Treatment of rare co‐occurrence of Epstein–Barr virus‐driven post‐transplant lymphoproliferative disorder and hemophagocytic lymphohistiocytosis after allogeneic stem cell transplantation. Issue 6 (1st September 2014)

• Record Type: Journal Article
• Authors: Weber, T.; Wickenhauser, C.; Monecke, A.; Gläser, C.; Stadler, M.; Desole, M.; Ligeti, K.; Behrmann, C.; Müller‐Tidow, C.; Müller, L.P.
• Is Part Of: Transplant infectious disease. Volume 16:Issue 6(2014)
• Page Start: 988
• Page End: 992
• Publication Date: 2014-09-01
• Subjects: Transplantation of organs, tissues, etc -- Complications -- Periodicals; Communicable diseases -- Periodicals; Infection -- Periodicals; 617.01
• DOI: 10.1111/tid.12287
• Languages: English
• ISSNs: 1398-2273

Abstract

<abstract abstract-type="main" id="tid12287-abs-0001"> <title>Abstract</title> <p>In both conditions, post‐transplant lymphoproliferative disorder (PTLD) and hemophagocytic lymphohistiocytosis (HLH), infection with Epstein–Barr virus (EBV) is a key mechanism: almost all PTLD in allogeneic stem cell transplantation (alloSCT) is caused by EBV‐related neoplastic lymphoproliferation, and secondary HLH is most frequently triggered by EBV infection. Therefore, concomitant EBV‐driven PTLD and HLH early after alloSCT require an approach to eliminate EBV and balance immune activation simultaneously. We report on a patient who developed simultaneous PTLD and signs of HLH on day 64 after alloSCT. Treatment was comprised of stopping cyclosporine, short‐course dexamethasone, and 3 courses of rituximab. The patient showed full recovery and complete remission of lymphadenopathy. This result indicates that immediate reduction in EBV‐carrying B cells by rituximab, suppression of general inflammation, and parallel support of reconstitution of long‐term T‐cell function, might be an appropriate therapeutic approach in this rare situation.</p> </abstract>