Acute promyelocytic leukaemia complicating multiple myeloma: Evidence of different cell lineages

The association of leukemia and multiple myeloma is well described usually as a complication of chemotherapy bur also in the absence of chemotherapy o r at diagnosis. Such leukemias are typically acute myeloid leukemia (AML), particularly myelomonocytic subtype, and cases of acute promyelocytic leuke (APL) are rarely reported. Controversy exists as to whether myeloma and AM L originate from a single haematopoietic progenitor or arise from different cell lineages. We report a case of a 58 year old female who developed APL 10 months following diagnosis of nonsecretory light chain (kappa) myeloma w hich had been treated with local spinal irradiation and low dose oral melph alan and prednisone. Clonality had originally been demonstrated by light ch ain restriction (kappa) of her bone marrow plasma cells whilst immunoglobul in heavy chain and T cell receptor genes were germ line. At development of APL cytogenetics revealed t(15;17) and PML-RAR fusion gene was detected by RT-PCR. The patient was treated with all-trans retinoic acid (ATRA) and rec eived 2 cycles of consolidation chemotherapy with Idarubicin. Following thi s therapy the t(15;17) and PML-RAR were both undetectable whilst the clonal population of kappa staining plasma cells persisted. This particular patie nt represents a rare case of APL complicating multiple myeloma with persist ence of the myeloma clone but disappearance of PML-RAR alpha RNA following therapy. This case study appears to support the argument that the APL and m yeloma originated from distinct cell lineages.