From the 1960s to 1980s, the morphological features of liver fibrosis and its important role in chronic liver disease were more clearly elaborated, but it was mostly considered as a passive and irreversible process. In the past 20 years, the research on liver fibrosis has made great progress, which is mainly reflected in: (1) Conceptually, it is clear that liver fibrosis is the body’s repair response to chronic injury and is an active stromal proliferation pathological process. (2) In terms of pathogenesis, it is clear that the cytological basis of liver fibrosis formation is hepatic stellate cell activation, and we basically understand the molecular mechanisms regulating hepatic stellate cell activation, such as free radicals, ECM environment and cytokines, especially transforming growth factor-β1 and other signal transduction mechanisms stimulating cell activation. (3) In terms of diagnosis, we have a basic understanding of the natural progression of liver fibrosis, especially hepatitis C liver fibrosis, the risk factors for its occurrence, genetic and environmental influencing factors, etc. The histopathological diagnostic criteria for liver fibrosis have been basically established, and significant progress has been made in comprehensive serological diagnosis. (4) In terms of treatment, symptomatic liver fibrosis and a certain degree of cirrhosis are reversible, and some drugs can promote the reversal of liver fibrosis, especially Chinese medicine has a better overall efficacy. Traditional Chinese medicine does not have the concept of liver fibrosis. Combined Chinese and Western medicine anti-liver fibrosis research has gone through 3 stages: (1) Clinical exploration period (1950s to 1970s). The understanding of liver fibrosis was often linked to its pathological outcome, cirrhosis, with reference to “Y cum”. (2) Experimental research period (late 1970s to early 1990s), i.e. experimental tests on the anti-liver fibrosis effects of Chinese herbal medicines, with representative studies including liver strengthening and softening soup, Salvia miltiorrhiza, peach kernel and its extract, cucurbitacin B, oleanolic acid, glycyrrhiza sweetener, hanfangji acephalin, etc. (3) The period of clinical trials of new drugs and mechanism of action research (after 1990s), that is, under the guidance of the principles of new drug research of traditional Chinese medicine and the principles of syndromic medicine, multi-center, randomized control, liver biopsy pathology and other methods were used to evaluate the clinical efficacy of traditional Chinese medicine against liver fibrosis, and modern life science methods were used to study the mechanism of action and the principle of compounding of effective traditional Chinese medicine. In September 2001, the first national conference on the combination of Chinese and Western medicine in the prevention and treatment of liver fibrosis was held in Shanghai, China, to exchange and summarize the research results on the combination of Chinese and Western medicine in liver fibrosis in China, which is of landmark significance. In order to fully understand the importance of the prevention and treatment of liver fibrosis, to summarize the research results on the diagnosis and treatment of liver fibrosis by combining Chinese and Western medicine, and to provide guidance for Chinese and Western medicine clinicians engaged in the prevention and treatment of liver diseases, the Society organized domestic experts and prepared this guideline for reference after several discussions and revisions since 2003. The main text is divided into 3 levels and 5 grades (Table 1), which are indicated by italicized Roman numerals in parentheses. I. Diagnosis (I) Clinical manifestations The clinical manifestations of patients with hepatic fibrosis are non-specific and vary widely. Common clinical manifestations include fatigue, loss of appetite, abnormal stools, discomfort or distension or pain in the liver area, dull complexion, dark red tongue, sublingual varices, and thin pulse. Some patients may have no obvious symptoms and signs, or may show other clinical manifestations with the primary disease. (1. Histopathological examination: Histopathological examination of the liver is the most important basis for making a definite diagnosis, measuring the degree of inflammation and fibrosis, and determining the efficacy of drugs. The basic requirements for liver biopsy include: aiming for a coarse needle puncture (preferably with 16G), a specimen length of 1 cm or more, and including at least 6 or more confluent areas under the microscope. Liver biopsy specimens should be serially sectioned and routinely stained with hematoxylin-eosin, Masson trichrome stain and/or reticulocutaneous fiber stain. The degree of liver fibrosis is classified into stages l to 4, respectively, according to the degree and site of fiber proliferation [4] (Stage, S, see Table 2). 2, Imaging: The rational choice of B-mode ultrasound, electronic computed tomography (CT) and/or magnetic resonance imaging (MRI) and the intercontrast test can help to dynamically observe the degree of fibrosis. Quantitative or semi-quantitative criteria to observe changes in liver elasticity, liver volume, morphology of the liver surface, thickness of the liver envelope, liver parenchyma, intrahepatic vessels and bile ducts, spleen and splenic vein, and gallbladder can provide valuable reference information for the diagnosis of fibrosis and assessment of the activity of the lesion. Available data show that changes in parameters such as the width of the internal diameter of the main trunk of the portal vein, the blood flow per minute in the portal vein, the thickness of the spleen, the width of the splenic vein and the maximum oblique diameter of the right lobe of the liver correlate well with the degree of liver fibrosis [4].CT and/or MRI examinations, the size of the left lobe of the liver and the spleen, as well as imaging changes in the morphology of the liver surface and the collateral vessels of the portal vein, are helpful in the observation of the degree and progression of liver fibrosis [9 ](II-3). 3.Serum fibrosis markers examination: It helps to reflect liver inflammation and fibrosis, mainly: (1) ECM metabolic components, including hyaluronic acid (HA), type III procollagen peptide or its metabolic fragments (including PIIIP or PCIII), type IV collagen or its metabolic fragments (including IVC, IV7S, IVNC1) and laminin (LN); (2) ECM metabolism-related enzymes and their inhibitors, such as (2) matrix metalloproteinase tissue inhibitor-1, etc.; (3) cytokines of fibrosis formation, such as transforming growth factor β1, etc. However, serum fibrosis markers still lack specificity and sensitivity and have no direct significance for the specific staging of fibrosis, so combined testing and dynamic observation are appropriate [4]. 4, other predictors and related risk factors: including serum aspartate aminotransferase (AST) level and AST/alanine aminotransferase (ALT) ratio, α2-macroglobulin and γ-globulin content, etc.. Elevated AST/ALT ratio, GGT, and APRI are particularly important. The associated risk factors include longer disease duration and older age of the patient, long-term heavy alcohol consumption, increased body mass index (BMI), insulin resistance and hepatic steatosis, human immunodeficiency virus infection and use of immunosuppressive drugs, and repeated schistosomiasis infections. In recent years, there have been more explorations and reports on the establishment of non-invasive diagnostic models based on liver histological fibrosis staging and comprehensive clinical data [10-12], and important progress has been made in the study of non-invasive diagnostic models for chronic hepatitis B liver fibrosis in China [13-15], which can be applied to accumulate more clinical evidence. (C) Diagnostic points 1. History of chronic liver disease: history of chronic viral hepatitis B, chronic viral hepatitis C, schistosomiasis, alcoholic liver disease, non-alcoholic fatty liver disease, drug or toxic liver disease, cholestasis and autoimmune liver disease, etc. The pathogenic diagnosis was made with reference to the relevant criteria established by the Chinese Medical Association Branch of Hepatology and the Infectious Diseases Branch [16-20]. 2. Clinical manifestations: Clinical symptoms are non-specific and can be asymptomatic. In addition to the clinical manifestations of the primary disease, there may be fatigue and weakness, discomfort or distension or pain in the liver area, loss of appetite, abnormal stools, dark red or dark tongue, and thin pulse. 3.Laboratory tests: abnormal increase in serum liver fibrosis markers (HA, PIIIP or PCIII, ⅣC, Ⅳ7S or ⅣNC1, LN), AST/ALT ratio, GGT, APRI, etc. 4.Imaging: Ultrasound examination reveals rough liver envelope, dense, thickened, enhanced and unevenly distributed echogenicity, unclear vascular orientation, etc., or widening of portal vein internal diameter, thickening of spleen, etc. 5. Histopathological examination of the liver: hematoxylin-eosin, Masson trichrome staining and/or reticulocyte staining of the liver tissue, with varying degrees of fibrous tissue hyperplasia (S1 to S4). 6. Risk factors: long-term heavy alcohol consumption, longer disease duration and older age of patients, increased body mass index (BMI), insulin resistance, hepatocellular steatosis, HIV infection and use of immunosuppressive drugs. The immediate goal of anti-liver fibrosis treatment is to inhibit the further development of liver fibrosis; the long-term goal is to reverse liver fibrosis, improve liver function and structure, delay the onset of cirrhosis and its decompensation, improve the quality of life and prolong the survival of patients. Liver fibrosis is a complex pathological process with active progression and dynamic changes, involving multiple links and factors. The treatment strategy should take into account all aspects of the occurrence and development of liver fibrosis, including treatment of the primary disease or removal of causative factors, anti-liver inflammation, inhibition of collagen fiber formation and promotion of collagen degradation, etc. This is actually a broad anti-liver fibrosis comprehensive therapy. Among them, etiologic treatment is the primary countermeasure against liver fibrosis, such as effective inhibition of hepatitis virus replication, killing schistosomes, and alcohol cessation can reduce persistent liver damage, thus promoting the repair of fibrotic liver tissue. Chronic inflammation is a prerequisite for the formation of fibrosis, and anti-inflammation is an important measure against liver fibrosis. “Guidelines for the treatment of alcoholic liver disease”, “Guidelines for the treatment of non-alcoholic fatty liver disease”, “Diagnostic criteria and treatment criteria for schistosomiasis in Japan” and other relevant guidelines and standards. However, etiology and anti-inflammatory therapy are not equivalent to, and cannot replace, narrowly defined anti-fibrotic therapy targeting ECM metabolism and hepatic stellate cell activation, and inhibiting hepatic ECM production and deposition and promoting its degradation are important countermeasures to anti-fibrotic therapy.