Bilirubin isBilirubinIt is one of the major pigments in human bile.Bilirubin isIron porphyrinThe main metabolite of the compound, toxic, can cause irreversible damage to the brain and nervous system, but also has antioxidant function, which can inhibitlinoleic acidandphospholipidOxidation of.Bilirubin is clinically determinedjaundiceIt is also an important indicator of liver function.
In 1847, Vichow first discovered bilirubin.[8]Pigment histochemistry actually started from Vichow's extensive research on hemoglobin decomposition products in tissues in 1847.He was the first person to use the term haematoitin (bilirubin) for the yellow crystalline pigment appearing in the bleeding area.[9]
In 1883, Ehrich discovered the azo reaction of bilirubin;From 1913 to 1916, van den Bergh discovered direct and indirect bilirubin;In 1942, Fischer and Plininger chemically synthesized bilirubin;In 1956, Watson applied the van den Bergh test to clinical practice.[8]
With the progress of biochemistry, immunology, molecular science and imaging, the molecular structure and chemical properties of bilirubin have been further understood, which has important clinical significance for understanding the normal metabolism and metabolic abnormalities of bilirubin.When bilirubin accumulates in the sclera, mucosa and skin to a certain extent, it will appear yellow staining, which is clinically calledjaundice。[8]
Physical and chemical properties
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Bilirubin belongs toDicarboxylinIt is a kind of bile pigment, which is reddish brown pigment body, insoluble in water, insoluble in alcohol, ether, and soluble in alkali. The maximum absorption is 432 nm (in alkali), 540 nm（chloroformMedium).Human and carnivorous animals have abundant bile.There are two types of blood bilirubin in the red purple Hijman van den Bergh reaction when diazo reagent is added: one is the direct type without alcohol, and the other is the indirect type when alcohol is added.The first type is mono or diglucuronic acid (ester), and the second type is free. It is the normal metabolite of hemoglobin, which can be formed by the reduction of biliverdin. If further reduction is made, it can be converted into ethyl middle bilirubin C through vinylthirtyHfortyOsixN，Methylene is completely saturated with hydrogen to form cholechrorane (urobilinogen).
Bilirubin is a pigment produced by hemoglobin in red blood cells. Red blood cells have a fixed life span (the average life span of normal red blood cells is about 120 days), and are destroyed every day.At this time, hemoglobin will be decomposed intoHeme(haem) andhemoglobin。The formation of n-heme under the action of NADPH and H ionBiliverdin, trivalent Fe ions, CO, biliverdin, and then generate bilirubin under the action of NADPH and H ions.Heme will be reprocessed into tissue protein.
Due to the toxicity of bilirubin, bilirubin forms a bilirubin albumin complex after entering the blood.The bilirubin albumin complex is separated into bilirubin andalbumin, i.eIndirect bilirubin。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.Bilirubin-Y protein and bilirubin-Z protein generate bilirubin glucuronate under the action of UDP glucuronate convertase, namelyConjugated bilirubin。The conjugated bilirubin enters the small intestine with bile, and the glucuronic acid is removed in the small intestine to generate bilirubin again. Bilirubin generates bilirubin, which is further oxidized to yellow brown bilirubin, which is the main color of feces.The bilirubin in the small intestine can reach the liver again through the enterohepatic circulation, but most of this bilirubin is still discharged into the intestine in its original form, which is calledFecal bilinogen。A small part of probilirubin enters the systemic circulation and is discharged with urine.It is one of the sources of urine color and the main pigment in urine. This part is calledUrobilinogen。
When red blood cells are damaged and hemolysis occurs, they will become indirect hyperbilirubinemia.In addition, when hepatocytes are abnormal, direct and indirect hyperbilirubinemia will be caused, and when bile duct and biliary system are blocked, direct hyperbilirubinemia will be caused.The treatment method in case of abnormal value shall be combined with other examination results to truly grasp the condition and then treat the cause of disease.According to different situations, we can take measures such as acute liver failure, hemodialysis, and emergency treatment of extrahepatic cholestasis.
Except for newborns, the average person's value is roughly fixed, and there is no age difference.In addition, diet and exercise will hardly change, but there will be an upward trend after a long hunger strike.[1]
Indirect bilirubin: it may beHemolytic jaundiceAs a result, the direct increase of bilirubin may also be caused by blood type incompatibility and anemia during blood transfusion.
In the liver function test, the normal value range of bilirubin
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Normal value range
total bilirubin
1.71～21 μmol/L（0.1mg/dl～1.0mg/dl）
Direct bilirubin
0～7.32 μmol/L （0～0.2mg/dl）
Indirect bilirubin
0～13.68 μmol/L（0～0.8mg/dl）[2]
source
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Porphyrin containing compounds in the body include hemoglobin, myoglobin, peroxidase, catalase and cytochrome.Adults produce about 250~350 mg of bilirubin every day. The main sources of bilirubin are:
① 65%~85% of bilirubin comes from the disintegration of aging red blood cells.
② About 15% is formed by the destruction of immature red blood cells in the bone marrow (invalid red blood cells in the bone marrow) during the hematopoietic process.
③ A small amount comes from the destruction and decomposition of heme containing proteins, such as myoglobin, peroxidase, cytochrome, etc.Some people call this bilirubin, which is not produced by the decomposition of aging red blood cells, "bypass bilirubin".[2]
formation
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The monocyte phagocyte system such as liver, spleen and bone marrow will be aging and abnormalred blood cellPhagocytosishemoglobin, produce and release free bilirubin, which is non binding (notGlucuronic acidFat soluble, very low solubility in waterPlasma albumincombination.Because its combination is very stable and insoluble in water, it cannot be excreted by the kidney.Bilirubin qualitative test is indirectpositive reaction。Therefore, this bilirubin is called unconjugated bilirubin.
The treatment of bilirubin by hepatocytes includes three processes.
"Uptake": unconjugated bilirubin goes to the liver with blood flow, and is quickly taken up by hepatocytes, and is passively delivered to the smooth endoplasmic reticulum by binding with Y protein and Z protein (the two carrier proteins, mainly Y protein, can specifically bind organic anions including bilirubin).
"Binding": Y protein bilirubin and Z protein bilirubin are in the smooth endoplasmic reticulum, and unconjugated bilirubin is combined with glucuronic acid through the action of microsomal UDP glucuronosyltransferase (UDPGA) and converted into conjugated bilirubin.The conjugated bilirubin is mainly bilirubin diglucuronate, and the other part of the conjugated bilirubin is bilirubin sulfate.This bilirubin is characterized by its high water solubility and can be discharged from the kidney. The qualitative test of bilirubin showed a direct positive reaction.Therefore, this bilirubin is called conjugated bilirubin.
"Secretion": conjugated bilirubin is secreted into the bile capillaries through the bile secretory organ (Golgi complex plays an important role in cell secretion) in the cytoplasm of liver cells, together with bile salts, and then discharged with bile.Due to the high concentration of bilirubin in the bile capillaries, the secretion of bilirubin from hepatocytes into the bile capillaries is a complex process of energy consumption.
The red blood cells in the body are constantly updated. The aging red blood cells are recognized and swallowed by the reticuloendothelial cells due to the changes of cell membrane. In the reticuloendothelial cells such as liver, spleen and bone marrow, hemoglobin is decomposed into globin and heme.Heme in microsomesHeme oxygenase(bemeoxygenase) catalyzed α - methylene bridge (=CH-）The two sides of the carbon atom of3+And biliverdin IX.Fe3+It can be reused and CO can be discharged from the body.The biliverdin of linear tetrapyrrole is further rapidly reduced to bilirubin under the catalysis of biliverdin reductase (NADPH) in the cytosol.Heme oxygenase is the rate limiting enzyme for bilirubin production and requires OtwoAnd NADPH, induced by the substrate heme.At the same time, heme can be used as the auxiliary group of enzyme to activate molecular oxygen.
X-ray diffraction analysis of the molecular structure of bilirubin shows that the hydrogen bond is formed in the bilirubin molecule and there is a single bond connection between the III and IV pyrrole rings in the molecule with a specific curly structure.Therefore, ring III and ring IV can rotate freely.At a certain spatial position, the carboxyl group of propionic acid group on ring III can form hydrogen bond with the hydrogen of imino group on ring IV, ring I and the carbonyl group on ring I;The carboxyl group of propionic acid group on ring IV also forms hydrogen bond with the hydrogen of imino group on ring II and III and the carbonyl group on ring II.The formation of these six hydrogen bonds curls the whole molecule into a stable conformation.The polar group is enclosed inside the molecule, so that bilirubin shows lipophilic and hydrophobic characteristics.[3]
transport
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Under physiological pH conditions, bilirubin is a fat soluble substance that is insoluble in water. Bilirubin generated in reticuloendothelial cells can freely enter the blood through the cell membrane. In the blood, it mainly combines with plasma albumin or α 1-globulin (mainly albumin) to form a complex for transportation.This combination increases the solubility of bilirubin in plasma and facilitates transportation;At the same time, it also restricts bilirubin to pass through various biomembranes freely, so that it will not have toxic effects on tissues and 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 20-25mg of bilirubin, while the plasma bilirubin concentration in normal people is only 0.1-1.0mg/dl, so under normal circumstances, the albumin in plasma is enough to bind all bilirubin.However, some organic anions such as sulfonamides, fatty acids, bile acids, salicylic acids, etc. can compete with bilirubin to bind to albumin, thus making bilirubin free and increasing the possibility of its penetration into cells.Excess free bilirubin can combine with lipids in the basal nuclei of the brain and interfere with the normal function of the brain, which is called bilirubin encephalopathy or nuclear jaundice.Therefore, in neonatal hyperbilirubinemia, a variety of organic anion drugs must be used with caution.
The conjugated bilirubin is discharged into the intestine along with bile through the biliary tract, and is reduced to pro urine (fecal) bilirubin by cells.Most of the urine (fecal) bilirubin is excreted with the feces, and a small part (about 1/10) is absorbed by the intestinal mucosa and reaches the hepatic sinus through the portal vein.Most of the pro urinary (fecal) bilirubin that reaches the hepatic sinuses passes through the liver and is discharged again with bile from the biliary tract (hepatointestinal circulation), while only a small part passes through the systemic circulation and is discharged through the kidney.
In the process of bilirubin metabolism, any obstacle in any link will cause the increase of bilirubin content in plasma and produce hyperbilirubinemia.[2]
physiological function
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Antioxidant function
In vitro experiments showed that bilirubin may be an endogenous antioxidant.[4]
For hepatocyte regeneration
The ratio of bilirubin to albumin in human body affects the regeneration of hepatocytes.[2]
Effect on traditional Chinese medicine
In China, bilirubin has always been an important part of artificial bezoar. The new discovery of the physiological function of bilirubin has brought dawn for us to explain the pharmacological mechanism of artificial bezoar at the molecular level.[2]
Measurement and evaluation
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Measurement principle
Diazo reagent method
The diazo reagent method, namely the improved J-G method, also known as the p-aminobenzene sulfonic acid method, is recommended by WHO and the clinical examination center of the Health and Family Planning Commission.The conjugated bilirubin in serum can directly react with diazo reagent to produce azobilirubin;Under the same conditions, free bilirubin breaks the hydrogen bond under the action of accelerators (caffeine and sodium benzoate) and reacts with diazo reagents to produce azobilirubin. Sodium acetate maintains pH and has an accelerating effect at the same time.Ascorbic acid (or sodium azide) destroys the remaining diazo reagent, stops the azo reaction of binding bilirubin, and prevents the slow reaction of free bilirubin;Add alkaline sodium tartrate to transfer the maximum absorbance from 530 nm to 598 nm, increasing the sensitivity and specificity. The final green color is the mixture of blue alkaline bilirubin and yellow pigment formed between caffeine and p-aminobenzenesulfonic acid.[10]
Bilirubin oxidase method
Bilirubin oxidase (B0) can catalyze the oxidation of bilirubin in samples to biliverdin, and further catalyze the oxidation of biliverdin to a purplish compound with unknown structure;At 460nm wavelength, the decrease in absorbance is proportional to the concentration of bilirubin in serum.Since B0 can oxidize all bilirubin components in alkaline environment, this characteristic can be used for determination of total bilirubin;Under acidic conditions, monoglucuronate bilirubin mBc (monoglucuronate bilirubin), diglucurate bilirubin dBc (diglucurate bilirubin) and most B8 (8-bilirubin) are oxidized, only Bu (unconjugated bilirubin) is not oxidized, which can be used for Be (conjugated bilirubin) (conjugated bilirubin or direct bilirubin)Determination of;Therefore, total/direct bilirubin can be measured quantitatively according to the optimal pH difference of different bilirubin reactions.[10]
Methodological evaluation
The improved J-G method has high sensitivity, good precision and accuracy. It can detect conjugated bilirubin and unconjugated bilirubin at the same time, with few error factors and little hemolytic interference. It is suitable for automatic analysis.Mild hemolysis has no effect on the method, but severe hemolysis can lower the result.Sodium azide can destroy diazo reagent. The quality control serum using sodium azide as antiseptic may cause incomplete reaction, or even no color.Lipid blood and lipolysin interfere with the determination, and fasting blood should be taken as far as possible.The determination of total bilirubin in serum by this method is not affected by temperature change at 10~37 ℃, and the color reaction is very stable within 2 hours.The bilirubin oxidation method has small amount of samples and reagents, good specificity, high sensitivity, good repeatability, simple and rapid manual operation, and higher precision than diazo reaction method;Anti interference ability is better than diazo method, hemolysis interference is small, suitable for automated instrument analysis, and may be developed as a reference method.Enzymatic determination of conjugated bilirubin solved the problem of large variation of conjugated bilirubin measurement value caused by different reagent types and concentrations, different pH and duration of complex reaction by diazo reaction method, and improved the specificity and accuracy of conjugated bilirubin analysis;TBIL, Bu and Be can be determined according to the optimal pH difference of different bilirubin reactions.However, this method often produces turbidity in the determination of jaundice serum or heparin anticoagulant plasma, which affects the results, so heparin anticoagulant should be avoided;In enzymatic determination, bilirubin oxidase is easily affected by serum protein, especially albumin. It can be inferred that bilirubin 8 bound to serum protein is resistant to the action of bilirubin oxidase within the pH range of maintaining albumin a spiral chain: commercial reagents are expensive.[10]
Abnormal metabolism
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Excessive production of unconjugated bilirubin
This is mainly due to the internal defects of red blood cells (such as the lack of some enzymes or abnormal hemoglobin) or the damage of red blood cells caused by external hemolytic factors (such as malaria, immune hemolysis, snake venom, aniline, etc.), resulting in the destruction of a large number of red blood cells and the production of a large number of unconjugated bilirubin. If the processing capacity of liver cells is exceeded, the unconjugated bilirubin in the blood will increase,Jaundice occurs.In some anemic patients, due to the proliferation of the bone marrow red cell system, invalid red blood cells in the bone marrow increase. Such red blood cells are mostly destroyed in "situ" and fail to enter the blood circulation, or the survival time of the red blood cells after entering the blood circulation is very short (several hours), resulting in the increase of unconjugated bilirubin.
Jaundice caused by excessive destruction of red blood cells and increase of unconjugated bilirubin is calledHemolytic jaundice（hemolytic jaundice）。The characteristics of bile pigment metabolism are:
1. Serum unconjugated bilirubin increases. Because the liver has a great reserve for unconjugated bilirubin treatment, the total serum bilirubin content generally does not exceed 3-5 mg%.The qualitative test of serum bilirubin showed indirect positive reaction.
2. The increase of pro urine (fecal) bilirubin in feces is due to the increased production of conjugated bilirubin by the liver and the increase of bilirubin discharged into the intestine.
3. Probilinogen in urine (feces) increased and bilirubin was negative.[5]
Obstruction of bilirubin uptake by hepatocytes
The disorder of unconjugated bilirubin uptake by hepatocytes can be seen in the following reasons:
1. The function of hepatocytes to absorb unconjugated bilirubin is reduced due to damage to hepatocytes (such as viral hepatitis or drug poisoning).
2. The development of newborn liver is not perfect, and the carrier protein in hepatocytes is less, so the ability of hepatocytes to absorb bilirubin is insufficient.
3. Gilbert's disease is a congenital, non hemolytic jaundice, which is caused by the obstruction of bilirubin uptake by the microvilli on the sinusoidal side of hepatocytes.The clinical test found that the liver clearance capacity of such patients to unconjugated bilirubin was only 1/3 of that of normal people, and their serum bilirubin generally did not exceed 3 mg% (in cases where the serum bilirubin was higher than 5 mg% and in severe cases, it was also found that the activity of UDP glucuronosyltransferase in liver tissue was reduced).
The characteristics of bilirubin metabolism in liver cell uptake disorder are: unconjugated bilirubin in blood is increased, and the qualitative test of serum bilirubin shows indirect positive reaction;No bilirubin in urine;The urine (fecal) bilinogen excreted from feces and urine is low.[5]
Bilirubin binding disorder in hepatocytes
Bilirubin binding disorder in hepatocytes can be found in the following reasons:
1. Liver cells are damaged (such as viral hepatitis or drug poisoning), which reduces the production of glucuronic acid in the liver or inhibits UDP glucuronosyltransferase.
2. The production of UDP glucuronosyltransferase in the liver of newborns is insufficient (it will be gradually perfected about 10 months after birth).Moreover, pregnanediol in maternal milk can inhibit UDP glucuronosyltransferase.
3. Crigler Najiar syndrome: it is a kind of neonatal non hemolytic and familial jaundice with nuclear jaundice.The experiments with isotope labeled bilirubin proved that the liver could not bind bilirubin to glucuronic acid.This is due to the lack of UDP glucuronosyltransferase in the liver.This kind of jaundice is very harmful. Most children die of nuclear jaundice, or bilirubin encephalopathy.Because unconjugated bilirubin is toxic, high concentrations of unconjugated bilirubin can inhibit oxidative phosphorylation.In addition, unconjugated bilirubin is fat soluble and has a large affinity with lipid rich tissues;In addition, the blood brain barrier of neonates or infants is not well developed, unconjugated bilirubin is easy to penetrate into brain tissue and deposit in nerve cells, especially in the basal nucleus of the brain, thalamus, and hippocampus, which are deeply stained by bilirubin (hence the name "nuclear jaundice"), causing functional impairment of the central nervous system, which is manifested in low spirit, lethargy, decreased or increased muscle tension, and even hyperkeratosisMuscle cramps and rigidity.
Bilirubin binding disorder in muscle cells, metabolic characteristics of bilirubin
(1) Serum unconjugated bilirubin is increased (Grigler Najiar syndrome type I, UDP glucuronosyltransferase is completely deficient, serum unconjugated bilirubin can be as high as 25-45mg%), and serum bilirubin qualitative test shows indirect positive reaction.
(2) There is no bilirubin in urine.
(3) As the production of conjugated bilirubin is reduced, the excretion of urine (fecal) bilirubin from feces and urine is significantly reduced.[5]
Obstruction of hepatocyte secretion of bilirubin
The conjugated bilirubin in hepatocytes is composed of liver bile with cholesterol, bile salts, lecithin, water and electrolytes, and secreted to the bile capillaries through Golgi complex and microvilli."Pure" or selective bilirubin secretion disorders are rare.Dubin Johnson syndrome and Rotor syndrome are two very similar chronic idiopathic jaundice, which can occur in the same family.The characteristics of its bile pigment metabolism are: the conjugated bilirubin in serum increases, showing direct positive reaction;Urine bilirubin is positive.At the same time, the excretion of sodium phenoltetrabromophthalide (BSP) by hepatocytes was also obstructed, but the secretion of bile salts and bile flow were normal, and there was no cholestasis.At present, it is believed that the secretion of bilirubin and anionic dyes by hepatocytes may have congenital defects, and bilirubin can not be secreted directionally into the bile capillaries and back into the sinuses, which increases the conjugated bilirubin in the serum.[5]
Hyperbilirubin
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1、 High bilirubin may be caused by liver disease.Because when liver cells become diseased or swollen (mostly caused by liver diseases such as acute icteric hepatitis, acute yellow liver necrosis, chronic active hepatitis, cirrhosis, etc.), the bile ducts in the liver may be compressed and the excretion of bile may be blocked, which may lead to the phenomenon of high bilirubin in the blood,However, hepatocyte jaundice occurred (both direct and indirect bilirubin increased).
2、 High bilirubin may also be caused by diseases of the biliary system.When tumors or stones occur 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]
Hyperphysia
According to research, the color of bilirubin is orange yellow, and when the bilirubin in the blood is high, it will be yellow in the sclera, skin, mucous membrane and other tissues and body fluids.Specifically:
1. When the concentration of serum bilirubin is far higher than the normal value of bilirubin, the skin, eyes and urine appear yellow, that is, jaundice.Among them, jaundice can be caused by inflammation, necrosis, poisoning and other damage to the liver, as well as biliary diseases and hemolytic diseases.
2. If the value of bilirubin is between 17.1-34.2 μ mol/L, there is no jaundice visible to the naked eye, which is called recessive jaundice.
3. If the value of bilirubin is greater than 34.2 μ mol/L, the eyes, skin and urine can be seen to be yellow with the naked eye, which is called dominant jaundice.The higher the value of total bilirubin, the heavier the jaundice.
Reasons for high
The life span of human red blood cells is generally 120 days.After death, red blood cells become indirect bilirubin (I-Bil), which is converted into direct bilirubin (D-Bil) through the liver to form bile, which is discharged into the biliary tract, and finally discharged through the stool.This is the normal transformation of bilirubin in the liver.
However, if other diseases occur, it will lead to abnormal liver metabolism, and then indirect bilirubin cannot be converted into direct bilirubin normally, resulting in high serum bilirubin.Hemolytic jaundice may occur at this time;When the liver cells are diseased, or because bilirubin cannot be converted into bile normally, or because the liver cells are swollen, the bile ducts in the liver are pressed, the excretion of bile is blocked, and the bilirubin in the blood is increased, then hepatocellular jaundice occurs;Once the extrahepatic biliary system has tumors or stones, the biliary tract will be blocked, bile can not be discharged smoothly, and obstructive jaundice will occur.The jaundice of hepatitis patients is generally hepatocyte jaundice, that is to say, both direct bilirubin and indirect bilirubin are increased, while the direct bilirubin is mainly increased in patients with cholestatic hepatitis.Pathologically, the high bilirubin in the blood mainly includes the following:
1. Increased total bilirubin and direct bilirubin: intrahepatic and extrahepatic obstructive jaundice, pancreatic head cancer, cholangiocapillary hepatitis and other bile stasis syndrome.
2. Increased total bilirubin and indirect bilirubin: hemolytic anemia, incompatible blood type transfusion, malignant disease, neonatal jaundice, etc.
3. Total bilirubin, direct bilirubin and indirect bilirubin increased: acute icteric hepatitis, chronic active hepatitis, cirrhosis, toxic hepatitis, etc.
4. The indirect bilirubin is on the high side, and the red blood cells in the body are destroyed too much, which will make the liver unable to completely convert the indirect bilirubin into direct bilirubin, leading to the high indirect bilirubin in the body. The common reasons for the high indirect bilirubin are hemolytic anemia, blood type incompatibility during blood transfusion, neonatal jaundice, etc;
5. Direct bilirubin is on the high side. If hepatocytes are damaged, direct bilirubin cannot be converted into bile normally, or bile excretion is blocked, it will cause direct bilirubin to be on the high side. The common causes of direct bilirubin on the high side include intrahepatic and extrahepatic obstructive jaundice, pancreatic head cancer, bile capillary hepatitis and other bile stasis syndrome.[5]
High hazard
Bilirubin is the waste of heme metabolism of red blood cells in blood.If the serum bilirubin is too high, it indicates abnormal information such as liver disease or bile duct obstruction. The value of serum bilirubin represents the severity of the abnormality.If the red blood cells are destroyed too much, the indirect bilirubin will be produced too much, which will make the liver unable to completely convert it into direct bilirubin, and then hemolytic jaundice will occur.
If bilirubin cannot be transformed into bile normally, liver cells become diseased, liver cells become swollen, bile ducts in the liver are pressed or bile excretion is blocked, the bilirubin in the blood will rise, and then hepatocyte jaundice will occur;The extrahepatic biliary system has tumors or stones, and the biliary tract is blocked, so the bile can not be discharged smoothly, and then obstructive jaundice occurs.The jaundice of hepatitis patients is mainly hepatocyte jaundice.
1) Hemolytic jaundice.Because of some hemolytic diseases, red blood cells can be destroyed too much, resulting in the increase of indirect bilirubin in blood.
2) Hepatocellular jaundice.
High projects
harm
High indirect bilirubin
Excessive destruction of red blood cells.
Indirect bilirubin can pass through the cell membrane and is toxic to cells. It cannot be discharged from the body through the kidney.
High indirect bilirubin indicates that the compensatory capacity of the liver is low or the liver has problems.
High direct bilirubin
It is usually caused by liver diseases, including acute icteric hepatitis, acute yellow liver necrosis, chronic active hepatitis, cirrhosis, etc.
If there is too much destruction of red blood cells in the patient's body and too much indirect bilirubin is produced, the liver will not be able to completely convert it into direct bilirubin, and hemolytic jaundice will occur.
High total bilirubin
It causes liver diseases, acute icteric hepatitis, acute liver necrosis, chronic active hepatitis, cirrhosis, etc.
It is suggested that patients with high bilirubin should go to the hospital for further examination to clarify and formulate medication plans according to specific conditions.For example, for the treatment of hepatitis B patients with high bilirubin, it is necessary to check the liver function, HBV DNA, etc., and carry out antiviral treatment or liver protection and jaundice reduction 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 their 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, E, have good antioxidant function and are easy to digest and absorb. Do not eat too many sweets and abstain from alcohol.
2. It is not suitable to eat more seafood, mushrooms, sesame, walnuts, jujube, lean meat and animal liver.
3. It is advisable to stay in bed for 1-2 hours after meals to ensure adequate blood supply to the liver, which is conducive to the repair and regeneration of liver cells and helps restore liver function.
It should be noted that patients with high bilirubin should regularly review their liver function, observe the treatment effect, and adjust the treatment plan in time.[4]
Infants with high bilirubin
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Normal value
Normal value range of infant bilirubin
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Range of normal values
Range of critical values
total bilirubin
3.4～17.1μmol/L
1.3 ～ 1.5mg/dl (if the infant exceeds this value, it can be regarded as abnormal)
Direct bilirubin
Below 0 ～ 6.8 μ mol/L
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Indirect bilirubin
1.7 ～ 10.2 μ mol/L below
——
Fluctuation range of infant's bilirubin in normal physiological period: after 24 hours of birth, the serum bilirubin of the infant can gradually rise from 17~51 μ mol/L at birth to 86 μ mol/L or more. Jaundice occurs clinically but no other symptoms, and it will subside automatically within 1~2 weeks, which is the biological jaundice period of normal infant's bilirubin.The serum bilirubin of infants with physiological jaundice should not exceed 204 μ mol/L in term infants and 255 μ mol/L in preterm infants, and attention should be paid to and prevention of bilirubin encephalopathy.
Physiological jaundice
After 24-72 hours of birth, the baby has yellow sclera, skin and urine, and indirect bilirubin is on the high side. At this time, the baby is in good spirits, feeding vigorously, and does not cry or make noise. After one week, it gradually decreases, and disappears within two weeks. Preterm babies generally subside within three weeks. Jaundice comes out late, and it goes out early. This is a normal phenomenon, and parents need not worry about it.
pathologic jaundice
Within one day of birth, the baby developed jaundice, indirect bilirubin was on the high side, and at this time, he was in poor spirits, refused milk, cried, and did not return after two weeks. He needed to go to the hospital for inspection and treatment according to his condition.[6]
matters needing attention
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Patients with high bilirubin should eat a light and nutritious diet.Such as bean products, fish, vegetables, fruits, etc., which contain a lot of vitamins A, B, C, E, have good antioxidant function and are easy to digest and absorb.It is advisable to eat more mushroom, sesame, walnut, jujube and lean meat, but patients with high bilirubin should not eat animal liver food.When the bilirubin of hepatitis B patients is on the high side, we must pay attention to it and go to the regular liver hospital for treatment in time.
Patients with high bilirubin should avoid drinking alcohol. Alcohol in alcohol is the most direct and the biggest damage to the liver.Research shows that more than 80% of heavy drinkers have fatty liver to some extent, 10% to 30% can develop alcoholic hepatitis, and 10% to 20% will develop cirrhosis.You should drink more water at ordinary times. Drinking water can supplement body fluid, enhance blood circulation, and promote metabolism. Drinking more water can also promote the secretion of glands. Patients with high bilirubin, especially digestive glands, pancreatic juice, and bile, are conducive to digestion, absorption, and the elimination of waste, and can reduce the damage of metabolites and toxins to the liver.
The patients with high bilirubin should take appropriate exercise to enhance the metabolism of the body, blood circulation, help the waste of liver and kidney metabolism, and excrete it more quickly -- sweating. This is good for the health of the patients with high bilirubin, and can also improve the ability of the human body to resist diseases. Therefore, the patients with high bilirubin usually need more outdoor activities, such as walking, hiking, playing ball gamesTaijiquan, etc., but it should be noted that people with poor liver should not take strenuous exercise.[2]
