Docetaxel-induced lymphopenia in patients with solid tumors

Abstract

BACKGROUND The quantitative abnormalities of the different peripheral blood lymphocyte subsets during docetaxel administration were prospectively studied. METHODS Forty‐six chemotherapy‐naive patients with solid tumors were treated with docetaxel either in a 3 weekly (n = 33) or weekly (n = 13) schedule. Twenty patients with central nervous system (CNS) metastatic disease as the first clinical presentation of cancer and 35 patients with metastatic colorectal carcinoma treated with chemotherapy were enrolled as controls. The phenotype of peripheral blood lymphocytes was determined by indirect immunofluorescence using appropriate monoclonal antibodies and fluorescent‐activated cell sorter analysis. RESULTS After the administration of the first docetaxel cycle, the absolute number of peripheral blood lymphocytes (P < 0.005), CD3⁺ (P < 0.01), CD4⁺ (P < 0.01), CD8⁺ (P < 0.01), and CD56⁺ (P < 0.01) but not CD20⁺ (P < 0.3) cells was significantly decreased compared with the pretreatment values. Further treatment resulted in a further decrease of these lymphocyte subsets including CD20⁺ cells (P < 0.01). Similarly, after the administration of the first weekly dose of docetaxel, the absolute number of total lymphocytes, CD3⁺, CD4⁺, and CD8⁺ cells was decreased. The administration of the second weekly docetaxel dose resulted in a further decrease of CD56⁺ (P = 0.012) and CD20⁺ (P = 0.007) cells. The administration of either high dose corticosteroids in patients with CNS metastases or an irrelevant chemotherapy (CPT‐11/5‐FU) did not result in similar abnormalities. The discontinuation of docetaxel was associated with a recovery of CD3⁺ and CD4⁺ lymphocytes within a 3‐month period. Eight (17%) patients developed nonneutropenic infections during docetaxel treatment. CONCLUSIONS Docetaxel has an important but reversible nonspecific lymphopenic effect that seems to be associated with an increased risk for nonneutropenic infections. Cancer 2000;89:1380–6. © 2000 American Cancer Society.