In recent years, with the accumulation of relevant clinical evidence, rapid progress has been made in the diagnosis and treatment of cholestatic liver disease. Recently, the Expert Committee on the Diagnosis and Treatment of Cholestatic Liver Disease has updated some of the contents of the 2009 edition of the Expert Consensus on the Diagnosis and Treatment of Cholestatic Liver Disease based on the latest achievements in the diagnosis and treatment of cholestatic liver disease and following the principles of evidence-based medicine. Diagnostic opinion of cholestatic liver disease Recommend: ① Detailed history and physical examination is important (III); ② Ultrasound and CT are the first-line noninvasive imaging methods to identify intrahepatic and extrahepatic cholestasis (III); ③ Serum AMA test is necessary for adult patients with chronic intrahepatic cholestasis (III); ④ MRCP, EUS, ERCP liver tissue biopsy are further tests that can be considered ( Ⅱ). Treatment of common cholestatic liver disease Primary biliary cirrhosis (PBC) It is recommended that: (i) patients with PBC, including asymptomatic patients, should be treated with UDCA [13-15 mg/(kgd)] (I) long-term (II); (ii) good long-term effects of UDCA are observed in patients with early disease and in patients with good biochemical response (II); this biochemical response is promised to be assessed after 1 years after treatment (II); ③ there is no consensus on how to treat patients with a poor biochemical response to UDCA (III); ④ except for other reasons, as demonstrated by patients with advanced disease with serum bilirubin levels above 6 mg/dl (dl (103 μmol/L) or patients with decompensated cirrhosis whose quality of life is intolerable, or due to refractory ascites and spontaneous bacterial peritonitis, Patients with life expectancy shorter than 1 year due to recurrent variceal rupture and bleeding, hepatic encephalopathy or hepatocellular carcinoma should be strongly recommended for liver transplantation (II); ⑤ The diagnosis of AMA-negative PBC requires liver tissue biopsy to confirm the presence of bile duct damage characteristic of PBC and no significant difference in biochemical response to UDCA compared with AMA-positive PBC (III). Primary biliary cirrhosis-autoimmune hepatitis (PBC-AIH) overlap syndrome Recommendations: ① Standardized diagnostic criteria regarding PBC-AIH overlap syndrome are still undefined. The existing diagnostic criteria are for reference (II); ② Once PBC is diagnosed, the presence of PBC-AIH overlap syndrome should be considered because of the important implications for treatment options (II); ③ For patients with PBC-AIH overlap syndrome, the combination of UDCA and glucocorticoids is the recommended treatment viewpoint (II), and another option is to start treatment with UDCA alone at an appropriate Another option is to start treatment with UDCA alone and add glucocorticoids at an appropriate time (e.g., at 3 months) if a satisfactory biochemical response does not occur (II). For patients requiring long-term treatment, low-dose steroid therapy (III) should be considered. Primary sclerosing cholangitis (PSC) Recommend: (i) MRC or ERCP cholangiography to clarify the diagnosis of PSC in patients with cholestasis biochemical features, and liver tissue biopsy to diagnose small bile duct PSC in patients with normal MRC or ERCP (I); (ii) ERCP is recommended immediately in patients with elevated serum bilirubin and/or increased pruritus with progressive bile duct dilatation and/or cholangitis to exclude significant strictures. Endoscopic dilatation or stent placement is recommended in patients with significant biliary strictures, and percutaneous cholangiography for bile duct dilatation or stent placement should be considered for unsuccessful endoscopic treatment (II); (III) surgical treatment is recommended in patients with significant strictures with unsatisfactory endoscopic and/or percutaneous treatment in the absence of cirrhosis (II); (IV) liver transplantation may be recommended in patients with advanced PSC (II) and in patients with cholangiocyte atypical hyperplasia (II) should be considered in patients with evidence of cholangiocytic atypia or severe recurrent bacterial cholangitis. Intrahepatic cholestasis in pregnancy (ICP) Recommendations: (1) The diagnosis of ICP is based on: (i) pruritus in pregnancy; (ii) elevated serum ALT and elevated serum glycolic or total bile acids; and (iii) exclusion of other diseases causing abnormal liver function or pruritus (II). The return of normal liver function after delivery helps in the diagnosis of ICP. (2) UDCA can reduce pruritus symptoms and improve liver function (I) and can be used in patients with symptoms in mid to late pregnancy (I) but there is insufficient evidence to reduce fetal complications (II). (3) SAMe can reduce the rate of cesarean delivery, prolong the gestational week, and improve liver biochemical indicators (I), and no adverse effects on the fetus or long-term adverse effects on the newborn have been found (III). (4) The efficacy of dexamethasone in improving symptoms and biochemical indices and improving pregnancy outcome is inexact, and it is mainly used in patients with ICP before 34 weeks of gestation who are estimated to be at risk of preterm delivery within 7 days, or in patients with severe disease requiring planned termination of pregnancy to promote fetal lung maturation (III). (5) Emphasis is placed on strengthening fetal monitoring during treatment and timing the termination of pregnancy (III). Drug-related cholestatic liver disease Recommendation: (1) Drugs can cause almost all types of liver injury, of which 20%-25% are cholestatic liver injury, characterized by AKP > 2× ULN or R value (R is the ratio of ALT/ULN to AKP/ULN) ≤ 2, with relatively good prognosis (Ⅰ); (2) The key to treatment is to discontinue and prevent the re-giving of drugs that cause liver injury, drugs belonging to the same biochemical family of drugs, most patients can gradually recover after discontinuation (Ⅲ); ③ therapeutic use should be simplified as much as possible, SAMe for drug-induced liver injury has definite efficacy (Ⅰ), and other drugs can be chosen from UDCA, polydiluted phosphatidylcholine, etc. (Ⅱ). For immune-mediated drug-induced cholestasis, corticosteroid therapy can be considered (III). Cholestatic liver disease due to various types of viral hepatitis Recommended: ① All types of viral infections can cause cholestatic hepatitis, with HBV and HEV predominating in adults, and prolonged severe jaundice that does not subside suggests a poor prognosis (Ⅲ); ② Treatment can be with SAMe, UDCA, and a combination of Chinese and Western medicine (Ⅱ); ③ When contraindications are excluded, adrenocorticosteroids can be used for a short period of time, but should be closely monitored for adverse effects (Ⅲ). Alcoholic liver disease combined with cholestasis Recommendation: ① chronic alcoholic liver disease combined with intrahepatic cholestasis indicates poor prognosis (Ⅱ); ② alcohol abstinence is the main treatment for alcoholic liver disease, and nutritional support therapy should be emphasized (Ⅲ); ③ adenosylmethionine can improve clinical symptoms and biochemical indices of alcoholic cholestatic liver disease, and long-term treatment can prolong survival or delay liver transplantation (Ⅰ), polyenylphosphatidylcholine It has a tendency to prevent histological deterioration in patients with alcoholic liver disease (I), glycyrrhetinic acid preparations, silymarin, polyenylphosphatidylcholine and reduced glutathione have different degrees of antioxidant, anti-infective, hepatocyte membrane and organelle protection effects, and clinical application can improve liver biochemical indexes (II); ④ severe cases with combined cholestasis, if MDF score > 32 and gastrointestinal tract is excluded bleeding, bacterial infection and other contraindications to hormones, adrenocorticosteroid treatment is recommended (Ⅰ).