Plerixafor is highly effective in the mobilisation of PBSC for autologous transplantation from patients failing to mobilise by conventional means: the initial Scottish experience in three transplant centres

• Published in: Bone marrow transplantation (Basingstoke) Vol. 43; no. S1; p. S113
• Main Authors: Gordon, W.C, Johnson, P.R.E, Roddie, P.H, Shepherd, P.C.A, Scott, Shepherd, Davies, J.M, Manson, L.M, Culligan, D, Chee, Y.-L, Parker, A, McQuaker, I.G, Clark, A, Soutar, R.L, Douglas, K.W
• Format: Journal Article
• Language: English
• Published: Nature Publishing Group 01.03.2009
• Subjects: Care and treatment; Hematopoietic stem cells; Lymphomas; Transplantation; United Kingdom
• ISSN: 0268-3369

The small molecule chemokine inhibitor Plerixafor has recently been used on a named-patient basis for PBSC mobilisation from patients failing to mobilise by conventional means. We present our initial experience with plerixafor in 18 mobilisation attempts in 17 patients, all of whom had previously failed to mobilise a transplantable PBSC dose, at three Scottish transplant centres. Patients had myeloma (n=10) or lymphoma (n=7). All had at least one previous attempt at PBSC mobilisation which failed or resulted in an insufficient cell dose for transplant (2 attempts in 2 patients). 5 of 17 patients had a pre-existing CD34+ dose from previous collections (range 0.98-2.32 x [10.sup.6]/kg; median 1.38); 12 patients had no cells collected before receiving plerixafor. As recommended by Genzyme, patients received four days of G-CSF 10 micrograms/kg followed by Plerixafor 240 micrograms/ kg subcutaneously in the evening, 11 hours prior to first apheresis, except for one patient with dialysis-dependent renal failure who received 160 micrograms/kg. G-CSF and plerixafor were repeated daily until a transplantable CD34+ dose was obtained (if possible). Apheresis was started without waiting for a day-of-collection peripheral CD34+ count. For patients with a peripheral CD34+count of less than 20/microlitre, 3 (rather than 2) blood volumes were processed. 16 of 17 patients achieved a transplantable PBSC dose (>2.5 x [10.sup.6]/kg CD34+ cells) after one (n=15) or two (n=1) courses of Plerixafor--a total success rate of 94%. The total number of apheresis procedures required was 1 (n=4), 2 (n=6), 3 (n=4) or 4 (n=2). One patient mobilised a cell dose of 1.89 x [10.sup.6]/kg in two procedures, but was unable to receive a third Plerixafor dose due to diarrhoea (a recognised side-effect)--a second treatment cycle one month later with antidiarrhoeal cover was successful. One patient was unable to undergo PBSC collection because of intercurrent infection (not thought to be plerixafor-related). No other immediate toxicities were seen. 7 patients have progressed to transplant. Median cell dose transplanted was 3.39, range 2.68-4.72. All seven patients have achieved sustained neutrophil and platelet engraftment (median 14 days to neutrophils >0.5; median 21 days to neutrophils >1.0; median 24 days to platelets >50). Plerixafor appears highly effective in the mobilisation of PBSC for transplant from patients failing to mobilise by conventional means, with generally acceptable toxicity.