Zusammenfassung
Die chronische Hepatitis-B-Virus (HBV)-Infektion kann niedrig-replikativ
mit günstiger Prognose oder hoch-replikativ mit dem Risiko
einer Leberzirrhose und eines Leberzellkarzinoms verlaufen. Eine
Immunsuppression im Rahmen einer lokalen oder systemischen Chemotherapie sowie
einer autoimmunen Krankheit erhöht signifikant das Risiko
der Reaktivierung einer HBV, zum Teil mit dem Bild einer akuten,
selten fulminanten Hepatitis. Unter intensiver Immunsuppression
z. B. im Rahmen einer Stammzelltransplantation kann eine
Re-Serokonversion auftreten mit Verlust von anti-HBs +/– anti-HBc
und erneutem Nachweis von HBsAg sowie HBV-DNA und dem Risiko einer
akuten (fulminanten) Hepatitis. Bestimmte Chemotherapeutika und
Immunsuppressiva begünstigen eine Reaktivierung. In Studien
konnte gezeigt werden, dass die Reaktivierung einer Hepatitis B
Virusinfektion erfolgreich mit dem Nukleosidanalogon Lamivudin behandelt
werden kann, eine prophylaktische Gabe scheint der Therapie einer
Re-Aktivierung überlegen zu sein. Für weitere
Nukleosid- (Telbivudin, Entecavir) oder Nukleotidanloga (Adefovir,
Tenofovir) liegen bislang keine größeren Erfahrungen
in dieser Indikation vor. Bei allen Patienten vor einer immunsuppressiven
Therapie muss daher der HBV Serostatus geprüft werden.
Patienten ohne HBV Infektion und ohne ausreichenden anti-HBs-Titer
müssen aktiv immunisiert werden. Bei Patienten mit chronischer HBV
Infektion und hochdosierter Immunsuppression besteht gemäß der
aktuellen Leitlinie der DGVS die Indikation zur antiviralen Therapie.
Bei Nachweis einer durchgemachten Hepatitis B Virusinfektion (anti-HBc
positiv, HBsAg negativ) muss eine Kontrolle vor und regelmäßig unter
immunsuppressiver Therapie sowie im Fall der Reaktivierung eine
Therapie mit Nukleos(t)idanaloga erfolgen. Bei Patienten vor Stammzelltransplantation
muss bereits bei Nachweis einer durchgemachten HBV Infektion eine
Prophylaxe mit einem Nukleos(t)idanalogon eingeleitet werden.
Abstract
Immunosuppression because of local or systemic chemotherapy or
immunosuppressive therapy of autoimmune diseases is an increasing
risk for reactivation of hepatitis B and may lead to acute hepatitis
and rarely to fulminant hepatitis. Intensive immunosuppression,
e. g. in advance of bone marrow transplantation, may lead
to re-seroconversion with loss of anti-HBs and detection of HBsAg
and HBV-DNA and a risk of (fulminant) hepatitis. Distinct chemotherapeutics
and immunosuppressive medication promote reactivation or re-seroconversion
of HBV infection. Several studies have shown a significant benefit
by antiviral therapy with nucleosidanalogue lamivudine to avoid reactivation.
For other nucleoside analogues (telbivudine, entecavir) or nucleotide
analogues (adefovir dipivoxil, tenofovir) larger experiences are
yet missing in this situation. Prophylaxis with antiviral agents
may be superior to therapy of reactivation. Prior to onset of immunosuppressive
treatment patients must be tested for HBV. Patients without detection
of HBsAg and without sufficient anti-HBs-titer should receive active
immunisation. In case of chronic HBV infection antiviral therapy
should be initiated before intense immunosuppression. In case of
HBV infection in medical history (anti-HBc positive, HBsAg negative) HBV
serostatus should be tested frequently. In case of reactivation,
therapy with nucleos(t)ide analogue should immediately be initiated.
In case of bone marrow transplantation prophylaxis with nucleos(t)idanalogue
has to be initiated before onset of treatment if anti-HBc is detectable,
independent from HBsAg result.
Schlüsselwörter
Hepatitis B Virus - Immunsuppression - Prophylaxe - Chemotherapie - TACE
Keywords
hepatitis B - immunosuppression - prophylaxis - chemotherapy - TACE
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Prof. Dr. Stefan Zeuzem
Klinikum der J.W. Goethe-Universität
Theodor-Stern-Kai 7
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