Hyperbilirubinemia

The significance of hyperbilirubinemia is mainly judged by daily life. It is also an important indicator of liver function. The serum bilirubin of normal people is mainly within a certain range. If hyperbilirubinemia exceeds a certain amount in daily life, the jaundice index will be found. Some symptoms of jaundice and high bilirubin in daily life are mainly caused by normal red blood cell production and transportation.

Therefore, high bilirubin is also very effective in the treatment and diagnosis of jaundice. The main manifestations of jaundice are skin changes, varicose veins, splenomegaly, liver cysts, breast development and increased bilirubin. Below we introduce the common diagnoses of this disease.

1. Source of bilirubin: The average lifespan of normal red blood cells is 120 days. Hemoglobin released by aging red blood cells is the main source of bilirubin, accounting for 80% to 85%. About 10% to 15% of bilirubin comes from hemoglobin of immature red blood cells in the bone marrow, and another 1% to 5% comes from free hemoglobin and hemoglobin-containing protein in the liver. Heme is converted into biliverdin by microsomal heme oxygenase, and biliverdin is reduced to bilirubin by biliverdin reductase.

2. Transport of bilirubin The above-mentioned bilirubin is free bilirubin. Because it is not taken up by liver cells and is not combined with glucuronic acid, it is called unconjugated bilirubin. Free bilirubin attaches to albumin in the blood circulation to form a bilirubin-albumin complex, which is transported to the liver.

3. Bilirubin uptake: In the liver sinusoids, bilirubin is taken up by the microprotrusions of the hepatocytes and albumin is separated from bilirubin. After bilirubin enters the hepatocyte, it is carried by the cytoplasmic carrier proteins Y and Z and transported to the microsome part in the smooth endoplasmic reticulum.

4. Conjugation of bilirubin: Free bilirubin is catalyzed by glucuronyl transferase in the microsomes and combines with glucuronic acid to form conjugated bilirubin. The main form is bilirubin glucuronide, which accounts for about 75% of the total conjugated bilirubin, and the rest is conjugated to glucose, xylose, disaccharides and glycine.

5. The mechanism of bilirubin excretion from liver cells after the formation of conjugated bilirubin is still not very clear. It may be transported to the capillary bile ductules, small bile ducts, and bile ducts through the Golgi apparatus and then discharged into the intestine, but it is undoubtedly an active transport, rate-limiting and energy-consuming process, during which bile salts and sodium ions are involved. After conjugated bilirubin enters the intestinal cavity, it is reduced to urobilinogen by dehydrogenation of intestinal bacteria. Most of it (the total daily amount is about 68 to 473 μmol) is excreted with feces and is called fecal bilirubin. A small part (10% to 20%) is reabsorbed by the lower ileum or colon, returns to the liver through the portal vein blood, and is converted into bilirubin, or is excreted into the intestine with bile without being converted. This process is called the "enterohepatic circulation" of bilirubin. A small part of the urobilinogen reabsorbed from the intestine (no more than 6.8 μmol per day) enters the systemic circulation and is excreted through the kidneys.

The above is a common introduction to hyperbilirubinemia. The serum bilirubin of a normal person is mainly within a certain range. If hyperbilirubinemia exceeds a certain amount in daily life, the jaundice index will be found. The main events in patients with cirrhosis are mainly skin changes, varicose veins, splenomegaly, liver cysts, breast development and increased bilirubin, so some medical examinations can be carried out in daily life.