What Is Hyperbilirubinemia?

Bilirubin is the waste product of the heme metabolism of red blood cells in the blood. It is mainly converted from hemoglobin, and one gram of hemoglobin can produce 34 mg of bilirubin. When red blood cells age (the life cycle of red blood cells is 120 days), spleen is destroyed to produce bilirubin. Bilirubin passes through the liver and is excreted from the bile ducts into the duodenum. Excreted. Normal people produce 250 to 350 mg of bilirubin daily, of which 80% to 85% come from aging red blood cells in the blood circulation, and the remaining 15% to 20% come from bone marrow and liver, which is called bypass bilirubin. Bilirubin is waste to the body. When the serum bilirubin is too high, abnormal information such as liver disease or bile duct obstruction is revealed. The level of serum bilirubin value represents the severity of the abnormality. Generally speaking, normal bilirubin (Bilirubin Direct) is below 0.5 mg / dl, and total bilirubin (Bilirubin Total) is below 1.3 mg / dl. Bilirubin is an important basis for judging jaundice clinically and an important indicator of liver function. The normal serum total bilirubin concentration is 1.7 17.1 mol / L, and one minute of bilirubin is lower than 3.4 mol / L.

Basic Information

Visiting department: Gastroenterology
Common causes: Direct bilirubin is high, total bilirubin, indirect bilirubin increase, erythrocyte rupture factors, etc.

Common symptoms: Sclera mild jaundice, splenomegaly, urine bilirubin positive, etc.

Causes of hyperbilirubinemia

The life span of human red blood cells is generally 120 days. After red blood cells die, they become indirect bilirubin, which is converted into direct bilirubin by the liver, forming bile, which is excreted into the biliary tract, and finally excreted in the stool. The sum of indirect bilirubin and direct bilirubin is total bilirubin. Obstacles in any of the above links can cause jaundice. If the red blood cells are destroyed too much, the indirect bilirubin produced is too much, and the liver cannot completely convert it into direct bilirubin, and hemolytic jaundice can occur; when liver cells become diseased, 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 bilirubin in the blood is increased. At this time, hepatic jaundice occurs; once the tumor or stones appear in the biliary system outside the liver , Blocking the biliary tract, bile can not be smoothly excreted, and obstructive jaundice occurs. The jaundice of patients with hepatitis is generally hepatocellular jaundice, with both direct bilirubin and indirect bilirubin increasing, while patients with cholestatic hepatitis are mainly elevated with direct bilirubin.

1. Direct bilirubin is high

If liver cells are damaged, bilirubin cannot be converted into bile normally, or bile excretion is blocked, it will cause direct high bilirubin, and common causes of high direct bilirubin are intrahepatic and extrahepatic obstructive jaundice, Pancreatic head cancer, capillary cholangitis, and other bile stasis syndromes;

2. Total bilirubin, direct bilirubin, and indirect bilirubin are all increased

Found in acute jaundice hepatitis, chronic active hepatitis, cirrhosis, and toxic hepatitis.

3. Increased total bilirubin and direct bilirubin

Found in intrahepatic and extrahepatic obstructive jaundice, pancreatic head cancer, capillary bile duct hepatitis, and other bile stasis syndromes.

4. Increased total bilirubin and indirect bilirubin

Found in hemolytic anemia, incompatible blood transfusions, malignant diseases, neonatal jaundice and so on.

5. RBC Rupture Factors

Liver damage can lead to the death and rupture of a large number of red blood cells in the liver of a patient. When the liver's metabolic function is not sufficient to convert it to direct bilirubin, it can cause symptoms of hemolytic jaundice.

6. Hepatocellular disease factors

When the liver cells of patients with hepatitis B become diseased or bilirubin cannot be converted into bile, it can lead to liver enlargement and compression of the intrahepatic bile ducts, resulting in impaired bile excretion, which causes the bilirubin content in the blood to rise.

7. Obstructive factors of bile excretion

For example, patients with hepatitis B have gallstones. Gallstones can block the excretion of bile in the liver, making bile unable to flow out of the liver smoothly, which can also cause bilirubin in the blood to rise.

8. Increased total bilirubin

(1) Liver disorders Acute jaundice hepatitis, acute yellow liver necrosis, chronic active hepatitis, cirrhosis, etc.

(2) Extrahepatic diseases Hemolytic jaundice, incompatible blood transfusion reactions, cholecystitis, cholelithiasis, etc.

(3) Others Found in toxic or viral hepatitis, hemolytic jaundice, malignant anemia, paroxysmal hemoglobinuria. Polycythemia, neonatal jaundice, internal bleeding, hemolytic jaundice after transfusion, acute yellow liver atrophy.

9. Indirect bilirubin elevation

(1) Hemolytic jaundice Because some hemolytic diseases cause excessive destruction of red blood cells, indirect bilirubin in the blood increases;

(2) Hepatocellular jaundice When hepatocellular disease occurs, bilirubin cannot be normally converted into bile, and hepatocytes are swollen, which compresses the bile ducts in the liver, prevents the excretion of bile, and increases bilirubin in the blood. .

(3) Blood transfusion error Blood transfusion caused by incompatible blood group causes hemolysis, which destroys a large number of red blood cells, and causes a large amount of indirect bilirubin to be released into the blood.

(4) Neonatal jaundice is mainly due to indirect bilirubin elevation in blood due to maternal and child blood type incompatibility or congenital biliary malformations in the newborn.
Regardless of the classification method, the occurrence of high bilirubin (jaundice) is ultimately due to one or several metabolic disorders of bilirubin.

Clinical manifestations of hyperbilirubinemia

Hemolytic jaundice

When a large number of red blood cells are destroyed (hemolyzed), an excessive amount of unbound bilirubin is generated, which exceeds the ability of liver cells to take up, bind, and excrete, causing unbound bilirubin to remain in the blood and cause jaundice. feature:

(1) Mild jaundice of sclera, fever, low back pain during acute attack (hemolytic crisis), skin and mucous membranes are often pale;

(2) No itching on the skin;

(3) Splenomegaly;

(4) Strong bone marrow hyperplasia, such as increased peripheral blood reticulocytes, nucleated red blood cells, and active proliferation of bone marrow red blood cell system;

(5) The total serum bilirubin is increased, generally not more than 85 mol / L, mainly due to the increase of unbound bilirubin;

(6) Increased urobilinogen in the urine without bilirubin, hemoglobinuria in acute episodes, and increased hemosiderin in urine during chronic hemolysis.

2. Hepatocellular jaundice

Due to hepatocyte lesions, bilirubin uptake, binding, and excretion are impaired, resulting in a significant amount of unbound bilirubin remaining in the blood, and at the same time due to liver cell damage and / or damage to the hepatic lobular structure, binding Erythromycin does not drain into the small bile ducts normally, and flows back into the liver lymph fluid and blood, resulting in jaundice. feature:

(1) The skin and sclera are pale yellow to deep golden yellow, and the skin sometimes has itching;

(2) Unbound and conjugated bilirubin in blood are increased;

(3) Urinary bilirubin is positive and urobilinogen is often increased, but at the peak of the disease, urobilinogen is reduced or absent due to intrahepatic cholestasis;

(4) The serum aminotransferase is significantly increased;

(5) Hepatitis virus markers in blood are often positive;

(6) Liver biopsy is of great significance in the diagnosis of diffuse liver disease.

3. Cholestatic jaundice

Intrahepatic cholestasis refers to molecular cytology of reduced bile production and secretion, as well as cholestasis and concentration. Intrahepatic cholestasis occurs either alone or concurrently with liver parenchymal damage. feature:

(1) The skin color is dark yellow, yellow-green or green-brown;

(2) The skin is itchy, which often occurs before the appearance of jaundice;

(3) The increase of bilirubin in blood is mainly combined with bilirubin, and the qualitative test of bilirubin showed a direct response;

(4) Urinary bilirubin is positive, but urobilinogen is reduced or absent;

(5) Decreased or absent urobilinogen in feces, and the feces are light gray or clay-colored;

(6) Serum total cholesterol, alkaline phosphatase, -glutamyl transpeptidase are increased, and lipoprotein-X is positive.

4. Congenital non-hemolytic jaundice

(1) Gilbert syndrome is caused by impaired uptake of free bilirubin by hepatocytes and insufficient glucuronyl transferase in microparticles. Serum non-conjugated bilirubin increased, liver function tests were normal, red blood cells were normal, the gallbladder was well-formed, and liver biopsy was normal.

(2) Dubin-Johnson syndrome is caused by the hepatocyte pair binding bilirubin and other organic anions (indocyanine green, X-ray contrast agent) to the bile duct. The uptake and binding are normal. Oral gallbladder contrast agent The gallbladder often does not develop. The appearance of the liver was green-black (black liver), and liver biopsy revealed diffuse tan pigment particles (melanin or adrenaline metabolite multimers) in liver cells.

(3) Rotor Syndrome, due to the congenital defects of uptake of free bilirubin and excretion combined with bilirubin in hepatocytes, mainly increase the combined bilirubin in the blood, and the indocyanine green (ICG) excretion test has decreased. Most of the cholecystograms are well developed, and a few do not. Liver biopsy was normal and no pigment particles were found in liver cells.

(4) Crigler-Najjar syndrome is due to the lack of glucuronyl transferase in hepatocytes, which prevents the formation of bound bilirubin. Therefore, the concentration of unbound bilirubin in the blood is high, and nuclear jaundice can be complicated; the prognosis is poor.

Hyperbilirubinemia test

Laboratory inspection

(1) Alkaline phosphatase (ALP) is significantly increased in extrahepatic and intrahepatic obstructive jaundice and intrahepatic cholestasis.

(2) Determination of serum total cholesterol, cholesterol esters, and lipoprotein-X (LP-X) In cholestatic jaundice, the total cholesterol content increases; hepatic jaundice, especially when there is extensive necrosis, the cholesterol ester decreases.

(3) Prothrombin time In hepatocellular and cholestatic jaundice, prothrombin production is reduced, so prothrombin time is prolonged, and the prothrombin time is rechecked 24 hours after the injection of vitamin K2 ~ 4mg. Significant shortening, indicating normal liver function, jaundice may be cholestasis; if not changed, it indicates that liver function to produce prothrombin is impaired, and jaundice may be hepatic.

2. Ultrasound imaging

If intrahepatic bile duct dilatation is found, it must be jaundice caused by extrahepatic bile duct obstruction.

3. Barium swallowing of esophagus and barium meal of gastrointestinal

Cirrhosis can be diagnosed if esophageal or gastric varices are found.

4.Retroduodenal cholangiography (ERCP)

It is important for the diagnosis of chronic pancreatitis, pancreatic cancer and understanding of the biliary system.

5.CT inspection

It has great diagnostic value for the diagnosis of hepatobiliary and pancreatic diseases and the location, scope and nature of extrahepatic obstruction.

6. Liver aspiration biopsy and laparoscopy

Can help diagnose hepatocellular jaundice, intrahepatic cholestasis and Dubin-Johson syndrome.

Hyperbilirubinemia diagnosis

Jaundice is an important symptom and sign of many diseases. The cause of jaundice is caused by abnormalities in the metabolism of bilirubin. Through the analysis of bilirubin, urobilinogen, and fecal bilirubin, the nature of jaundice can be initially classified. In order to make an accurate determination of the cause, it still depends on the clinician's comprehensive analysis and judgment based on the results obtained by the medical history, signs, laboratory and other auxiliary examinations, in order to obtain a correct diagnosis.

Hyperbilirubinemia complications

Bilirubin encephalopathy, also known as nuclear jaundice, is a hemolytic disease of the newborn. Because unbound bilirubin crosses the blood-brain barrier, inhibits the use of oxygen in brain tissues, affects cell oxidation, and inhibits brain cell energy production leading to brain damage. Due to the destruction of red blood cells, a large amount of bilirubin is produced. At the same time, the defense function of brain tissue is poor about one week after birth, and free bilirubin easily enters the brain, which mainly damages the basal ganglia and cerebellum, as well as the nucleus related to hearing. The patient developed deep jaundice, drowsiness, decreased muscle tone, and quickly developed into increased muscle tone, screaming, hearing impairment, eye movement disorders, mental retardation, and hand, foot movement. Such children are poorly treated, but the cerebral cortex is less damaged, so these children may have better intelligence. Therefore, we must do perinatal health care to prevent nuclear jaundice. Once hyperbilirubinemia occurs within one week after birth, it should be detected early, and blue light irradiation, drugs, and blood exchange therapy should be taken early to prevent nuclear jaundice.

Hyperbilirubinemia treatment

Patients with high bilirubin are recommended to check for alanine aminotransferase and aspartate aminotransferase. If the two are elevated, the primary disease needs to be identified for liver protection and other treatments; if glutamine and aspartate aminotransferase are within the normal range, bilirubin is high No treatment is needed for the time being. Pay attention to rest, eat properly, check liver function regularly, and monitor the development of the disease at all times. For the treatment of hyperbilirubinemia, it is recommended to go to a regular hospital for treatment because the root cause must be identified while treating the symptoms.

Prognosis of hyperbilirubinemia

Hyperbilirubinemia is that the liver's ability to metabolize and transform bilirubin decreases after the liver of the patient is damaged, causing bilirubin not to be discharged normally and flowing back into the blood. Hyperbilirubinemia is very harmful to the human body, because bilirubin itself has a certain degree of toxicity, and a large amount of bilirubin accumulates in the blood. The light can cause severe jaundice in the patient, and the severe can also endanger the patient's life. Bilirubinemia may indicate that the patient has hemolytic jaundice, hepatocellular jaundice, obstructive jaundice, etc. At this time, the patient's liver appears to be diseased or the bile duct is blocked, resulting in a sharp increase in blood bilirubin. In severe jaundice, liver damage and metabolic function decline, and a large amount of bilirubin accumulates in the liver, which will definitely aggravate liver damage. The patient has symptoms such as indigestion, itching of the skin, and abdominal pain, accompanied by changes in the color of the stool. At this time, the patient should seek medical treatment in a timely manner, without delay, and if necessary, perform the necessary hemodialysis to reduce the symptoms.

Hyperbilirubinemia prevention

Reasonable arrangement of diet, life should be regular, the spirit should be pleasant, pay attention to the combination of movement and static, do not have a disorder to take medicine and abuse drugs. Please note the following:

1. It should be light and rich in vitamins A, B, C, and E. It has a good antioxidant function and is easy to digest and absorb, such as legumes, fish, vegetables, fruits, etc.

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

3. Avoid drinking, avoid too many sweets.

4. It is advisable to rest in bed for 1 to 2 hours after meals to ensure that the liver has sufficient blood supply and is conducive to liver cell repair.