What Is Unconjugated Bilirubin?

Bilirubin is a type of bile pigment. It is the main pigment in human bile and is orange-yellow. Bilirubin is the main metabolite of iron porphyrin compounds in the body. It is toxic and can cause irreversible damage to the brain and nervous system, but it also has an antioxidant function that can inhibit the oxidation of linoleic acid and phospholipids. Bilirubin is an important basis for judging jaundice clinically and an important indicator of liver function.

Chinese name: Bilirubin
Foreign name: Bilirubin

CAS: 635-65-4
EINECS: 211-239-7

Physiochemical properties of bilirubin

Bilirubin is a bile pigment of biladiene. It is a red-brown pigment body, insoluble in water, hardly soluble in alcohol, ether, and easily soluble in alkali. The maximum absorption is 432 nm (in alkali) and 540 nm (in chloroform). Bile is abundant in humans and carnivores. Blood bilirubin, in the red-purple Hijman van den Bergh reaction caused by the addition of diazo reagents, there are two types: one is a direct type that appears positive without alcohol, and the other is an alcohol Indirect color rendering. The first type is mono- or di-glucuronic acid (ester), and the second is a free type, which is a normal metabolite of hemoglobin. It can be formed by reduction of bilirubin. If further reduced, it becomes ethyl through vinyl Mesobilirubin C ₃₀ H ₄₀ O ₆ N, all methine is saturated with hydrogen to form mesobilirubinogen (urobilinogen).

Bilirubin is a pigment made by hemoglobin in red blood cells. Red blood cells have a fixed life span (the average life expectancy of normal red blood cells is about 120 days) and is destroyed every day. At this time, hemoglobin is broken down into haem and heme. Bilirubin is produced under the action of NADPH and H ions. Trivalent Fe ions and CO, and bilirubin is produced by NADPH and H ions. Heme is then reconstituted into tissue protein.

Due to the toxic nature of bilirubin, bilirubin forms a bilirubin-albumin complex when it is introduced into the blood. The bilirubin-albumin complex is separated into bilirubin and albumin, indirect bilirubin, before entering the liver. After entering the liver, bilirubin will combine with Y protein and Z protein in the liver to form bilirubin-Y protein and bilirubin-Z protein. This reaction is reversible. The bilirubin-Y protein and bilirubin-Z protein generate glucuronate bilirubin under the action of UDP-glucuronidase, which binds bilirubin. Combined with bilirubin entering the small intestine with bile, glucuronic acid is removed in the small intestine to produce bilirubin again, bilirubin generates probilirubin, and probilirubin is further oxidized to yellow-brown bile, which is the main color of stool . Choline in the small intestine can pass through the enterohepatic circulation to reach the liver again, but most of this part of choline is still discharged to the intestine in the original form. This part is called fecal bile. A small portion of procholin enters the systemic circulation and is excreted with urine. It is one of the sources of urine color and is the main pigment in urine. This part is called urobilinogen.

When the red blood cells are damaged and there is hemolysis, it will become indirect hyperbilirubinemia. In addition, direct and indirect hyperbilirubinemia can be caused when liver cells are abnormal, and direct hyperbilirubinemia can be caused when the bile duct and biliary system are blocked. The treatment method when there are outliers, together with other test results, truly grasp the condition, and then treat the cause of the disease. Depending on the situation, treatments such as acute liver failure, hemodialysis, and emergency treatment of extrahepatic bile stasis can be taken separately.

Except for newborns, the average person's value is roughly fixed, and there is no difference in age. In addition, diet and exercise hardly cause changes, but they tend to rise after a long hunger strike. ^[1]

Bilirubin classification

total

Bilirubin Bilirubin: High indirect bilirubin, high direct bilirubin, indicating hepatocellular jaundice, damage to liver cells, and impaired liver function. The liver cannot completely convert indirect bilirubin into direct bilirubin, while the liver Compression of the inner bile duct causes excretion disorders, and direct biliary red cannot be completely discharged to the biliary tract. At the same time, it may be accompanied by acute jaundice hepatitis, chronic active hepatitis, cirrhosis, liver cancer and other diseases.

Direct bilirubin: indicates that it is caused by obstructive jaundice.

Indirect bilirubin: It may be caused by hemolytic jaundice, direct bilirubin elevation may also cause blood group incompatibility during blood transfusion, anemia and other reasons.

The normal range of bilirubin in liver function tests is as follows:

[Total bilirubin] 1.71 21mol / L (0.1mg / dl 1.0mg / dl)

[Direct bilirubin] 0 7.32mol / L (0 0.2mg / dl)

[Indirect bilirubin 0 to 13.68 mol / L (0 to 0.8 mg / dl) ^[2]

Bilirubin source

Porphyrin-containing compounds in the body include hemoglobin, myoglobin, peroxidase, catalase, and cytochrome. Adults produce about 250 to 350 mg of bilirubin daily. The main sources of bilirubin are:

65% to 85% of bilirubin comes from the disintegration of aging red blood cells.

About 15% are formed by the immature red blood cells being destroyed in the bone marrow during the hematopoietic process (ineffective red blood cell production in the bone marrow).

A small amount comes from the destruction and decomposition of hemoprotein, such as myoglobin, peroxidase, and cytochrome. Some people call this bilirubin not produced by the breakdown of senescent red blood cells as "bypass bilirubin." ^[2]

Bilirubin formation

Liver, spleen, bone marrow and other mononuclear phagocytic cell systems engulf aging and abnormal red blood cells, break down hemoglobin, and generate and release free bilirubin. This bilirubin is non-binding (not combined with glucuronic acid, etc.) It is fat-soluble, has little solubility in water, and binds to plasma albumin in blood. Because of its stable binding and poor solubility in water, it cannot be excreted by the kidneys. The qualitative test of bilirubin showed an indirect positive response. Therefore, this bilirubin is called unbound bilirubin.

The processing of bilirubin by liver cells involves three processes.

"Uptake": Unbound bilirubin flows to the liver with the blood, and is quickly taken up by hepatocytes. It binds to the hepatocyte carrier proteins Y and Z (the two carrier proteins, mainly Y protein, can specifically (Combined with organic anions including bilirubin) are passively sent to the smooth endoplasmic reticulum.

"Binding": Y protein-bilirubin and Z protein-bilirubin are in the endoplasmic reticulum of the slippery surface and do not bind bilirubin through the action of UDP-glucuronosyltransferase (UDPGA) of microsomes, and glucose Alkyd binds to conjugated bilirubin. The main bilirubin binding agent is bilirubin diglucuronide, and a part of the bilirubin binding agent is bilirubin sulfate. This bilirubin is characterized by high water solubility and can be excreted from the kidneys. The qualitative test of bilirubin showed a direct positive response. Therefore, this bilirubin is called bound bilirubin.

"Secretion": Combined with bilirubin in the hepatocyte cytoplasm, it is secreted into the capillary bile duct through the bile secretion device (the Golgi complex plays an important role in the cell secretion process) and is excreted with bile. Due to the high concentration of bilirubin in the capillary bile duct, bilirubin secreted from the liver cells into the capillary bile duct is a more complex energy-consuming process.

Red blood cells in the body are constantly renewed, and senescent red blood cells are recognized and engulfed by reticuloendothelial cells due to changes in cell membranes. In reticuloendothelial cells such as the liver, spleen, and bone marrow, hemoglobin is broken down into globin and heme. Heme is catalyzed by heme oxygenase (bemeoxygenase) in the microsomes, and the carbon atoms on the -methine bridge (= CH-) on the heme protoporphyrin IX ring are cleaved to open the protoporphyrin IX ring. And releases CO and Fe ³⁺ and biliverdin IX (biliverdin). Fe ³⁺ can be reused and CO can be excreted from the body. The linear tetrapyrrole bilirubin is further rapidly reduced to bilirubin under the catalysis of bilirubin reductase (NADPH) in the cytosol. Heme oxygenase is the rate-limiting enzyme for bilirubin production, which requires O2 and NADPH to participate, and is induced by the substrate heme. At the same time, heme can also act as a prosthetic group of the enzyme to activate molecular oxygen.

X-ray diffraction analysis of the molecular structure of bilirubin showed that hydrogen bonds were formed within the bilirubin molecule and a specific coil structure was formed between the two pyrrole rings III and IV. Therefore, the III and IV rings can rotate freely. At a certain spatial position, the carboxyl group of the propionate group on the ring III can form a hydrogen bond with the hydrogen of the imino group on the ring I and the carbonyl group on the ring I; The hydrogen of the imino group on ring III and the carbonyl group on ring II form a hydrogen bond. The formation of these six hydrogen bonds causes the entire molecule to curl into a stable conformation. Encapsulating polar groups inside the molecule makes bilirubin show lipophilic and hydrophobic properties. ^[3]

Bilirubin transport

Bilirubin is a fat-soluble substance that is hardly soluble in water under physiological pH conditions. Bilirubin produced in reticuloendothelial cells can enter the blood through the cell membrane, and is mainly associated with plasma albumin or 1 globulin in the blood ( Albumin-based) binds to complexes for transport. This combination increases the solubility of bilirubin in the plasma and facilitates transportation; at the same time, it restricts the free passage of bilirubin through various biological membranes, so that it does not cause toxic effects on tissue cells. Each albumin molecule has a high Affinity binding site and a low affinity binding site. Each molecule of albumin can bind two molecules of bilirubin. In normal people, the plasma albumin per 100ml of plasma can bind to 20-25mg bilirubin, while the normal human plasma bilirubin concentration is only 0.1-1.0mg / dl, so under normal circumstances, the albumin in the plasma is sufficient to bind all Bilirubin. However, certain organic anions such as sulfonamides, fatty acids, bile acids, and salicylic acids can compete with bilirubin and bind to albumin, thereby freeing bilirubin and increasing the possibility of its penetration into cells. Too much free bilirubin can bind to lipids in the basal nucleus of the brain and interfere with the normal function of the brain, called bilirubin encephalopathy or nuclear jaundice. Therefore, in neonatal hyperbilirubinemia, a variety of organic anion drugs must be used with caution.

Combined with bilirubin, it is excreted into the intestine along with bile through the biliary tract, and is reduced to urinary (fecal) procholin by the cells. Most of the urine (faeces) procholin is excreted with feces, and a small part (about 1/10) is absorbed by the intestinal mucosa through the portal vein and reaches the sinus. Most of the urine (faeces) probilirubin that reaches the liver sinus is discharged from the biliary tract with the bile through the liver (liver-intestinal circulation), and only a small part is excreted through the system and excreted through the kidneys.

In the process of bilirubin metabolism, any obstacle occurs in any part of the process, it will cause the bilirubin content in plasma to rise, and produce hyperbilirubinemia. ^[2]

Bilirubin physiological function

Antioxidant function of bilirubin

In vitro tests indicate that bilirubin may be an endogenous antioxidant. ^[4]

Bilirubin for liver cell regeneration

The ratio of bilirubin to albumin in the human body affects liver cell regeneration. ^[2]

Effect of bilirubin on traditional Chinese medicine

In China, bilirubin has always been an important part of artificial bezoar, and the new discovery of the physiological function of bilirubin has brought us the dawn of elaborating the pharmacological mechanism of artificial bezoar at the molecular level. ^[2]

Abnormal bilirubin metabolism

Unbound bilirubin overproduction

This is mainly due to the internal defects of red blood cells (such as the lack of certain enzymes or abnormal hemoglobin) or the damage of red blood cells by exogenous hemolytic factors (such as malaria, immune hemolysis, snake venom, aniline, etc.), causing a large number of red blood cell destruction. A large amount of unbound bilirubin is produced. If the processing capacity of hepatocytes is exceeded, unbound bilirubin in the blood increases, and jaundice occurs. In some patients with anemia, due to the proliferation of the bone marrow red blood cell system, the production of ineffective red blood cells in the bone marrow increases. Such red blood cells are mostly destroyed in situ, failing to enter the blood circulation, or the survival time of red blood cells after entering the blood circulation is very short. Hours) while increasing unbound bilirubin.

Jaundice caused by excessive destruction of red blood cells and increased unbound bilirubin is called hemolytic jaundice. Its bile pigment metabolism is characterized by:

1. Increase in serum unbound bilirubin. Because the liver has a large reserve capacity for processing unbound bilirubin, the total serum bilirubin content generally does not exceed 3-5 mg%. The qualitative test of serum bilirubin showed an indirect positive response.

2. Increased bilirubin in feces (feces) This is due to the increased production of bilirubin by the liver and increased bilirubin excretion into the intestine.

3 Urinary urinary (fecal) procholin is increased and bilirubin is negative. ^[5]

Impaired bilirubin uptake by liver cells

Unbound bilirubin disorders in hepatocyte uptake can be seen for the following reasons:

1. Damage to liver cells (such as viral hepatitis or drug poisoning) reduces the ability of liver cells to take up unbound bilirubin.

2. The development of newborn liver is not perfect, and there are few carrier proteins in hepatocytes, so the ability of hepatocytes to take up bilirubin is insufficient.

3 Gibert's disease is a type of congenital, non-hemolytic jaundice, which is caused by a disorder in the uptake of bilirubin by the sinusoidal microvilli of hepatocytes. Clinical tests found that the liver of such patients has an ability to clear unbound bilirubin only 1/3 of normal people, and its serum bilirubin generally does not exceed 3 mg% (in serum bilirubin above 5 mg% and heavy In the case, it was also found that UDP-glucuronyltransferase activity was reduced in liver tissue).

Bile pigment metabolism of liver cell uptake disorders is characterized by an increase in unbound bilirubin in the blood and an indirect positive response to the qualitative test of serum bilirubin; no bilirubin in the urine; urinary (fecal) bilirubin excreted by feces and urine On the low side. ^[5]

Bilirubin binding disorder in hepatocytes

Obstruction of bilirubin binding in hepatocytes can be seen for the following reasons:

1. Damaged liver cells (such as viral hepatitis or drug poisoning), reduced glucuronide production in the liver, or inhibited UDP-glucuronyl transferase.

2. Inadequate production of UDP-glucuronosyltransferase in the liver of newborns (to be perfected around 10 months after birth). And progesterone in breast milk has inhibitory effect on UDP-glucuronyl transferase.

3 Crigler-Najiar Second Syndrome: This is a non-hemolytic, familial jaundice of neonates with nuclear jaundice. Experiments with isotopically labeled bilirubin have shown that the liver cannot bind bilirubin to glucuronic acid. This is due to the lack of UDP-glucuronyl transferase in the liver. This type of jaundice is very harmful, and most children die from nuclear jaundice, or bilirubin encephalopathy. Because unbound bilirubin is relatively toxic, high concentrations of unbound bilirubin can inhibit oxidative phosphorylation. In addition, unconjugated bilirubin is fat-soluble and has a strong affinity for lipid-rich tissues. In addition, the development of the blood-brain barrier of newborns or infants is not yet perfect. Unconjugated bilirubin easily penetrates into brain tissue and is deposited on nerves. Intracellular, especially in the basal nucleus of the brain, thalamus, and hippocampus are deeply stained by bilirubin (hence the name nuclear jaundice), causing central nervous system dysfunction, which is manifested as loss of energy, lethargy, decreased or enhanced muscle tone, and even angle Arch tension, muscle spasms, and rigidity.

Disturbance of bilirubin binding in muscle cells and bile pigment metabolism

(1) Increased serum unbound bilirubin (Grigler-Najiar type 2 syndrome, UDP-glucuronyl transferase is completely deficient, serum unbound bilirubin can reach 25-45 mg%), serum bilirubin Qualitative tests were indirect positive.

(2) No bilirubin in the urine.

(3) Due to the reduction of combined bilirubin production, the excretion of urine (feces) probilirubin from feces and urine is significantly reduced. ^[5]

Impaired bilirubin secretion by liver cells

Hepatocyte-bound bilirubin is composed of cholesterol, bile acid salts, lecithin, water, and electrolytes to form bile liver, which is secreted into the capillary bile ducts through the Golgi complex and microvilli. "Pure" or selective bilirubin secretion disorders are rare. Dubin-Johnson syndrome and Rotor syndrome are two very similar chronic idiopathic jaundices that can occur in the same family. Bile pigment metabolism is characterized by an increase in serum bilirubin and a direct positive reaction; urinary bilirubin is positive. At the same time, the excretion of sodium phenol tetrabromide (BSP) by liver cells is also impaired, but bile acid salt secretion and bile flow are normal, and there is no cholestasis. At present, it is thought that it may be due to congenital defects in the secretion of bilirubin and negative ion-containing dyes by hepatocytes. Bilirubin cannot be secreted to the capillary bile ducts and flows back into the sinuses, which increases the binding of bilirubin in serum. ^[5]

Bilirubin is too high

First, high bilirubin may be caused by liver disease. Because when liver cells become diseased or due to hepatocyte swelling (mostly caused by liver diseases such as acute jaundice hepatitis, acute yellow liver necrosis, chronic active hepatitis, cirrhosis), the bile ducts in the liver can be compressed. , The excretion of bile is blocked, which can cause the phenomenon of high bilirubin in the blood, and hepatic jaundice occurs (expressed as an increase in both direct bilirubin and indirect bilirubin).

Second, high bilirubin may also be caused by diseases of the biliary system. When tumors or stones appear in the extrahepatic biliary system and the biliary tract is blocked, bile cannot be excreted smoothly, which can cause high bilirubin and obstructive jaundice. ^[5]

Bilirubin hypertensive disease

According to research, the color of bilirubin is orange-yellow, and when the bilirubin in the blood is high, it will show yellowing of the sclera, yellowing of the skin, yellowing of the mucous membrane and other tissues and body fluids, and yellow staining. Specifically:

1. When the serum bilirubin concentration is much higher than the normal value of bilirubin, the skin, eyes, and urine appear yellow, that is, jaundice. Among them, liver inflammation, necrosis, poisoning and other damage can cause jaundice, biliary diseases and hemolytic diseases can also cause jaundice.

2. If the value of bilirubin is between 17.1-34.2 mol / L, jaundice is not visible to the naked eye, which is called hidden jaundice.

3. If the value of bilirubin is greater than 34.2 mol / L, the eyes can see that the eyes are yellow, the skin is yellow, and the urine is yellow. This is called overt jaundice. The higher the value of total bilirubin, the more severe the jaundice.

Causes of high bilirubin

The life span of human red blood cells is generally 120 days. After red blood cells die, they become indirect bilirubin (I-Bil), which is converted into direct bilirubin (D-Bil) by the liver, forming bile, which is excreted into the biliary tract, and finally excreted in the stool. This is the normal conversion of bilirubin in the liver.

However, if other diseases occur, liver metabolism will be abnormal, and indirect bilirubin cannot be normally converted into direct bilirubin, resulting in high bilirubin in serum. Hemolytic jaundice may occur at this time; when liver cells are diseased, or bilirubin cannot be normally converted into bile, or due to swelling of the liver cells, the bile ducts in the liver are compressed, the excretion of bile is blocked, and the bile in the blood is blocked Erythromycin rises, and hepatic jaundice occurs at this time; once a tumor or stone appears in the biliary system outside the liver, the biliary tract is blocked, bile cannot be excreted smoothly, and obstructive jaundice occurs. The jaundice of hepatitis patients is generally hepatocellular jaundice, which means that both direct bilirubin and indirect bilirubin are increased, while patients with cholestatic hepatitis are mainly elevated in direct bilirubin. So pathologically, the conditions that cause high bilirubin in the blood mainly include the following:

1. Total bilirubin and direct bilirubin increase: intrahepatic and extrahepatic obstructive jaundice, pancreatic head cancer, capillary bile duct hepatitis, and other bile stasis syndromes.

2. Increase in total bilirubin and indirect bilirubin: hemolytic anemia, incompatible blood transfusion, malignant disease, neonatal jaundice, etc.

3. Total bilirubin, direct bilirubin, and indirect bilirubin are all increased: acute jaundice hepatitis, chronic active hepatitis, cirrhosis, and toxic hepatitis.

4. High indirect bilirubin, excessive destruction of red blood cells in the body, will prevent the liver from completely converting indirect bilirubin into direct bilirubin, resulting in high indirect bilirubin in the body, causing high indirect bilirubin. The reasons are hemolytic anemia, blood group incompatibility during transfusion, neonatal jaundice, etc .;

5. Direct bilirubin is high. If liver cells are damaged, direct bilirubin cannot be converted into bile normally, or bile excretion is blocked, it will cause high direct bilirubin and common causes of high direct bilirubin. There are intrahepatic and extrahepatic obstructive jaundice, pancreatic head cancer, capillary bile duct hepatitis, and other bile stasis syndromes. ^[5]

High bilirubin harm

Bilirubin is the waste product of the heme metabolism of red blood cells in the blood. If the serum bilirubin is too high, it may indicate abnormal information such as liver disease or bile duct obstruction. The level of serum bilirubin value represents the severity of the abnormality. If the red blood cells are destroyed too much, too much indirect bilirubin is produced, which will prevent the liver from completely converting it into direct bilirubin, which will cause hemolytic jaundice.

Bilirubin cannot be normally converted into bile, liver cell lesions, hepatocyte swelling, compression of the bile ducts in the liver, or obstruction of bile excretion will increase bilirubin in the blood, and then cause hepatocellular jaundice; extrahepatic Tumors or stones in the biliary system, obstruction of the biliary tract, bile cannot be smoothly excreted, and obstructive jaundice occurs. The jaundice of hepatitis patients is mainly hepatocellular jaundice.

1) Hemolytic jaundice. Due to some hemolytic diseases, red blood cells can be destroyed too much, leading to an increase in indirect bilirubin in the blood.

2) Hepatocellular jaundice.

Harm of indirect high bilirubin:

1) Excessive destruction of red blood cells.

2) Indirect bilirubin can penetrate cell membranes, has toxic effects on cells, and cannot be excreted through the kidneys.

3) Indirect bilirubin is high, which indicates that the liver's compensatory ability is low or the liver has a problem.

The harm of high direct bilirubin:

1) Direct high bilirubin is usually caused by liver disease. Acute jaundice hepatitis, acute yellow liver necrosis, chronic active hepatitis, and cirrhosis are common.

2) If the patient's red blood cells are destroyed too much and indirect bilirubin is produced too much, the liver cannot completely convert it into direct bilirubin, and hemolytic jaundice will occur.

Harm of high total bilirubin:

1) High total bilirubin causes liver diseases, acute jaundice hepatitis, acute liver necrosis, chronic active hepatitis, cirrhosis, etc.

2) Extrahepatic diseases caused by high total bilirubin, hemolytic jaundice, neonatal jaundice, gallstone disease, pancreatic head disease, etc. ^[5]

High bilirubin treatment

It is recommended that patients with high bilirubin go to the hospital for further examination to clarify and formulate a medication plan according to specific conditions. For example, in the treatment of patients with hepatitis B with high bilirubin, it is necessary to check liver function, HBVDNA, etc., and perform antiviral treatment or liver protection and yellowing treatment according to the test results. In addition, it is also recommended that patients with high bilirubin develop good habits and pay attention to the following aspects in daily life:

1. The diet should be light. Eat more legumes, fish, vegetables, fruits and other foods that contain a lot of vitamins A, B, C, and E. They have good antioxidant functions and are easy to digest and absorb. Do not eat too many sweets. , Alcohol.

2. Eat more seafood, shiitake mushrooms, sesame, walnuts, jujube, lean meat and animal liver.

3. It is advisable to rest in bed for 1-2 hours after a meal to ensure that the liver has sufficient blood supply, which is beneficial to the repair and regeneration of liver cells and helps restore liver function.

It should be noted that patients with high bilirubin should pay attention to regular review of liver function during the treatment process, observe the treatment effect, and adjust the treatment plan in time. ^[4]

Bilirubin is high in infant bilirubin

Normal bilirubin

The normal range of infant bilirubin is 3.4 to 17.1 mol / L of total bilirubin, direct bilirubin is below 0 to 6.8 mol / L, and indirect bilirubin is below 1.7 to 10.2 mol / L.

Infant bilirubin threshold value range: The critical value of total bilirubin is 1.3 to 1.5 mg / dl. If the infant exceeds this value, it can be regarded as abnormal.

The normal physiological period of infant bilirubin fluctuates: serum bilirubin gradually increases from 17 to 51 mol / L at birth to 86 mol / L or more after 24 hours of birth, clinically jaundice occurs without other symptoms, 1 to 2 Automatically subsides within the week, which is the normal physiological jaundice period of infant bilirubin. The serum bilirubin in infants with physiological jaundice does not exceed 204 mol / L in term infants, and the preterm infant does not exceed 255 mol / L, and the occurrence of bilirubin encephalopathy should be noted and prevented.

Bilirubin physiological jaundice

After the baby is born for 24-72 hours, sclera, skin, and urine appear yellow, and indirect bilirubin is high. At this time, the baby is in good spirits, has strong milk, does not cry and does not cry, and gradually decreases after one week, and subsides cleanly within two weeks. Premature babies usually subside within 3 weeks, jaundice appears late, and early retreat. This is a normal phenomenon, and parents need not worry.

Bilirubin pathological jaundice

Within one day after the baby was born, jaundice occurred, and the indirect bilirubin level was too high. At this time, the baby was in a bad mood, refused milk, and cried. He would not return after two weeks. He needed to go to the hospital for examination and treat according to the condition. ^[6]

Bilirubin considerations

Patients with high bilirubin should have a light diet and be nutritious. Such as legume products, fish, vegetables, fruits, etc., contain a lot of vitamins A, B, C, E, have good antioxidant function and easy digestion and absorption. Should eat more mushrooms, sesame, walnuts, jujube, lean meat, but patients with high bilirubin should not eat animal liver foods. Hepatitis B patients must pay attention to high bilirubin, and go to regular liver disease hospitals for treatment in a timely manner.

Patients with high bilirubin should refrain from drinking alcohol. Alcohol in alcohol is the most direct and most harmful to the liver. Studies have shown that more than 80% of heavy drinkers have a degree of fatty liver, 10% to 30% can develop alcoholic hepatitis, and 10% to 20% will develop cirrhosis. Usually drink plenty of water. Drinking water can replenish body fluids, enhance blood circulation and promote metabolism. Drinking more water can also promote glands. Patients with high bilirubin, especially digestive glands and secretion of pancreatic juice and bile, will help digestion, absorption and Elimination of waste can reduce liver damage caused by metabolites and toxins.

Patients with high bilirubin should exercise properly to allow the body's metabolism, blood circulation to increase, help waste of liver and kidney metabolism, and excrete them quickly-sweating, which is good for the health of patients with high bilirubin. It can also improve the human body's ability to resist diseases, so patients with high bilirubin usually have more outdoor activities, such as walking, walking, playing basketball, playing Taijiquan, etc. However, people with poor liver should not exercise vigorously. ^[2]