演題詳細

ポスター / Poster

ポスター 12 (Poster 12) :MDS:臨床 1

print

日程
2013年10月11日(金)
時間
16:50 - 17:50
会場
ポスター会場 / Poster (ロイトン札幌 3F ロイトンホールABCD)
座長・司会
波多 智子 (Tomoko Hata):1
1:長崎大学原爆後障害医療研究所 血液内科学研究分野(原研内科)
 
前へ戻る

Successful auto-SCT for t-MDS with der(1;7) using a stem cell graft harvested before developing MDS

演題番号 : PS-1-90

出島 彰宏 (Akihiro Dejima):1、澤崎 愛子 (Aiko Sawazaki):1、杉森 千春 (Chiharu Sugimori):1、上田 幹夫 (Mikio Ueda):1、山口 正木 (Masaki Yamaguchi):1、中尾 眞二 (Shinji Nakao):2

1:Ishikawa Prefectural Central Hospital,Japan、2:Cellular Transplantation Biology,Kanazawa University Graduate School , Japan.

 

(Case) A 74 year-old man was diagnosed to have AITL in June, 2006. 3 cycles of CHOP induced complete remission (CR). Autologous PBSCs (1.72x107 CD34+ cells/kg) were harvested after administration of VP16 in August, 2006. The patient was treated with MCEC followed by infusion of 1.1x107 CD34+ cells/kg in November, 2006. He remained in CR with normal blood cell counts until January, 2010, when anemia and thrombocytopenia developed. Bone marrow examination showed dysplastic signs in neutrophils and megakaryocytes and 2.4% blast cells. G-banding revealed 46,XY,+1,der(1;7)(q10;p10),del(20)(q1) in 4 of 20 dividing cells. He was diagnosed with RCMD. 6 cycles of azacitidine induced cytogenetic CR in July, 2011, but pancytopenia recurred in June, 2012 and 4.0% blast cells appeared in the peripheral blood. RAEB-1 was diagnosed. Bone marrow karyotype was 47,XY,+1,der(1;7)(q10;p10),+8,del(20)(q1) in 6 of 14 dividing cells. Because he developed recurrent febrile neutropenia and was considered to have a dismal prognosis, he was treated with BEA followed by infusion of 6.2x106 CD34+ cells/kg that had been cryopreserved for 6 years in November, 2012. Neutrophil engraftment occurred on day 11 and he has been in CR with normal karyotype after the second auto-SCT. (Conclusion) To our knowledge, this is the first case of t-MDS successfully treated with auto-SCT using stem cells that were harvested prior to developing the secondary MDS. Collecting as many CD34+ cells as possible and saving excess CD34+ cells for the possible use for a second SCT may be an effective strategy for managing t-MDS.

前へ戻る