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HBV reactivation
donor. Decisions to stop prophylaxis will likely need to be made on an individual basis, aided by regular monitoring of viral markers, including anti-HBs antibody titers. For all patients, monitoring including ALT, HBsAg and HBV DNA should continue for at least six months after prophylaxis has been stopped, as cases of reactivation after stopping antiviral treatment have been reported.79
Hepatitis B virus vaccination
Given the importance of anti-HBs in potentially reduc- ing the risk of HBV reactivation, the role of HBV vaccina- tion has been investigated, specifically in the setting of HSCT.80,81 In one study of 46 patients with past HBV infec- tion undergoing HSCT, 21 patients received a standard 3- dose regimen of HBV vaccine post transplant. None of these patients developed HBV reverse seroconversion compared with 12 out of 25 patients in the non-vaccine group (P=0.0003), even after a median follow up of 67 months. Further studies are required, but vaccination, in its simplicity, presents an attractive strategy to manage reactivation.
Conclusion
Hepatitis B virus reactivation is not uncommon in
and ongoing reports of significant morbidity, or even fatalities, make this an important topic to understand and manage appropriately. Given the efficacy of antiviral prophylaxis, the key to preventing reactivation is identi- fying patients at risk. All patients need to be screened for HBV, including HBsAg and anti-HBc antibody, before any immunosuppressive therapy is initiated. Furthermore, it is important to assess and understand the risk posed by individual treatment regimens in order to determine the need for antiviral prophylaxis and the duration of treatment. For those patients identified as requiring antiviral treatment or prophylaxis, a shift towards newer nucleoside / nucleotide analogs tenofovir and entecavir is recommended, especially in high-risk and prolonged regimens. Areas worthy of future research include identifying more sensitive ways of stratifying risk, especially for the large number of patients with resolved HBV infection; these may be serological viral markers that better reflect the burden of latent forms of HBV DNA in the liver and their transcriptional activity, or, indeed, immune markers that indicate the strength or type of immune control and whether they are likely to be affected by immunosuppression. Better risk stratifica- tion may allow us to be more selective about who requires prophylaxis, but until then, a low threshold approach is required to prevent the significant morbidity and mortality associated with reactivation.
patients with hematologic disorders and
malignancies,
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