Addition of granulocyte colony-stimulating factor to chemotherapy in patients with AIDS-related lymphoma: effects on neutrophil Fcg receptor expression and soluble FcgRIII plasma levels
M. J. K Ersten
Abstract
M. J. K Ersten
Abstract
Summary. AIDS-related neutropenia and neutrophil dysfunction can (partly) be reversed by granulocyte-colony stimulating factor (G-CSF). We studied the effect of G-CSF on neutrophil increment and levels of soluble Fcg receptor type III in 15 patients with AIDS-related lymphoma (ARL) undergoing chemotherapy. In six of these patients we performed a detailed kinetic analysis of the membrane expression of the functionally important Fcg-receptors type I, II and III. In all these patients G-CSF induced FcgRI positive neutrophils with a decreased expression of the FcgRIII receptor. These changes were similar to those seen both in healthy volunteers and in non-HIV-infected individuals treated with chemotherapy. Interestingly, the mean neutrophil and sFcgRIII increment were significantly lower and more patients had a nadir granulocyte count < 0.5 〈 10 9 /l after the first cycle than after the second cycle of chemotherapy. This may be related to a therapy-associated decrease in HIV-1 viral load. The conclusion is that patients treated with chemotherapy for ARL have a qualitatively normal response to G-CSF.
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Summary. AIDS-related neutropenia and neutrophil dysfunction can (partly) be reversed by granulocyte-colony stimulating factor (G-CSF). We studied the effect of G-CSF on neutrophil increment and levels of soluble Fcg receptor type III in 15 patients with AIDS-related lymphoma (ARL) undergoing chemotherapy. In six of these patients we performed a detailed kinetic analysis of the membrane expression of the functionally important Fcg-receptors type I, II and III. In all these patients G-CSF induced FcgRI positive neutrophils with a decreased expression of the FcgRIII receptor. These changes were similar to those seen both in healthy volunteers and in non-HIV-infected individuals treated with chemotherapy. Interestingly, the mean neutrophil and sFcgRIII increment were significantly lower and more patients had a nadir granulocyte count < 0.5 〈 10 9 /l after the first cycle than after the second cycle of chemotherapy. This may be related to a therapy-associated decrease in HIV-1 viral load. The conclusion is that patients treated with chemotherapy for ARL have a qualitatively normal response to G-CSF.
Key concepts: Granulocyte colony-stimulating factor, Lymphoma, Chemotherapy, Neutropenia, Granulocyte, Medicine, Absolute neutrophil count, Internal medicine