Abstract
Abstract 3882
Poster Board III-818
Introduction
Patients with hepatitis B virus (HBV) infection, defined by the presence of HBV surface antigen (HBsAg), have an increased risk of HBV reactivation when they are on immunosuppressive treatment for multiple myeloma (MM). Although there is no guideline for MM patients with HBV infection, current lymphoma guidelines do recommend that these patients should receive antiviral prophylaxis during and after chemotherapy. Of late, the advent of bortezomib in the management of MM has resulted in a high reported incidence of variecella-zoster reactivation. The risk of HBV reactivation in MM patients with HBV infection undergoing treatment has not been previously studied. As HBV infection is endemic in Asia, we sought to evaluate the prevalence of HBV infection in our patients, the incidence of its reactivation especially in patients receiving bortezomib and the role of anti-viral prophylaxis.
Methods
Previously untreated MM patients diagnosed from 2000-2008 who were tested for HBsAg in our institution were included. Hepatitis attributable to HBV reactivation was defined as an increase in HBV DNA levels of tenfold, or an absolute increase greater than105 copies/ml in the HBV DNA level. HBV infected patients were prospectively followed. 33% of all patients have been exposed to bortezomib, while 26% received high dose therapy with autologous stem cell transplantation (HDT/ASCT).
Results
243 untreated MM patients were identified. The prevalence of HBV infection is 5.8% (14/243). 6 (43%) HBV infected patients had detectable HBV DNA viral load (>3 log) at baseline. All 6 patients had normal baseline liver function tests and received lamivudine prophylaxis. All 14 HBV infected patients went on to receive systemic therapy for MM, with continual monitoring of HBV DNA viral load and liver enzymes for viral reactivation. 4 patients with undetectable HBV DNA load did not receive anti-viral prophylaxis. Of these 14 patients, 3 (21%) who had been on lamivudine prophylaxis had reactivation of the virus, with 1 dying from it, and 1 having emergence of a mutant viral strain. Two of them had no detectable viral load at presentation. Two patients reactivated 3 and 5 months after HDT/ASCT, while 1 reactivated immediately after a bortezomib/ doxil salvage regimen.
Conclusion
The risk of HBV reactivation appeared to be commonest during the immune reconstitution phase after HDT/ASCT. Although the majority of patients with HBV infection and not receiving HDT/ASCT do not reactivate, the risk may not negligible when bortezomib is used (7%). Undetectable HBV DNA and the use of anti-viral prophylaxis do not appear to preclude reactivation. The optimal use of anti-viral prophylaxis, particularly if bortezomib is given, should be further evaluated. This is particularly relevant in the current era where bortezomib plays a dominant role in the treatment of MM, and especially in endemic regions where the incidence of HBV infection is high.
Disclosures:
No relevant conflicts of interest to declare.
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