What is Gilbert's syndrome: a disease or an individual feature? Gilbert's syndrome - what it is, causes and symptoms, diagnosis, treatment methods and prognosis Gilbert's syndrome, the latest developments, watch online.

A condition when a person himself or his relatives notice a yellow coloration of the skin or eyes (often this happens after a feast with the use of a variety of foods), with a more thorough study, it may turn out to be Gilbert's syndrome.

A doctor of any specialty can also suspect the presence of a pathology, if during the period of its exacerbation it was necessary either to take an analysis called "liver tests" or undergo an examination.

Definition of the term

Gilbert's syndrome (Gilbert's disease) is a chronic benign liver disease, accompanied by episodic icteric staining of the sclera and skin, and sometimes other symptoms associated with an increase in the concentration of bilirubin in the blood. The disease flows in waves: periods without pathological signs are replaced by exacerbations, which mainly appear after taking certain foods or alcohol. With the constant use of food “inappropriate” for liver enzymes, a chronic course of the disease may be noted.

This pathology is associated with a defect in the gene transmitted from the parents. It does not lead to severe destruction of the liver, as it happens with, but can be complicated by inflammation of the bile ducts or (see).

Some doctors consider Gilbert's syndrome not a disease, but an organismal genetic feature. This is not true: the enzyme, the violation of the synthesis of which underlies the pathology, is involved in the neutralization of various toxic substances. That is, if some function of the organ suffers, then the condition can be safely called a disease.

What happens in the body with this syndrome

Bilirubin, which causes the human skin and eye proteins to turn sunlight, is a substance formed from hemoglobin. After living for 120 days, a red blood cell, an erythrocyte, decomposes in the spleen, heme is released from it - an iron-containing non-protein compound, and globin - a protein. The latter, breaking up into components, is absorbed by the blood. Heme also forms fat-soluble indirect bilirubin.

With exacerbation, the skin has a more icteric color. It can turn yellow both the skin of the whole body and certain areas - feet, palms, nasolabial triangle, armpits.

Since it is a toxic substrate (mainly for the brain), the body tries to neutralize it as soon as possible. To do this, it is associated with the main blood protein - albumin, which transfers bilirubin (its indirect fraction) to the liver.

There, part of it is waiting for the enzyme UDP-glucuronyl transferase, which, by attaching glucuronate to it, makes it water-soluble and less toxic. Such bilirubin (it is already called direct, bound) is excreted with the contents of the intestine and urine.

Gilbert's syndrome is pathognomonic in violation of:

• penetration of indirect bilirubin into hepatocytes (liver cells);
• delivering it to those areas where UDP-glucuronyl transferase works;
• binding to glucuronate.

This means that in the blood with Gilbert's syndrome, the level of fat-soluble, indirect bilirubin increases. It easily penetrates into many cells (the membranes of all cells are represented by a double lipid layer). There he finds mitochondria, sneaks inside them (their shell also mostly consists of lipids) and temporarily disrupts the processes that are most important for cells: tissue respiration, oxidative phosphorylation, protein synthesis, and others.

While indirect bilirubin is increased within 60 μmol / l (at a rate of 1.70 - 8.51 μmol / l), mitochondria of peripheral tissues are affected. If its level is higher, the fat-soluble substance gets a chance to penetrate the brain and hit those of its structures that are responsible for performing various vital functions. important processes. The most life-threatening bilirubin impregnation of the centers responsible for respiration and heart function. Although the latter is not inherent in this syndrome (here bilirubin occasionally rises to high numbers), but when combined with a drug, viral or alcoholic lesion, such a picture is possible.

When the syndrome manifested quite recently, there are no changes in the liver yet. But when it has been observed in a person for a long time, a golden-brown pigment begins to be deposited in its cells. They themselves undergo protein degeneration, and the extracellular matrix begins to undergo scarring.

Disease statistics

Gilbert's syndrome is a fairly common pathology among the population of the whole world. It occurs in 2 - 10% of Europeans, every thirtieth Asian, while Africans get sick most often - the disease is recorded in every third.

The disease manifests itself at the age of 12 - 30, when a surge of sex hormones is noted in the body. Men get sick 5-7 times more often: this is due to the effect of male sex hormones on bilirubin metabolism.

Many have suffered famous people, which, however, did not prevent them from achieving success in life. Among them are Napoleon Bonaparte, tennis player Henry Austin, and possibly Mikhail Lermontov.

The reasons

The causes of the development of Gilbert's syndrome are genetic. It develops in people who have inherited a certain defect of the second chromosome from both parents: in the place that is responsible for the formation of one of the liver enzymes - uridine diphosphate-glucuronyl transferase (or bilirubin-UGT1A1) - two extra "bricks" appear. These are the nucleic acids thymine and adenine, which can be inserted one or more times. The severity of the course of the disease, the duration of its periods of exacerbation and well-being will depend on the number of "inserts".

As a result, the content of the enzyme is reduced to 80%, which is why its task - the conversion of indirect bilirubin, which is more toxic to the brain, into a bound fraction - is performed much worse.

This chromosomal defect often makes itself felt only starting from adolescence when the metabolism of bilirubin changes under the influence of sex hormones. Due to the active influence of androgens on this process, Gilbert's syndrome is recorded more often in the male population.

How is this gene passed on?

The transmission mechanism is called autosomal recessive. This means the following:

• there is no connection with the X and Y chromosomes, that is, an abnormal gene can manifest in a person of any gender;
• each person has a pair of each chromosome. If he has 2 defective second chromosomes, then the symptoms of Gilbert's syndrome will appear. When a healthy gene is located on the paired chromosome at the same locus, the pathology has no chance, but a person with such a gene anomaly becomes a carrier and can pass it on to his children.

The probability of manifestation of most diseases associated with a recessive genome is not very significant, because if there is a dominant allele on the second similar chromosome, a person will only become a carrier of the defect. This does not apply to Gilbert's syndrome: up to 45% of the population has a defective gene, so the chance of passing it on from both parents is quite high.

trigger factors

Usually, the syndrome does not develop from scratch, since 20-30% of UDP-glucouronyltransferase provides the body's needs under normal conditions. The first symptoms of Gilbert's disease appear after:

• alcohol abuse;
• taking anabolic drugs;
• severe physical activity;
• taking drugs containing paracetamol, aspirin; the use of antibiotics rifampicin or streptomycin;
• fasting;
• overwork and stress;
• dehydration;
• operations;
• treatment with drugs "Prednisolone", "Dexamethasone", "Diprospan" or others, based on glucocorticoid hormones;
• eating large amounts of food, especially fatty.

These same factors exacerbate the course of the disease and provoke its relapse.

Types of the syndrome

The disease is classified according to two criteria:

• The presence of additional destruction of red blood cells (hemolysis). If the disease proceeds with hemolysis, indirect bilirubin is initially elevated, even before the collision with the block in the form of a defect in the UDP-glucuronyltransferase enzyme.
• Relationship with viral hepatitis (Botkin's disease, hepatitis B, C). If a person who has two defective second chromosomes transfers acute hepatitis viral genesis, pathology manifests earlier, up to 13 years. Otherwise, it manifests itself in 12 - 30 years.

Symptoms

Mandatory for the exacerbation of Gilbert's syndrome symptoms are the following:

• periodically appearing and / or the whites of the eyes (the sclera turn yellow already at a smaller one). The skin of the whole body or a separate area may turn yellow (nasolabial triangle, palms, armpits or feet);
• fast fatiguability;
• decreased quality of sleep;
• loss of appetite;
• xanthelasma - yellow plaques in the eyelids.

You may also see:

• sweating;
• heartburn;
• heaviness in the hypochondrium on the right;
• nausea;
• flatulence;
• headache;
• muscle pain;
• diarrhea or, conversely, constipation;
• weakness;
• apathy or, conversely, irritability;
• dizziness;
• trembling of the limbs;
• compressive pain in the right hypochondrium;
• feeling that the stomach is "standing";
• sleep disturbance;
• disorders of the autonomic nervous system: cold sweat, with increased heart rate and nausea;

During the period of well-being, any signs are completely absent, and in a third of people they are not observed even during an exacerbation.

Exacerbations occur with varying frequency: from once every five years to five times a year - it all depends on the nature of the food taken, physical activity and lifestyle. Most often, relapses occur in spring and autumn, without treatment they last about 2 weeks.

In people with a chronic course of the disease, the character often changes. This is due to the discomfort they experience due to the fact that their eye or skin color is different from others. He also suffers from the need for constant examinations.

How to determine what a syndrome is

A doctor can assume that a person has Gilbert's syndrome and its symptoms already by the way the disease began, as well as by an increase in the level of total bilirubin in venous blood due to its indirect fraction - up to 85 µmol / l. At the same time, enzymes that indicate damage to the liver tissue - ALT and AST - are within the normal range. Others: albumin level, coagulogram parameters, alkaline phosphatase and gamma-glutamyl transferase - within the normal range:

It is important that with Gilbert's syndrome, all tests that are prescribed to determine the cause of jaundice will be negative. It:

• markers of viral hepatitis: A, B, C, E, F (it makes no sense to test for hepatitis D with unconfirmed hepatitis B);
• Epstein-Barr virus DNA;
• cytomegalovirus DNA;
• antinuclear antibodies and antibodies to liver microsomes are markers of autoimmune hepatitis.

The hemogram should not show a decrease in the level of erythrocytes and hemoglobin, the form should not prescribe "microcytosis", "anisocytosis" or "microspherocytosis" (this indicates hemolytic anemia, not Gilbert's syndrome). Anti-erythrocyte antibodies determined in the Coombs reaction should also not occur.

Other organs do not suffer either (as, for example, in severe hepatitis B), as can be seen from the indicators of urea, amylase, and creatinine. There is no change and electrolyte balance. Bromsulfalein test: the release of bilirubin is reduced by 1/5. Genome of hepatitis viruses (DNA and RNA) PCR method from the blood - a negative result.

The result of stool stercobilin is negative. Bile pigments are not found in the urine.

The syndrome can be indirectly confirmed by such functional tests:

• phenobarbital test: reception with this name for 5 days reduces the concentration of indirect bilirubin. Phenobarbital is selected at the rate of 3 mg / kg of body weight per day.
• fasting test: if a person eats 400 kcal / day for two days, after that his bilirubin increases by 50 - 100%;
• nicotinic acid test(the agent reduces the resistance of the erythrocyte membrane): if this drug is administered intravenously, the concentration of bilirubin in the unconjugated fraction will increase.

Genetic analysis

The diagnosis is confirmed by an analysis for Gilbert's syndrome. This is the name of the study of human DNA obtained either from venous blood or from buccal scrapings. When the disease is written: UGT1A1 (TA) 6 / (TA) 7 or UGT1A1 (TA) 7 / (TA) 7. If after the abbreviation "TA" (this means 2 nucleic acids - thymine and adenine) both times there is a figure 6 - this excludes Gilbert's syndrome, which leads a diagnostic search in the direction of other hereditary jaundices and hemolytic anemias. This analysis is quite expensive (about 5000 rubles).

After establishing the diagnosis, instrumental studies can be performed:

• : the size, condition of the working hepatic surface, cholecystitis, inflammation of the intra- and extrahepatic bile ducts, stones in the biliary organs are determined;
• Radioisotope study of liver tissue: Gilbert's disease is characterized by a violation of the excretory and absorbing functions;
• Liver biopsy: no evidence of inflammation, cirrhosis, or lipid deposition in the liver cells, but a decrease in UDP-glucuronyltransferase activity can be determined.
• Elastometry of the liver- Obtaining data on the structure of the liver by measuring its elasticity. Manufacturers of the Fibroscan device, on which the procedure is performed, say that the method is an alternative to a liver biopsy.

Treatment

The question of the need for therapy is decided by the doctor based on the condition of the person, the frequency of remissions, and the level of bilirubin.

Up to 60 µmol/l

Treatment of Gilbert's syndrome, if the unconjugated bilirubin fraction does not exceed 60 μmol / l, there are no signs such as drowsiness, behavioral changes, bleeding gums, nausea or vomiting, but only slight yellowness is noted, medication is not prescribed. Can only be applied:

• phototherapy: illumination of the skin with blue light, which helps water-insoluble indirect bilirubin to turn into water-soluble lumirubin and be excreted in the blood;
• diet therapy with the exclusion of the product provoking the disease, as well as the exclusion of fatty and fried foods;
• sorbents: intake of activated carbon, or another sorbent.

In addition, a person will need to avoid sunburn, and when going out in the sun, protect the skin with sunscreen.

Treatment if above 80 µmol/l

If indirect bilirubin is above 80 µmol / l, Phenobarbital is prescribed at a dose of 50-200 mg per day, for 2-3 weeks (it causes drowsiness, so driving and going to work during treatment are prohibited). Can be used drugs with phenobarbital, which have a less hypnotic effect: "Valocordin", "Barboval" and "Corvalol".

The drug "Zixorin" ("Flumecinol", "Synclit") is also recommended: it activates individual liver enzymes, including glucuronyl transferase. It does not cause such a hypnotic effect as phenobarbital, and after its withdrawal it is more quickly excreted from the body.

In addition, other drugs are prescribed:

• sorbents;
• proton pump inhibitors ("Omeprazole", "Rabeprazole"), which will not allow large amounts of hydrochloric acid to be produced;
• drugs that normalize intestinal motility: "Domperidone" ("Dormicum", "Motilium").

Diet for Gilbert's disease

The diet for the syndrome with hyperbilirubinemia more than 80 µmol / l is already more strict. Allowed:

• lean meats and fish;
• low-fat sour-milk drinks and cottage cheese;
• dried bread;
• biscuit cookies;
• non-acidic juices;
• fruit drinks;
• sweet teas;
• vegetables and fruits fresh, baked, boiled.

It is forbidden to eat fatty, spicy, canned and smoked foods, muffins and chocolate. You can also not drink alcohol, cocoa and.

Treatment in a hospital

If the level of bilirubin is high, or the person began to sleep worse, he is worried about nightmares, nausea, loss of appetite, and hospitalization is necessary. In the hospital, he will be helped to reduce bilirubinemia with the help of:

• intravenous administration polyionic solutions
• powerful
• monitor the correct intake of sorbents
• blocking the action of toxic substances arising from liver damage, lactulose preparations will also be prescribed: Normaze, or others.
• importantly, they will be able to carry out intravenous administration of albumin or blood transfusion.

In this case, the diet is extremely organic. Animal proteins (meat, offal, eggs, cottage cheese or fish) are removed from it, fresh vegetables, fruits and berries, fats are excluded. You can only eat cereals, soups without frying, baked apples, biscuit cookies, bananas and low-fat sour-milk products.

Remission period

In the period outside the exacerbation, you need to protect your biliary tract from stagnation of bile in them and the formation of stones. To do this, take choleretic herbs, preparations Gepabene, Ursofalk, Urocholum. Once every 2 weeks, "blind probing" is performed, when xylitol, sorbitol or Karlovy Vary salt are taken on an empty stomach, then they lie on their right side and warm the gallbladder area for half an hour.

The period of remission does not require patients to follow a strict diet, you just need to exclude foods that cause exacerbation (each person has a different set). The diet should have enough vegetables rich in fiber, necessarily - small amounts of meat and fish, less sweets, carbonated drinks and fast food. Alcohol is best avoided completely: even if you do not turn yellow after it, in combination with a fatty and heavy snack, it can lead to hepatitis.

The desire to keep bilirubin at normal levels with an unbalanced diet is also dangerous. It can lead a person to deceptive well-being: this pigment will decrease, but not due to improved liver function, but due to a decrease in the content of red blood cells, and anemia will lead to completely different complications.

Forecast

Gilbert's disease proceeds favorably, without causing an increase in mortality, even if indirect bilirubin in the blood is constantly elevated. Over the years, inflammation of the bile ducts develops, passing both inside the liver and outside it, cholelithiasis, which negatively affects the ability to work, but is not an indication for the issuance of disability.

If a couple has already had a child with Gilbert's syndrome, they should consult a medical geneticist before planning their next conception. The same must be done if one of the parents clearly suffers from this pathology.

If Gilbert's syndrome is combined with other syndromes in which bilirubin utilization is impaired (for example, with Dubin-Johnson or Crigler-Nayar syndrome), then the person's prognosis is quite serious.

A person suffering from this disease is more difficult to tolerate diseases of the liver and biliary tract, especially viral hepatitis.

Military service

Regarding Gilbert's syndrome and the army, the legislation indicates that a person is fit for service, but he should be assigned to such conditions where he will not need to work hard physically, starve or take products toxic to the liver (for example, headquarters). If the patient wants to devote himself to a professional military career, then this is not allowed for him.

Prevention

It is impossible to somehow prevent the appearance of a genetic disease, which is this syndrome. You can only delay the onset of the disease or make periods of exacerbation more rare if:

• eat healthy foods, including more plant-based foods in the diet;
• harden in order to be less sick with viral diseases;
• monitor the quality of food so as not to cause poisoning (with vomiting, the syndrome worsens)
• do not use heavy physical activity;
• less exposure to the sun;
• eliminate those factors that can lead to viral hepatitis (injecting drugs, unprotected sex, piercing / tattooing, and so on).

Vaccinations with Gilbert's syndrome are not contraindicated.

Thus, Gilbert's syndrome is a disease, although, in the vast majority of cases, it is not life-threatening, but it requires certain lifestyle restrictions. If you do not want to soon suffer from its complications, identify the factors that provoke an exacerbation and avoid them. Also discuss with a hepatologist or therapist all questions regarding the rules of nutrition, drinking regimen, medication or alternative treatment.

Reizis A.R.

Oksana Mikhailovna Drapkina,

In our section "Hepatology" Professor Reyzis Anna Romanovna. Gilbert's syndrome.

It usually raises a lot of questions.

"Gilbert's Syndrome. Contemporary Perspectives, Outcomes and Therapy.

Ara Romanovna Reyzis, professor, doctor of medical sciences:

Dear Colleagues.

There are diseases that run through the whole life of a person - from childhood and adolescence to the most advanced years. On this way, they come into the field of view of doctors of various specialties, a very wide range of doctors. It is important that this wide circle be aware of what is new in our understanding of this disease.

These diseases include Gilbert's syndrome (GS). More than a century has passed since Augustine Gilbert described this syndrome in 1901. During this time, a lot of new things have appeared in our ideas about this disease. It is in the aspect of this new that I would like to present this pathology today.

We remember what it is from our institute days. Gilbert's syndrome is a hereditary disorder of bilirubin metabolism, which consists in the insufficiency of its glucuronidation (mandatory for its entry into the biliary tract) and the development in connection with this benign unconjugated hyperbilirubinemia.

We also know the set of clinical and laboratory criteria that have always underpinned our diagnosis. It is known that it is detected mainly in adolescents in prepubertal and pubertal age. Most often in the family we have some data on hereditary family predisposition to this syndrome.

As a rule, the intensity of jaundice is small. Maximum - subicteric skin and icteric sclera. The appearance or intensification of jaundice is often associated with intercurrent diseases or with starvation, physical or psycho-emotional overstrain. And also with the use of a number of drugs. Especially the so-called aglucones, sulfamides, the salicylates group. We will talk about this a little further in more detail.

Most often, hepatomegaly is absent or insignificant. In laboratory tests, an increase in bilirubin by 2-5 (rarely more) times due to the predominantly free fraction. With normal activity of transaminases and the absence of markers of viral hepatitis and data for hemolytic anemia.

This set of clinical and laboratory data was enough for us to diagnose this syndrome.

Recently, the situation has changed in the sense that we have received the possibility of an objective genetic analysis that confirms or does not confirm this diagnosis.

The genetic face of SF has become known, which consists in the fact that a mutation occurs in the promoter region of the coding enzyme glucuronyl transferase. It consists in a dinucleotic insert tyrosine-arginine. This insertion is repeated a different number of times. Depending on this, we have either the classic variant of SF or its variations (alleles).

The possibility of objective confirmation of this diagnosis, its objective statement in many ways radically changed our understanding of this syndrome. Changed some of the myths that have been fairly persistent throughout the century that we are familiar with this syndrome.

The first is the prevalence of SA. It was believed that this is a fairly rare disease. With the help of a genetic diagnosis, it became clear that this is a fairly common disease. Between 7% and 10% of the world suffer from GS. This is every tenth. For a hereditary disease, this is an extraordinary frequency.

In the African population up to 36%. In our population (European and Asian) 2-5%. In our country and in our population, this diagnosis is becoming more frequent.

(Slide show).

Data from our clinic, where we encounter SF as an object differential diagnosis viral hepatitis. For 20 years we have (from the 1990s to the present time) an increase in the frequency of this diagnosis by more than 4 times.

The second myth that goes into the past with the possibility of a genetic diagnosis of GS. It is a myth that SF is primarily jaundice. This is a completely optional symptom for SJ. This is just the tip, the visible part of the iceberg. The main part of patients with GS does not have jaundice or manifests it in some special life situations. This is not a mandatory symptom, which is also very important.

The third myth with which we must part in our time. The myth that GS is a completely harmless disease. We are used to the fact that this is so. It does not lead to fibrosis or transition to cirrhosis of the liver. In this regard, it does not require our attention.

In fact, it has recently become clear that he makes a very serious contribution to the development and frequency of development cholelithiasis(ZHKB) in the world. In particular, a number of studies speak about this on a fairly large scale.

Genetic study in 2009, where about two hundred patients with cholelithiasis and about 150 patients without it were genetically examined for GS. It turned out with high reliability that among those who have GS, cholelithiasis is significantly more common.

In 2010, an even larger study appeared. This is a meta-analysis of a number of studies. It covers about three thousand patients with cholelithiasis and about one and a half thousand patients without it. It turned out that patients in whom GS is genetically confirmed have a full risk of cholelithiasis. Mainly, men have this brew.

Women generally suffer from gallstone disease more often due to the hormonal device, estrogens, and so on. Men, on the other hand, fall into this category mainly if they have FS. The increase in cholelithiasis in men with SF occurs by 21%.

Another new direction, a completely new aspect in our contemporary ideas about SJ. This fact that the study of the characteristics of drug metabolism against the background of SF formed the basis for the emergence of a completely new direction in pharmacology. The so-called pharmacogenetics, which are of great importance for the development medicines and their practical use.

Many drugs, the so-called aglucones, must also combine with glucuronic acid, like bilirubin, in order to be eliminated from the body and generally go through their metabolism in the body. Load the same enzyme - glucuronyl transferase.

Accordingly, bilirubin is displaced from the bond with glucuronic acid. Violate its excretion into the bile ducts, resulting in jaundice.

When developing and testing a number of drugs on a large contingent of patients, pharmacologists are faced with the fact that a number of patients reveal severe jaundice. This could be interpreted as a true hepatotoxicity of the drug, which sometimes cast a shadow on very important and promising drugs that are essential for the corresponding category of patients.

A 2011 paper shows how the trial of Tocilizumab, a promising drug used in rheumatoid arthritis, two patients had a high rise in bilirubin levels. When these patients were examined, it turned out that both of these patients (and only they of all those participating in the test) had a genotype characteristic of GS.

This removed this drug from suspicion in terms of true hepatotoxicity.

But the number of relevant publications is multiplying. Here is another indication of this. With a disease such as acromegaly, there is now often resistance to somatostatin. New drug, which was tested at the same time, showed a high degree, a high incidence of jaundice. It turned out that all these patients had GS.

A much closer example to us is antiviral therapy chronic hepatitis C interferons with "Ribavirin" ("Ribavirin"). The same picture. Two patients gave a 17-fold rise in bilirubin levels. But it turned out that these two patients had GS. The abolition of "Ribavirin" led to the normalization of bilirubin. No additional shadow was cast on Ribavirin.

So far, we have dealt mainly with world literature data. I want to give my own data for 20 years of a children's clinic. During this time, we observed 181 children and adolescents with GS. It turned out that a very high percentage of these patients (more than half of them) had biliary dyskinesia with and without sludge syndrome, had the development of cholelithiasis, despite the fact that these are children.

But we received especially important and interesting information when we divided our patients into two groups, for two decades: 1992-2000 and 2001-2010. These decades were distinguished by the fact that at the first stage they did not receive drugs "Ursodeoxycholic acid" ("Ursodeoxycholic acid"). Or they received it according to indications, when we already had a developed picture of the lesion of the biliary tract.

In these patients, the normal state of the biliary tract was only in 11.8% of children. 76.5% had biliary dyskinesia, almost half of them with sludge syndrome. Almost 12% of children have already developed cholelithiasis.

At the second stage (second decade) 105 patients. Already from the first steps, as soon as the diagnosis of GS was made, preventive courses of "Ursodeoxycholic acid" (UDCA) were carried out twice a year in the form of the drug "Ursosan" ("Ursosan"), with which we have been working for many years.

Results. In these patients, in almost 65% of cases, the normal state of the biliary tract. The number of patients with cholelithiasis decreased by 4.5 times (up to 2.8%).

This suggests that, nevertheless, SJ deserves our attention and some therapeutic impact. It is aimed at reducing the overall level of bilirubin, as indirect, free to reduce general intoxication (since indirect bilirubin is toxic to the nervous system). As well as a decrease in direct bound bilirubin to prevent damage to the biliary tract.

What do we have for this today. In terms of reducing the level of indirect bilirubin, the drug "Phenobarbital" ("Phenobarbital") is still used. It is known that it has some ability to increase the activity of glucuranyl transferases. Due to this, the level of indirect hyperbilirubinemia decreases to some extent and intoxication, the effect on the central nervous system(CNS).

In order to reduce or prevent damage to the biliary tract, we consider correct application UDKhK ("Ursosan", in particular). According to our data, it significantly reduces or even prevents complications from the biliary tract, including cholelithiasis.

(Slide show).

There is an arrow here from UDCA to a decrease in the effect on the central nervous system. We have come across some interesting data so far experimental studies. They say that UDCA can reduce sensitivity nerve cells to the damaging effect of indirect bilirubin.

The culture of rat nerve cells (astrocytes and neurons) were incubated with indirect bilirubin or with indirect bilirubin in the presence of UDCA. In the case of mono incubation, there was a 4-7 fold increase in apoptosis in these cells.

In the case when they were incubated with indirect bilirubin in the presence of UDCA, there was a significant protection (60%). Reducing the level of apoptosis less than 7%.

Thus, the treatment of SF today, in our opinion, should contain. As for dietary restrictions, they can only be associated with a possible foliopathy and be of such a nature. They should not be strict enough, but in the order of a healthy lifestyle.

As for the second point - the mode of sparing - it is very important. Patients should be well aware of this. Physical and psycho-emotional overstrain is extremely unfavorable and will directly lead to yellowing.

A very important point is medication sparing - minimizing medicinal effects in all directions. First of all, this applies to glucocorticosteroids, which are direct aglucones. Salicylates - the whole group. Sulfonamides. "Diakarb" ("Diacarb"), quite often used. "Menthol" ("Mentholum") and a number of other drugs.

In general, on the banner of a patient with SF should be written: "Minimization of medicinal effects."

Concerning drug therapy of the syndrome itself, then "Phenobarbital" in the age dosage is used only in cases of a high rise in bilirubin (above five or more norms). With a lower level of bilirubin rise - "Valocordin" ("Valocordin"), which contains phenobarbital in small quantities. In children or adolescents, 1 drop per year of life, 20-30 drops in adults 3 times a day.

As for UDCA, 10 - 12 mg per kilogram per day. Preventive courses for 3 months (spring-autumn) are useful annually and, as I have shown in our experience, they are quite effective in terms of preventing lesions of the biliary tract and cholelithiasis.

It is shown with an increase in direct bilirubin to its normalization. In the event of biliary dyskinesia with sludge syndrome before their elimination and 1-2 months after to keep the received.

Thus, SF is a hereditary disorder of bilirubin metabolism, the timely recognition and correction of which is essential, both for the patient and for the population as a whole.

The current stage in the development of medicine, which has made it possible to objectively confirm the diagnosis of SF by genetic methods, puts its diagnosis on a new level.

The benignity of the syndrome, which consists in the absence of fibrosis and outcome in liver cirrhosis, does not exclude such adverse consequences as diseases of the biliary tract, up to cholelithiasis.

Last thing. For the prevention and treatment of these adverse effects, it is advisable to use UDCA, in particular Ursosan.

Thank you for attention.

A violation in the process of neutralizing the liver pigment, in which bilirubin accumulates in the body, is called Gilbert's syndrome. The disease was first discovered in the early 20th century and is also known as constitutional liver dysfunction and familial benign jaundice.

This defect is transmitted at the genetic level, most often through the male line. For this pathology characteristic symptom is yellowing skin and mucous membranes, against the background of the absence of damage to liver tissues. Special measures for the treatment of Gilbert's Syndrome are not required.

Methods for diagnosing Gilbert's syndrome

Most people live with such a pathology for many years and are unaware of its existence. Usually the disease is detected during a random examination and most often during adolescence.

For reference! More than 7% of people suffer from Gilbert's Syndrome.

Diagnosis of Gilbert's Syndrome is based on patient complaints and on the results of additional studies.

During mental overstrain, in violation of the water balance in the body or against the background of an infectious or viral disease Patients may experience the following symptoms:

1. Memory difficulties.
2. Sleep problems.
3. Mental instability.
4. Headache and bouts of nausea.
5. Pain in the abdomen and in the region of the liver.
6. Increased yellowness of the skin.
7. Muscle pain.
8. Difficulty breathing and rapid pulse.

Based on such complaints, tests are prescribed to exclude possible causes, in which increased bilirubin may appear:

• Hepatitis and other pathologies of the liver.
• Diseases of the biliary tract.
• enzymopathic jaundice.
• Excess content in the body of beta-carotene.
• cholestasis.

For this, the following studies are used:

• Blood test for hemoglobin. In the presence of Gilbert's Syndrome, its concentration will exceed 160 g / l.
• liver tests. The level of indirect bilirubin will be above the acceptable value, while other liver enzymes will remain within the normal range.
• DNA research. Sometimes this genetic analysis is enough to make a diagnosis.
• Analysis of urine. A characteristic indicator will be the presence of bilirubin in it.

Tests can be used to confirm the diagnosis:

• The concentration of bilirubin is checked in the morning on an empty stomach. After that, the patient should consume no more than 400 calories per day for two days. The bilirubin test is repeated. Gilbert's Syndrome is indicated by an increase in the level of pigment by more than 50%.
• The disease is confirmed by an increase in the concentration of bilirubin after intravenous administration. nicotinic acid.
• The same results are noted after the introduction of rifampicin.
• After taking phenobarbital, a decrease in the content of pigment in the blood will have a positive value.

If necessary, obtain additional information using computed tomography or ultrasound of the liver, pancreas, and bile ducts.

Important! Gilbert's syndrome is an incurable pathology that does not pose a threat to life.

Acceptable blood bilirubin results

The permissible norm of total bilirubin is considered to be 3.4-20.5 µmol / l. This value consists of two components - direct and indirect bilirubin. With an increase in the concentration of the pigment, it is important to know due to which bilirubin the coefficient increased.

Direct bilirubin is in a bound state and does not pose a threat. Indirect bilirubin freely moves through the body and, having accumulated in large quantities, has a toxic effect on internal organs. An increase in the level by several tens of times already poses a threat even to life.

Up to 60 µmol/l

Indirect bilirubin is able to freely penetrate into the cells and have a negative impact on the processes taking place in them. The rate of this enzyme is not higher than 8.5 µmol/l. If its level has increased, but does not exceed 60 µmol/l, then only peripheral tissues are damaged.

In such cases, in the absence of symptoms such as drowsiness, vomiting, unstable mental state, drug treatment is not used. Absorbents, blue light treatment and dietary nutrition are used as therapy.

Over 80 µmol/l

With an increase in indicators above 80 μmol / l, bilirubin may penetrate into more significant organs. Brain cells, heart and respiratory system. Patients with Gilbert's Syndrome can provoke such a jump by abusing drugs, alcoholic beverages, or having a viral illness.

Symptoms include loss of appetite, bouts of vomiting, insomnia, and nightmares. Such patients are in medical institution under the constant supervision of a doctor, where they are prescribed phenobarbital, hepatoprotectors, antitoxic drugs and absorbents. In particularly difficult cases, blood transfusion is used.

In patients, protein products, fats and vegetables are removed from the diet, allowing only cereals, biscuits and fat-free kefir to be eaten. Such a diet must be followed until a stable remission is established, subsequently refusing only dishes that can lead to an exacerbation.

Gilbert's syndrome is not life-threatening, but eventually leads to the development of gallstone disease.

Ways to lower bilirubin

After finding a high liver pigment ratio in a blood test, patients are concerned about how to lower bilirubin.

First of all, it is necessary to establish and eliminate the cause that caused the increase in the level of the enzyme. If this is a concomitant disease, then it must be cured, otherwise the jumps in the level of bilirubin will be repeated.

The doctor will select the appropriate complex therapy and prescribe treatment based on symptoms, medical history and general state patient's health.

To drug treatment a mandatory item will be recommended to follow a strict diet:

1. The basis of the diet should be various cereals and cereal side dishes.
2. It is advisable to cook the first dishes only on vegetable broth.
3. More dairy products and sweet fruits.
4. It is allowed to use fresh juices, jelly, compotes, herbal teas.
5. Use meat and fish products with a low percentage of fat.
6. Fractional nutrition in small portions.
7. Exclude citrus fruits, spicy vegetables and spices from the menu.
8. Alcohol, soda, strong tea and coffee are also prohibited.
9. smoked, fatty foods, as well as fried foods will only exacerbate the problem.

As ancillary measures, you can turn to traditional medicine.

Medical treatment

Main task drug therapy, prescribed by a doctor, will be the treatment of a concomitant disease, the removal of symptoms and the reduction of the load on the liver. As a result, drugs such as:

1. Hepatoprotectors. Pancreatin, Essentiale will help restore liver cells.
2. Cholagogue. normalizes the outflow of bile.
3. Antibiotics will reduce inflammation.
4. Drugs that improve digestion, for example, Mezim.
5. Absorbents and antiemetics to relieve symptoms.
6. Preparations plant origin to cleanse and support the liver.

Treatment with folk remedies

Effective help can be provided by:

• Birch leaves, if you brew them with two glasses of boiled water and drink after 30 minutes of settling for about 7 days at night.
• Drinking twice a day, 100 ml of beet juice.
• Dry motherwort brew in boiling water for 30 minutes and drink on an empty stomach for 14 days.
• Corn. Dried stigmas insist in boiling water and drink a quarter cup before meals.

Prevention

Proper lifestyle has always helped to maintain and restore health at any age. Therefore, you should not ignore the doctor's recommendations for dieting. An adjusted diet, combined with moderate outdoor exercise, will not only be an excellent addition to your complex treatment high levels of bilirubin, but also effective prevention against relapses.

For the best result of bad habits like alcohol and cigarettes should also be forgotten. It will also be useful to avoid stressful situations, and to exclude products containing artificial colors and preservatives from consumption.

Gilbert's syndrome - genetic disease, which is characterized by a violation of the utilization of bilirubin. The liver of patients does not properly neutralize bilirubin, and it begins to accumulate in the body, causing various manifestations of the disease.

Gilbert's syndrome was first described by the French gastroenterologist Augustin Nicolas Gilbert (1958-1927) and his colleagues in 1901. This pathology has several names: familial non-hemolytic jaundice, benign familial jaundice, constitutional liver dysfunction or Gilbert's syndrome. Occurs as a result of an increase in the amount of unconjugated bilirubin in the blood plasma, without signs of liver damage, biliary obstruction or hemolysis. This disease is familial and is inherited. The disease occurs due to a genetic defect that leads to a disruption in the formation of an enzyme that promotes the utilization of bilirubin. People with Gilbert's syndrome have moderate elevated level bilirubin in the blood, which can sometimes cause yellowing of the sclera of the eyes and skin. Gilbert's syndrome does not require radical methods treatment. Since this syndrome has a large number of symptoms and manifestations, it is not considered a disease, and most people do not know that they have this pathology until a blood test shows an elevated level of bilirubin. In the United States, approximately 3% to 7% of the population has Gilbert's syndrome, according to National Institute Health - Some gastroenterologists believe that the prevalence may be higher, as high as 10%. The syndrome appears more often among men.

Cause of Gilbert's syndrome.

Main functions of the liver

The liver is the largest organ in the human body. Some of the key functions of the liver are:
Converts thyroxine hormone thyroid gland(T4) to the more active form of triiodothyronine (T3). Insufficient conversion can lead to hypothyroidism, chronic fatigue, weight gain, poor memory, and other symptoms.
Creates GTF (glucose tolerance factor) from chromium, niacin and possibly glutathione. GTFs are required for insulin to properly regulate blood sugar levels.
The liver synthesizes bile salts, which emulsify fats and fat-soluble vitamins A, D, E, K for better absorption. The liver also removes some fat-soluble toxins from the body.
Activation of vitamins in their biologically active forms- coenzymes. Virtually every nutrient must be biotransformed in the liver into its proper biochemical form before being stored, transported, or incorporated into metabolic processes.
Accumulation of nutrients, especially vitamins A, D, B-12 and iron for use as needed.
Produces carnitine from lysine and other nutrients. Carnitine is the only known bionutrient that can transport fats to the mitochondria, where they are used to generate ATP energy. Mitochondria generate 90% of ATP energy at the cellular level.
The main regulator of protein metabolism. The liver converts various amino acids into each other as needed.
Produces cholesterol and converts it to various forms needed to transport substances to tissues.
The function of detoxification is one of the most important functions of the liver. Most harmful substances and metabolic products are neutralized in the liver. So the decay products of the cellular elements of the body undergo a series of transformations, in particular, the products of erythrocyte decay.

Hyperbilirubinemia - an increased content of bilirubin in the blood - occurs because the activity of the enzyme glucuronyl transferase, which conjugates bilirubin, decreases. The neutralization that takes place in the liver makes the bilirubin water soluble so that it can dissolve in the bile and enter the body. duodenum and eventually be eliminated from the body. The average lifespan of an erythrocyte is 120 days, after which it is utilized and decomposed into bilirubin and hemoglobin. Directly in the liver, the insoluble form of bilirubin is converted into a water-soluble form. Gilbert's syndrome is caused by a gene defect - a mutation of UDP-glucuronosyltransferase, the gene responsible for the production of this enzyme. People inherit the syndrome from their parents. Bilirubin is not neutralized and accumulates in the blood. When the level reaches a certain point, the patient may experience symptoms of jaundice.

Symptoms of Gilbert's syndrome

Most people who have a disease do not know they have it. The level of bilirubin usually remains within the normal range, and sometimes rises slightly. One of the earliest and pathognomonic symptoms is jaundice. Jaundice of the sclera or skin may appear when the amount of bilirubin in the blood rises. Symptoms may worsen and become more obvious in association with: another illness, infection, dehydration, stress, or menstruation. Although the level of bilirubin is unlikely to ever reach dangerous levels, jaundice is one of the important and alarming symptoms.

Yellowness of the skin (left - normal, right - pathology)

Yellowness of the sclera

The following symptoms may also be pathognomonic, but to a lesser extent. Often patients describe: fatigue, blurred consciousness, headaches, memory impairment, dizziness, depression, irritability, anxiety, nausea, loss of appetite, irritable bowel syndrome, abdominal pain and cramps, pain in the liver / gallbladder, tremors, itchy skin insomnia, difficulty concentrating, panic attacks, hypoglycemic reaction to food, intolerance to carbohydrates, alcohol.

Food intolerances can cause liquid stool or diarrhea, bloating. Symptoms of respiratory and heart failure may appear: labored or shallow breathing, heart palpitations. Due to metabolic disorders, muscle and joint pain, weakness, weight loss and taste perversion occur.

The following symptoms (very rarely observed and with a pronounced violation of bilirubin metabolism), which urgently require medical intervention: difficulty in choosing words, feeling intoxicated, uncontrollable vomiting, excessive thirst, chest pains, muscle twitching (tremor), enlargement lymph nodes, bitter or metallic taste in the mouth. These symptoms indicate the development of acute liver failure.

Diagnosis of Gilbert's syndrome

This diagnosis is most often made in late adolescence. The diagnosis is easy if the history of the disease is taken correctly, genetic typing is not necessary in this case. A sample of a blood test is taken from the patient, which examines liver function and the level of direct and indirect bilirubin. If the results of the test show a high level of insoluble bilirubin in the blood, and other indicators are normal, the doctor may diagnose Gilbert's Syndrome. In the presence of severe jaundice, a number of differential diagnostic tests may be required to exclude other pathologies, which may be, for example:

1. Sharp inflammatory diseases liver (hepatitis) - they can impair the ability of the liver to utilize bilirubin.
2. Inflammation of the bile ducts - may interfere with the release of bile and removal of bilirubin.
3. Obstruction of the bile ducts - also prevents the flow of bile and contributes to the accumulation of bilirubin.
4. Hemolytic anemia- leads to an increase in bilirubin due to increased breakdown of red blood cells.
5. Cholestasis - the flow of bile from the liver is interrupted. Bile containing bilirubin remains in the liver.
6. Crigler-Najar syndrome - congenital non-hemolytic non-conjugated bilirubinemia.
7. Dubin-Johnson syndrome - enzymopathic jaundice, a rare pigmentary hepatosis, characterized by impaired excretion of conjugated bilirubin from hepatocytes into the bile capillaries.
8. False jaundice - a harmless form of jaundice, in which yellowing of the skin is associated with an excess of beta-carotene.

Additional tests may include: ultrasound scan abdominal cavity to exclude obstruction of the biliary tract or diffuse pathology of the liver, a diet for 24 hours to exclude the alimentary cause of the increase in bilirubin and genetic typing.

Treatment of Gilbert's syndrome.

Gilbert's syndrome is considered a harmless disease - as a rule, it does not cause any health problems. At the moment, the development of medical technologies for effective etiotropic treatment does not exist. Although the symptoms of jaundice may be alarming for the patient, the physician should explain that jaundice is not a regular symptom and should not be cause for concern. Long-term follow-up of a patient with Gilbert's syndrome is usually not required. If the patient notices a worsening of the symptoms of jaundice, he should tell his doctor about it so that he can rule out various other causes. Patients whose symptoms of jaundice are very distressing may take small amounts of phenobarbital. It has a slight antihyperbilirubinemia effect. Along with its positive effect, this drug causes a sedative effect on the nervous system, and with prolonged use causes a toxic effect on the liver. Therefore, an effective and balanced dosing of this drug is important.

Diet can relieve symptoms: foods with a long shelf life and containing a large amount of preservatives should be excluded from the diet, multivitamin complexes should be used to strengthen overall immunity, all foods should be boiled, baked or steamed (minimum fat).

Complications of Gilbert's syndrome

By itself, Gilbert's syndrome does not cause any complications and does not damage the liver, but it is important to differentiate one type of jaundice from another in time. This group of patients had hypersensitivity liver cells to hepatotoxic factors such as alcohol, drugs, some groups of antibiotics. Therefore, in the presence of the above factors, it is necessary to control the level of liver enzymes.

Therapist Zhumagaziev E.N.

Content

Gilbert's disease or syndrome is a benign disorder of the liver, which is associated with the neutralization of indirect bilirubin by the organ, which is released during the natural breakdown of hemoglobin. The disease has an undulating character and a hereditary constitutional feature. It affects up to 10% of the population, more often men suffer from the disease, the syndrome is widespread among Africans.

General information about Gilbert's syndrome

Familial simple cholemia, hyperbilirubinemia or Gilbert's disease is a pigmented benign hepatosis, which is characterized by an increase in the level of indirect bilirubin in the blood. The reason for the development of the syndrome is a violation of the intracellular transport of a substance in hepatocytes, a decrease in the degree of its absorption and transformation. The disease was first diagnosed in 1901. Main Features chronic disease are a violation of the synthesis of proteins, hemoglobin, jaundice.

The reasons

Gilbert's jaundice is a hereditary disease caused by a defect in the second chromosome gene responsible for the production of the liver enzyme glucuronyl transferase. It helps indirect bilirubin bind to glucuronic acid in the liver, resulting in a direct pigment fraction that can be excreted in the bile. Lack of the enzyme leads to hyperbilirubinemia and jaundice. Factors causing an exacerbation of the syndrome are:

• viral, infectious diseases;
• trauma;
• menses;
• violations of the diet, diet, starvation;
• insolation (excessive exposure to the sun);
• lack of sleep;
• dehydration of the body;
• stress;
• medication: Ampicillin, Rifampicin, Paracetamol, Levomycetin, Caffeine, anabolics, hormonal drugs, sulfonamides;
• alcohol abuse;
• surgical interventions.

Symptoms of Gilbert's syndrome

Up to a third of patients do not even suspect that they have Gilbert's syndrome. Elevated bilirubin levels are noted from birth, but in newborns, diagnosis is difficult due to possible congenital physiological jaundice. The disease is detected in men 20-30 years old during various examinations. The main signs of the disease are:

• icterus (icterus) of the sclera, skin - most cases of jaundice are of a periodic mild nature;
• pain in the right hypochondrium;
• heartburn;
• metallic taste in the mouth;
• loss of appetite;
• nausea, vomiting, especially after sweet foods;
• flatulence;
• decreased concentration;
• feeling of a bloated, full stomach;
• constipation, diarrhea;
• general weakness, malaise, fatigue;
• dizziness;
• cardiopalmus;
• insomnia;
• chills, but the temperature does not rise;
• muscle pain;
• depression, antisocial behavior;
• causeless fear, panic;
• irritability.

Diagnosis of Gilbert's syndrome

To make an accurate diagnosis, a diagnosis is made. Popular examination methods are:

1. A general blood test for Gilbert's syndrome - reticulocytosis (an increase in the level of immature erythrocytes), a mild degree of anemia is noted in the blood.
2. Urinalysis - in the presence of bilirubin and urobilinogen, we can talk about a violation of the liver.
3. Biochemical analysis in the blood - sugar is slightly reduced, normal level proteins, alkaline phosphatase, negative thymol test.
4. The level of bilirubin in the blood - an increase above the norm (8.5-20.5 mmol / l) due to the indirect fraction.
5. Blood clotting - normal prothrombin index and time.
6. Viral hepatitis markers are absent.
7. Ultrasound (ultrasound examination) of the liver - during exacerbation, the organ is slightly enlarged. Often the disease is combined with cholangitis, chronic pancreatitis, stones in gallbladder in history.

Doctors recommend that patients check thyroid function, donate blood to determine serum iron, total iron-binding ability, transferrin. To confirm the diagnosis, additional tests are carried out:

1. Fasting test- refusal of food for 48 hours or its restriction to 400 kcal per day. This dramatically increases the concentration of free bilirubin by 200-300%. The unbound substance is tested on an empty stomach on the first day of the study and two days later. If indirect bilirubin increases by 50-100%, the test is positive.
2. A test with Phenobarbital - a dose of 3 mg / kg per day for a course of 5 days leads to a decrease in the concentration of unbound bilirubin.
3. Test with nicotinic acid- make an intravenous injection of 50 mg of nicotinic acid, which leads to an increase in indirect bilirubin by 200-300% in three hours.
4. Rifampicin test- the introduction of 900 mg of the substance increases the concentration of unbound bilirubin.

Another popular method of diagnosis is percutaneous puncture of the liver. The doctor receives a punctate, examines it for signs chronic course hepatitis and cirrhosis of the liver. An expensive diagnostic method is a genetic-molecular analysis of blood from a vein. It allows you to determine the defective DNA, due to which the disease develops.

Treatment of Gilbert's syndrome

Therapies are subjected to attacks of exacerbation of Gilbert's syndrome. Doctors prescribe complex drug therapy:

1. Taking Phenobarbital and Zixorin (Flumecinol) in doses of 0.05-0.2 g per day for a course of 2-4 weeks. This leads to a decrease in the concentration of bilirubin in the blood, the elimination of dyspeptic disorders. Phenobarbitle is recommended to be taken at a minimum dose at bedtime to avoid drowsiness, ataxia, and lethargy. At a bilirubin level of 50 µmol/l and feeling unwell the patient is prescribed a course of Phenobarbital at a dose of 30-200 mg per day. Since the component is part of the drops Corvalol, Barboval and Valocordin, you can take them 20-25 drops three times a day.
2. Cordiamin - 30-40 drops 2-3 times a day for a course of seven days.
3. To eliminate cholecystitis and cholelithiasis, the use of infusions of choleretic herbs, procedures for using tubages from sorbitol or xylitol, Karlovy Vary and Barbara salt are indicated.
4. To remove bound bilirubin, enhanced diuresis is carried out, the adsorbent of the substance in the intestine is Activated carbon. To bind the already circulating bilirubin in the blood, 1 g / kg of body weight of albumin is administered for an hour. This procedure is advisable before a blood transfusion.
5. To destroy bilirubin fixed in tissues, phototherapy with a wavelength of 450 nm is used, lamps with blue color are used. The eyes are protected by goggles.
6. During therapy, provoking factors (alcohol intake, hepatotoxic drugs, infections, mental and physical stress), insolation should be avoided.
7. Vitamin therapy is useful, especially the intake of B vitamins.
8. Sanitation of chronic foci of infection.
9. In critical situations, he conducts an exchange transfusion of blood.
10. After removing the exacerbation, a course of hepatoprotectors is shown: Legalon, Bonjigar, Hofitol, Karsil, Essentiale Forte, Silymarin, Heptral.
11. During exacerbations, choleretic agents, enzymes (Mezim, Festal) are prescribed, and ursodeoxycholic acid preparations are used to lower the level of free bilirubin.
12. To restore intestinal motility and eliminate nausea or vomiting, Domperidone, Cerucal, Metoclopromide is indicated.

Diet

With Gilbert's syndrome, a lifelong diet is indicated, which is tightened during exacerbations. The food includes fruits, vegetables, oatmeal and buckwheat, low-fat cottage cheese, mild hard cheese, powdered or condensed milk. A day you can eat one egg and a little sour cream. Reception of low-fat meat, a bird, fish, plentiful drink is shown. Black tea and coffee are replaced with green tea, unsweetened lingonberry, cranberry or cherry fruit drinks. Food should be taken 4-5 times a day in small portions. Removed from the diet:

• bakery products;
• sweet food;
• fatty creams;
• chocolate;
• spicy foods;
• food with preservatives;
• alcohol, especially strong.

Forecast

With Gilbert's syndrome, the prognosis is favorable. If you follow the diet and the rules of behavior (avoid the sun, starvation, stress), then the life expectancy of such patients does not differ from healthy ones. It contributes to its increase healthy lifestyle life, refusal of alcohol, junk food. When treated with Phenobarbital or Cordiamin, the level of bilirubin returns to normal.

Jaundice may appear after infections, vomiting, missed meals. Before planning a pregnancy, patients should consult a geneticist. To prevent the onset of the disease, compliance with the diet, work and rest, water balance, avoidance of insolation, dehydration is shown. Illness is not a reason to refuse vaccinations.

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