In the past, scholars generally believed that patients with cirrhosis were ineffective for antiviral therapy and that treatment with IFNα was dangerous for post-hepatitis decompensated cirrhosis. However, since the introduction of lamivudine (3TC), its low side effects and strong antiviral power have led to a change in the view of antiviral therapy for cirrhotic patients. Recent clinical trials have shown that lamivudine can still be expected to have good results in patients with cirrhosis or even decompensated cirrhosis, and decompensated cirrhosis is not a contraindication to antiviral therapy. 1 . Necessity of antiviral therapy for cirrhosis after viral hepatitis In chronic viral hepatitis, the hepatitis virus continues to replicate in the body, continuously expressing and releasing antigens, thus continuously causing inflammatory activity in the liver, causing increasing fibrosis in the liver and eventually leading to cirrhosis. Therefore, the treatment of cirrhotic patients with viral replication, in addition to anti-fibrotic drugs, should theoretically be based on antiviral therapy, which is the only way to eliminate the initiating factor (antigen) that causes hepatocellular damage and fundamentally curb the host’s immune response, acting as a kettle of fire. Recent clinical trials have shown that if antiviral therapy is used correctly in the early stages of cirrhosis, not only can liver function and clinical symptoms improve, but also the process of cirrhosis can be expected to be reversed. In some patients, despite the advanced stage of cirrhosis, antiviral therapy may still stabilize the disease, prolong survival and improve the quality of life of patients, so it is very necessary to give antiviral therapy to patients with post-hepatitis cirrhosis. 2 .Efficacy of lamivudine in post-hepatitis decompensated cirrhosis Lamivudine is a new type of nucleoside oral antiviral drug with strong inhibitory effect on hepatitis B virus (HBV) replication. Results of clinical trials in chronic hepatitis B without cirrhosis have demonstrated that lamivudine rapidly reduces HBV DNA concentrations and improves liver histological lesions. Although randomized, double-blind controlled trials of lamivudine for cirrhosis are lacking in large numbers of cases, there are increasing reports of encouraging efficacy of lamivudine for the treatment of post-hepatitis decompensated cirrhosis, bringing a ray of hope to patients with advanced cirrhosis. Because of its efficacy and low side effects, it has been advocated that this drug should be the first choice of antiviral therapy for patients with post-hepatitis cirrhosis. Kapoor et al. gave lamivudine 150 mg/d for at least 9 months (mean 17.9 months) to 18 patients with hepatitis B cirrhosis in the decompensated stage (all HBV DNA positive, 10 HBeAg positive). RESULTS: After 8 weeks of treatment, all patients had HBV DNA conversion and 1 case had HBsAg disappearance. Serum ALT, AST and Child-Pugh score (Note: Child-Pugh score is a scoring of the different degrees of five indicators, including hepatic encephalopathy, serum bilirubin, ascites, serum albumin concentration and prothrombin time, with grade A being 5-6, less severe and less risky for surgery; grade B being 7-9, moderate risk for surgery; grade C being 10-15, more severe and There was a significant improvement in the number of patients hospitalized due to complications. No significant side effects were observed. Only one case of drug-resistant mutation YMDD variant beads occurred. Buti et al. gave 100 mg of oral lamivudine daily for 1 year to 16 patients with chronic hepatitis B, 4 with decompensated cirrhosis, and 4 who had experienced recurrent HBV infection after liver transplantation. RESULTS: All patients with decompensated cirrhosis and liver transplantation had negative serum HBV DNA after treatment, and lamivudine was well tolerated in all cases. yao et al. treated 13 patients with chronic hepatitis B cirrhosis with positive serum HBV DNA with lamivudine, giving 150 mg daily, and all patients had Child’s-Pugh scores ≥10 (mean 11), 9 of whom were HBeAg-positive. Results: 69% (9/13) of the patients showed significant improvement in liver function, as evidenced by a mean reduction in Child’s-Pugh score of more than 3 points, and 5 cases had a Child’s-Pugh score of less than 7 points (no longer requiring liver transplantation), and all patients remained HBV DNA negative and had stable liver function, except for one patient who suddenly developed viral replication 12 months after treatment. Sponseller et al. reported the effect of long-term lamivudine treatment in 5 patients with clinically and biopsy-confirmed post-hepatitis B cirrhosis in the decompensated phase, with pre-treatment Child’s score of C in 2 cases, B in 2 cases, and A in 1 case. After treatment, all five cases had negative HBV DNA, improved clinical and biochemical tests, significantly reduced Child’s score (from 12 to 5 in one patient with Child’s grade C), and recovered from the original hepatic encephalopathy. 35 patients with chronic hepatitis B decompensated cirrhosis were treated with lamivudine by Villeneuve et al. Before treatment, all patients were positive for serum HBV DNA, 10 had Child-Pugh class B and 25 had Child-Pugh class C. Most patients’ liver function gradually improved after treatment, and the most significant improvement in liver function was observed after 9 months of treatment, with serum total bilirubin decreasing from (67 ± 13) μmol/L to (30 ± 4) μmol/L before treatment, serum albumin increasing from (27 ± 1) g/L to (34 ± 1) g/L, and Child-Pugh score decreasing from (10.3 ± 0.4) to (7.5 ± 0.5). 0.5) (all P values < .05). The above clinical findings suggest that lamivudine can be safely applied to patients with post-hepatitis B decompensated cirrhosis with a significant effect of inhibiting HBV replication, thus delaying or even reversing the pathological process of cirrhosis. The author applied lamivudine in the past two years to treat 2 patients with severe decompensated post-hepatitis B cirrhosis, who had positive serum HBsAg, HBeAg and HBV DNA and obvious abnormal liver function before treatment. These 2 cases had recurrent complications such as hepatic encephalopathy, intractable massive ascites and recurrent bacterial peritonitis. After 12 weeks of treatment with lamivudine (100 mg daily), the serum HBeAg and HBV DNA of the 2 cases turned negative and seroconversion of anti-HBe occurred, and clinical and biochemical tests gradually improved; after 9 months of treatment, ascites basically disappeared, and hepatic encephalopathy and bacterial After 9 months of treatment, ascites basically disappeared, hepatic encephalopathy and bacterial peritonitis did not recur, and the disease was very stable and well tolerated to the drug (data to be published). According to the author's clinical experience, these two patients would never have achieved such good results if they had not been treated with lamivudine. It is reasonable to assume that lamivudine is an important antiviral therapy for patients with post-hepatitis cirrhosis, and its long-term use may significantly improve the prognosis of patients with advanced cirrhosis.