We report 4 cases of extramedullary myeloma at cutaneous trauma sites, including central venous catheter tunnel, growth-factor-injection sites, & marrow biopsy sites.

Case 1 (centre 1) presented with stage IIIA IgG BJ+ medullary myeloma aged 57. Induction was with cyclophosphamide/thalidomide/dexamethasone (CTD), followed by 200mg/m2 melphalan autologous cyclophosphamide-mobilised PBSCT in VGPR1. Within 3 months of PBSCT, 4 violaceous subcutaneous nodules developed; in CVC line scar, marrow biopsy scar, abdominal GCSF-injection site on left abdominal wall & thoracic skin. Biopsy showed atypical CD56-CD138+ lambda-restricted decohesive plasmablasts; marrow was clear of infiltrate. Plasma cells infiltrated pleura & omentum, & a large pelvic mass rapidly led to hydronephrosis. She has commenced bortezomib & dexamethasone with initial response of both cutaneous deposits & renal improvement.

Case 2 (centre 2) presented with stage IIIA light chain myeloma aged 59, on 2 year background of cytopaenias. CTD induced PR1, followed by 200mg/m2 Melphalan autologous cyclophosphamide-mobilised PBSCT. 3 months later nodules in CVC line scar appeared & biopsy showed CD56-CD138+MUM-1+ plasma cell infiltrates; concommitant marrow showed CD56+ atypical plasma cell infiltrate. Despite salvage therapy he died within 2 months.

Case 3 (centre 1) had stage IIIA myeloma at 63 years & relapsed after cyclophosphamide-mobilised PBSC harvest post CTD induction; ESHAP salvage & remobilisation of PBSC allowed 200mg/m2 Melphalan autologous PBSCT to VGPR2. Within 4 months of PBSCT plasma cells were apparent in peripheral blood at routine visit, followed by linear plasmacytomata along CVC line track, despite VAD chemotherapy. Despite transient response to salvage bortezomib the exit site lesions regrew together with abdominal wall plasmacytomata, & she died 6 months after emergence of extramedullary disease.

Case 4 (centre 1) had stage IIA light chain myeloma with minor response to VAD & radiotherapy, & was reinduced with CTD. 3 months after 200mg/m2 Melphalan ESHAP-mobilised PBSCT CR1 was achieved, but 6 months post-PBSCT oligosecretory disease reappeared in marrow. Despite bortezomib & dexamethasone subcutaneous deposits occured at sites of prior GCSF & heparin injections, & she died within 6 months of 2nd relapse.

These cases exemplify early post high-dose chemotherapy emergence of high-grade extramedullary disease arising within tissue trauma sites, including CVC tunnels, GSCF injection & biopsy sites. Common to all cases are thalidomide-containing regimens, GCSF pre-PBSCH & post-PBSC reinfusion. Such skin deposits & atypical extramedullary manifestations are previously described only as late events in myeloma evolution. The period between PBSCT & trauma-site lesions is 3–6 months; prior report of surgical scar plasmacytomata also had a 4 month lag phase. The time interval & clinical history suggests circulating plasma cells may be seeding into trauma sites around the time of autologous PBSCT, & growing (possibly from single cell or cell clumps) to clinical appearance 3–4 months thereafter. Trauma-induced cytokines/chemokines may facilitate migration of circulating plasma cells to line/infection/biopsy sites; alternatively extravasated blood with even low level plasma cell circulation could lead to subsequent plasmacytomas. Potential role of thalidomide in selecting this behaviour in predisposed individuals, through effects upon adhesion & neovascularisation, will be examined & putative role of GCSF, which has implications for mobilisation.

Disclosures: Advisory Board Meeting in June 2006 for Pharmion.

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