Hyperbilirubinemia: forms, symptoms, treatment. Hyperbilirubinemia: what danger does this pathology pose? Surgical treatment of bilirubinemia

Hyperbilirubinemia is a condition of the body in which the level of bilirubin in the blood is elevated. After exceeding a certain concentration, bilirubin penetrates the body tissues, turning them yellow. Bilirubin is formed from the breakdown of red blood cells. After this, it is found in the body in free and non-free form.

Free (indirect, unconjugated) bilirubin is formed immediately after the breakdown of red cells and has a harmful effect on the body, manifested by various symptoms. Unfree bilirubin is contained in the body in a transformed form and is prepared for removal from it by the organs of the excretory system.

Forms of the disease

Hyperbilirubinemia can be of the following forms:

• Prehepatic hyperbilirubinemia is associated with an increase in the level of bilirubin in the blood.
  This form of the disease manifests itself in the form of the following symptoms: the skin, sclera of the eyes and mucous membrane of the patient’s mouth turns yellow. The level of bilirubin in the blood is two or more times higher than normal. The color of the patient's urine becomes rich yellow, the feces acquire a brown tint. The patient may have a decreased mood and increased fatigue. A more rare symptom is disturbances in consciousness and sleep.
• Hepatic hyperbilirubinemia – caused by damage to liver tissue.
  The skin, sclera of the eyes and mucous membranes of the patient acquire a reddish color. The level of bilirubin in the blood increases more than twice the normal level. The patient is bothered by pain or discomfort in the right hypochondrium. The patient may complain of nausea and vomiting. After eating, the patient may feel heartburn. There may be a feeling of bitterness in the mouth. The patient's urine becomes darker, almost brown. The patient feels weak and tired even with light exertion. After some time, the patient's skin color acquires a greenish tint.
• Subhepatic hyperbilirubinemia is caused by difficulty passing bile, which contains conjugated bilirubin, into the intestine.
  The skin, sclera of the eyes and mucous membranes of the oral cavity acquire a yellowish tint. The level of bilirubin in the blood is more than twice the normal level. Discoloration of urine, up to white, is observed. The patient is bothered by itchy skin. Feeling of bitterness in the mouth. Symptoms such as pain and discomfort appear in the right hypochondrium. The patient feels unwell, lethargy and apathy. The patient's body weight decreases. The intake of vitamins into the body is impaired.

If the liver tissue is not damaged, the diagnosis is functional or benign hyperbilirubinemia. In this case, heredity is considered the main factor. Benign hyperbilirubinemia can be of various types; they are caused by an increase in the level of bilirubin in the blood.

Functional hyperbilirubinemia is manifested by a icteric tint of the patient’s skin and eyeballs, as well as an increase in the level of bilirubin in the blood in a blood test. Such a disorder may appear after severe stress, after surgery, or as a complication after suffering a viral disease during pregnancy.

Unconjugated hyperbilirubinemia is manifested by an increase in the level of free bilirubin in a blood test. This disease most often occurs in newborns with hemolytic disease.

Hyperbilirubinemia in newborns is a physiological variant of the norm; it is caused by the immature state of the liver. Indirect hyperbilirubinemia can be observed in a child in the first days after birth and does not cause him discomfort. Hyperbilirubinemia in newborns occurs under the constant supervision of medical specialists and is accompanied by tests for blood bilirubin levels. This analysis is carried out to prevent severe cases of the disease.

In other cases, this hyperbilirubinemia syndrome can be observed with mechanical damage to red cells. In this case, such damage can occur if the body is exposed to various harmful factors, such as exposure to heavy metals.

Conjugative hyperbilirubinemia is characterized by an increase in the level of direct bilirubin. This is a variant of physiological jaundice of newborns born prematurely. Symptoms of the disease disappear after two to three weeks.

Transient hyperbilirubinemia appears in most children in the first days after birth. This happens because the baby’s internal organs are still functionally immature and are adapting to the environment. This form of hyperbillirubinemia does not require special treatment with medications; usually medical specialists give recommendations regarding adherence to the daily regimen. Signs of this form of hyperbilirubinemia pass without consequences for the newborn, liver function is not impaired.

Causes of hyperbilirubinemia

Patients are interested in the reasons for hyperbilirubinemia and what leads to its occurrence. Various factors can lead to the development of a certain form of hyperbilirubinemia.

Prehepatic hyperbilirubinemia can occur for the following reasons:

• Heredity. The structure of red blood cells (erythrocytes) may have deviations from the norm due to genetics.
• Intoxication as a result of poisoning with harmful or toxic substances, alcohol.
• Anemia caused by various factors.
• Viral diseases.
• Sepsis.
• Blood group incompatibility that occurs as a result of blood transfusion to a patient.
• Autoimmune diseases such as systemic lupus erythematosus, autoimmune hepatitis, autoimmune hemolytic anemia.
• Extensive hemorrhages in the abdominal cavity.
• Leukemia.

Hepatic hyperbilirubinemia can occur for the following reasons:

• Hepatitis of viral origin or caused by the use of drugs.
• Dubin-Johnson syndrome.
• Tumors, abscesses, cirrhosis of the liver.
• Gilbert's syndrome.
• Rotor syndrome.

Subhepatic hyperbilirubinemia can occur for the following reasons:

• The bile duct is blocked by a stone.
• The bile duct is narrowed as a result of its injury.
• Inflammation of the duct.
• Pancreas cancer.

Treatment of the disease

Hyperbilirubinemia (see also jaundice) is a pathological condition, the treatment of which begins with the elimination of the underlying disease. It is very important to conduct a primary diagnosis in order to identify the main cause of hyperbilirubinemia, this will build a bridge to a complete cure for the patient. Examination and treatment of the patient is carried out in the gastroenterology department of the hospital.

If the examination revealed benign hyperbilirubinemia, the use of medications is not required. In this case, this condition is corrected by following the daily routine and diet prescribed by the doctor.

If the patient requires medical assistance, the following groups of drugs are used:

• Antioxidants for the purpose of detoxification, since the products of bilirubin metabolism have a toxic effect on the nervous system, especially the brain. It could be Cystamine or Tocopherol.
• Glucocorticosteroids. If the patient has a variant of hyperbilirubinemia in which damage to the liver parenchyma is observed, Prednisolone is prescribed.
  External use products. This group of drugs is used if the patient’s complaints include a symptom of itching. In this case, wiping with camphor alcohol may be prescribed.
• Sometimes the use of surgical treatment methods is required. If the lumen of the bile ducts has been narrowed as a result of mechanical damage, surgical correction of the defect may be required.

In addition to using medications, doctors recommend following a special diet. In accordance with it, spicy, salty and smoked foods are prohibited for consumption. Fatty foods are also not recommended for cooking.

A cooking method such as frying while cooking is also not suitable. The patient should also give up alcohol. Doctors also recommend leading a healthy lifestyle, refraining from heavy physical activity and avoiding severe stress.

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Treatment of hyperbilirubinemia primarily depends on its pathogenetic variant, symptoms and should be aimed at treating the underlying disease that caused the symptoms of hyperbilirubinemia. Patients with symptoms of hyperbilirubinemia are immediately hospitalized in order to definitively clarify the diagnosis and carry out active treatment. An exception to this rule is patients with Gilbert's syndrome with hyperbilirubinemia, in whom it is not necessary to specifically reduce hyperbilirubinemia. In these patients, the main focus is on preventing symptoms of liver disease, as well as reducing physical and neuropsychic stress. For the treatment of hyperbilirubinemia, it is recommended to eat 4 full meals a day and 1-2 times a year monthly courses of treatment with choleretic tea.

All other patients with hyperbilirubinemia are prescribed diet No. 5, which limits fats but contains carbohydrates, proteins and vitamins in sufficient quantities. Drinking plenty of water is beneficial, especially mineral waters (“Borjomi”, “Essentuki” No. 4, No. 17, etc.). Food should be taken at least 5 to 6 times a day when treating hyperbilirubinemia.

Hyperbilirubinemia - treatment in the clinic

The regime of patients with hyperbilirubinemia should be bed or semi-bed. The toxic effect of high concentrations of bilirubin during hyperbilirubinemia can be reduced by including antioxidant drugs (tocopherol, ascorbate, cystamine, ionol, etc.) in the complex of drug treatment of symptoms of hyperbilirubinemia. In severe forms of hyperbilirubinemia, intravenous glucose, sometimes in combination with subcutaneous insulin injections, is recommended to treat symptoms; hemodesis.

To prevent and treat symptoms of hemorrhagic syndrome, vitamin K, vikasol, ascorbic acid, B vitamins, and calcium chloride are administered. For symptoms of parenchymal and intrahepatic hyperbilirubinemia caused by an immunoinflammatory process, a relatively short course of treatment with glucocorticosteroids (12–30 days) in small doses (30 mg/day) is administered.

In the absence of symptoms of mechanical hyperbilirubinemia, choleretic agents (holosas, etc.) can be prescribed for treatment, and in the presence of infection in the biliary tract, antibiotics can be prescribed to treat hyperbilirubinemia. Bile secretion can be improved with duodenal intubation. Such a symptom as painful and persistent skin itching in patients with cholestatic jaundice is alleviated by treatment with warm baths with the addition of vinegar, soda, carbolic acid; rubbing with a weak solution of carbolic acid or camphor alcohol. For the same purpose, bromine preparations, atropine, and pilocarpine can be prescribed internally.

The concentration of bile acids in the blood with symptoms of hyperbilirubinemia can be tried to be reduced by influencing the mechanism of their hepatic-intestinal circulation. For this, patients are prescribed drugs that bind bile acids in the intestines - cholestyramine 12 - 16 g per day, bilignin 5 - 10 g (1 - 2 teaspoons) 3 times a day 30 - 40 minutes before meals, washed down with water. Treatment of patients with obstructive jaundice is usually surgical.

Gilbert's syndrome in the treatment of symptoms of hyperbilirubinemia

Among enzymatic hyperbilirubinemias, the most common is Gilbert's syndrome (disease) and the adjacent Calque's syndrome (post-hepatitis variant of Gilbert's syndrome). This syndrome (disease) with symptoms of hyperbilirubinemia occurs more often in men in the second and third decades of life. It is characterized by symptoms: a periodic increase in the content of unconjugated plasma bilirubin to 85 - 140 µmol/l and in most cases appears for the first time in acute diseases of various nature (acute viral hepatitis, infectious mononucleosis, toxic liver damage of various etiologies, malaria, etc.), as well as after significant physical or emotional stress, hypothermia, injury, surgery, etc.

Symptoms of hyperbilirubinemia due to inflammatory (hepatitis, cirrhosis) or toxic (chemical poisoning, drug intolerance, etc.) hepatocellular damage is called hepatic (hepatocellular), or parenchymal. Damaged hepatocytes are not able to fully capture bilirubin from the blood, bind to glucuronic acid and release it into the bile ducts and require treatment.

As a result, without treatment, the content of unconjugated (indirect) bilirubin increases in the blood serum. In addition, with symptoms of liver cell dystrophy, reverse diffusion of conjugated (direct) bilirubin from the bile canaliculi into the blood capillaries is observed. This pathological mechanism causes an increase in the level of conjugated (direct) bilirubin in the blood serum, as well as symptoms of hyperbilirubinuria and a decrease in the excretion of stercobilin in feces.

In total, when liver parenchyma cells are damaged, the content of unconjugated and conjugated bilirubin in the blood serum can increase 4–10 times or more. With parenchymal lesions of the liver, the ability of liver cells to capture bile acids from the blood sharply decreases, as a result of which they accumulate in the blood and are excreted in the urine.

Hyperbilirubinemia - symptoms of the disease

Development of symptoms of hyperbilirubinemia

Symptoms of hyperbilirubinemia occur when there is increased formation of bilirubin, as well as when its transport into liver cells and excretion by these cells is impaired, or when the binding processes of free bilirubin are impaired (glucuronidation, sulfurization, etc.). Free (unconjugated) bilirubin in hyperbilirubinemia is poorly soluble and toxic; it is neutralized in the liver by the formation of soluble diglucuronide - a paired compound of bilirubin with glucuronic acid (conjugated, or direct bilirubin).

High concentrations of bilirubin with symptoms of hyperbilirubinemia inhibit the processes of oxidative phosphorylation and reduce oxygen consumption, which leads to tissue damage and the need for treatment. The toxic effect of high concentrations of bilirubin is manifested by symptoms of damage to the central nervous system, the occurrence of foci of necrosis in parenchymal organs, suppression of the cellular immune response, the development of anemia due to hemolysis of red blood cells, etc.

Symptoms of hyperbilirubinemia due to increased formation of bilirubin are observed with excessive hemolysis (for example, with hemolytic anemia during a hemolytic crisis, extensive hemorrhages, heart attacks, lobar pneumonia). This form of hyperbilirubinemia is called suprahepatic or hemolytic hyperbilirubinemia. If it causes symptoms of jaundice, then the latter has similar names.

Stages of hemolysis of hyperbilirubinemia

In the initial stage of hemolysis, there may be no symptoms of hyperbilirubinemia, since the liver is able to metabolize and secrete bilirubin into bile in an amount that is 3 to 4 times greater than its production under physiological conditions. Overhepatic (hemolytic) hyperbilirubinemia develops when the reserve capacity of the liver is exhausted. With moderate hemolysis, the symptoms of hyperbilirubinemia are caused mainly by unconjugated bilirubin, and with massive hemolysis - by unconjugated and conjugated bilirubin. The latter can cause symptoms of hyperbilirubinuria. Unconjugated bilirubin does not pass through the healthy kidney filter and does not appear in the urine.

Hyperbilirubinemia caused by genetic defects in liver enzymes involved in the elimination from plasma and glucuronidation of free bilirubin are called enzymopathic (constitutional). They usually occur without symptoms of liver damage and hemolysis, are not accompanied by loss of ability to work and do not end in death with adequate treatment.

Hyperbilirubinemia is a disease characterized by increased bilirubin levels in the blood serum. Bilirubin is one of the pigments of bile, which has a yellow-red color. This substance is synthesized from hemoglobin of erythrocytes, which break down as a result of volutive changes, in the reticuloendothelial system, that is, in the cells of the spleen, bone marrow, liver, as well as in the connective tissues of organs (histiocytes).

Causes of hyperbilirubinemia

There are many reasons for the increase in bilirubin content, starting with its excessive formation (massive simultaneous destruction of a large number of red blood cells) and ending with disturbances in the removal of the substance itself from the body or the process of uptake from the blood plasma and metabolism in liver cells. A distinction is made between direct and indirect bilirubin and depending on what stage of metabolism the conversion process is at - these concepts show whether this substance is in close contact with blood serum proteins for transport, or whether the compound has already completed metabolism in liver cells.

An increase in indirect bilirubin is called unconjugated hyperbilirubinemia. This disease is associated with increased hemolysis, and it received its name as a result of the fact that bilirubin enters the liver in an unbound form. An increase in the level of unconjugated bilirubin is observed in the presence of hemolytic disease of the fetus or newborn, as well as in hereditary and acquired hemolytic anemia. Also, the manifestation of unconjugated hyperbilirubinemia is promoted by poisoning and mechanical damage to red blood cells, as well as some liver diseases.

An increase in the content of direct, conjugated bilirubin is called “conjugative hyperbilirubinemia.” The main cause of development is disturbances in the removal of bilirubin from the body. Present in various forms of hepatitis, cirrhosis of the liver and in cases of obstructions to the outflow of bile (gallbladder stones, etc.). Also, an increase in direct bilirubin is facilitated by long-term use of hormonal contraceptives or the use of steroids (prescribed for the treatment of diseases of the body, as well as in athletes involved in bodybuilding).

Symptoms of the disease

With an increased level of bilirubin in the blood, there is a threat of disturbances from the central nervous system, namely, the person becomes lethargic, lethargic, and easily overtired. A complication is also possible when bilirubin enters the nuclei of the brain stem and has a toxic effect on them. This is especially true for newborns. Crigler-Nayjar syndrome (congenital malignant hyperbilirubinemia of an unconjugated nature, which is inherited) usually leads to the death of sick children.

With a mild course of the disease, general weakness and fatigue are observed. In such cases, the liver is not enlarged in size and is painless, the treatment will be effective and the ability to work will be maintained.

Benign hyperbilirubinemia, as a rule, is congenital in nature as a result of a congenital disorder of the liver, which does not have a serious effect on the functioning of the body as a whole. A characteristic sign of the disease is a yellow (icteric) coloration of the skin and whites of the eyes, especially pronounced as a result of overwork and stress. Sometimes, during an exacerbation, pain in the right hypochondrium, general weakness, nausea and appetite disturbances appear.

Methods of treatment and therapy

If the study revealed benign hyperbilirubinemia, treatment consists of following a diet. During remission and if you do not have concomitant disorders in the gastrointestinal tract, diet No. 15 is prescribed; during exacerbations, as well as in the presence of gallbladder diseases, doctors recommend using diet No. 5 (prescribed for most acute and chronic liver diseases).

Special liver therapy is not needed for this form of the disease. As a rule, patients are prescribed a course of vitamin therapy and choleretic drugs. If there are disturbances in the synthesis or excretion of bilirubin, thermal and electrical procedures in the liver area are contraindicated. It is necessary to limit physical and nervous stress to avoid the acute form of the disease.

Hyperbilirubinemia in newborns is treated primarily with phototherapy, which uses ultraviolet fluorescent light to transform bilirubin and accelerate its elimination from the baby's body. Standard phototherapy is used in hospitals. But newborns who have jaundice and no other signs of illness can be treated at home using a fiber-optic blanket. This blanket reduces bilirubin content more slowly than a fluorescent lamp, so it is only applicable in mild forms of the disease.

Fluorescent light, which is used for phototherapy, is not dangerous if the treatment is carried out correctly. Children wear a blindfold over their eyes during the procedure to avoid damaging their visual organs (to prevent burns to the retina). The bandage is removed while feeding the baby. As a rule, the light irradiation procedure is carried out at short intervals of 2-4 hours until the bilirubin returns to normal. Children are not at all bothered by dark blindfolds, since before birth, in the womb, they were in complete darkness and this is a familiar environment for them.

Hyperbilirubinemia syndrome is a congenital form of the disease, so its treatment consists of maintaining the body and ensuring normal functioning. In congenital forms, exacerbations occur, during which it is necessary to undergo a course of treatment with the Sorbovit-K sorbent, and after a decrease in bilirubin levels, one should return to preventive measures, that is, taking vitamins, choleretic drugs and following a diet.

In most patients, the increase in bilirubin (a breakdown product of red blood cells) is asymptomatic. Among the common symptoms of hyperbilirubinemia, several are distinguished.

• Prehepatic hyperbilirubinemia – develops with increased formation of bilirubin in the blood.
  • Coloration of the skin, mucous membranes of the mouth and pharynx, and whites of the eyes lemon-yellow. It occurs only when bilirubin increases by more than 2 times (the norm is 8.5-20.5 µmol/l).
  • General weakness, lethargy.
  • Paleness of the mucous membranes of the mouth and pharynx against the background of the skin.
  • The stool is an intense dark brown color.
  • Apathy, bad mood.
  • Loss of consciousness, neurological disorders (rarely - speech difficulties, drowsiness, decreased visual acuity).
  • Darkening of urine.
• Hepatic hyperibilirubinemia – associated with damage to liver tissue.
  • Coloring of the skin, mucous membranes of the mouth and pharynx, and whites of the eyes into a saffron-yellow, reddish skin color (“red jaundice”) occurs only when bilirubin increases by more than 2 times.
  • General weakness, lethargy.
  • Bitter taste in the mouth.
  • Slight skin itching all over the body.
  • Discomfort, pain in the right hypochondrium.
  • Single (more often) or repeated vomiting.
  • Possible heartburn (a burning sensation in the chest after eating).
  • Periodic nausea.
  • Darkening of urine (it becomes the color of dark beer).
  • Over time, the skin color may take on a greenish tint.

• Subhepatic hyperbilirubinemia - associated with blockage or difficulty in the passage of bile (rich in direct bilirubin - non-toxic, bound) into the intestines.
  • Yellow coloration of the skin, mucous membranes of the mouth and pharynx, and the whites of the eyes. Occurs only when bilirubin increases more than 2 times.
  • Disturbing skin itching all over the body.
  • Discomfort, possible pain in the right hypochondrium.
  • Discoloration of the stool (even turning it white).
  • Large amounts of fat in the stool.
  • Bitter taste in the mouth.
  • Loss of body weight.
  • Hypovitaminosis A, D, E, K – decreased supply of vitamins to the body.

Forms

Highlight 3 forms diseases.

• Prehepatic hyperbilirubinemia – develops with increased formation of bilirubin (a breakdown product of erythrocytes (red blood cells)) in the blood.
• Hepatic hyperibilirubinemia – associated with damage to liver tissue.
• Subhepatic hyperbilirubinemia – associated with blockage or difficulty in the passage of bile (rich in direct bilirubin - non-toxic, bound) into the intestines.

Causes

• Prehepatic hyperbilirubinemia.
  • Anemia (anemia):
    • hemolytic (destruction of erythrocytes (red blood cells));
    • pernicious (insufficient supply of vitamin B12 associated with stomach disease and leading to anemia);
    • hemoglobinopathies (disturbed structure of hemoglobin (oxygen carrier protein in the blood)).
  • Hereditary (passed from parents to children) disorders of the structure of red blood cells (for example, spherocytosis - a defect in the cell wall of the red blood cell).
  • Intoxication (poisoning) medications and alcohol.
  • Infections:
    • sepsis (severe general inflammation of the body caused by the spread of bacteria in the blood);
    • viruses.
  • Blood transfusion (blood group incompatibility).
  • Autoimmune diseases (in which the immune system perceives its cells as foreign and begins to attack them):
    • systemic lupus erythematosus (a chronic disease of connective tissue (participating in the protective and supporting function) and medium-sized blood vessels. Characterized by multiple rashes on the body, joint pain and kidney damage);
    • autoimmune hepatitis (liver inflammation);
    • autoimmune hemolytic anemia.
  • Blood cancer (leukemia).
  • Massive hemorrhages (for example, into the abdominal cavity after abdominal trauma).

• Hepatic hyperibilirubinemia.
  • Hepatitis:
    • viral (caused by hepatitis viruses A, B, C, D, E);
    • medicinal (caused by anabolic steroids (drugs used by professional athletes for elite athletic performance), certain antibacterial drugs and antipyretics).
  • Tumors (neoplasms) and abscesses (ulcers) of the liver.
  • Cirrhosis of the liver (terminal (final) stage of liver disease, in which connective (scar) tissue forms in the liver).
  • Gilbert's syndrome. It is characterized by periodically occurring yellowness of the skin and whites of the eyes without other characteristic and pronounced complaints. Very rarely, short-term pain may occur in the right hypochondrium. It proceeds quite calmly and does not have much impact on a person’s life.
  • Dubin-Johnson syndrome. It is characterized by periodically occurring yellowing of the skin and whites of the eyes along with slight itching. During the period of jaundice, there are feelings of weakness, increased fatigue, loss of appetite, bitterness in the mouth, and rarely, dull aching pain in the right hypochondrium.
  • Rotor syndrome. It is characterized by periodically occurring yellowing of the skin and whites of the eyes along with slight itching. During the period of jaundice, there are feelings of weakness, increased fatigue, loss of appetite, bitterness in the mouth, rarely - dull aching pain in the right hypochondrium, darkening of urine.

• Subhepatic hyperbilirubinemia.
  • Blockage of the common bile duct (bile duct) stone.
  • Cholangitis (inflammation of the bile duct).
  • Narrowing (stricture) of the duct after traumatic injury.
  • Cancer (a rapidly progressing, fast-growing tumor) of the pancreas or the bile duct itself.

Treatment of hyperbilirubinemia

Treatment depends on the cause of hyperbilirubinemia syndrome.

• Antibacterial and antiviral drugs (eliminating the bacterial or viral cause of hyperbilirubinemia).
• Hepatoprotectors (drugs that preserve the activity of liver cells).
• Choleretic agents (increasing the excretion of bile from the gallbladder).
• Immunomodulators (drugs that stimulate your own immune system to fight the disease).
• Anti-inflammatory drugs (reducing or eliminating inflammation in the liver).
• Antioxidants (drugs that reduce and/or eliminate the damaging effects of toxic (poisonous) substances and metabolic products in the body).
• Drugs from the group of barbiturates - drugs that reduce the level of bilirubin (a breakdown product of red blood cells) in the blood.
• Enterosorbents (drugs to enhance the excretion of bilirubin from the intestine).
• Phototherapy can be used - the destruction of bilirubin accumulated in tissues by exposure to light, usually blue lamps. Eye protection is required to prevent burns.

• Diet No. 5 (meals 5-6 times a day, limiting protein to 30-40 g per day with the development of hepatic encephalopathy (a complex of neurological disorders that occurs with liver diseases), excluding spicy, fatty, fried, smoked foods, table salt from the diet ).
• Taking vitamin (B vitamins, folic acid, ascorbic acid, lipoic acid) complexes in courses lasting 1-2 months.
• Enzyme (digestion aid) preparations that do not contain bile.
• Limiting intense physical and psycho-emotional stress.

Complications and consequences

• The development of hypovitaminosis (deficiency of vitamins and microelements in the body associated with disorders of the digestive function).
• The occurrence of liver failure (a set of symptoms associated with a violation of one or more liver functions (detoxification, participation in digestion, participation in the formation of proteins and many others), which develop as a result of acute or chronic destruction of liver cells).
• Development of cholecystitis (inflammation of the gallbladder).
• The occurrence of cholelithiasis (formation of stones in the gall bladder).

Prevention of hyperbilirubinemia

• Diagnosis and timely treatment of the disease(s) that caused the development of hyperbilirubinemia.
  • Anemia (anemia):
    • hemolytic (destruction of erythrocytes (red blood cells));
    • pernicious (insufficient supply of vitamin B12 associated with stomach disease and leading to anemia);
    • hemoglobinopathies (disturbed structure of hemoglobin (oxygen carrier protein in the blood)).
  • Intoxication (poisoning) with drugs and alcohol.
  • Infections:
    • sepsis (severe general inflammation of the body caused by the spread of bacteria in the blood);
    • viruses.
  • Tumors (neoplasms) and abscesses (ulcers) of the liver.
  • Blockage of the common bile duct (bile duct) with a stone.
  • Cholangitis (inflammation of the bile duct).

• A rational and balanced diet (eating foods rich in fiber (vegetables, fruits, herbs), avoiding fried, smoked, too hot or spicy foods).
• Quitting smoking and drinking alcohol.
• Strict control over the intake of medications during various courses of treatment, the expiration date of the drugs, and the exclusion of exceeding the dosage.

Hyperbilirubinemia - what is it? Hyperbilirubinemia is a disease in which the level of bilirubin in the blood increases. The disease often causes diseases of the internal organs (liver failure and cholelithiasis), and in some cases can even lead to serious inflammation of the gallbladder. However, specific treatment for mild stages of the disease is not required.

By the way, many experts do not consider hyperbilirubinemia to be an independent disease. They relate this concept rather to the symptoms of a disease, for example, similar to a headache or an increase in a person’s body temperature in response to the cause of the disease. Nevertheless, every symptom is closely related to a pathological change in the body. But with which one? The answer to this question can only be given by a specialist after a thorough examination of the patient’s condition and after the necessary examinations.

There is a group of diseases in which the skin is characterized by a yellowish tint, but the functioning of the liver and other internal organs remains within normal limits.

In such cases, any morphological changes in the liver are completely absent. When such syndromes occur, doctors talk about the presence of congenital (functional) or benign hyperbilirubinemia.

• Benign hyperbilirubinemia often manifests itself as chronic jaundice. Rarely, it may have the character of intermittent jaundice. If we talk about the causes of such a disease, then this is often a hereditary (family) factor. The medical term “benign hyperbilirubinemia” is a concept of a certain collective nature, talking about various pathologies of metabolic processes associated with the production of bilirubin and an increase in its 1111 level. In people with history of such a disease, the defining signs of the pathology are icteric discoloration of the skin, eye sclera, as well as a high level of bilirubin. This kind of jaundice can appear against the background of severe mental stress, after surgery, or after an infection during pregnancy. It is immediately necessary to clarify that hyperbilirubinemia of this kind during pregnancy does not pose any danger to life and is not a recommendation for termination of pregnancy. Special treatment in such cases is not prescribed.
• Unconjugated hyperbilirubinemia is a disease in which the content of so-called indirect bilirubin in the blood increases. This happens mainly during hemolysis, and is closely related to its intensification. This disease can often be observed in newborns diagnosed with hemolytic disease, with a hereditary form of hemolytic anemia, and also due to damage (mechanical impact) of red blood cells. This often happens when the body is poisoned with toxic substances and heavy metals. An increase in the level of indirect bilirubin in the blood is associated with glucuronidation processes (the main reaction of phase II metabolism of the lymphatic system). Occurs with liver cirrhosis, chronic and acute hepatitis.

• If we are talking about an increased concentration of direct bilirubin, then this disease is called conjugative hyperbilirubinemia, which in principle is a concept such as physiological jaundice. The disease is more common in children born prematurely (premature), because the liver enzyme system in such children is still immature. Hyperbilirubinemia in newborns of this kind, as a rule, does not appear immediately, but only on the 3rd day, progresses for a week, and then gradually declines. At the age of two weeks in full-term infants and three weeks or a little more in premature infants, the conjugative form of jaundice completely disappears.
• Transient hyperbilirubinemia is recorded in most newborns in the very first days of life (60-70%). In such babies, transient jaundice is observed, caused by the processes of hemolysis of red blood cells due to the immaturity of the functions of the internal organs, mainly due to a weak reduction of bile pigments. This form of the disease manifests itself on days 2-3, the color of the stool does not change, and the urine does not change color either. True, increased drowsiness, inactive sucking, and occasional vomiting may be observed. Signs of the disease persist for a week, sometimes a little more. Treatment in such cases is prescribed by a pediatrician. The prognosis of the disease is always favorable and there are generally no consequences. In rare cases, transient jaundice can develop into pathology. This occurs when there is a malfunction in the body against the background of an increase in the concentration of bilirubin, called unconjugated.

Reasons for increased bilirubin levels (direct and indirect):

• anemia (congenital and acquired hemolytic anemia);
• hereditary factor (the structure of red blood cells is impaired);
• poisoning with drugs and alcohol (intoxication of the body);
• infections of various origins (viruses, sepsis);
• blood transfusion, when a patient is mistakenly given blood that is incompatible with his group and Rh factor;
• diseases of an autoimmune nature (in patients, the native immune system considers native cells to be foreign and begins to reject them);
• chronic form of lupus erythematosus;
• inflammation of the liver tissue;
• leukemia;
• tumors;
• hemorrhages in the peritoneum, for example, after severe trauma;
• medications (anabolic steroids), which are often used when playing sports to improve their records;
• medications with antibacterial and antipyretic effects.

Hyperbilirubinemia can have a significant adverse effect on the central nervous system and cause intoxication of the body.

The described causes (hepatitis, cirrhosis), as well as a rapid increase in the level of direct bilirubin in the blood, indicate that the patient’s condition is pathologically severe.

The reasons for high levels of direct bilirubin during pregnancy are stagnation of bile caused by the influence of estrogens. As a rule, this pathology is very rare and develops in the third trimester of pregnancy. If such a disease is detected in a woman during pregnancy, it is necessary to undergo all the necessary examinations to exclude the presence of serious disorders and other dangerous diseases. All therapeutic measures in this case should be aimed at combating the underlying disease.

Symptoms of the disease

Many biochemical blood parameters cannot be visually determined, but hyperbilirubinemia can be determined even with the naked eye, because the symptoms of the disease are too obvious.

Characteristic symptoms are a yellowish (lemon) color of the skin, oral mucosa, whites of the eyes, dark urine (reminiscent of beer), as well as mild but persistent itching of the entire body.

Jaundice discoloration tends to worsen under stress. Obvious jaundice appears only when the bilirubin level increases several times (2 times or more).

Patients may often experience other symptoms:

• discomfort under the right rib;
• nausea, vomiting (profuse or scanty, single, less often repeated);
• heartburn, bitter taste in the mouth (increases after eating);
• weakness, apathy, loss of appetite;
• mood swings;
• drowsiness (mainly during pregnancy);
• stool becomes greasy, colorless, similar to white clay (sometimes it can become dark brown);
• short-term loss of consciousness (rare);
• disorders of the neurological system (difficulty speaking, sharp deterioration of vision);
• sudden weight loss.

During pregnancy, a woman diagnosed with hyperbilirubinemia quickly gets tired, wants to sleep all the time, and becomes slightly lethargic.

Women in an “interesting situation” are advised to follow a diet consisting of gentle foods and not eat a lot of fatty, salty foods. Naturally, we are not talking about any physical activity, especially beyond measure, during pregnancy. Each woman herself should be responsible for her own and her baby’s health, not neglect these recommendations, and, if necessary, undergo treatment prescribed by a therapist.

In patients with a mild form of the disease, liver enlargement and pain on pressure are not observed. But in the moderate and severe stages, during palpation the doctor detects an enlargement of the organ. If, along with pain, there are numerous symptoms, then delaying treatment is extremely irresponsible.

Treatment

When a person is diagnosed with high bilirubin levels, he needs to visit a physician. After the doctor talks with the patient and conducts a thorough examination, he will give a referral for examination, including an ultrasound. Based on the test data, the doctor will be able to determine the causes of the disease and prescribe the necessary treatment.

If the patient suspects hemolytic anemia, he will need to contact a hematologist. Consultation with such a doctor during pregnancy is especially important, because not only the health of the expectant mother, but also the baby’s is at stake.

During pregnancy, treatment is prescribed only after a thorough examination and all necessary studies. Medicines are prescribed based on benefit to the mother and minimal risk to the fetus.

1. If it turns out that the main cause of the disease is bacterial or viral in nature, then the therapist, as a rule, prescribes treatment with antiviral and antibacterial drugs. In addition, the patient will be advised to take medications that stimulate bile secretion.
2. But to boost immunity, drugs called immunomodulators can be prescribed.
3. Anti-inflammatory drugs should be included in complex treatment if there is an inflammatory process in the liver.
4. You may need to take a course of antioxidants to cleanse your body (mainly your intestines) of toxins.
5. In addition to drug therapy, phototherapy is prescribed, which consists of irradiation procedures with blue light from special lamps (such a stream of rays can destroy even persistent bilirubin).

Each patient, on the doctor’s recommendation, must rearrange their diet, namely, remove from the table all foods that do not benefit the body and aggravate the course of the disease.