Objective. Drugs can induce almost the entire spectrum of hematologic disorders, affecting white cells, red cells, platelets, and the coagulation system. This paper aims to emphasize the broad range of drug-induced hematological syndromes and to highlight some of the newer drugs and syndromes. Methods. Medline literature on drug-induced hematologic syndromes was reviewed. Most reports and reviews focus on individual drugs or cytopenias. Results. Drug-induced syndromes include hemolytic anemias, methemoglobinemia, red cell aplasia, sideroblastic anemia, megaloblastic anemia, polycythemia, aplastic anemia, leukocytosis, neutropenia, eosinophilia, immune thrombocytopenia, microangiopathic syndromes, hypercoagulability, hypoprothrombinemia, circulating anticoagulants, myelodysplasia, and acute leukemia. Some of the classic drugs known to cause hematologic abnormalities have been replaced by newer drugs, including biologics, accompanied by their own syndromes and unintended side effects. Conclusions. Drugs can induce toxicities spanning many hematologic syndromes, mediated by a variety of mechanisms. Physicians need to be alert to the potential for iatrogenic drug-induced hematologic complications.

Lenalidomide can be effective in treatment of MDS, particularly in patients with isolated 5q deletion, as well as in patients with 5q− with other karyotypic abnormalities (List et. al. NEJM355, 1456; 2006). However, there is little data for secondary MDS. We report two patients with chemotherapy-induced MDS with 5q−, both treated with lenalidomide, one of whom responded. Case 1: An 81-year-old female with multiple myeloma who had been treated with melphalan and prednisone developed worsening anemia despite continued biochemical remission of her myeloma. Three years after melphalan treatment, a bone marrow revealed MDS with only 2% plasma cells. Cytogenetics showed: 46, XX, del(5)(q13q33), del(14)(q1?3), add(22)(q13)[1]/46, sl, del(20)(q13.1) [9]/47, sdl1, +8[10]. The patient was transfusion dependent despite treatment with EPO. She was treated with lenalidomide 10 mg daily and began responding after eight weeks of therapy. Her anemia improved, and she became transfusion independent until her death 6 months later from infection. Figure 1. HCT before and after lenalidomide treatment (patient 1) Figure 1. HCT before and after lenalidomide treatment (patient 1) Case 2: A 54-year-old male developed MDS after multiple therapies for low grade non-Hodgkins lymphoma, including rituximab, ibritumomab tiuxetan, chlorambucil, and CHOP. While in remission for lymphoma, he developed pancytopenia. A bone marrow revealed no lymphoma, but demonstrated evidence of MDS. Cytogenetics showed: 46, XY, del (5)(q13q33) [3]/44, idem, −7, add(19)(q13), −21[3]/46, XY [14]. The patient was transfusion dependent. He was treated with lenalidomide 10mg daily, demonstrating no significant benefit after 10 weeks. We report that one of our two patients with secondary MDS and 5q− responded to lenalidomide with a resolution of her transfusion requirement. Two prior cases of improvement in secondary MDS with 5q− after lenalidomide treatment have been reported (Melchert et. al. Leukemia21: 1576–78, 2007). Lenalidomide is active in some cases of secondary MDS with 5q−. Further studies are needed to better define the activity of lenalidomide in secondary MDS with and without 5q−.