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Chronic hepatitis B: symptoms
Last reviewed: 23.04.2024
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Chronic hepatitis B is found predominantly in men.
Possible links with HBV include ethnicity (countries with a high level of carrier status), sexual contact with infected people, work related to contact with human blood, transplantation of organs and tissues, or immunodepressant therapy in history, homosexuality and drug addiction. The likelihood of developing a chronic infection in a child born to an HBeAg-positive mother is 80-90%. In healthy adults, the risk of chronic after acute hepatitis is very low (about 5%). There may be no history of any of these risk factors.
Chronic hepatitis B may be a continuation of unresolved acute hepatitis B. Acute attack is usually mild. The patient with a bright onset of the disease and severe jaundice usually comes to full recovery. In surviving patients with fulminant hepatitis, the progression of the disease is rare or it is not observed at all.
Following an acute attack, the activity of serum transaminases "fluctuates" against intermittent jaundice. Complaints can be practically absent, and patients only have biochemical signs of an active process or complaints of weakness and malaise are possible; while the diagnosis is established after a routine examination.
Chronic hepatitis B can be diagnosed in donors at the time of blood donation or routine blood screening based on the detection of HBsAg and a moderate increase in serum transaminase activity.
Chronic hepatitis is often a "mute" disease. Symptoms do not correlate with the severity of liver damage.
Approximately half of patients when referring to a doctor there are jaundice, ascites or portal hypertension, which indicate a far-gone process. Encephalopathy when treated is uncharacteristic. The patient usually can not point to the previous acute attack of hepatitis. At some patients at handling reveal hepatocellular carcinoma.
Clinical signs of exacerbation and reactivation of the virus
Patients with a fairly stable course of chronic hepatitis B can develop clinical signs of exacerbation. This is expressed in the aggravation of weakness and usually in increasing the activity of serum transaminases.
An exacerbation may be associated with seroconversion from HBeAg-positive to HBeAg-negative state. Liver biopsy reveals acute lobular hepatitis, which eventually subsides, and the activity of serum transaminases decreases. Seroconversion can be spontaneous and occurs annually in 10-15% of patients or is the result of antiviral therapy. The test for HBV-DNA can remain positive even when anti-HBe appears. In some HBeAg-positive patients, "outbreaks" of viral replication and increased activity of serum transaminases occur without the disappearance of HBeAg.
Spontaneous reactivation of the virus with the transition from HBeAg-negative state to HBeAg- and HBV-DNA-positive is also described. The clinical picture varies from minimal manifestations to fulminant hepatic insufficiency.
Reactivation of the virus is especially severe in HIV-infected patients.
Reactivation can be established serologically by the appearance of anti-HBc IgM in the blood.
Reactivation can be a consequence of cancer chemotherapy, the use of low doses of methotrexate for the treatment of rheumatoid arthritis, organ transplantation, or the administration of corticosteroids to HBeAg-positive patients.
Severe disorders are associated with mutations in the prre-core-region of the virus, when there is no e- antigen in the presence of HBV-DNA .
Possible superinfection of HDV. This leads to a significant acceleration in the progression of chronic hepatitis.
It is also possible superinfection of HAV and HCV.
As a result, any deviations in the course of the disease in carriers of HBV increase the possibility of developing hepatocellular carcinoma.
Chronic hepatitis B, associated with the replicative phase (HBeAg-positive replicative chronic hepatitis B)
Clinical and laboratory data for this variant of chronic hepatitis B correspond to active hepatitis.
Patients complain of general weakness, fatigue, fever (up to 37.5 ° C), weight loss, irritability, poor appetite, a feeling of heaviness and pain in the right upper quadrant after eating, a feeling of bitterness in the mouth, bloating, unstable stools. The higher the activity of the pathological process, the more pronounced the subjective manifestations of the disease.
When examining patients, attention is drawn to transient jaundice of the skin and sclera (not often), weight loss, with high activity of chronic hepatitis, hemorrhagic phenomena (nasal bleeding, hemorrhagic rashes on the skin) are possible. The appearance of "vascular asterisks", skin pruritus, "hepatic palms", transit ascites in the skin usually indicates a transformation into cirrhosis of the liver, but the same symptoms can also be observed with a pronounced activity of chronic hepatitis.
Objective studies reveal in all patients hepatomegaly of varying degrees. The liver is painful, tight-elastic consistency, its edge is rounded. An enlarged spleen may be palpable, but the degree of enlargement is often insignificant. Pronounced hepatosplenomegaly with hypersplenism is more common in liver cirrhosis.
In some cases, a cholestatic variant of chronic hepatitis B can be observed. It is characterized by jaundice, skin itching, hyperbilirubinemia, hypercholesterolemia, high blood levels of y-glutamyltranspeptidase, alkaline phosphatase.
In a small number of patients with chronic hepatitis B, extrahepatic systemic lesions are detected involving the inflammatory process of the digestive system (pancreatitis), exocrine glands (Sjogren's syndrome), the thyroid gland (autoimmune Hashimoto thyroiditis), joints (polyartralgia, synovitis), lungs (fibrosing alveolitis) muscles (polymyositis, polymyalgia), vessels (nodular periarteritis and other vasculitis), peripheral nervous system (polyneuropathy), kidneys (glomerulonephritis).
However, it should be emphasized that the expressed extra-systemic lesions are much more characteristic for autoimmune hepatitis and for the transformation of chronic hepatitis into cirrhosis of the liver.
[10], [11], [12], [13], [14], [15], [16]
Chronic hepatitis B, associated with integrative phase (HBeAg-negative integrative chronic hepatitis B)
HBeAg-negative integrative chronic hepatitis B has a favorable course. As a rule, this is an inactive phase of the disease. This variant of chronic hepatitis usually proceeds without pronounced subjective manifestations. Only a few patients complain of mild weakness, decreased appetite, and inadequate pain in the liver. With an objective study of patients, no significant changes in their condition are found (there is no jaundice, weight loss, lymphadenopathy and system extrahepatic manifestations). However, almost always there is hepatomegaly and very rarely insignificant splenomegaly. As a rule, the spleen is not enlarged. Laboratory indicators are usually normal or at the upper limit of normal, the level of alanine aminotransferase is not increased or elevated insignificantly, there are no significant changes in immunological parameters.
In liver biopsies, lymphocytic-macrophagal infiltration of portal fields, vnichridolkovy and portal fibrosis, necrosis of hepatocytes are absent.
In the blood serum, the markers for the integration phase of the hepatitis virus are found: HBsAg, anti-HBe, anti-HBdgG.
Radioisotope and ultrasound scanning of the liver reveals hepatomegaly of varying severity.
Chronic HBeAg-negative (integrative) hepatitis with a high level of alanine aminotransferase in the blood - integrative mixed-hepatitis
In this variant of HBeAg-negative (integrative) chronic hepatitis, despite the absence of markers for replication of the hepatitis B virus, high levels of alanine aminotransferase in the blood persist, indicating a continuing pronounced cytolysis of hepatocytes. It is generally believed that maintaining a high level of alanine aminotransferase in the absence of signs of viral replication requires the exclusion of the addition of other hepatotropic viruses (integrative mixed hepatitis B + C, B + D, B + A, etc.) or may indicate a combination of viral hepatitis B in the phase integration with other liver diseases (alcoholic, medicamentous liver damage, liver cancer, etc.).
[20], [21], [22], [23], [24], [25], [26], [27]
HBeAg-negative hepatitis with preserved viral replication (mutant HBeAg-negative variant of chronic hepatitis B)
In recent years, the ability of the hepatitis B virus to produce mutant strains has been described. They differ from typical "wild" strains by the lack of the ability to produce specific antigens. Mutations of the hepatitis B virus are due to an inadequate weakened reaction of the body to infection, as well as the introduction of vaccinations against hepatitis B. The termination of the synthesis of antigens is seen as the adaptation of the virus to the mechanisms of protecting the macroorganism, as an attempt to escape immunological surveillance.
Mutant HBeAg-negative variant of chronic hepatitis B is characterized by a loss of the ability of the virus to synthesize HBeAg and occurs mainly in patients in whom the immune response is weakened.
Mutant HBeAg-negative variant of chronic hepatitis B is characterized by the following features:
- absence of HBeAg in the blood serum (due to low production, it remains in hepatitis) in the presence of HBV replication markers;
- detection of HBV DNA in the blood serum of patients;
- presence of HBeAb in the blood serum;
- presence of HBs-antigenemia in high concentration;
- Detection of HBeAg in hepatocytes;
- more severe clinical course of the disease and a much less pronounced response to interferon treatment compared to HBeAg-positive chronic hepatitis B.
F. Bonito, M. Brunetto (1993), Nonaka et al. (1992) report a severe, clinically manifested flow of MGB HBeAg-negative chronic hepatitis B. The morphological pattern of liver biopsy corresponds to HBeAg-positive chronic hepatitis B, possibly the development of destructive liver damage according to the type of chronic active hepatitis.
It is assumed that in the mutant HBeAg-negative chronic hepatitis, the risk of malignancy with the development of hepatocarcinoma is great.