Drug‐induced leukopenia and aplastic anemia

Hematopoietic damage following treatment with certain medications remains a major problem of drug therapy. As long as drugs remain indispensable in the treatment of disease, this problem cannot be resolved simply by avoiding their use. Instead, development of information that pertains to the mechanism and prediction of drug‐induced blood dyscrasias must be acquired for the safe use of drugs. Forewarned is forearmed; if it were possible to identify a susceptible patient or a potentially dangerous drug, then the potential risk of producing a serious blood re action with treatment would be minimized. A precedent for this concept was established with the discovery that patients whose erythrocytes are deficient in glucose‐6‐phosphate dehydrogenase are unusually susceptible to hemolytic anemia if treated with oxidant drugs. 41 For most of the other toxic blood dyscrasias, knowledge of the pathogenesis remains obscure because certain difficulties limit acquisition of such information. The mechanisms of a drug reaction produced by one drug may differ from that produced by another drug. Also, the rare incidence of druginduced blood dyscrasias has made very few patients available for studies. Few papers have appeared which deal with the mechanism of drug‐induced hematopoietic disease. In addition, the difficulties entailed in obtaining bone marrow and other specimens in sufficient quantity has restricted effective investigation. Since the technique required to study mechanisms of drug reactions may be complex and expensive, it may be logistically unsound for a laboratory to “tool up” and then sit back and wait for the first patient to arrive.