Reaktivace chronické hepatitidy B
[Reactivation of chronic hepatitis B]
Jazyk čeština Země Česko Médium print
Typ dokumentu časopisecké články, přehledy
PubMed
23909265
PII: 41154
- MeSH
- adenin analogy a deriváty terapeutické užití MeSH
- aktivace viru * MeSH
- antivirové látky terapeutické užití MeSH
- biologické markery MeSH
- chronická hepatitida B diagnóza imunologie prevence a kontrola MeSH
- guanin analogy a deriváty terapeutické užití MeSH
- hepatitida B - antigeny povrchové imunologie MeSH
- imunokompromitovaný pacient * MeSH
- imunosupresiva škodlivé účinky MeSH
- lamivudin terapeutické užití MeSH
- lidé MeSH
- myší monoklonální protilátky škodlivé účinky MeSH
- organofosfonáty terapeutické užití MeSH
- protinádorové látky škodlivé účinky MeSH
- rituximab MeSH
- tenofovir MeSH
- virus hepatitidy B imunologie MeSH
- zánět MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- přehledy MeSH
- Názvy látek
- adenin MeSH
- antivirové látky MeSH
- biologické markery MeSH
- entecavir MeSH Prohlížeč
- guanin MeSH
- hepatitida B - antigeny povrchové MeSH
- imunosupresiva MeSH
- lamivudin MeSH
- myší monoklonální protilátky MeSH
- organofosfonáty MeSH
- protinádorové látky 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.