If it is higher than 1,000 copies/ml, the probability of hepatitis outbreak within three years is about 12%; if it is between 10,000 copies and one million copies, the probability of hepatitis outbreak within three years is about 43%; high With one million copies, the probability of hepatitis outbreak within three years is about 66.7%. If the number continues to be less than 1,000 copies, it can be diagnosed as an inactive hepatitis B surface antigen carrier and does not require any drug treatment. It is recommended to review it every six months. A study in Taiwan showed that if the HBV DNA of inactive hepatitis B surface antigen carriers continues to be less than 1,000 copies, 45% of patients will become negative for hepatitis B surface antigen after 25 years. How can I turn my hepatitis B surface antigen negative?
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Teacher Liu is 35 years old this year and has Dasan Yang hepatitis
After 3 months of treatment with PegIntron interferon, The HBVDNA quantification dropped from the seventh power of 10 to less than 100IU/ml. Six months later, the liver function returned to normal and the E antigen also turned negative. Teacher Liu was so happy to achieve such a good effect! Nine months later, an even bigger surprise occurred. His hepatitis B surface antigen also turned negative. Teacher Liu continued to take interferon for a full year, but a test before stopping the medication found that hepatitis B surface antigen had become positive again. I suggest that he continue to use interferon treatment for 3 months. If he is still positive, he should stop taking the medicine and observe it. Teacher Liu's attitude is very firm. He plans to continue interferon treatment and will not stop until the surface antigen turns negative. Can antiviral treatment target hepatitis B surface antigen negative conversion? To clarify this issue, we must first start with what hepatitis B surface antigen is.
Hepatitis B surface antigen is the eggshell of an egg. Hepatitis B virus must use this layer of eggshell to closely connect with liver cells and invade liver cells.
Hepatitis B surface antigen is produced by hepatitis B virus. If hepatitis B surface antigen is detected in the patient's blood, it means that hepatitis B virus must be present in the patient's liver cells. Moreover, the higher the surface antigen titer in the blood, the greater the amount of hepatitis B virus in the liver. The hepatitis B virus in liver cells can produce massive amounts of hepatitis B surface antigen. If there is one copy of the virus in the liver, there will be hundreds of units of surface antigen in the blood. People who are surface antigen positive must have current hepatitis B virus infection.
Approximately 8% of patients with major triple positive HBV DNA who have reached HBV DNA below the lower limit of detection and experienced E antigen seroconversion after Pegasys treatment will become negative for hepatitis B surface antigen. The liver is the base camp for hepatitis B virus replication, and the HBVcccDNA (hepatitis B virus highly-valent closed circular DNA) in the nucleus of liver cells is the seed for hepatitis B virus replication. Current nucleoside (acid) drugs can only eliminate hepatitis B virus in the blood circulation and inhibit the production of new hepatitis B viruses, but have little effect on HBVcccDNA in the nucleus of liver cells. The results calculated using mathematical models show that it will take at least 14.5 years of effective antiviral treatment to completely eliminate HBVcccDNA in the liver cell nucleus. It can be seen that it is difficult for current antiviral drugs to achieve the so-called ideal goal of "conversion of hepatitis B surface antigen to negative", which is an elusive goal for most patients with chronic hepatitis B. Does the conversion of hepatitis B surface antigen to negative mean that hepatitis B has been completely cured and will it never recur?
No. Even if hepatitis B surface antigen becomes negative, it does not mean that hepatitis B is completely cured. HBVcccDNA still exists in the nucleus of the patient's liver cells, and there is still a risk of hepatitis B recurrence. In clinical practice, it is not uncommon for hepatitis B surface antigen to turn negative and then relapse after treatment with interferon. Therefore, it is difficult to achieve the goal of completely curing hepatitis B with the current level of treatment.
Although it is currently difficult for us to completely eliminate hepatitis B virus, through standardized antiviral treatment, we can maximize the long-term suppression of viral replication, minimize the incidence of cirrhosis, liver cancer, and liver failure, so that Hepatitis B patients live well and long, and in this way the purpose of our treatment is achieved. Through standardized antiviral treatment, your liver will be well protected. With the current level of scientific and technological development, in five or ten years, humans will definitely find a treatment method to completely eliminate the hepatitis B virus!
After standard antiviral treatment, HBV DNA quantification continues to be lower than the lower limit of detection, and liver function is normal for a long time. The vast majority of hepatitis B patients can live a safe, healthy and long life. It's just that hepatitis B surface antigen is positive, but a small amount of hepatitis B virus remains in the liver cells. What does it matter if it is checked regularly? Why should we go beyond the current level of hepatitis B treatment and pursue the perfect treatment goal of hepatitis B surface antigen negative conversion? Looking at the famous people in history at home and abroad, how many of them had perfect lives? Not to mention us ordinary people.
It should be noted that life is inherently imperfect, and imperfection is life!