SIR—As described by Verdonck and colleagues1 and also reported by Tricot and colleagues, 2 there is an apparent antitumour effect of donor lymphocyte infusions when multiple myeloma recurs after allogeneic bone marrow transplantation. We report two additional cases. A 51-year-old woman was diagnosed as having multiple myeloma, IgG-κ stage IIIA, in June, 1987. She underwent bone marrow transplantation in November, 1987, with a graft from her HLA-identical sister, after cyclophosphamide and whole body irradiation. In the following years, plasma M protein gradually decreased from 34 g/L to 14 g/L by November, 1990, and her marrow became normal. In December, 1992, she had a pathological fracture and the M protein increased to 21 g/L. M protein was detected in urine, and pathological plasma cells (4%) reappeared in marrow. She received donor leucocyte infusions in March, 1993, achieving a partial remission, with fall in M protein to 14 g/L and normal marrow. However, M protein in urine did not decrease and, in October, 1994, M protein in plasma rose. In January, 1995, VAD therapy (vincristine, doxorubicin, and dexamethasone) was begun because of a rise in M protein to 28 g/L. The patient responded to chemotherapy and, after three courses, M protein was 15 g/L. In March, 1995, she received, for a second time, donor leucocyte infusions (total 3· 1108/kg lymphocytes), This time, intravenous interleukin-2 (9106 IU continuously for 24 h followed by 0· 9106 IU twice daily for 1 mo) was started after infusion of the first leucopheresis product. However, despite this treatment, M protein concentration slowly increased to 20 g/L in December, 1995.

Our second patient, a 38-year-old man, presented in March, 1988, with an eyelid plasmocytoma, which was successfully removed. In April, 1989, the plasmocytoma relapsed in the right parotid gland and, after surgery with postoperative irradiation, he was regarded as in remission. In July, 1989, he had a spontaneous costal fracture and radiography showed multiple osteolytic lesions. Aspirate from bone marrow contained 50% plasma cells, and there was a trace of Bence-Jones proteinuria of κ-type. There was no M protein in plasma. After intermittent melphalan/prednisone courses for 1 year, on February 12, 1991, he underwent bone marrow transplantation, with his HLA-identical brother as donor, after conditioning with busulphan and cyclophosphamide. Repeated tests for bone marrow morphology and Bence-Jones proteinuria were normal, and skeletal surveys showed no osteolytic lesions until April, 1993, when he had a traumatic fracture that did not heal. To correct pseudoarthrosis, he underwent surgery in September, 1994, when a marrow transplant was taken from the iliac crest. Morphology showed a relapse, with infiltrating plasma cells and κ positivity in the iliac crest, and also in a specimen from a new lesion in the right acromion. After local irradiation he was given donor leucocyte infusions in June, 1995 (total 4· 6108/kg lymphocytes), together with interleukin-2. However, new osteolytic lesions were detected in August, 1995, and treated with local irradiation. In September, 1995, the patient developed graft-versus-host disease (GVHD) of the liver and gut necessitating intervention with prednisone and cyclosporin. GVHD