Melphalan

Abstract

Mucositis, febrile neutropenia and line-associated internal jugular vein thrombosis: 2 case reports In a series of 2 cases, a 65-year-old man developed mucositis and febrile neutropenia and a 52-year-old man developed lineassociated internal jugular vein thrombosis during treatment with melphalan used as a conditioning regimen [route, duration of treatment to reaction onsets and outcomes not stated]. Case 1: A 65-year-old man was referred for assessment after a full blood count identified a platelet count of 165 × 109/L and WBC count of 119 × 109/L in December 2013. He was diagnosed with chronic myeloid leukaemia (CML) in chronic phase and initiated on nilotinib. At 3 months, he achieved a complete cytogenetic response. Bone marrow biopsy performed 3 years after the diagnosis of CML identified an increase in the plasma cell count to 15% of nucleated cells with a concurrent increase in paraprotein. A MRI of the thoracolumbar spine identified extensive marrow infiltration and discrete spinal lesions. A diagnosis of multiple myeloma was considered, and he was initiated on cyclophosphamide, bortezomib and dexamethasone induction therapy. Following completion of four cycles of induction therapy, he achieved a partial response (PR). His nilotinib was interrupted 2 days before cyclophosphamide stem cell mobilisation. He achieved an adequate CD34+ cells/kg cell yield of 11.89 × 109/L. He underwent a melphalan 200 mg/m2 conditioned autologous stem cell transplant (ASCT) with the expected complications of febrile neutropenia and mucositis. At day 100 post ASCT, he had minimal amelioration in his paraprotein, and bone marrow biopsy identified 3% plasma cells. He was initiated on maintenance lenalidomide, and nilotinib was interrupted. He remained alive 7 years following the diagnosis of CML. Case 2: The 52-year-old man was diagnosed with chronic myeloid leukaemia (CML) in chronic phase in December 2000. He was initiated on imatinib on clinical trial and achieved a complete cytogenetic response at 3 months. Ten years after his diagnosis of CML, bone marrow trephine identified monoclonal plasma cells accounting for 25% of nucleated cells. At approximately the same time, therapy with imatinib was stopped as he had been in a molecular remission for a protracted period of time. Over the following 5 years, his BCR-ABL became detectable but remained below 0.01%, and his paraprotein increased with lambda free light chains of 262 mg/L. A repeat bone marrow biopsy revealed 50% plasma cells on trephine. Cytogenetics identified an abnormal hypodiploid clone in 3 of 20 cells with gain of 1q. A diagnosis of multiple myeloma was considered, and he was initiated on cyclophosphamide, bortezomib and dexamethasone induction therapy. After four cycles of induction therapy, he achieved a partial response. After completion of induction therapy, he underwent stem cell mobilisation with plerixafor and filgrastim. He underwent a melphalan 200 mg/m2 conditioned autologous stem cell transplant (ASCT), which was complicated by a line-associated internal jugular vein thrombosis but was otherwise well tolerated. At day 100 post ASCT, he achieved a very good partial response with a paraprotein of 2 g/L. He remained alive 20 years after the diagnosis of CML.