PMC:2778502 / 33135-34967 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/2778502","sourcedb":"PMC","sourceid":"2778502","source_url":"http://www.ncbi.nlm.nih.gov/pmc/2778502","text":"20. Conclusions\nThe wide spectrum of drug-induced hematologic syndromes is mediated by a variety of mechanisms, including immune effects, interactions with enzymatic pathways, and direct inhibition of hematopoiesis. The table summarizes the drug-induced hematological syndromes discussed above. Providing proof that a drug causes a particular hematologic syndrome is frequently impossible. Many patients simultaneously receive multiple drugs, making it difficult to be certain of causality. Rechallenge with a drug suspected of causing toxicity is usually not advisable. For some drugs, such as heparin, quinidine, and vancomyin, in vitro testing has been performed and mechanisms for cytopenias elucidated. However, such testing is not always possible given that for most there are no standardized, commercially available assays and that reactions may be related to metabolites as opposed to more easily tested parent compounds.\nAs medicine advances, older drugs become obsolete and are replaced by newer formulations. Many drugs formerly associated with hematologic toxicities (e.g., penicillin, alpha methyl-dopa, quinidine, gold, and chloramphenical) are no longer in common use. However, newer drugs are found to be associated with their own potential hematologic toxicities (e.g., clopidogel, linezolid, ribavirin, rituximab, and GPIIb/IIIa inhibitors). Furthermore, in addition to classic drug-induced cytopenias, we are increasingly seeing thrombosis as a common theme with a number of diverse agents (e.g., heparin, COX-2 inhibitors, bevacizumab, hormone replacement therapy, tamoxifen, erythropoietin, thalidomide and lenalidomide). Physicians from a wide variety of specialties need to understand the hematological consequences of drugs and be prepared for the occurrence and correction of these events in their 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