334 CMV and EBV Reactivation after Allogeneic Transplantation

Track: Poster Abstracts
Wednesday, February 11, 2015, 6:45 PM-7:45 PM
Grand Hall CD (Manchester Grand Hyatt)
Andrew Butler, Dr , Canterbury Health Laboratories, Christchurch, New Zealand
Andrew Thurston, Dr , Christchurch Hospital, Christcurch, New Zealand
Presentation recording not available for download or distribution as requested by the presenting author.
Background: Reactivation of cytomegalovirus (CMV) and Epstein-Barr virus (EBV) following allogeneic stem cell transplant occurs in 60-70% and 5-15% of patients respectively.  CMV disease can present as pancytopenia, disordered liver function, pneumonitis, retinitis or neurological disorders. EBV reactivation can result in post transplant lymphoproliferative disorder (PTLD).  At risk patients are monitored using DNA PCR assays and pre-emptive therapy commenced. The optimum timing for intervention has not been established.

Methods: We identified at-risk patients receiving an allogeneic transplant during the period 2012-2013 from our institutional database and retrospectively collected data from the electronic and paper records.

Results: Complete data was available for 27 patients. The diagnoses were AML/MDS (14), ALL (6), CLL (3), CML (1), aplastic anaemia (1) and myelofibrosis (1). 26 were at risk for EBV reactivation and 13 were at risk for CMV reactivation.  5/13 (38%) patients developed CMV reactivation at a median of 26 days post transplant (range 22-49). The median CMV DNA peak titre was 3647 IU/ml (range 603-62616). 4/5 patients were treated with valganciclovir and none developed CMV disease. Valganciclovir was well tolerated and effective in all cases. 7/26 patients (27%) developed EBV reactivation after a median 60 days (range 10-221).  2 patients (12.5%) developed lymphadenopathy and received rituximab with a complete response.  Two patients developed late onset recurrent EBV reactivation following treatment with rituximab. One patient had a rising titre from day +165, continuing to rise from <137 to 37944 IU/ml on day +494. The second patient reactivated on day +225 with a titre continuing to rise to 23693 IU/ml on day +264. Neither patient was on immunosuppression or has developed clinical or radiological evidence of PTLD.

Conclusion: CMV reactivation was less frequent than previously reported andpre-emptive therapy was effective. It is possible that some patients were treated unnecessarily although treatment was well tolerated. EBV reactivation rates were consistent with those previously reported.  Two cases of PTLD highlight the importance of regular EBV titre monitoring and early treatment. The late re-emergence of EBV reactivation in patients who are not on immuno-suppression is not well described in the literature and its pathogenesis and clinical significance may be different from early reactivation.


Disclosures:
Nothing To Disclose