Cholestatic liver disease is a group of common clinical diseases with cholestasis as the main manifestation. In recent years, rapid progress has been made in the diagnosis and treatment of this disease. Following the 2009 and 2013 editions of the Expert Consensus on the Diagnosis and Treatment of Cholestatic Liver Disease, the information on the diagnosis and treatment of cholestatic liver disease has been further accumulated in the past 2 years, and after summarizing and analyzing the relevant data death. The diagnosis and treatment of cholestatic liver disease are influenced by various factors and should be individualized on the basis of standardization to achieve the best treatment effect. With the accumulation of relevant clinical evidence, the Expert Committee is now updating parts of the Consensus. 2015 updates were made in the diagnosis and treatment of cholestatic liver disease, and the main points are organized as follows: Pharmacological treatment of cholestatic liver disease adds TUDCA TUDCA is a combined form of taurine and ursodeoxycholic acid (UDCA), a naturally occurring hydrophilic bile acid in human bile, and is It is the physiologically active form of ursodeoxycholic acid and is involved in the “enterohepatic circulation” and is absorbed and utilized by active transport at the end of the ileum. Oral TUDCA is better enriched than UDCA and can more effectively promote the hydrophilic transformation of the bile pool and protect the hepatic parenchymal cells and bile duct cells. UDCA The results of the study by Fengchun Zhang et al. showed that TBil, ALB, AKP, GGT, AST, and ALT improved most significantly after 3 months of UDCA treatment in PBC patients, and the above indicators leveled off after several months to 1 year of follow-up. The analysis of these indicators after 3, 6 and 12 months of UDCA treatment using the Paris and Barcelona criteria showed that the Paris and Barcelona criteria significantly differentiated the long-term prognosis of patients. Compared to 1 year, the above biochemical indicators at 6 months of treatment showed higher or equal positive and negative predictive values and lower negative likelihood ratios. Biochemical parameters after 6 months of TUDCA can be used to predict the long-term prognosis of PBC as a substitute for those after 1 year, which can help to determine the prognosis of PBC at an earlier stage and to decide whether to try other treatments. The efficacy of TUDCA in the treatment of PBC was investigated in a study by Setchell et al. who administered 500-1500 mg of TUDCA daily to 24 patients with PBC and confirmed that the bile contained 34-41% ursodeoxycholic acid, accompanied by a decrease in hydrophobic native bile acids, suggesting that TUDCA administration resulted in a greater conversion of the bile acid pool to This suggests that TUDCA administration resulted in a greater hydrophilic conversion of the bile acid pool and significantly improved the biochemical response in PBC patients. The study then further examined the metabolism of TUDCA in PBC patients using gas chromatography-mass spectrometry and confirmed that even the highest dose of TUDCA (1500 mg/d) did not lead to an increase in the harmful bile acid lithophanic bile acids. Treatment of patients with poor UDCA response There is no consensus on how to treat patients with a poor biochemical response to UDCA (B2), and budesonide and obeticholic acid are expected to be treatment options for patients with a poor response to UDCA. New advances in PBC treatment Obeticholic acid (OCA) is a semi-synthetic analogue of the primary bile acid goose deoxycholic acid that selectively activates the bile acid nuclear receptor FXR. studies suggest that OCA has good anti-cholestatic, anti-inflammatory and anti-fibrotic effects. To evaluate the safety and efficacy of OCA for the treatment of patients with PBC who do not respond to UDCA therapy, a randomized double-blind controlled clinical study by Hirschfield et al [31] suggested that OCA significantly reduced AKP, GGT, and ALT levels in patients with PBC who do not respond to UDCA therapy compared with placebo, and doses of 10-50 mg were effective. Considering that the hematobiochemical therapeutic response induced by OCA persisted in the 12-month unblinded extension trial, researchers are still working to evaluate the safety and efficacy of OCA for long-term use, and OCA is expected to be a new therapeutic agent for PBC.