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[Basic factors affecting the development of chronic hepatitis B virus infection]
Insights
Hepatitis B carriers experienced relapses due to various causes including HBeAg seroconversion and viral superinfections. Many relapses were transient, with some improving spontaneously, while others indicated disease progression.
Area of Science:
- Hepatology and Virology
- Infectious Diseases
- Immunology
Context:
- Study followed 276 individuals with persistent Hepatitis B surface antigen (HBsAg) positivity for five years.
- Included patients with chronic persisting hepatitis, chronic active hepatitis, liver cirrhosis, and asymptomatic HBsAg carriers.
- Focused on the subgroup of 128 patients with chronic active hepatitis who were initially positive for Hepatitis B e-antigen (HBeAg).
Purpose:
- To investigate the long-term outcomes of HBsAg carriers after viral hepatitis B.
- To determine the incidence and causes of acute relapses in HBeAg-positive patients over a five-year period.
- To analyze the relationship between HBeAg seroconversion and disease exacerbation.
Summary:
- Over five years, 43 out of 128 HBeAg-positive patients achieved HBeAg seroconversion (negativity), at an annual rate of 6.7%.
- 38 patients experienced acute relapses, attributed to factors including Hepatitis A virus, Hepatitis non-A non-B virus, EB virus, cytomegalovirus, HBeAg to anti-HBe seroconversion (36.8%), and corticotherapy discontinuation (15.8%).
- HBeAg to anti-HBe seroconversion was linked to acute exacerbations in about one-third of cases, typically transient with subsequent improvement. Relapses post-corticotherapy also often resolved spontaneously.
Impact:
- Provides insights into the complex natural history of chronic Hepatitis B infection.
- Highlights the multifactorial nature of disease relapses in HBsAg carriers.
- Suggests that while HBeAg seroconversion can trigger transient exacerbations, it may ultimately contribute to improved outcomes in some chronic hepatitis B patients.
Abstract:
The authors followed up for a period of five years 276 convalescents after viral hepatitis B where all remained carriers of HBsAg. The group comprised 108 cases of chronic persisting hepatitis, 134 cases of chronic active hepatitis, 13 cirrhoses of the liver and 21 symptom-free carriers of HBsAg. In the group of chronic active hepatitis at the onset of the investigation 128 were HBeAg positive. In the course of five years in 43 patients seroconversion to HBeAg negativity occurred. Thus an annual index of seroconversion from HBeAg of 6.7% was recorded. In the course of five years in 38 patients of 128 HBeAg positive ones an acute relapse was observed. The causes of the relapse were explained by detailed serological examination. Superinfection with the hepatitis A virus participated three times (7.9%), probable superinfection with the hepatitis non-A non-B virus six times (15.8%), superinfection with the EB virus three times (7.9%), superinfection with cytomegalovirus twice (5.3%), seroconversion HBeAg to anti-HBe 14 times (36.8%), discontinuation of corticotherapy six times (15.8%), superinfection with the delta virus in none of the patients and relapses due to other causes four times (10.5%). Seroconversion of HBeAg to anti-HBe was in cca one third of the patients associated with acute exacerbation of the hepatic process. These relapses were, however, transient and their regression was followed by a further improvement of the chronic inflammation. Also relapses after discontinuation of corticotherapy usually improved spontaneously after a certain time interval. When the cause of the relapse was superinfection with the EB virus or cytomegalovirusas as a rule acceleration and further progress of the inflammatory process occurred.