Chronic hepatitis B is the most common of the chronic infectious diseases in Asia and has probably the highest prevalence of infection. The natural population infection rate in China reached 10 per cent at the time of the 2000 survey. Although most people are asymptomatic, the implied prevalence may be very high. For example: in reality, some patients say that their liver function has been normal for so many years, and this physical examination suddenly reveals that they have cirrhosis of Hepatitis B. Even some patients come to the clinic and say, “I am a small triple Yang, the virus has been negative, liver function has been normal. How did cirrhosis occur directly? Of course, these patients are in the minority. But these few patients illustrate a basic fact. As long as hepatitis B is not completely eradicated, it may cause damage to our health, and our road to treatment is not really over. In addition, many more patients are suffering from recurrent liver function abnormalities for a myriad of reasons. Some are the patient’s own stubborn view that antiviral therapy is dangerous. Some of them think that I used to be fine, but now my liver function is a bit abnormal, and I will soon go back to my previous state after taking some liver-protecting drugs. There are also some who hope to cure themselves through some magical prescriptions. There are also those whose condition fluctuates repeatedly due to unreasonable treatment by doctors. Although the treatment of hepatitis B in the last 10 years has many more treatment means than that of more than 10 years ago. There are many nucleoside analogs to fight against the virus, and liver-protecting drugs are also emerging, however, the results of hepatitis B treatment are not satisfactory. Why is this so? One of the big reasons is because the treatment is not standardized, in addition, because some of the reasons are because the patient can not adhere to, there are also some reasons, because the doctor of hepatitis B this disease, the pathogenesis of insufficient understanding, simply think, as long as the liver or as long as the anti-virus, can achieve its therapeutic purpose. Let’s first look at the pathogenesis of acute hepatitis B. The first thing we see is the elevation of aminotransferase, at this time, the patient’s virus is often positive, the patient manifested as triple positive, with the progress of the disease, the patient’s aminotransferase began to decline, the viral DNA turned negative, the viral serology manifested as triple positive, with the condition of the disease improves, at this time, triple positive, began to change, triple positive, with the prolongation of time, hepatitis B, the gradual disappearance of the surface antigen, the surface antibody gradually appeared, the appearance of surface antibody means that the surface antigen gradually disappeared, the surface antibody gradually appeared. Gradually appear, the appearance of surface antibodies means that hepatitis B is cured, hepatitis B serology is 245 positive, then the fourth and fifth antibodies, respectively, represent what is the significance of it! The appearance of the fourth antibody suggests that the replication ability of the virus is reduced or disappeared, while the fifth antibody, if it persists, not only can’t indicate that hepatitis B continues to improve, it may suggest that hepatitis B is fixed in the patient’s liver for a long time, so the real meaning of hepatitis B self-cure should be followed by the disappearance of the fourth item of the hepatitis B serology, which changes into the second and fifth positive items, with the prolongation of time Just as it will also fade away, leaving only the second positive item, which is positive for surface antibodies, only patients who are positive for surface antibodies alone can be considered completely cured of complete Hepatitis B. Currently on the transplant and immunocompromised patients can occasionally see 45-positive patients with the phenomenon of hepatitis B virus re-vitalization. Although it is an individual case, it fully illustrates the factual basis of this situation. Therefore, from the acute onset of hepatitis B to the process of healing. The complete cure of hepatitis B needs to achieve at least surface antigen turn negative and surface antibody appear. So, how can a patient with slow hepatitis B reach this state. I use a few cases to illustrate. Patient 1, the patient (Wang) slow hepatitis B for many years, major triple Yang. 8 years ago due to severe hepatitis hospitalization. After recovery, long-term use of entecavir. 1 year ago review, the patient HBVDNA negative, small triple positive. Surface antigen titer was less than 50. Liver function is normal. There is no obvious cirrhosis. At this time, the conventional choice is to continue to use entecavir antiviral. However, we convinced the patient to use interferon. After 3 months of interferon treatment, the surface antigen turned negative. After 3 months of continued use, the patient’s surface antibody reached 28 IU/ML, and the patient requested another 3 months of interferon. One year after stopping the drug, the patient still had normal liver function and negative HBVDNA. The two halves were 25 positive. Patient 2. Patient (Shen) had recurrent liver function abnormalities with ALT fluctuating within 100. Minor triple positive, HBVDNA negative. The outpatient doctors in various hospitals over the past 5 years said he had a fatty liver. Repeatedly use liver-protecting drugs. Liver function is normalized with the medication, and recurrence occurs soon after the medication is stopped. The patient was very confused. We gave the patient a liver tissue biopsy. Pathology suggests viral hepatitis with no fat accumulation in the liver. After interferon treatment, the patient’s liver function was normalized after 3 months. By 9 months the patient’s surface antigen disappeared surface antibodies appeared. Patient 3. Patient (Xu) was infected by vertical mother-to-child transmission. The viral load was greater than 8 times. Repeated liver function abnormalities and ineffective hepatoprotective therapy. Major triple positive. Surface antigen was found to be 45000IU/ML. patient was given entecavir treatment for 6 months, patient’s viral DNA was negative but still had abnormal liver function. alt 100IU/ML was about. ALT100IU/ML. Liver function was still not normalized with hepatoprotective drugs. The patient was given interferon antiviral therapy. 9 months later the interferon was stopped and the antiviral drugs were continued. Currently, liver function is normal, virus negative, and minor triple positive. Surface antigen titer is more than 4300. Seeing the hope of a complete cure, but the treatment is not yet complete. Patient 4, patient (Cao) for mother-to-child vertical transmission of infection. Viral load 7 times. Repeated liver function abnormalities, large triple Yang. Surface antigen was found to be 22,000 IU/ML. the patient hoped for a one-time cure. Direct treatment with interferon. His doctor followed the patient’s wishes and used interferon. 6 months later, the patient’s viral load was 5 times higher. Surface antigen 18,000 IU/ML, still a major triple. The efficacy of the treatment is not good. Whether to continue to adhere to, or give up becomes a dilemma. Patient 5: The patient is triple positive with normal liver function. Viral load 4 times. The patient is unwilling to take antiviral therapy. The patient was given a long-term oral immunity-enhancing drug. After 1 year of oral intake, the patient’s liver function was normal and HBVDNA was negative. The two halves became small triple positive. Patient 6, the patient is triple positive, mild liver function abnormalities, viral load 6 times, surface antigen 4900 more. Nine months after the use of interferon the patient was negative for virus and had normal liver function. Minor triple positive. Surface antigen is more than 800. Many people will choose to stop the drug at this time for observation. However, we suggested the patient to continue to use interferon. 2 years later, the patient’s surface antigen was only 10. We continued to encourage the patient to persist. By 2.5 years, the patient’s surface antigen had turned negative. Surface antibody titer was 30 IU/ML, and the patient continued the treatment for half a year. The patient’s surface antigen titer reached more than 100IU. Patient 7: In 2009, the patient had hepatitis B teratitis III, the virus was greater than 9 times, and the liver function was normal. Use lamivudine antiviral, 2 years later appeared abnormal liver function, virus 6 times square. Adefovir was added. By 2012 the patient again developed mildly abnormal liver function. Virus 4 times square. Switched to entecavir. After 1 year of use the virus still could not be converted. Liver function mildly abnormal. Doctor gave entecavir in combination with adefovir for 1 year. Patient still has virus 5 times. Liver function is abnormal. No classical viral variant locus mutations have been detected. Surface antigen was found to be 29,000 IU/ML. 3 months after we switched the patient to tenofovir, the patient’s virus was 3 times more virulent. Still no conversion. Currently still in treatment communication. From the above 7 cases, the treatment of hepatitis B is not an overnight solution. Of course these are individual cases and cannot fully represent the overall. However, antiviral and immune regulation is the key to completely curing hepatitis B. How to choose the treatment plan is very important, inappropriate treatment plan not only wastes the patient’s money, but also increases the patient’s pain. In addition, the goal of the treatment should be clear before the treatment, without the goal of the treatment, it is ultimately impossible to evaluate the efficacy of the treatment. It is not clear when one should continue to persevere. When to give up. In general, the ultimate goal of hepatitis B treatment is the conversion of surface antigen and the appearance of surface antibody. Hepatitis B is difficult to cure, mainly because CCCDNA is difficult to remove, which is an important reason for patients to relapse after stopping the drug. And CCCDNA is inside the liver cells. Clearing it sometimes damages liver cells. Therefore the treatment needs to come to a balance between the liver cells and the virus. This requires the doctor to observe the patient’s response to treatment thoroughly and carefully. In addition, surface antigen and CCCDNA are positively correlated. Therefore, the removal of surface antigen is the only way to clear CCCDNA from hepatitis B. Clearing CCCDNA is a long process that requires regular treatment and patience. It requires standardized treatment and patience. Inappropriate choice of antivirals will only increase the difficulty of treatment (Case 7 is representative of unregulated treatment, which makes follow-up difficult). All the previous talk is about antivirals, which on the surface only use interferon and nucleoside analogs. It seems simple, but the timing of treatment is very important. Personal experience is that you must choose the right treatment at the right time. And there should be key observables to react to the outcome of the treatment. Choosing inappropriate observations can lead to misjudgment of the condition. There is also the fact that the body’s immune regulation in the treatment of hepatitis B has a role that can not be ignored.