Z Gastroenterol 2018; 56(01): E2-E89
DOI: 10.1055/s-0037-1612891
Poster Visit Session V Viral Hepatitis and Immunology – Saturday, January 27, 2018, 11:00am – 11:45am, Foyer area East Wing
Georg Thieme Verlag KG Stuttgart · New York

HBV reactivation in allogeneic stem cell transplant recipients: risk factors, outcome and role of HBV mutations

O Anastasiou
1   University Hospital Essen, Gastroenterology and Hepatology, Essen
,
F Almpani
2   Institute of Virology, Essen
,
A Herrmann
2   Institute of Virology, Essen
,
G Gerken
1   University Hospital Essen, Gastroenterology and Hepatology, Essen
,
M Ditschkowski
3   University Hospital of Essen, Department of Bone Marrow Transplantation, Essen
,
S Ciesek
2   Institute of Virology, Essen
› Author Affiliations
Further Information

Publication History

Publication Date:
03 January 2018 (online)

 

Background:

HBV reactivation (HBVr) in allogeneic hematopoetic stem cell (aHSC) recipients appears heterogeneously concerning its frequency, manifestation and outcome. Aim of this study was to present data from a large German cohort of aHSCT recipients, focusing on the incidence of HBVr in anti-HBc aHSCT recipients, its clinical outcome and the role of mutations in HBV.

Patients and methods:

Between 2005 and 2015, 1.871 patients received aHSCT at University Hospital Essen. A follow up of at least 6 months after transplant was available in 55 anti-HBc patients; clinical and virological data were analyzed. HBV genome was sequenced with NGS in serum samples of 8 HBVr patients.

Results:

Thirteen out of 55 (23.6%) patients developed HBVr at a median of 26 months after aHSCT. After initiation of antiviral treatment, complete HBV DNA suppression was achieved in 7/10 (70%) patients 1 to 40 months after HBVr. Nine out of 13 patients had increased ALT. Three patients had compromised coagulation and model for end-stage liver disease (MELD) scores of 18 – 27. One of them died due to liver failure 5 weeks after HBVr. As a risk factor for HBVr, we identified an anti-HBc S/CO ≥7.5 before transplantation. Complete HBV DNA suppression was achieved in 7/10 (70%) patients. Therapy relevant mutations were found in one patient. In 4/8 patients, immune escape mutations have been detected either as majority or minority variants.

Conclusion:

HBVr is common in anti-HBc positive aHRCT recipients and can lead to severe hepatitis with compromised coagulation. Level of anti-HBc S/CO before transplantation is a risk factor for HBVr. Complete virological response under adequate antiviral treatment could not be achieved in all patients.