Reaktivace chronické hepatitidy B
[Reactivation of chronic hepatitis B]
Language Czech Country Czech Republic Media print
Document type Journal Article, Review
PubMed
23909265
PII: 41154
- MeSH
- Adenine analogs & derivatives therapeutic use MeSH
- Virus Activation * MeSH
- Antiviral Agents therapeutic use MeSH
- Biomarkers MeSH
- Hepatitis B, Chronic diagnosis immunology prevention & control MeSH
- Guanine analogs & derivatives therapeutic use MeSH
- Hepatitis B Surface Antigens immunology MeSH
- Immunocompromised Host * MeSH
- Immunosuppressive Agents adverse effects MeSH
- Lamivudine therapeutic use MeSH
- Humans MeSH
- Antibodies, Monoclonal, Murine-Derived adverse effects MeSH
- Organophosphonates therapeutic use MeSH
- Antineoplastic Agents adverse effects MeSH
- Rituximab MeSH
- Tenofovir MeSH
- Hepatitis B virus immunology MeSH
- Inflammation MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
- Review MeSH
- Names of Substances
- Adenine MeSH
- Antiviral Agents MeSH
- Biomarkers MeSH
- entecavir MeSH Browser
- Guanine MeSH
- Hepatitis B Surface Antigens MeSH
- Immunosuppressive Agents MeSH
- Lamivudine MeSH
- Antibodies, Monoclonal, Murine-Derived MeSH
- Organophosphonates MeSH
- Antineoplastic Agents MeSH
- Rituximab MeSH
- Tenofovir MeSH
Hepatitis B (HBV) is a DNA virus, which cannot be eradicated completely from the organism by treatment, only its replication can be suppressed to low levels. The pathogenesis of liver damage due to HBV is immune mediated, the infected hepatocytes represent the target structures of immune reaction. In individuals who spontaneously achieved the state of inactive carriage of the virus or even achieved HBsAg negativity, we deal only with immune control of viral replication. Chemotherapy or immunosuppressive treatment disrupt the immune control of HBV infection, the virus replication substantially increases and hepatitis B reactivates. HBV reactivation manifests as further flareup of chronic inflammation with rapid progression of liver cirrhosis or even as a fulminant hepatitis with liver failure. The risk of reactivation increases with degree of induced immunosuppression, the highest risk is associated with corticosteroid and rituximab therapy. HBV reactivation threatens patients during solid tumours treatment as well as haemato oncological malignancies, patients treated with immunosuppressive and bio-logical therapies for systemic inflammatory diseases and inflammatory bowel diseases, as well as patients on maintenance haemodialysis, after kidney transplantation and patients with HBV/ HIV co infection. HBV reactivation increases both morbidity and mortality in listed groups of patients. The patients threatened by HBV reactivation can be identified easily based on HBV serological markers assessment. Preemptive therapy with nucleos(t)ide analogues significantly reduces the risk of HBV reactivation, the effect of longterm antiviral therapy is described in detail in kidney transplant recipients in whom the 3rd generation antivirals (entecavir and tenofovir) completely obviate the negative impact of HBV on longterm survival. In oncological patients who are treated for a determined time period, we can use lamivudine, which is not suitable for longterm treatment due to high risk of resistance emergence.