Reactive thrombocytosis might contribute to chemotherapy-related thrombophilia in patients with lung cancer

Abstract Purpose Thrombotic risk is increased in patients with cancer and further potentiated by chemotherapy. We assessed whether early hemostatic alterations could represent a risk factor for thrombosis in patients undergoing chemotherapy for lung cancer. Patients and Methods Forty-nine patients receiving chemotherapy for unresectable, locally advanced, or metastatic lung cancer were included. Blood cell count, prothrombin time, partial thromboplastin time, fibrinogen, antithrombin, D-dimers, protein C, protein S, homocysteine, folates, vitamin B 12 , and activated protein-C resistance were measured at day 0, +7, +15, and +21 of the first chemotherapy cycle. Factor V Leiden and FII G20210A mutations were assessed. Follow-up of patients was prospectively performed for thrombosis during all chemotherapy treatment. Factor V Leiden and FII G20210A frequency were the same as in controls. Results Average basal levels of prothrombin time, partial thromboplastin time, antithrombin, protein C, protein S, folates, vitamin B 12 , and activated protein-C resistance were normal and remained stable during chemotherapy. Homocysteine, D-dimers, and fibrinogen basal levels were high but remained constant after chemotherapy. An average reduction in platelet count was recorded at day +14 in all patients after a striking increase (5.2-fold) at day +21 in the group of patients treated with gemcitabine ( P Conclusion Our findings exclude alterations of coagulation inhibitors or activation of difused intravascular coagulation/fibrinolysis as factors that induce chemotherapy-related thrombosis in lung cancer. The temporal relationship between thrombocytosis at the time of chemotherapy administration and the clinical onset of thrombotic events suggests that thrombocytosis plays a role in triggering thrombotic complications.