With the launch of lamivudine (Herceptin) in China in 1998, a new milestone in the treatment of chronic hepatitis B began in China. Over 3 years of clinical studies have shown that lamivudine treatment has slowed or even reversed the progression of chronic hepatitis B disease, followed by the launch of adefovir, entecavir, and telbivudine, which have provided more options for the treatment of chronic hepatitis B with nucleoside analogues. However, with the widespread use of nucleoside analogues in the treatment of chronic hepatitis B, the exact duration of treatment has become increasingly difficult to determine: how to determine the target population for long-term treatment with nucleoside analogues, the “safe” time to discontinue nucleoside analogues with poor efficacy, the time to discontinue nucleoside analogues with satisfactory efficacy, and the time to discontinue nucleoside analogues with satisfactory efficacy. How to determine the timing of “sustainable” drug discontinuation? The majority of hepatitis B comrades are eagerly awaiting the answers to these questions. In the author’s specialist clinic, the above questions are always present among hepatitis B patients using nucleoside (acid) drugs, so I have been thinking about the above questions as well. Who needs long-term nucleoside (acid) medication? The answer is simple and clear! Whether in developed Europe and the United States or in the Asia-Pacific region, where the economy is relatively backward, the goal of nucleoside (acid) drug therapy is clear: to slow down or even reverse the progression of liver disease and prevent cirrhosis, liver cancer and even liver disease-related death. Based on the serious consequences of liver cirrhosis, such as ascites, gastrointestinal bleeding, liver cancer and eventual liver disease-related death, patients with cirrhosis, especially decompensated cirrhosis, are rightfully the first target of long-term nucleoside (acid) drug therapy. The only way to get “long-term treatment” is to get “long-term peace”! Based on the high risk of severe liver fibrosis developing into cirrhosis, hepatitis B warriors with liver puncture biopsies clearly identified as severe liver fibrosis or liver hardness higher than 12 kPa should receive a longer period of nucleoside (acid) drug therapy, on this aspect, warriors can refer to the author’s article “Prevention of liver cancer and cirrhosis complications requires early detection and intervention of cirrhosis trends! and will not repeat it here. The second question we are concerned about is how to achieve “safe” discontinuation of the drug for those who are not doing well and are eager to stop the drug for various reasons. The so-called “safety” is a relative term. It seems inevitable that a relapse of hepatitis after discontinuation of the drug with poor efficacy is the end, but our concern is whether the relapse of hepatitis after discontinuation is “fatal”? Is there a short-term risk of cirrhosis or even liver disease failure? The answer to these questions requires addressing the issue of liver fibrosis assessment prior to treatment. If a pre-treatment liver puncture biopsy shows no liver fibrosis or only mild liver fibrosis (fibrosis in the confluent area or a small amount of interfibrillation, or if liver stiffness is less than 7.4 kPa (except for those with cirrhosis on ultrasound), it should be “safe” to discontinue the drug with poor efficacy; if neither a liver puncture biopsy nor a liver stiffness test has been performed before treatment, it should be “safe” to discontinue the drug. If neither liver aspiration biopsy nor liver stiffness examination has been performed before treatment, it is wise to perform liver aspiration biopsy to determine the status of liver fibrosis before discontinuing the drug! The reason why liver aspiration biopsy is recommended to determine the status of liver fibrosis after treatment is because the liver is a silent organ that “goes against the grain” and an apparently “safe” liver may hide the risk of cirrhosis, and the existing diagnostic criteria are derived from untreated patients who have undergone The existing diagnostic criteria for liver fibrosis, which are derived from untreated patients, and those for liver fibrosis, where the inflammatory tendency of the liver is restored by antiviral therapy, would be very different, and there is a lack of data; we have found liver stiffness within the normal range in patients with cirrhosis whose liver inflammation has been absorbed. The final question: If nucleoside (acid) therapy is satisfactory, when do we stop the drug to obtain “sustained” benefit? What is satisfactory efficacy? For hepatitis B E antigen-positive (i.e., “major triple-positive”) patients, after a period of treatment, “E antigen seroconversion” (a term used by hepatitis B specialists) occurs, i.e., a change from “major triple-positive” to “major triple-positive”. The “major triple-positive” transformation to “minor triple-positive”, while using imported reagents to test HBVDNA negative! It should be noted that we emphasize the “small triplet”, while the frequent “small two-positive” does not meet the criteria, because these warriors are basically low-level “large triplet” ( If conditions allow, it is recommended to confirm the “small three yang” through imported reagents, not to be a fan of foreigners, but the gap is indeed so!) The difference is real! Once the “minor triplet” appears, we will see the light of day to stop the medication! However, how long does “small triple yang” last (let’s call it “consolidation time”) is the “insurance” strategy to stop medication, there are different opinions, but it is clear that consolidation treatment The longer the duration, the better the “benefit” of stopping the drug! In the author’s experience, combined with the available research data, consolidation therapy for more than 2 years seems to be the preferred course of action! Again, the so-called consolidation treatment time should be calculated from the “major triplet” to “minor triplet” (confirmed by imported reagents), and imported reagents to test negative for HBVDNA. For E antigen-negative hepatitis B comrades, the time to stop the medication seems to be far away! Since there is no “E antigen seroconversion” standard, the quantitative surface antigen (HBsAg) test has become the judgment indicator, the current more consistent statement is: HBsAg quantitative below 1000IU/mL, you can consider stopping the drug, but if the HBsAg is lower than then stop the drug, of course, the best The “benefit” is naturally to stop the drug after HBsAg turns negative. It should be emphasized that no matter what, the possibility of relapse of the disease after stopping the medication always exists, thus regular checkups after stopping the medication is crucial! For those without cirrhosis, whether or not to re-treat depends on whether or not there is hepatitis activity, and the duration of recurrent hepatitis activity, while for those with cirrhosis before treatment, HBVDNA should be checked every 2 months for six months after stopping medication, and can be adjusted to every 3 months after six months, and once HBVDNA exceeds 10,000 copies/mL, regardless of whether or not the transaminases are elevated, it is necessary to restart antiviral therapy!