In fact, most of the approximately 30 million patients with chronic hepatitis B in China are not receiving regular treatment. Do you think I’m being alarmist? Anyone with the disease should actively seek the best possible treatment, but this is not the case. Because chronic hepatitis B is often insidious, the onset of the disease is not known for many years without regular checkups, so of course they don’t seek treatment; many people think that as long as liver function is normal, it’s OK, and not clearing the virus is not considered standard treatment. Thus, there is the question in the title.
Hepatitis B virus infection can have different progressions and outcomes, which are determined by both viral and human factors. Viral factors include the number of infections and the replicative activity of the viral strain; human factors are mainly the immune status, including age, genetic quality and underlying health status that determine the immune status.
Is chronic hepatitis B transformed from acute hepatitis B?
It cannot be taken for granted that the vast majority of chronic hepatitis B does not come from acute hepatitis B, but develops in people who are chronic hepatitis B carriers, with approximately 25% of carriers developing hepatitis.
The majority of chronic carriers were infected with the hepatitis B virus during childhood, when the immune system was not fully developed and the hepatitis B virus was not easily cleared after infection.
Of course, there are a very small number of adults with acute hepatitis B who will become chronic, and that is only possible for those with pre-existing immune deficiency diseases such as chronic nephritis, or those with a deficient constitution due to drug or alcohol abuse.
What factors are associated with the progression of chronic hepatitis B to cirrhosis?
Chronic hepatitis B is characterized by long-lasting and recurrent inflammatory lesions, and the main factors for progression are gender, age, active viral replication, long-term lesion activity and overlapping infections with other hepatitis viruses.
More men have severe disease and more men have progressive cirrhosis. About 15% of adults with chronic hepatitis B spontaneously go into remission each year from “major triplet” to “minor triplet”. Pediatric cases have a high immune tolerance (the characteristic of tolerating viral replication without morbidity) and rarely convert from “major triplet” to “minor triplet”, although the lesions are mild but rarely remit spontaneously. The number of adult cirrhosis is many times higher than the number of adult hepatitis. There are more severe hepatitis in the elderly, more cardiovascular, respiratory and diabetic co-morbidities, and more cirrhosis develops, and more liver cancer occurs in the elderly with cirrhosis.
HBeAg (+) chronic hepatitis B with prolonged disease, immune activity is also increasing, higher levels of virus will be more aggressive lesions, may progress faster. hBeAg (C) chronic hepatitis B is derived from HBeAg (+) cases by long-term activity, immune activity is higher, so the level of virus and the degree of lesions consistent. hBeAg (C) patients, although the lesions progress more slowly, but the eventual development of liver failure. Although the progression of lesions in HBeAg(C) patients is slower, liver failure, cirrhosis and hepatocellular carcinoma eventually occur in far more cases than in HBeAg(+) cases.
People with chronic hepatitis B overlapping hepatitis A or C viruses have faster progression of disease and more often develop cirrhosis and hepatocellular carcinoma.
What factors are associated with the development of decompensation in compensated cirrhosis
From chronic hepatitis B to active cirrhosis, there is a progression from mild to severe, in 2 stages: compensated cirrhosis is when liver function can afford daily life and general work; otherwise, it is decompensated. Mild compensated cirrhosis is often unconscious and can be missed when visiting a hospital; heavier cases may have some vague symptoms, including easy fatigue, abdominal discomfort, or stuffiness in the right upper abdomen, abnormal liver function tests, and ultrasound findings of splenomegaly; more severe cases may have slightly more symptoms, with elevated serum transaminases in liver function tests, lower albumin, liver palms, spider nevi, and ultrasound showing uneven liver surface and Widening of portal vein and splenic vein, etc.
If the disease progresses to a more severe form, it reaches decompensated cirrhosis: jaundice, ascites, encephalopathy, bleeding and reduced albumin. Loss of compensation is the result of prolonged viral replication and inflammatory activity, and is an advanced form of active cirrhosis.
The continued progression of cirrhosis depends on the level of viral replication (expressed as quantitative serum HBV DNA) and the activity of the lesion (expressed as serum transaminases, transpeptidases and jaundice).
Blood flow from our intra-abdominal organs is concentrated in a vessel called the portal vein, which flows to the liver and then back to the heart from the hepatic vein. After cirrhosis, there is resistance to blood flow in the portal vein and the blood pressure in the vein increases, which is called portal hypertension. The heavier the cirrhosis, the higher the pressure within the portal vein, and serious comorbidities can occur: one is esophageal varices, which can rupture and bleed when the varices are heavy, and the consequences can be catastrophic if there is a lot of bleeding; the other is hyperfunction because the spleen is bruised and enlarged. The spleen is a small blood bank, when normal, it removes some aging blood cells, but hypersplenism will destroy some blood cells that have not yet aged, and the reduction of platelets and white blood cells is more obvious. Too few platelets can cause bleeding everywhere; too few white blood cells can cause various bacterial infections. As a result, these comorbidities will occur when the cirrhosis is heavy; with the comorbidities will make the cirrhosis even heavier and may make the compensated cirrhosis progress to decompensated cirrhosis.
What factors are associated with the development of liver cancer in patients with cirrhosis
Liver cancer occurs in 1% to 6% of cirrhotic patients each year, with a five-year cumulative incidence of 15% to 20%. Liver cancer can occur sooner in cirrhosis with high viral levels and active lesions; however, a very small number of patients with quiescent lesions may become cancerous in a longer natural course, so it is necessary to insist on regular checkups.
What are the common factors for the progression of chronic hepatitis B lesions?
Chronic hepatitis B varies in severity and is characterized by continuous viral replication during the long course of the disease, which leads to recurrent activity. Without standardized antiviral therapy, most of the disease will gradually worsen; some gradually progress to cirrhosis, decompensation and hepatocellular carcinoma. Without antiviral treatment, many will eventually progress to catastrophic advanced liver disease. Chronic hepatitis B is a chronic liver disease with a more serious prognosis.
There are many “liver protection” drugs available in China that can effectively control symptoms, and many doctors and more patients are satisfied with normal liver function tests. The current rate of patients receiving antiviral therapy is still very low due to lack of affordability.
Anti-viral treatment for chronic hepatitis B can rarely cure the disease within three to five years with the disappearance of “small triplets”, but most of them can control the progress of the disease and put it into remission. Antiviral therapy is much more effective and economical for HBeAg(+) chronic hepatitis than for HBeAg(C) chronic hepatitis; it is much more effective and economical for treating chronic hepatitis than for treating active cirrhosis; it is much more effective and economical for treating active compensated cirrhosis than for treating cirrhosis with loss of liver function. Moreover, the more the disease progresses, the less the components that can be reversed, so why not actively treat the disease with antiviral therapy as early as possible to prevent its progress?