Granulocyte Colonystimulating Factor And Granulocytemacrophage Colonystimulating Factor For Chemotherapyinduced Myelosuppression

Granulocyte colony-stimulating factor (G-CSF) and granulocyte-macrophage colony-stimulating factor (GM-CSF) are endogenous glycoproteins that participate in the differentiation and proliferation of granulocytes, monocyte-macrophages, and other cells for hematopoeisis (17). Myelosuppresion is the major toxicity of chemotherapy for solid organ tumors, and prolonged myelosuppression and neutropenia lead to a reduction in chemotherapy dose intensity. Therefore, with the discovery, cloning, and production of recombinant human forms of G-CSF and GM-CSF (rHuG-CSF and

Fig. 1. The relationship between absolute neutrophil count (ANC) and neutropenic fever after salvage chemotherapy is shown for patients with metastatic breast carcinoma. When the ANC decreases to a level below the threshold of 500/|mL, the incidence of neutropenic fever increases in a linear trend (p < 0.01). *, Number of courses with fever/number of courses with nadir ANC in the same range.

Fig. 1. The relationship between absolute neutrophil count (ANC) and neutropenic fever after salvage chemotherapy is shown for patients with metastatic breast carcinoma. When the ANC decreases to a level below the threshold of 500/|mL, the incidence of neutropenic fever increases in a linear trend (p < 0.01). *, Number of courses with fever/number of courses with nadir ANC in the same range.

rHuGM-CSF), patients could receive cytotoxic chemotherapy with white blood cell growth factors to counteract the subsequent myelosuppression.

Several studies were performed to evaluate the effect of filgrastim (an rHuG-CSF) and rHuGM-CSF on neutropenia and overall disease outcome in patients receiving chemotherapy for solid tumors. Gabrilove et al. (18) performed a study evaluating fil-grastim in patients with transitional cell carcinoma of the urothelium. Twenty-seven patients who were receiving MVAC (methotrexate, vinblastine, doxorubicin, and cisplatin) chemotherapy were given filgrastim 60 Mg/kg on one of three schedules: before, after, or before and after chemotherapy. Treatment given before chemotherapy increased ANC. Treatment after chemotherapy decreased both the number of days the ANC was <1.0 x 109/L and the number of days antibiotics were given compared with fiilgrastim use before chemotherapy. Furthermore, patients who received filgrastim after chemotherapy were able to receive the next course of chemotherapy on the planned day of treatment.

Crawford et al. (19) did a randomized, double-blind, placebo-controlled trial in patients with small-cell lung cancer (SCLC) to evaluate the incidence of fever and neutropenia in patients treated with chemotherapy. Two-hundred eleven patients receiving chemotherapy with cyclophosphamide, doxorubicin, and etoposide (CAE)

were randomly assigned to placebo or filgrastim on d 4-17 of a 21-d cycle. Patients who received filgrastim experienced a significant reduction in the incidence of fever and neutropenia, duration of grade IV neutropenia defined as ANC < 0.5 x 109/L, days of treatment with intravenous (iv) antibiotics, and culture-confirmed infection. Both studies showed a significant reduction in the incidence of neutropenia in patients receiving chemotherapy who also received filgrastim after chemotherapy and an apparent inferiority, in the first study, of filgrastim administered before chemotherapy. When filgrastim was given prophylactically, patients had less toxicity from myelosuppression and were able to maintain the planned treatment schedule; however, not all patients in these studies developed significant neutropenia and therefore would not require growth factor support.

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