BACKGROUND: Neutropenic fever is the commonest complication of cladribine therapy for hairy-cell leukemia (HCL), leading to a 3% mortality rate. Our aim was to identify predictive factors and evaluate the effects of concomitant granulocyte-macrophage colony-stimulating factor (GM-CSF). PATIENTS AND METHODS: We studied 102 patients with active HCL given cladribine for 7 days. Pretreatment parameters predicting neutropenic fever were analysed. Twelve patients at high risk for febrile complications also received 400 micrograms GM-CSF per day on days 1 through 21. RESULTS: Pretreatment anemia, hypocholesterolemia, bone marrow differential with a high percentage of hairy cells and a low percentage of myelopoietic cells, low albumin, and high C-reactive protein predicted neutropenic fever. The addition of GM-CSF did not improve the kinetics of recovery for neutrophils, hemoglobin or platelets, as compared to matched control patients. However, GM-CSF significantly reduced cladribine-induced lymphopenia, but not the incidence of neutropenic fever. CONCLUSION: Factors predicting febrile neutropenia were identified. GM-CSF protected from cladribine lymphotoxicity but did not improve neutropenia or febrile episodes.
BACKGROUND:Neutropenic fever is the commonest complication of cladribine therapy for hairy-cell leukemia (HCL), leading to a 3% mortality rate. Our aim was to identify predictive factors and evaluate the effects of concomitant granulocyte-macrophage colony-stimulating factor (GM-CSF). PATIENTS AND METHODS: We studied 102 patients with active HCL given cladribine for 7 days. Pretreatment parameters predicting neutropenic fever were analysed. Twelve patients at high risk for febrile complications also received 400 micrograms GM-CSF per day on days 1 through 21. RESULTS: Pretreatment anemia, hypocholesterolemia, bone marrow differential with a high percentage of hairy cells and a low percentage of myelopoietic cells, low albumin, and high C-reactive protein predicted neutropenic fever. The addition of GM-CSF did not improve the kinetics of recovery for neutrophils, hemoglobin or platelets, as compared to matched control patients. However, GM-CSF significantly reduced cladribine-induced lymphopenia, but not the incidence of neutropenic fever. CONCLUSION: Factors predicting febrile neutropenia were identified. GM-CSF protected from cladribine lymphotoxicity but did not improve neutropenia or febrile episodes.