Liver Fibrosis

Introduction to liver fibrosis Hepatic fibrosis refers to the excessive deposition of fibrous connective tissue in the liver, which is the result of imbalance between fibrosis and fibrosis. Fibrosis is a kind of repairing reaction of the body to the injury. Repeated or persistent chronic liver parenchymal inflammation caused by various causes, necrosis can lead to continuous fibrosis of the liver to form liver fibrosis. From the clinical and pathological evolution of many chronic liver diseases, especially chronic viral hepatitis, liver fibrosis is the inevitable stage of the development of chronic liver disease to cirrhosis. It is believed that liver fibrosis still has the possibility of reversing to normal, while cirrhosis is not. basic knowledge The proportion of illness: 0.001% Susceptible people: no specific population Mode of infection: non-infectious Complications: D-type viral hepatitis Schistosomiasis Hemochromatosis Alcoholic liver disease Biliary cirrhosis Primary sclerosing cholangitis

Cause of liver fibrosis

Virus infection (30%):

Pathogenic factors as antigens, such as hepatitis B virus (HBV), hepatitis C virus (HCV), soluble antigen (SEA) substances secreted by Manchus and Schistosoma japonicum eggs, mainly cause liver damage through immune response. Directly acts on hepatocytes to cause liver damage, such as carbon tetrachloride. The combination of certain drugs and poisons, hepatocyte damage and inflammatory reaction are the response of liver tissue to pathogenic factors, but the inflammatory reaction, hepatocyte regeneration and repair are anti-injury reactions, usually according to necrosis inflammation fiber The pattern of hyperplasia is now thought to play a central role in the initiation of liver fibrosis in the process of liver inflammation (chronic liver injury).

Body factor (30%):

In recent years, immune effector cells and related cells such as fibroblasts and endothelial cells have been produced, and hormone-like proteins that transmit interactions between different cells and tissues are collectively referred to as cytokines (including lymphokines and mononuclear factors) or peptides. Regulatory factors, in addition to a variety of biological activities, various cytokines also have inducing, receptor regulation and biological effects interactions, thus forming a network of complex cytokines, known by research Cytokines are involved in the regulation of liver fibrosis formation, and once the cytokine network is dysregulated, it plays an important role in the formation of liver fibrosis.

Liver fibrosis prevention

Emotional stability

The relationship between the liver and mental emotions is very close. Poor mood, depression, and anger can affect the function of the liver and accelerate the development of the disease. Establishing a strong will, a cheerful mood, refreshing the spirit, and eliminating the burden of thought will be beneficial to the improvement of the condition.

2. Dynamic and static combination

Hepatic fibrosis compensatory function decline, and should be absolutely bed rest when taking ascites or infection. In the period of adequate compensation and stable period, you can do some light work or appropriate activities, such as walking, doing exercises, Tai Chi, qigong and so on. The amount of activity is not to feel fatigue.

3. medication from Jane

Blind excessive abuse of general drugs can increase the burden on the liver and is not conducive to liver recovery. Drugs harmful to the liver such as isoniazid and barbiturates should be used with caution or hanged.

4. Quit smoking and avoid alcohol

Alcohol can help the fire and blood, long-term drinking, especially hard alcohol, can lead to alcoholic cirrhosis. Therefore, drinking alcohol can make patients with cirrhosis worse, and easily cause bleeding. Long-term smoking is not conducive to the stability and recovery of liver disease, can accelerate the process of cirrhosis, and has the risk of promoting liver cancer.

5. Dietary care

It is suitable for low fat, high protein, high vitamin and easy to digest diet. Timely, quantitative, and temperate. In the early stage, you can eat more soy products, fruits, fresh vegetables, and eat sugar, eggs, fish, and lean meat. When liver function is significantly reduced and there is a sign of hepatic coma, you should properly control protein intake and promote low-salt diet or avoid Salt diet. The daily intake of salt should not exceed 1 to 1.5 grams, and the water consumption should be within 2000 ml. In severe ascites, the salt intake should be controlled within 500 mg and the water intake should be less than 1000 ml. Should avoid spicy and stimulating products and hard and cold food, it is not advisable to eat overheated food to prevent and emit blood.

6. Active prevention

Cirrhosis is a consequence of the progressive development of the liver due to different causes.

It is necessary to pay attention to the prevention and treatment of various primary diseases, actively prevent and treat chronic hepatitis, schistosomiasis, gastrointestinal infections, avoid contact with and use substances that are toxic to the liver, and reduce the pathogenic factors.

Hepatic fibrosis complications Complications D-type viral hepatitis schistosomiasis hemochromatosis alcoholic liver disease biliary cirrhosis primary sclerosing cholangitis

Concurrent infectious (chronic B, C and D viral hepatitis, schistosomiasis, etc.), congenital metabolic defects (hepatolenticular degeneration, hemochromatosis, 1-antitrypsin deficiency, etc.) and chemical toxicities (chronic alcoholic liver disease, chronic drug-induced liver disease) and autoimmune hepatitis, primary biliary cirrhosis and primary sclerosing cholangitis.

Symptoms of liver fibrosis Common symptoms Portal collateral circulation abdominal pain with jaundice upper abdominal mass and abdominal distension jaundice abdominal mass upper abdominal mass liver fibrosis liver stellate cell hyperplasia liver disease diffuse liver nodules

Most of the pathological changes of human liver fibrosis develop slowly, from liver cell damage, inflammation, necrosis, abnormal proliferation and deposition of extracellular matrix, and some need to go through several months to several years, with an average of about 3 to 5 years. Time, because the liver has a strong compensatory function, even if liver fibrosis is active, the patient's clinical performance is not typical; even if the patient has symptoms, often lacks characteristics, many patients are in physical examination or due to other diseases Exploratory laparotomy, even when the autopsy was discovered, the possible clinical manifestations should refer to the "cirrhosis" related content.

Liver fibrosis examination

Laboratory inspection

1. An indicator of the response to extracellular matrix metabolism

(1) Detection of enzymes involved in collagen and matrix metabolism:

1 proline-4-hydroxylase (PH): PH is a glycoprotein, serum PH level is related to the degree of liver fibrosis, but non-hepatic fibrosis, such as obstructive jaundice can also rise High, there is now prepared PH sub-monoclonal antibody, immunological method to detect serum PH content, so that the sensitivity is increased by about 20 times.

2 Monoamine oxidase (MAO): MAO is involved in the cross-linking of collagen, causing covalent cross-linking in the soluble collagen fibers to form insoluble collagen fibers. The increase in serum MAO activity is parallel to the degree of liver fibrosis. It has been found that MAO has four isoenzymes, of which MAO1 is significantly increased in liver fibrosis, but MAO has low sensitivity and complicated operation, so it has not been widely used.

3P-Z peptidase: This enzyme is an endonuclease whose activity can be used as an indicator of collagen degradation. It is often detected simultaneously with P-III-P. The ratio of P-III-P/PZ-peptidase is used as liver in foreign countries. The dynamic non-invasive index of fibrosis, the Chinese Yin Weiwei et al., found that the serum P-III-P/PZ peptidase ratio increased with the degree of liver fibrosis, indicating the P-III-P/PZ peptidase ratio It is a useful indicator reflecting the degree of collagen metabolism and liver fibrosis.

(2) Detection of collagen, procollagen peptide and collagen metabolites:

Type 1 procollagen (PC-III) and type III procollagen terminal peptide (P-III-P): When PC-III is secreted into the blood by the cell, the amino (N) and carboxyl (C) peptides are inscribed. The enzyme is excised in the blood and increases with the active synthesis of collagen. The diameter of P-III-P is 60 nm. These peptide ends can regulate the diameter of collagen fibers. In 1985, Galambos et al. extracted PC-III from goat skin and established The RIA test method was used to determine the serum PC-III of 50 patients with liver disease. The results showed that the PC-III value was related to the degree of liver fiber activity. In 1990, Li Weida et al. established PC-III RIA method by extracting PC-III from human fetal skin. Its normal limit is 120g/L. In 1979, Rohde first extracted the amino terminal polypeptide of type III procollagen from fetal cowhide, and established a radioimmunoassay method. The significance of P-III-P determination in the diagnosis of liver disease was reported. At present, there are many reports on P-III-P at home and abroad. It is believed that P-III-P is still a good indicator of the degree of liver fibrosis activity, and a good indicator for judging the antihyperline drug course and the prognosis of chronic liver disease. However, there are still some problems to be explored. First of all, it has no organ specificity. Therefore, when diagnosing liver disease, Excluding the increase in P-III-P caused by other diseases, and secondly, the serum P-III-P content in various liver diseases has a large overlap, so it is difficult to determine the type of liver disease.

2 Type IV collagen and its decomposition fragments (7S fragment and NC1 fragment): Type IV collagen is distributed under the sinusoidal endothelial cells, which is the main component of the basement membrane. It has a high affinity with LN, and excessive deposition makes the liver sinus capillar. Vascularization, changes in hepatic sinus structure and hepatic blood flow, restricting liver nutrition, thereby aggravating liver lesions, deposition of IV collagen in the early stage of liver fibrosis, P-III-P, 7S, NC-1 in blood The content is increased, 7S and CN-1 are obvious. Some people think that serum 7S and NC1 content are sensitive indicators reflecting collagen synthesis. It has also been reported that serum IV collagen test kit (Japan) has been supplied to the market by enzyme-linked method. .

(3) Relevant indicators for changes in matrix composition:

1 layer of laminin (LN): LN, also known as laminin, is a non-collagen structural glycoprotein in the matrix. It is a unique component of the basement membrane and is broken down into 7 peptide fragments by digestive enzymes. The epitope is present in Fragment I (LNP1) and has a molecular weight of approximately 250KD. The RIA assay is now established using the antigen-antibody system of LNPI, which can obtain sufficient antigen without affecting the specificity and sensitivity of the assay, and making serum LN. The promotion and use of the level detection method became possible. Misoki et al. used the RIA method to measure the serum LN levels of normal people and patients with different liver diseases. The results showed that normal people, slow-moving liver, slow-lived liver and cirrhosis were 1340, 1600, 2060 and 2200 ng/ L. At present, most scholars believe that serum LN can be used as one of the indicators for early diagnosis of liver fibrosis, but non-specific, malignant tumors and pancreatic diseases can also increase serum LN, so LN still has some limitations.

2 Fibronectin (FN) and its receptor (FNR): In the liver, FN mainly exists in the wall of the hepatic sinus and coexists with type I, III, and IV collagen, acting as a scaffold, and also constitutes a component of the basement membrane, serum. There are many reports on the determination of FN in China. The serum FN is increased in patients with acute and chronic hepatitis by single expansion method, blood coagulation method and rocket electrophoresis. The FN of early cirrhosis is also significantly increased, but it is decreased after decompensation. Most scholars believe that it is not a good indicator for early diagnosis of liver fibrosis. It has been reported in foreign countries that 75 cases of serum -subunit FNR confirmed by liver biopsy were detected by enzyme-linked method, and serum FNR level was closely related to liver fibrosis. However, no more reports have been confirmed.

3 hyaluronic acid (HA): HA is one of the most single glycosaminoglycans. It is synthesized by mesenchymal cells, lymphatic to lymph nodes, and finally enters the blood. Most of the HA is taken up by liver endothelial cells and is interstitial cells. It was degraded into acetic acid and lactic acid and excreted by the kidney. It was reported that among 117 patients with liver disease, 47 patients with pathologically diagnosed cirrhosis had higher blood HA than 100 g/L, and most of them were higher than 200 g/L; 70 cases were non- Only 26 cases of cirrhosis were higher than 100g/L; only 5 of 207 normal controls were higher than 100g/L. There are many reports on the application of HA in liver disease at home and abroad. The results can be summarized as Acute hepatitis, slow-moving liver, slow-lived liver and cirrhosis serum HA have increased to varying degrees, which is related to the degree of liver damage and liver fibrosis activity, but attention should be paid to malignant tumors, rheumatoid arthritis and respiratory distress syndrome. The patient's serum HA is elevated.

2. Involved in the regulation of cytokine formation in the formation of hepatic fibrosis In the repair process of acute hepatitis, TGF-1 may have the synthesis of collagen and other interstitial. Some people think that TGF-1 may be a joint inflammatory process and liver fibrosis. There are many reports on the relationship between serum and TNF-. Some animal experiments and clinical studies have concluded that the degree of liver fibrosis activity of schistosomiasis is related to serum TNF-, HA, if it is based on extensive research. Predicting the level of serum cytokines as an auxiliary indicator for the diagnosis of active liver fibrosis is worthy of further study.

Film degree exam

1. Ultrasound examination of liver fibrosis has abnormal changes in liver echo.

2. CT CT can be found in the thickening of the liver capsule, the contour of the liver surface is irregular or nodular, the echo of the liver parenchyma is uneven or the CT value is increased, the proportion of each leaf is changed, the thickness of the spleen is increased, and the portal vein and spleen vein are increased. Wide, color Doppler can measure hepatic artery and portal vein blood flow and functional portal-body shunt, but overall imaging examination is not sensitive enough to diagnose liver fibrosis.

Diagnosis and differentiation of liver fibrosis

diagnosis

Liver vascularization is an extremely complex dynamic process. In terms of diagnosis, it is necessary to combine clinical and fibrosis-related biochemical indicators for comprehensive analysis in order to make a realistic diagnosis. The following points are for reference during diagnosis.

1. Liver fibrosis occurs and develops on the basis of chronic liver disease. Therefore, when we consider the diagnosis of liver fibrosis, we must first analyze the presence or absence of chronic liver disease and chronic liver disease, so the relevant etiological tests and liver Functional tests should be done. Some people recommend ADA (adenosine deaminase), GST (glutathione S transferase) and other indicators, which are considered sensitive and simple.

2. Serum indicators for the detection of biochemical indicators of liver fibrosis have more than 20 kinds of domestic and foreign comprehensive, the above listed tests are more commonly used, it is recommended that P-III-P/PC-III, HA, LN, TNF-, The sensitivity is considered to be high, but it is still not specific.

3. Ultrasound examination.

Liver biopsy is the most direct and accurate method for diagnosing liver fibrosis, but it is difficult to be accepted by patients for invasive examination, and it cannot be used as a dynamic indicator to observe changes in liver fibrosis and to judge curative effect.

Differential diagnosis

Should pay attention to the identification of liver cysts, liver tumors and other diseases.

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