Using entecavir to treat hepatitis B, how can we reduce the risk of progression to fibrosis and cirrhosis?

alopah Date:2021-09-09 17:06:55
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A few days ago, I was asked by Internet users to use entecavir against hepatitis B virus. How can we avoid liver fibrosis and cirrhosis? How can we reduce the further development of intrahepatic inflammation? Before answering this question, we need to know that the most important factor in the treatment of hepatitis B is antiviral treatment. No matter whether nucleoside analogues or interferons are selected, active and effective antiviral treatment can inhibit hepatitis B replication to the maximum extent, delay or reduce the risk of hepatitis B progression to cirrhosis and even liver cancer.


What aspects should be done to reduce the progression of hepatitis B to cirrhosis and liver cancer?


First, standardize the use of entecavir

Entecavir is a guanine nucleoside analogue that inhibits hepatitis B virus polymerase. It can be phosphorylated into active triphosphate. The half-life of triphosphate in cells is 15 hours. By competing with deoxyguanine nucleoside triphosphate, the natural substrate of HBV polymerase, entecavir triphosphate can inhibit all three activities of viral polymerase (reverse transcriptase): (1) initiation of HBV polymerase; (2) Formation of negative chain of pre genomic mRNA reverse transcription; (3) Synthesis of HBV DNA positive strand.


A large number of clinical data have confirmed that entree Cave is the first-line antiviral therapy, and the ability to inhibit hepatitis B virus replication is strong. If standardized use, there is no second-line drug and its cross resistance risk exists. Generally speaking, entree Cave is rarely resistant to chronic viral suppression.


Currently, entecavir is required to be taken on an empty stomach for a relatively fixed time. The purpose is to ensure sufficient and stable blood drug concentration. In order to avoid the delay of drug coefficient after eating and maximize its curative effect, entecavir on an empty stomach is the best choice.


Second, strengthen the follow-up and reexamination during the antiviral period of entecavir

Although entecavir is the first-line antiviral drug, in clinical practice, there are still a few people with poor response and even drug resistance. The main reasons are non-standard medication and insufficient self phosphatase, resulting in insufficient phosphorylation of entecavir and cross resistance after previous drug resistance.


In addition to ensuring the compliance of medication, regular review and follow-up can be done to find the response results of treatment in time. If entecavir can not turn negative within one year after anti-virus treatment, it is necessary to actively find out the reasons for poor response and whether it is caused by non-standard medication. If it is not for this reason, the virus level decreases, but it can not turn negative, We need to actively adjust drug treatment.


What is the reason why liver disease doctors suggest that hepatitis B patients can not achieve viral conversion within 1 years, and need to actively adjust the treatment? Mainly because the virus can not turn negative, prone to repeated hepatitis activities, leading to disease progression. The red line of our antiviral treatment is that the virus turns negative. Instead of turning negative, it is a drop in the bucket to pay attention to other adjuvant treatments.


entecavir against hepatitis B virus


Third, pay attention to the regression of intrahepatic inflammation during anti-virus

Why should we pay attention to intrahepatic inflammation? Most hepatitis B patients begin antiviral therapy at the time of hepatitis activity. The most common feature is abnormal liver function, especially when alanine aminotransferase is elevated. The persistent abnormality of alanine aminotransferase can reflect the injury and necrosis of hepatocytes, which indicates the emergence of immune-mediated hepatocyte injury. Although the liver will be repaired in time after hepatocyte necrosis, with the absorption and regression of inflammation, the liver is prone to a large amount of extracellular matrix deposition and the risk of fibrosis.


Clinically, it is found that abnormal liver function occurs in the early stage of disease resistance, especially the increase of alanine aminotransferase, which generally indicates the existence of hepatitis activity, indicating good immune activation. At this time, the immune ability to clear the virus is stronger, but the liver specific immune recovery and even after enhancement, the immune damage to hepatocytes is more obvious. For persistent abnormal liver function, active anti-inflammatory and liver protection treatment should be considered, which can partially reduce the duration and intensity of liver inflammation, accelerate the absorption and regression of inflammation, and further reduce the risk of fibrosis formation or progression.


Even a few patients, after anti-virus and liver protection treatment, although the liver function is normal, the liver inflammation has not completely subsided and absorbed in the short term. It can be found in clinical practice that after the liver function is normal, the liver hardness value indicated by the follow-up liver elasticity has not decreased immediately, and the liver hardness value will decrease for a period of time after the liver function is stable. Therefore, we all suggest to use liver bomb to evaluate the degree of liver fibrosis. We all need to do liver bomb 3 months after transaminase normalization, considering that intrahepatic inflammation will not be completely absorbed and subsided immediately after transaminase is normal.


Fourth, pay attention to the optimal treatment of entecavir during anti-virus treatment

The optimization of entecavir antiviral therapy is mainly due to the fact that many hepatitis B patients are able to get rid of the hepatitis B virus after the use of entecavir through active self-regulation. However, many large Sanyang patients have achieved serological conversion of e antigen or have undergone seroconversion of e antigen despite the virus turning negative. However, it is not stable and lasting enough, and it is prone to re Yang of e antigen, that is, after the big three Yang changes to the small three yang, it will soon return to the big three yang. Similarly, many small Sanyang patients used entecavir to achieve virus negative conversion, but it is difficult for surface antigen to achieve negative conversion.


The above phenomenon is mainly due to the fact that hepatitis B patients have certain immune control ability to achieve negative virus, but the immune response is still not ideal, and there is no stronger immune response and continuous control ability. It is difficult to achieve the ideal response of viral markers.


In order to further improve the effect of hepatitis B treatment, in addition to the mistress of the virus, it is necessary for the patients to achieve the e antigen conversion at an early date. The patients will soon disappear and the long-term negative symptoms of the virus should be maintained during the whole follow-up period. In other words, to treat hepatitis B, in order to minimize the risk of hepatitis B progression to liver fibrosis, cirrhosis and even liver cancer, it is still necessary to achieve virus conversion, e antigen conversion, and even surface antigen conversion. At present, to achieve this higher therapeutic goal, entecavir combined with other antiviral drugs is an option that can be considered.


From the current treatment system, entecavir combined with sequential interferon or even intermittent interferon are the embodiment of individualized management. When we find that entecavir has achieved the primary goal of anti-virus (virus turning negative), we need to focus on higher goals. Many times, nucleoside analogues can not be completed independently, and it needs to be combined with interferon to meet this requirement.


This requires that some hepatitis B patients, especially the entecavir anti virus, do regular review and follow up. Only when entecavir is difficult to achieve e antigen conversion or surface antigen turn negative, if we find the optimal treatment time (lower HBV DNA level, lower e antigen level or lower surface antigen level), choose the suitable plan. Strive to achieve better treatment goals. Only in this way, the risk of hepatitis B progression to cirrhosis will be lower, and the risk of liver cancer will be even smaller.


In short, patients with chronic hepatitis B need to choose individualized antiviral strategies on the basis of standardized treatment in order to maximize the therapeutic effect and avoid progression to liver cirrhosis and liver cancer to the greatest extent.

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