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Autologous (ASCT) and allogeneic stem cell transplantations (alloBMT) are well-established therapies for multiple myeloma. However, patients continue to relapse at a constant rate. We present here 15 out of 163 patients who underwent SCT and relapsed with plasmacytomas only without evidence of bone marrow disease progression (14/147 post-ASCT and 1/16 post-alloBMT). The median time from SCT to plasmacytoma relapse was 24 months. The sites of plasmacytoma included bone, skin, rectum, and testicles. Five patients were treated with local radiotherapy, while seven patients received a combination of radiotherapy and chemotherapy or thalidomide, and two patients received chemotherapy alone with or without thalidomide. The recipient of alloBMT was initially treated with VAD-chemotherapy and local radiotherapy followed by a mini-allograft from the original donor. Eleven patients died at a median of 10 months following diagnosis of the plasmacytoma. Four are still alive, 12-20 months post-plasmacytoma diagnosis. These cases of unconventional disease recurrence are likely to be seen due to sub-clinical seeding of tumour cells suggestive of the presence of an extramedullary (EM) clone of plasma cells with a high degree of chemoresistance. We also review all the available data in the literature for the optimal therapy for patients with isolated EM relapse.

Secondary leukaemia following treatment of M3 acute promyelocytic leukaemia (APL) is a rare event. We describe a patient in remission following chemotherapy for APL who relapsed with M2 acute non-lymphoblastic leukaemia (ANLL). The original t(15;17) (q22;q21) chromosome translocation was lost and replaced by a clone containing a dic(5;17) (q11;p11) abnormality. Southern genomic analysis demonstrated re-arrangements of the retinoic acid receptor varies; is directly proportional to (RAR varies; is directly proportional to) and PML genes in the APL blasts at presentation but not in the M2 ANLL marrow at relapse. The significance of unbalanced 5;17 translocations as markers for therapy-related secondary leukaemia is discussed.

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Summary. Some aspects of red‐cell membrane structure and function have been investigated in patients with haemolysis due to dapsone (4,4′ diaminodiphenylsulphone). Osmotic fragility and potassium flux were not increased but red‐cell membrane changes occurred which suggested instability. These included loss of phospholipid, decrease in acetylcholinesterase activity and increased autohaemolysis. In addition, there was evidence for lipid peroxidation, which might have been the primary lesion. Red‐cell membrane sulphydryl group activity was either reduced or altered because these cells were abnormally sensitive to the action of the sulphydryl group inhibitor p‐chloromercuribenzoate, as measured by increased potassium leakage aiid haemolysis. Dapsone also caused abnormal peroxide lysis in the presence of normal hydrogen peroxide detoxification mechanisms and in the absence of vitamin E deficiency. This was prevented by excess vitamin E but not by the sulphydryl compounds, reduced glutathione or cysteine, and it was increased by previous treatment with p‐chloromercuribenzoate. It is suggested that reduced membrane sulphydryl group activity, probably due to the formation of mixed disulphides with precipitated haemoglobin, and lipid peroxidation may be responsible for in vitro and, possibly, in vivo dapsone‐induced haemolysis.