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


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 B12, 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 B12, 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 < 0.001). Four thrombotic events were recorded. In all cases, thrombosis occurred within 10 days of the second or the following chemotherapy cycle with gemcitabine and cisplatin. One patient had Factor V Leiden heterozygous disease.


CONCLUSIONS
Our findings exclude alterations of coagulation inhibitors or activation of disseminated intravascular coagulopathy/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.
Zecchina
Gabriella
G
Division of Hematology, San Luigi Hospital, University of Turin, Orbassano, Italy. gabriella.zecchina@unito.it
Ghio
Paolo
P
Bosio
Sandra
S
Cravino
Marta
M
Camaschella
Clara
C
Scagliotti
Giorgio V
GV
D000328:Adult; D000368:Aged; D000970:Antineoplastic Agents / Q000009:adverse effects*; D005260:Female; D006801:Humans; D008175:Lung Neoplasms / Q000097:blood / Q000188:drug therapy*; D008297:Male; D008875:Middle Aged; D010976:Platelet Count; D013922:Thrombocytosis / Q000150:complications*; D019851:Thrombophilia / Q000139:chemically induced*; D013927:Thrombosis / Q000139:chemically induced
D000970:Antineoplastic Agents