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35th Annual Meeting of the European Group for Blood and Marrow Transplantation
25th Meeting of the EBMT Nurses Group
8th Meeting of the EBMT Data Management Group
3rd Patient & Family Day
Göteborg, Sweden
29.03.2009 - 01.04.2009 |
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Multiple myelomaMonday, March 30, 2009, 17:30 - 19:00Lenalidomide as salvage therapy after allogeneic transplant for primary plasma cell leukaemia: a case reportI. Attolico, M. Cimminiello, G. Discepoli, R.A. Cifarelli, M. Pizzuti, N. Filardi, M. Poggiaspalla, D. Vertone, A. Olivieri (Potenza, Ancona, Metaponto (MT), IT)
Primary Plasma Cell Leukemia (PPCL) is an aggressive and rare variant of Multiple Myeloma (MM). Allogeneic haematopoietic stem-cell transplantation (HSCT) results in sustained long-term OS, suggesting a possible graft-versus-leukemia (GVL) effect. Relapse or progression after HSCT are common and outcome is poor. No data are available about Lenalidomide as salvage therapy for PPCL relapsed after HSCT. We report a 41 year-old woman with PPCL (IgA kappa monoclonal component (MC), 32% immature plasmacells in peripheral blood, 50% immature plasmacells CD38/CD138/sIgkappa+, CD19/CD56/CD45- in the bone marrow). She received six Hyper-CVAD courses achieving Complete Remission (CR) and, after blood stem cells collection, underwent ASCT (Melphalan 200mg/m˛ followed by reduced intensity conditioning HSCT from HLA identical brother (thiotepa 5mg/Kg, fludarabine 30mg/m˛, melphalan 140mg/m˛. Full donor chimerism was documented at day +90. At day +138 she relapsed with cytogenetics showing a complex hyperdiploid karyotype. Bortezomib (1,3mg/m˛) and Dexamethasone (40mg) (days 1,4,8,11) were started without response; as a second-line, cyclophosphamide (300 mg/m˛ on days 1,8,15) was added to Bortezomib and Dexamethasone. Nevertheless disease progressed and full donor chimerism was lost; therefore Lenalidomide (25mg/day, 1-21) and Dexamethasone (40 mg/day 1,8,15,22) were administered. At the end of the first course the patient developed a skin rash, hyperbilirubinemia and increased liver enzymes, compatible with acute GVHD, treated with methilprednisolone (2 mg/Kg/day). The patient showed a quick improvement with reduction of MC and abnormal plasmacells in the bone marrow. After six courses of Lenalidomide the patient is in CCR, with complete donor chimerism and normal cytogenetics; a mild cGVHD persists, requiring low dose steroids. We describe here the first case of a patient with relapsed and chemorefractory PPCL after allogeneic HSCT, who achieved a CCR with Lenalidomide; moreover, this is the first case of response to Lenalidomide associated with development of GVHD. The mechanism of the GVL/GVM is largely unknown. T and NK cells might exert an alloimmune reaction. In this case we hypothesize that the strong antiproliferative effect of Lenalidomide could have reduced the leukemia burden, making the GVL effect stronger. Furthermore Lenalidomide could have stimulated donor T/NK cells,as suggested by experimental data.
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