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

AbstractPURPOSE:
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 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.
CONCLUSION:
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.
AuthorsGabriella Zecchina, Paolo Ghio, Sandra Bosio, Marta Cravino, Clara Camaschella, Giorgio V Scagliotti
JournalClinical lung cancer (Clin Lung Cancer) Vol. 8 Issue 4 Pg. 264-7 (Jan 2007) ISSN: 1525-7304 [Print] United States
PMID17311691 (Publication Type: Journal Article)
Chemical References
  • Antineoplastic Agents
Topics
  • Adult
  • Aged
  • Antineoplastic Agents (adverse effects)
  • Female
  • Humans
  • Lung Neoplasms (blood, drug therapy)
  • Male
  • Middle Aged
  • Platelet Count
  • Thrombocytosis (complications)
  • Thrombophilia (chemically induced)
  • Thrombosis (chemically induced)

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