How far is it from chronic hepatitis to mild cirrhosis?

Many patients usually do not care about it, and when cirrhosis is accidentally detected in medical checkups, they are unable to eat or sleep, and ask themselves how long they have to live. Cirrhosis is actually very common, and there are different stages of development with great differences in severity. Most patients can have different degrees of reversal as long as they are actively treated. In 2009, I found out that I had “triple III”, and I didn’t pay attention to it because I didn’t have any physical discomfort. In recent years, there have been a few abnormal liver function in the physical examination of the unit, and took some drugs to protect the liver and reduce enzymes. In June this year, the physical examination found that the spleen enlarged to 4.2cm, the viral DNA was 5.76E+07 iu/ml, the glutamic enzyme was 86, the glutamic enzyme was 91, and the liver puncture found that it was already G3S4, which was diagnosed as early stage of liver cirrhosis. How come? I don’t smoke, drink heavily or stay up late, I had a nervous breakdown. I have an old man and a young man, what should I do? Where is cirrhosis in the progression of chronic hepatitis B liver disease? Chronic hepatitis B virus infection has a slow development process, from light to heavy in the following order: 1. “Triple sun” chronic asymptomatic carriage → mild hepatitis → hepatitis with varying degrees of fibrosis → chronic inactive carriage → re-activation of the “triple sun” hepatitis → 3 to 5 years after the occurrence of mild compensatory cirrhosis. Mild compensated cirrhosis → moderate compensated cirrhosis → early decompensated cirrhosis → advanced decompensated cirrhosis. 2. 2. “Major triple positive” hepatitis with fibrosis → “Minor triple positive” hepatitis → (very few) small hepatocellular carcinoma → hepatocellular carcinoma → giant hepatocellular carcinoma. 3. “Triple positive” hepatitis with fibrosis → (after 2-3 years) mild compensated cirrhosis, moderate compensated cirrhosis → decompensated cirrhosis → (the incidence increases with the severity of the lesion) small hepatocellular carcinoma → hepatocellular carcinoma → giant hepatocellular carcinoma. 4. In any stage of chronic hepatitis B virus infection, acute liver failure (the so-called “slow and urgent”) may occur, and the condition will return to the original point before the “urgent” in time for treatment; and cirrhosis of varying degrees may occur at the earliest in 6 months after the untimely treatment or the original cirrhosis will be aggravated. Cirrhosis aggravated. “Major Triple Positive” has a higher level of viral replication, and the condition should develop faster. “Minor triple positive” is caused by mutated virus, the virus replication level is lower, the development of the disease is slower, but many people are delayed and potential development, cirrhosis and liver cancer instead, accounting for about 80% of the overall. How does chronic hepatitis progress to mild compensated cirrhosis? Chronic hepatitis B causes active cirrhosis, with clinical features of both hepatitis and cirrhosis. The progression from chronic hepatitis to cirrhosis goes through different stages: from mild compensated cirrhosis to advanced uncompensated cirrhosis, it takes a variable period of time depending on the severity of the inflammation: those with heavy inflammation develop quickly and may have obvious symptoms; those with mild inflammation develop slowly and often worsen slowly without symptoms. Chronic hepatitis liver cells are destroyed by inflammation, and fibrous tissue is used to repair the damage, which is liver fibrosis. Enzyme-lowering drugs and traditional Chinese medicine can slow down the inflammation, because they can not clear the virus, many patients’ inflammation is still slow and asymptomatic, hepatocyte destruction does not rest, and liver fibrosis will of course develop gradually. Only antiviral treatment can stop the inflammatory destruction of hepatocytes, thus blocking liver fibrosis, and hepatocytes have vigorous new vitality to reverse fibrosis. There is no substitute for antifibrosis possible only with antiviral! Cooked pig liver cut surface can be seen dense gray-white dots, each dot is a hepatic lobule, the entity of the liver is composed of countless hepatic lobules. If hepatitis patients do not antiviral treatment, hepatocytes are gradually destroyed, liver fibrosis slowly accumulates, and will eventually destroy (normal) liver lobules? and become (diseased) nodules. If most of the liver lobules become nodules, hepatitis with fibrosis becomes mild compensated cirrhosis. This is a slow and gradual evolution, just from quantitative to qualitative changes. In fact, mild compensated cirrhosis is not fundamentally different from more severe fibrotic hepatitis. Current antiviral therapy is more successful, liver fibrosis can be reversed, and cirrhosis can be reversed to varying degrees.