynormal bilirubin level in urineis the absence of bile pigment.

Increased bilirubin in urine

In various diseases, direct and indirect bilirubin fractions can be detected in urine samples. This condition is called bilirubinuria.

Indirect bilirubin appears if its content in the blood significantly exceeds the norm and at the same time the permeability of the glomerular membrane is increased. This occurs in the following diseases:

of various etiologies.
Ga nephropathy (Berger disease)
systemic lupus erythematosus;
Henoch-Schönlein purple
periarteritis nodosa;
hemolytic-uremic syndrome (HUS);
idiopathic thrombocytopenic purpura (ITP).

The cause of increased direct bilirubin in urine is jaundice. A positive reaction is already detected in cases where the bilirubin content in the blood is within 30– 34 µmol/l. This indicates a violation of the excretion of bile into the duodenum and an excess of bilirubin in the plasma in adults and children. If the general blood test for bilirubin is normal, there will be no this pigment in the urine.

The presence and absence of this bile pigment in urine in various forms of hepatitis is shown in the table:

Type of jaundice	Try
Normal (healthy person)	Negative
Hemolytic	Negative
Parenchymatous, at the onset of the disease	Weakly positive
Parenchymatous, at the height of the disease	Strongly positive
Parenchymatous, in the recovery stage	Weakly positive
Obstructive	Positive

How are tests done for bilirubinuria?

To determine bilirubin in urine, special tests are performed:

Gmelin's test (Rosenbach's modification) is carried out as follows: add 1-2 drops of acetic acid to 100–150 ml of urine and filter the solution several times through a paper filter. After this, the wet filter is left on the Petri dish to dry, after which a drop of a mixture of nitrous and nitric acids is applied to its surface. Increased bilirubin in the urine causes the paper to stain in the form of multi-colored concentric rings, including green, blue, purple, red on the outside and yellow in the center. Without the presence of a green ring, the sample is considered negative.

Rosin's test is carried out by adding a few drops of a 1% alcohol solution of iodine or Lugol's solution to 9–10 ml of urine taken for research. If there are bilirubin fractions in the sample, a persistent, noticeable green ring forms at the liquid interface.

To determine the amount of direct bilirubin fraction, a screening test on standard strips is also used. The level of content of this pigment is determined after applying urine to it and assessing the resulting color using the attached scale.

Urine test for the presence This liver enzyme provides excellent capabilities:

for early detection of hepatitis and differential diagnosis of various types of jaundice;
to determine the effectiveness of treatment in the treatment of many liver diseases;
in the diagnosis of kidney pathologies accompanied by an increase in the permeability of the glomerular membrane;
for monitoring the presence of pigment in urine during pregnancy and for preventive examination of persons working with harmful substances;
as a quick test for liver condition in patients taking medications that can cause liver dysfunction.

Urine tests for bilirubin are very simple, but quite informative.

Stool test for bilirubin

The bile pigment, bilirubin, is normally found only in the stool of very young children who are breastfed. The presence of this pigment in the feces of infants gives the feces a greenish tint. This is an absolutely normal phenomenon and has nothing to do with high bilirubin in the blood of a newborn or newborn and with infantile jaundice, which is characterized by increased indirect bilirubin.

By the fourth month, microflora begins to appear in the baby’s intestines, partially metabolizing this pigment to stercobilinogen, and around nine months this substance is completely metabolized in the intestines to stercobilin and stercobilinogen.

Reasons for the presence of bilirubin fractions in stool

In older children, positive bilirubin should not be detected in the stool, although small amounts of this substance are sometimes observed in the feces during the first year of a child's life. This is due to the instability and underdevelopment of the children's intestinal microflora.
In adults in coprogram, bilirubin readings should be negative. Its presence, especially in combination with a decrease in the concentration of stercobilinogen, indicates the existing dysbiosis (overt or hidden) and the presence of pathogenic and microflora in the intestines.
Another reason for the appearance of this substance in feces is dyspepsia. In the event of gastrointestinal pathologies accompanied by frequent stool upset, the microflora is “washed out” and traces of bilirubin appear in the stool. This condition is observed in acute and chronic disorders of the gastrointestinal tract or conditions accompanied by impaired digestion of food. In such cases, in a biochemical blood test, the rate of bilirubin fractions is also increased.
This substance may appear in the results of coprograms in acute poisoning. In this case, the functioning of the gastrointestinal tract and liver is disrupted, due to which the content of bilirubin compounds in the body increases and the evacuation of intestinal contents is accelerated. As a result, a large amount of this pigment enters the intestinal lumen and it leaves the intestine too quickly, not having time to be metabolized into stercobilin and stercobilinogen, and is found in the feces. In this case, indirect bilirubin in the blood is often increased.

How is bilirubin in stool determined?

The content of bilirubin pigment in feces is determined using the Fouche reaction; for this, a reagent is made from 100 ml of distilled water, 25 g of trichloroacetic acid and 10 ml of a 10% ferric chloride solution. A piece of feces is ground with water in a ratio of 1:20 and the reagent is added drop by drop. If there are traces of bilirubin, the test sample turns blue.

The sublimate reaction can also detect the content of bilirubin in feces, but it is less sensitive. To do this, a small lump of feces is ground in a mortar with 3–4 ml of a solution of mercury bichloride (mercuric chloride) and left in a fume hood for a day. The color of stool indicates the presence of bilirubin. Normally, the biomaterial should turn pink or reddish, however, with a positive reaction, the color of the stool turns greenish.

If even a small amount of this pigment is detected in the feces of an adult, consultation with a gastroenterologist and an infectious disease specialist is necessary, especially if at the same time the total bilirubin indicator in the blood test is increased.

Bilirubin and acute and chronic liver failure (hepatargia)

Liver failure occurs with pronounced changes in the liver parenchyma (fibrous, dystrophic or necrotic). Depending on the speed of occurrence, acute and chronic forms are distinguished.

With hepatargia, the detoxification function of the liver sharply decreases, due to which endotoxins, which should have been eliminated, penetrate into the blood and cause poisoning of the body. In the blood, direct and total bilirubin increases to critical levels (260–350 µmol/l), which causes damage to the central nervous system. The mortality rate is 50–80%. Liver failure can be acute or chronic. The degree of danger is determined through tests for bilirubin.

Causes of hepatargia

The condition is often a consequence of the development of viral hepatitis and liver cirrhosis. In this case, the presence of slowly progressive hepatargia is characteristic. Hepatitis and cirrhosis can be asymptomatic for a long time, and the norm of direct bilirubin in the blood may not be exceeded for a long time;
Sometimes the reason is human infection with Epstein-Barr viruses, herpes, adenovirus, etc. When a woman is infected with cytomegalovirus, intrauterine infection of the fetus occurs and its death. In this case, total bilirubin is increased during pregnancy.
The most common cause of this condition is exposure to poisons and medications. In some cases, poisoning occurs due to the use of drugs in the wrong dosage, and sometimes it is a consequence of a failed suicide. In this case, the process develops acutely and is accompanied by nausea, vomiting, hemorrhagic syndrome, “hepatic” bad breath, neuropsychiatric disorders, and increased total bilirubin in the blood.
Very often this condition is associated with the presence of malignant tumors in the body. Both the main focus and metastasis to this organ can be observed in the liver. In cancer, symptoms increase gradually, accompanied by severe jaundice, nausea, vomiting and cachexia. At the beginning of the development of the tumor process, there may be a normal level of bilirubin - 7-18%, but gradually its concentration in the blood increases and it begins to exceed the norm by 10-15 times.
Another cause of liver failure is alcohol and drug abuse. In this case, the process can proceed either quickly or slowly, it all depends on the specific version of the “predilection”. However, over time, the increased bilirubin still exceeds the norm many times over.

Symptoms of hepatargia

With this pathology, they gradually increase; jaundice, edema, weight loss, fever, telangiectasia, and dull abdominal pain. “Liver signs” appear on the body: palmar erythema, hemorrhages, Chistovich’s stars, varicose veins of the abdomen in the form of a “jellyfish head”.

Later they are joined by: severe bad breath, neurosis, apathy, and unstable emotional state. Slurred speech, writing problems, finger tremors, and poor coordination may occur. A general blood test and biochemistry show significant deviations from the norm.

With further progression of failure, hepatic coma occurs. Its precursors are: drowsiness, lethargy, rigidity of skeletal muscles, confusion, muscle twitching, convulsions, uncontrolled urination. Very high levels of liver tests are observed in the blood. A general blood test for bilirubin can show up to 500 µmol/l. Patients fall into a coma and die.

In order not to become victims of this disease, you need to take care of your liver, monitor your health, periodically get tested, and if the biochemistry is “bad” and total bilirubin is increased, the reasons for this phenomenon need to be found out. You should not self-medicate, because only a doctor knows exactly what bilirubin and other blood parameters should be.

Physiological and pathological jaundice in newborns

Jaundice (jaundice) in newborns is associated with the breakdown of fertile hemoglobin in the first days of life. It can be physiological and pathological. With physiological jaundice, its manifestations go away on their own and the general condition of the newborn does not suffer. The concentration of total bilirubin is normal in children in this case; it increases only due to its unbound fraction. To determine the extent of the problem, children are tested for bilirubin.

Severe physiological jaundice

If the norm of free bilirubin is significantly exceeded, the general condition of the child may suffer. Such babies are lethargic, lethargic, suck poorly, they may develop a fever and vomit. However, the condition of the newborn should be judged not by these signs, but by the bilirubin level.

When total bilirubin in newborns exceeds the norm significantly, albumin produced by the children's liver cannot completely conjugate it and it penetrates the central nervous system through the blood-brain barrier. In this case, this pigment, which is, in fact, poison, has a toxic effect on the brain. As a result, the baby may subsequently develop paralysis, mental retardation, deafness and blindness.

Treatment of jaundice

In order to prevent such complications, in case of severe and protracted jaundice, it is necessary to carry out specific treatment.

Previously, children were infused with various solutions to normalize bilirubin levels, but this has now been abandoned. Now light therapy is carried out, during which the newborn’s skin is illuminated with a special installation. Under the influence of light, the pigment decomposes and is removed from the body. Such children are monitored by neonatologists until direct bilirubin returns to normal. Most often, it is possible to normalize bilirubin in 9 days or less.

A great way to overcome jaundice is to start breastfeeding your baby as early as possible, because colostrum helps to pass meconium and cleanse the newborn’s intestines.

It has been noted that this condition is more often observed in children born prematurely, with multiple pregnancies and difficult births. Children born to mothers suffering from chronic diseases such as diabetes are susceptible to jaundice. Contrary to popular belief, an increased bilirubin level in the mother during pregnancy and yellowing of the skin in the newborn baby are absolutely unrelated.

Bilirubin tests reveal pathological jaundice

This type of pathology in newborns manifests itself in the first days of life. Such a baby may have: acholic feces, dark urine, hemorrhages and bright yellowness of the skin and sclera. In contrast to physiological hyperbilirubinemia, when it occurs pathologically, the norm of direct bilirubin in the blood is noticeably exceeded. In this case, a comprehensive examination and treatment is necessary.

The causes of the phenomenon are most often known:

Incompatibility of the blood of mother and baby by group and Rh factor can cause hemolysis of red blood cells and icteric staining of the sclera of the newborn.
Sometimes a child becomes infected with the hepatitis virus or protozoa from the mother and develops an infection. In this case, specific therapy is carried out for mother and baby, since the rate of total bilirubin in a woman is also increased in this case due to infection.
Due to congenital abnormalities of the liver and biliary tract, obstructive jaundice may occur, characterized by an increase in direct bilirubin levels by 6 or more times. Only surgeons can help here.
There is a large group of hereditary hyperglobulinemias (Crigler-Najjar, Dabin-Johnson, Rotor syndromes), which are caused by genetic metabolic defects. In this case, you need to prepare for long-term diagnostics and lifelong maintenance therapy.

Only a doctor can accurately diagnose jaundice in newborns and find out its cause. The diagnosis can only be made based on test results.

Where to get tested for bilirubin in St. Petersburg, prices

You can take any tests in St. Petersburg, including bilirubin, in a modern one. You can also go here. We work seven days a week. Prices for tests are low, and a discount is provided for diagnosing infections.