HYPERCOAGULABILITY IN PATIENTS WITH LUNG CANCER UNDERGOING CHEMOTHERAPY

Authors

  • Mariani Mariani Division of Hematology, Department of Clinical Pathology, School of Medicine, University of North Sumatra/Adam Malik Hospital, Medan,
  • Herman Hariman Division of Hematology, Department of Clinical Pathology, School of Medicine, University of North Sumatra/Adam Malik Hospital, Medan
  • Noni Sari Soeroso Division of Oncology, Department of Chest and Respiratory Medicine, School of Medicine, University of North Sumatra/Adam Malik Hospital, Medan

DOI:

https://doi.org/10.24293/ijcpml.v24i3.1404

Keywords:

, Lung cancer thrombosis, hypercoagulability, D-dimer, PT, APTT, TT

Abstract

There is evidence that in the case of malignancies including lung cancer, that there is hypercoagulability. In spite of this, it is still not clear whether the course of chemotherapy alters the risk. This study aimed to investigate whether there was state of pre-thrombosis and hypercoagulability in patients with lung cancers and the underlying effect of chemotherapy during the treatment. Twelve lung cancer patients were recruited. Their stages and clinical performances were determined. The blood sample was taken before the chemotherapy, shortly after the first- and third-chemotherapy cycles, for the investigation of D-dimer, platelet count, PT (INR), ratios of APTT, and TT. The chemotherapy protocols vary from one patient to the others as well as between the 1st and the 3rd chemotherapy regimens although most of the protocols consist of carboplatin + gemcitabine or carboplatin + paclitaxel. From the thrombosis view of point, they were all asymptomatic and remained so during the period of investigation. Thrombosis is defined as an increase of D-dimer and hypercoagulability as finding one or more of PT (INR), ratio APTT, ratio TT <1.0. The trend of the result in the three sampling points was carried out by ANOVA, while Wilcoxon test for small samples did univariate analysis between two investigations. The result of PT, APTT, and TT indicating hypercoagulability showed that they remained unchanged until the third cycle of chemotherapy (p>0.05). The platelets of patients dropped significantly; median (range) 422 to 287 x 109/L before the chemotherapy to the end of the third cycle respectively. The D-Dimer of patients remained unchanged, however when it was investigated by univariate analysis in the group with D-Dimer >500 ng/mL, this group showed a decreased D-Dimer towards the end of the third cycle (p <0.05). This study demonstrated that there was hypercoagulability in patients with lung cancers before the chemotherapy until the 3rd cycle of chemotherapy. The course of chemotherapy did not alter hypercoagulability. However, in the group where pre-thrombosis had already happen as evidenced by high D-dimer (>500 ng/mL), the chemotherapy showed benefit regarding of reduction of the D-dimer which may lead to the possible breakdown of the existing thrombus.

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References

Heit JA, Silverstein MD, Mohr DN, Mohr DN, Petterson TM, et al. Risk factors for deep vein thrombosis and pulmonary embolism: A population-based control study. Arch Intern Med 2000; 160:809-15.

Samama MM. An epidemiology study of risk factors for deep vein thrombosis in medical outpatients: The Sirus study. Arch Intern Med 2000; 160:3415-20.

Rickles FR, Edwards RL. Activation of blood coagulation in cancer. Trousseau's syndrome revisited. Blood 1983; 62:14-31.

Donati B. Cancer and thrombosis: From phlegmasia alba dolens to transgenic mice. Thromb Haemost, 1995; 74:278-81.

Rickles FR, Levine MN, Edwards RL. Haemostatic alterations in cancer patients. Cancer Metastasis Rev, 1992; 11:237-48.

Falanga A, Ofosu FA, Delaini F, Oldani E, Dewar L, et al. The hypercoagulable state in cancer: Evidence for impaired thrombin inhibition. Blood Coagul Fibrinolysis 1994; 1 (suppl): 19-23.

Kakkar AK, Levine M, Pinedo HM, Wolff R, Wong J. Venous thrombosis in cancer patients: Insight from the FRONTLINE survey. The Oncologist, 2003; 8:31-8.

Nakashima MO, Rogers HJ. Hypercoagulable State: An algorithmic approach to laboratory testing and on monitoring of direct oral anticoagulants. Blood research 2014; 29(2): 85-94.

Dipasco PJ, Misra S, Koniaris LG, Moffat FL Jr. Thrombophilic state in cancer, part I: Biology, incidence and risk factors. J SurgOncol 2011; 104(3): 316-22.

Cleveland Clinic. Hypercoagulable state (Blood Clotting Disorders) from http://myclevelandclinic 2015; 1-4.

Caine GJ, Stonelake PS, Lip GY, Kehoe ST. The hypercoagulable state of malignancy: Pathogenesis and current debate. Neoplasia 2002; 4:465-73.

Blom JW, Osanto S, Rosendaal FR. The risk of venous thrombotic event in lung cancer patients: Higher risk for adenocarcinoma than squamous cell carcinoma. J Thromb Haemost, 2004; 2:1760-5.

Donati MB, Falanga A. Pathogenetic mechanisms of thrombosis in malignancy. Acta Hematol 2001; 106:18-24

Levine MN, Gent M, Hirsh J, Arnold A, Goodyear MD, Hryniuk W, De Pauw S. The thrombogenic effect of anticancer drug therapy in women with stage II breast cancer. N Engl J Med, 1988; 318(7): 404-7.

Falanga AM, Marchett M, Vignoli A. Coagulation and cancer: Biological and clinical aspects. J Thromb Haemost, 2013; 11(2): 223-233.

Otten HM, Mathijssen J, Ten Cate H, Soesan M, Inghels M, et al. Symptomatic venous thromboembolism in cancer patients treated with chemotherapy: An underestimated phenomenon. Arch Intern Med, 2004; 164(2): 190-4.

Ruiz MA, Marugan I, Estelles AF. The influence of chemotherapy on plasma coagulation and fibrinolytic systems in lung cancer patients. Cancer, 1989; 63:643-8.

Zacharski LR. Anticoagulants in cancer treatment: Malignancy as a solid phase coagulopathy. Cancer Lett. 2002; 186(1): 1-9.

Prisco D, Grifori E. The role of D-dimer testing in patients with suspected venous thromboembolism. Semin Thromb Hemost, 2009; 35:50-59.

Kleinegris MC, Ten Cate H, Ten Cate HAJ. D-dimer as a marker for cardiovascular and arterial thrombotic events in patients with peripheral arterial disease. A systematic review. Thromb Haemostas, 2013; 110(2): 233-243.

Gomez K, Tudderham EGD, McVey JH. Normal haemostasis. Post graduate hematology, 6thEd., Boston, WileyBlackwell, 2011; 747-771.

Glassman AB. Hemostatic abnormalities associates with cancer and its therapy. Ann Clin Lab Sci 1997; 27:191-5.

Kamath S, LipGYH. Fibrinogen: Biochemistry, epidemiology and determinants. QJM: An Inter J of Med 2003; 96(10): 711-9.

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Submitted

2018-12-07

Accepted

2018-12-07

Published

2018-07-01

How to Cite

[1]
Mariani, M., Hariman, H. and Soeroso, N.S. 2018. HYPERCOAGULABILITY IN PATIENTS WITH LUNG CANCER UNDERGOING CHEMOTHERAPY. INDONESIAN JOURNAL OF CLINICAL PATHOLOGY AND MEDICAL LABORATORY. 24, 3 (Jul. 2018), 214–218. DOI:https://doi.org/10.24293/ijcpml.v24i3.1404.

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