A 55‐year‐old white woman presented in July 1984 with severe aplastic anemia refractory to anti‐thymocyte globulin, corticosteroids, and danazol. In December 1984, oral cyclosporine therapy was begun, and a partial remission was achieved with persistent thrombocytopenia and transfusion independence. The cyclosporine dosage was tapered and then stopped in May 1986 when the platelet count was 35,000/L. In October 1986 the platelet count was only 16,000/L, and the bone marrow showed evidence of a myelodysplastic syndrome; cytogenetic analysis revealed deletion of the long arm of chromosome 13 (previous cytogenetic findings had been normal). After cyclosporine therapy was resumed, platelet count promptly increased to 36,000/L. A subsequent attempt to taper the cyclosporine dosage resulted in a decreased platelet count. The platelet count responded to cyclosporine again and was maintained at 54,000/L and higher with cyclosporine therapy at only 25 mg/day. This information suggests that, despite the development of a myelodysplastic syndrome, immune mechanisms were still operative in the pathogenesis of our patient's thrombocytopenia. Immune modulation may have an important role in preventing progression of myelodysplastic syndromes to more severe forms or to acute leukemia.
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