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Hemophagocytic Syndrome after Cord Blood Transplantation; Possible Implication of Severe Pre-Engraftment Immune Reactions

Track: Poster Abstracts
Wednesday, February 26, 2014, 6:45 PM-7:45 PM
Longhorn Hall E (Exhibit Level 1) (Gaylord Texan)
Hisashi Yamamoto, MD , Department of Hematology, Toranomon Hospital, Tokyo, Japan
Shinsuke Takagi , Department of Hematology, Toranomon Hospital, Tokyo, Japan
Naoyuki Uchida, MD , Department of Hematology, Toranomon Hospital, Tokyo, Japan
Kosei Kageyama , Department of Hematology, Toranomon Hospital, Tokyo, Japan
Daisuke Kaji , Department of Hematology, Toranomon Hospital, Tokyo, Japan
Sachie Wada , Department of Hematology, Toranomon Hospital, Tokyo, Japan
Aya Nishida, MD , Department of Hematology, Toranomon Hospital, Tokyo, Japan
Hikari Ota, MD , Department of Hematology, Toranomon Hospital, Tokyo, Japan
Kazuya Ishiwata, MD , Department of Hematology, Toranomon Hospital, Tokyo, Japan
Masanori Tsuji, MD , Department of Hematology, Toranomon Hospital, Tokyo, Japan
Go Yamamoto, MD, PhD , Department of Hematology, Toranomon Hospital, Tokyo, Japan
Yuki Asano-Mori, MD, PhD , Department of Hematology, Toranomon Hospital, Tokyo, Japan
Koji Izutsu, MD, PhD , Department of Hematology, Toranomon Hospital, Tokyo, Japan
Atsushi Wake, MD , Department of Hematology, Toranomon Hospital, Tokyo, Japan
Shuichi Taniguchi, MD, PhD , Department of Hematology, Toranomon Hospital, Tokyo, Japan
[Aims] We reported the impact of hemophagocytic syndrome (HPS) on engraftment failure in cord blood transplantation (CBT).  The aim of this study was to explore pathogenesis underlying HPS.  [Methods] We retrospectively reviewed 351 patients who underwent single CBT using fludarabine-based regimens at our institute from January 2002 to July 2011 consecutively.  [Results] Median age was 58 years (range, 17-82).Diagnoses were AML/MDS (n=209), ALL/ML (n=103), and others (n=36).  Tacrolimus plus MMF (TAC+MMF) were used in 196 cases as GVHD prophylaxis, while TAC alone in 155.  HPS developed in 33 patients at a median of 19 days post-CBT.  The cumulative incidence of HPS was 9.4%.  Development of HPS had a negative impact significantly on neutrophil engraftment (33.3% with HPS vs 83.3% without HPS, p=<0.01), which resulted in inferior overall survival rate.  Majority of the HPS patients (25/30) showed donor-dominant chimerism at the diagnosis of HPS.  Patients with severe form of pre-engraftment immune reactions (sPIR) showed significantly higher incidence of HPS than those without PIR (51.9% vs 6.6% p=<0.01).  Patients who received cord blood unit with higher degree of HLA antigen mismatch in GVH direction (2 vs 0-1) also showed higher incidence of HPS (11.5% vs 4.8% p=<0.04).  TAC+MMF decreased the incidence of sPIR and HPS compared to TAC alone (2.8% vs 15.3% p=<0.01 and 4.6% vs 15.5% p= <0.01, respectively), which had a trend toward higher engraftment rate (83.7% vs 72.3% p=0.07).  In multivariate analysis, GVHD prophylaxis using TAC alone, lower number of CD34+ cells infused (>0.8x105/kg vs <0.8x105/kg) and higher degree of HLA antigen mismatch in GVH direction were significantly associated with HPS development.  [Conclusion] HPS was closely associated with engraftment failure in our CBT cohort.  sPIR plays an crucial role of developing HPS and was possibly controlled by intensification of GVHD prophylaxis.
Disclosures:
Nothing To Disclose