Common culprits include chemotherapeutic agents such as alkylating compounds, antimetabolites, and topoisomerase inhibitors, which disrupt DNA replication in rapidly dividing stem cells. Radiation therapy at therapeutic doses can also damage marrow microenvironments, leading to cytopenias. Other sources are heavy metals (arsenic, cobalt, beryllium), industrial solvents, and certain pesticides. In some cases, viral infections (e.g., HIV, hepatitis C) or autoimmune diseases can produce secondary hematotoxicity by targeting marrow precursors or immune effector cells.
Diagnostic evaluation typically involves a complete blood count with differential and peripheral blood smear examination. Bone marrow aspirate and biopsy are performed when significant cytopenia persists, to assess cellularity, dysplasia, or infiltrative processes. Serum levels of the suspected toxin, imaging for organ involvement, and drug monitoring may aid in confirming a causal relationship.
Management focuses on removing the offending agent, when feasible, and providing symptomatic support. Transfusions of packed red cells, platelets, or fresh frozen plasma are used in severe anemia or bleeding. Growth factors such as granulocyte colony‐stimulating factor or erythropoietin can stimulate recovery of neutrophils or red cells, respectively. In chemotherapy-induced neutropenia, prophylactic antibiotics and dose adjustment are often required. Preventive strategies involve meticulous drug dosing, monitoring protocols, and patient education regarding signs of bleeding or infection.
Research continues to clarify the molecular pathways of hematotoxicity, with particular emphasis on oxidative stress, DNA repair deficits, and epigenetic modifications. Understanding these mechanisms informs the development of more targeted therapies and protective agents that may mitigate blood cell damage while preserving the efficacy of life‐saving interventions.