What Is Hepatocellular Jaundice?

Hepatocellular jaundice refers to jaundice caused by damage to liver cells, bilirubin uptake, binding, and excretion, and bilirubin accumulation in the blood. The mechanism of hepatocellular jaundice can be both retention of unbound bilirubin and reflux of bilirubin.

Hepatocellular jaundice refers to jaundice caused by damage to liver cells, bilirubin uptake, binding, and excretion, and bilirubin accumulation in the blood. The mechanism of hepatocellular jaundice can be both retention of unbound bilirubin and reflux of bilirubin.

Chinese name

Hepatocellular jaundice

Foreign name

hepatocellular jaundice

Hepatocellular jaundice I. Overview

In cases of viral hepatitis, leptospirosis, sepsis, liver abscess, or phosphorous poisoning, the jaundice that occurs is hepatocellular jaundice. Uninjured or lightly damaged liver cells can still form bound bilirubin, but a part of the formed bound bilirubin can flow back into the blood, so there is also bound bilirubin in the blood. In addition, swelling of the liver cells, inflammatory exudate in the portal vein area, and the presence of bile ducts in the small bile ducts can prevent bile excretion and promote the reverse flow of bound bilirubin into the blood. Because there is both unbound bilirubin and conjugated bilirubin accumulation in the blood, there is a biphasic response in the qualitative test of bilirubin. Bilirubin is excreted through the kidneys, so bilirubin appears in the urine. Since the amount of bound bilirubin formed by the liver is reduced, and a part of the formed bound bilirubin flows back into the blood, the amount of bilirubin entering the intestine is reduced. Although the amount of urobilinogen absorbed from the intestine is not more than usual, due to poor liver function, the ability to take urobilinogen from the blood is reduced, and the function of excreting it into the biliary tract is also reduced. Increase in protozoin, urobilinogen in the urine also increased.

Hepatocellular jaundice 2. Causes and common diseases

Jaundice due to damaged liver cells. When liver cells are damaged and the ability to process bilirubin is reduced, all indirect bilirubin produced by normal metabolism cannot be converted into direct bilirubin, which causes an increase in indirect bilirubin in the serum, and undamaged liver cells can still Indirect bilirubin is converted into direct bilirubin into the capillary bile duct. However, because the bile excretion pathway is blocked or flows through the necrotic liver cells, the blood flows back into the blood, which directly increases the serum bilirubin and penetrates into the tissue to form jaundice.

Hepatocellular jaundice III. Differential diagnosis

The differential diagnosis of hepatocellular jaundice needs to pay attention to clinical symptoms and signs, and ask whether there are accompanying symptoms such as fever, rash, itching of the skin, fatigue, appetite and abnormal urine and stool, bleeding tendency, and corresponding symptoms of various organ systems. Examination should be comprehensive and meticulous without omissions. Pay special attention to the yellow color of the skin and mucous membranes (hemolytic jaundice is often lemon-colored, hepatocellular jaundice is mostly golden yellow or light yellow, and obstructive jaundice is mostly dark yellow or yellow-green), whether the lymph nodes, liver, gallbladder, and spleen are enlarged Wait. The signs and symptoms of different primary diseases are different. Most patients with hepatomegaly and portal hypertension are decompensated for liver cirrhosis. Physical examination of liver cancer patients with jaundice can detect hepatomegaly with nodularity. Spider nevus is found in chronic hepatitis and cirrhosis. . The course of hepatocellular jaundice can also be used as a reference for diagnosis. For example, jaundice of viral hepatitis A and E usually lasts 3 to 4 weeks. Jaundice of chronic hepatitis B, C, and D can last for months or become chronic liver. Cholestasis inside. Other acute jaundice can be resolved in a short time after the cause is relieved or the disease has been alleviated, and jaundice caused by cancer is mostly progressive.

Hepatocellular jaundice

1. The skin and mucous membranes are golden yellow and sometimes itchy;

2. Unbound and bound bilirubin in blood are increased, and bilirubin (that is, conjugated bilirubin) accounts for more than 35% of the total bilirubin in one minute;

3. Bilirubin is positive in urine. The content of urobilinogen depends on the degree of liver cell damage and / or intrahepatic cholestasis. When liver cell damage is severe, urobilinogen reabsorbed from the intestinal cavity is in liver cells. It cannot be oxidized into bilirubin, so urobilinogen increases in the urine, but when cholestasis occurs in the liver at the peak of the disease, although hepatocyte damage is severe, the urobilinogen can be reduced or even absent;

4. The content of urobilinogen in feces can be normal, reduced or absent, and it also varies depending on the degree of intrahepatic cholestasis;

5. Serum transaminase was significantly increased, and the turbidity test result was positive;

6, liver biopsy has obvious hepatocellular lesions (necrosis, steatosis, etc.).

Hepatocellular jaundice V. Principles of treatment

The treatment of hepatocellular jaundice can be divided into two parts: general treatment and treatment for the etiology of primary liver disease.

In the case of liver disease compensatory period and inactive condition, the patient can move slightly, but when there is liver damage or liver disease decompensated period and concurrent infection, the patient needs bed rest to ensure adequate liver blood flow. The diet of patients with hepatocellular jaundice should be high-calorie, high-protein, high-sugar, low-fat, low-cholesterol, and vitamin-rich digestible foods. When liver function is significantly reduced or there is a sign of hepatic encephalopathy, the intake of protein must be strictly restricted. For patients with ascites and edema, it is necessary to strictly limit sodium intake, avoid eating rough and hard food, and prohibit drinking and taking drugs that are harmful to the liver. Patients with severe liver disease are at risk of concurrent infection, and broad-spectrum antibiotics can be used to prevent infection.

The treatment of primary liver disease is more important for the relief of hepatocellular jaundice, and symptomatic treatment should be performed on the basis of clarifying the primary cause. The most important treatment for alcoholic liver disease is to quit drinking. For patients with viral hepatitis, such as chronic hepatitis B, nucleoside analogs are generally required for antiviral treatment. Hepatitis C requires direct antiviral drugs and antiviral treatment. At the same time to regulate immunity, appropriate combination of liver protection drugs. Jaundice hepatitis caused by other non-hepadnaviruses (such as cytomegalovirus, Epstein-Barr virus, etc.) should focus on the primary disease, plus liver protection, enzyme reduction, and yellowing treatment. Cirrhosis requires treatment for the cause of cirrhosis, and treatment of complications, such as ascites, upper gastrointestinal bleeding, hepatic encephalopathy, and hepatorenal syndrome, needs to be addressed. Jaundice caused by primary liver cancer can be either hepatocellular jaundice or obstructive jaundice, which is more common in the latter. For these patients, active comprehensive medical and surgical treatment of primary liver tumors should be allowed under the circumstances This is the fundamental measure to control and eliminate jaundice. Artificial liver, liver cell transplantation, liver transplantation and gene therapy have gradually attracted public attention in recent years. The artificial liver support system has become an ideal auxiliary supportive treatment method for patients with severe jaundice. It can compensate or partially compensate for the detoxification and biosynthetic functions of the liver, providing time and opportunities for the recovery of liver cells, and waiting for donor livers. Transplant patients fight for time. Hepatocyte transplantation refers to planting isolated and cultured hepatocytes in patients to replace or partially replace patients with liver insufficiency. It is suitable for acute and chronic liver failure and hereditary liver diseases. Orthotopic liver transplantation is the best treatment option for patients with end-stage liver disease. Gene therapy has achieved remarkable achievements in recent years. The effects of various gene vectors have achieved certain results in animal models, but its safety remains to be studied due to potential side effects.