SECONDARY MYELODYSPLASTIC-SYNDROME IN MULTIPLE-MYELOMA - A STUDY OF 9PATIENTS WITH AN ATTEMPT TO DETECT MYELOMA PATIENTS AT RISK

Citation
M. Mittelman et al., SECONDARY MYELODYSPLASTIC-SYNDROME IN MULTIPLE-MYELOMA - A STUDY OF 9PATIENTS WITH AN ATTEMPT TO DETECT MYELOMA PATIENTS AT RISK, Haematologia, 26(2), 1994, pp. 67-74
Citations number
NO
Categorie Soggetti
Hematology
Journal title
ISSN journal
00176559
Volume
26
Issue
2
Year of publication
1994
Pages
67 - 74
Database
ISI
SICI code
0017-6559(1994)26:2<67:SMIM-A>2.0.ZU;2-W
Abstract
Over a follow-up period of ten years, nine of our 100 patients with mu ltiple myeloma (MM), developed myelodysplastic syndrome (MDS, preleuka emia). MDS occurred 19-156 (median 35) months from the diagnosis of MM . Six patients presented with pancytopenia and no patients had active MM at the time of MDS diagnosis. Three patients were defined as having refractory anaemia (RA) and six as refractory anaemia with excess bla sts (RAEB) or RAEB in transformation (RAEBT), according to the FAB cla ssification. The clinical course is characterized by increasing red bl ood cell and platelet transfusion requirements, recurrent infections a nd bleeding episodes. All patients, except for one, died within 3 to 8 (median 5) months from MDS diagnosis. The causes of death were sepsis or bleeding; three patients underwent leukaemic transformation. Thus, the clinical course of this small group of myeloma patients who devel oped secondary MDS (sMDS), was similar to other series of patients wit h sMDS. Serial bone marrow examinations suggest an initial hypercellul ar phase, followed by a rapidly evolving preterminal hypocellular marr ow. In an attempt to detect MM patients at risk of developing sMDS, th e epidemiological (including ethnic), clinical and laboratory data of the 9 MDS patients at the time of the MM presentation were reviewed an d compared to the other MM patients. No significant differences were o bserved between the two groups in most parameters, except for two. All MDS patients were Ashkenazi Jews and no patients of Sepharadic origin developed MDS. Also, no IgA-myeloma patient developed MDS. If these f indings are confirmed in a larger series, it may point to subgroups at risk which may require a different approach. We also tested the well- known association of sMDS in MM patients with the administration of al keran (melphalan) to these patients. No difference was found in the cu mulative dose of alkeran used in our 9 MDS patients, compared with oth er myeloma patients. On the other hand, the MDS patients in our series received higher cumulative dose of prednisone per person then the oth ers. Although this is a preliminary observation in a small number of p atients, taking these data together with some recent reports associati ng corticosteroids with leukaemogenesis as well as the known effects o f these agents on the immune system, it is tempting to speculate that corticosteroids may play a role in the pathogenesis of this complicati on in patients with MM.