Abstract

SUMMARY OF CHEMOTHERAPY -INDUCED ANEMIA

Parvathi M. L.*

ABSTRACT

Anemia is commonly encountered in cancer patients especially so among those undergoing active chemotherapy with or without radiation therapy. Both radiotherapy and chemotherapy can be immunosuppressive and inhibit erythropoiesis; some, however, may cause a greater degree of anemia than others. The underlying mechanisms responsible for this type of anemia are unclear, but are thought to involve the activation of cytokines such as Interferon-γ, Interleukin-1 and tissue necrosis factor (TNF). These cytokines may suppress endogenous erythropoietin (EPO) production, impair iron utilization and reduce erythroid precursor proliferation. Several treatment modalities including blood transfusion, erythropoietin-stimulating agents and intravenous (IV) iron therapy was discussed. Anemia is commonly encountered in cancer patients especially so among those undergoing active chemotherapy with or without radiation therapy. Both radiotherapy and chemotherapy can be immunosuppressive and inhibit erythropoiesis; some, however, may cause a greater degree of anemia than others. The underlying mechanisms responsible for this type of anemia are unclear, but are thought to involve the activation of cytokines such as Interferon-γ, Interleukin-1 and tissue necrosis factor (TNF). These cytokines may suppress endogenous erythropoietin (EPO) production, impair iron utilization and reduce erythroid precursor proliferation. Several treatment modalities including blood transfusion, erythropoietin-stimulating agents and intravenous (IV) iron therapy was discussed. Anemia is commonly encountered in cancer patients especially so among those undergoing active chemotherapy with or without radiation therapy. Both radiotherapy and chemotherapy can be immunosuppressive and inhibit erythropoiesis; some, however, may cause a greater degree of anemia than others. The underlying mechanisms responsible for this type of anemia are unclear, but are thought to involve the activation of cytokines such as Interferon-γ, Interleukin-1 and tissue necrosis factor (TNF). These cytokines may suppress endogenous erythropoietin (EPO) production, impair iron utilization and reduce erythroid precursor proliferation. Several treatment modalities including blood transfusion, erythropoietin-stimulating agents and intravenous (IV) iron therapy was discussed.

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