Discussion

Abstract

Dr. HELLRIEGEL opened the discussion with a question about acute leukemia following aplastic anemia and remarked that — acccording to the series of SAARNI and LINMAN — one quarter of patients with preleukemia have a hypoplastic bone marrow. He stressed that patients with drug-induced bone marrow aplasia, e. g., chloramphenicol-induced bone marrow dyscrasias, run a particularly high risk of developing acute leukemia. In his study, two cases with a primary aplastic bone marrow, demonstrated by biopsy, developed acute leukemia. Dr. SULTAN mentioned cases with true aplastic anemia — proven by marrow biopsy — which start with aplasia without a PNH clone, go through a phase of dysplasia, and finally develop acute leukemia. During treatment with androgens, the marrow becomes more and more cellular. The cytological aspects of dysplasia are exactly the same as those seen in refractory or sideroblastic anemia; many years later these patients develop acute leukemia. Androgen therapy may trigger the differentiation of the remaining clones of myeloid stem cells — incapable of differentiation in cases of aplastic anemia — but is probably not responsible for the development of acute leukemia. Dr. NAJEAN added a further type of preleukemia associated with aplastic anemia. This disease is only observed by acute lymphoblastic leukemia. Dr. HEIMPEL answered that the incidence of leukemia in true hypoplastic anemia is very low. In studies of the history of some time before the diagnosis of leukemia was established, it would be rare to find cases with bone marrow hypoplasia. He tended to put aplastic anemia among the conditions with a not-too-high risk of acute leukemia. Dr. SULTAN stressed that for technical reasons, the frequency of aplastic anemias developing acute leukemia cannot be judged in older series, because the cases are less well documented.