Background: Multifactor affect the pathogenesis of thrombosis in solid malignancy; however, a significant role is attributed to the cancer cells ability to interact with and activate the host hemostatic system. [1] 

Hemostasis is highly correlated to tumor growth, angiogenesis and metastasis, modulation of these pathways reflects interesting and promising treatment options in the future. [1]

Most patients with cancer frequently suffer from chronic compensated DIC and have abnormal laboratory coagulation tests without clinical manifestations of thrombosis, which is a subclinical hypercoagulable state that can be detected by varying degrees of activation of blood clotting. The results of laboratory tests in these patients reflect continuous fibrin formation and lysis during the course of malignancy. [1]

Aim of study: To study the effect of solid malignant tumors on blood coagulation via measurements of plasma fibrinogen and D-dimer.

Subjects and methods: Thirty patients (9 males and 21 females) attending the oncology consultatory out-patient clinic at Baghdad Teaching Hospital/ Medical City were randomly selected and included in this study.

These patients were newly diagnosed as having malignant solid tumors depending on histopathological reports from private and governmental sectors.

All the laboratory tests were done at the hematology and biochemistry departments of Teaching Laboratories/ Medical City.

Results: Plasma fibrinogen level was significantly higher in patients group rather than control group (3.863 ±0.706) Vs (2.497±0.457 g/L} respectively, (P-value 0.001).The mean value of factor VIII activity was {181% ±58.4)and (99.3% ±11.1)for patient and control groups respectively, the P-Value was significant ( > 0.001 ).D-dimer was negative for all members of control group, for patients group ( 66.7 %) of them showed positive D-dimer and (33.3)were negative for D-dimer ,P-value was significant ( >0.001 ). Conclusions: There was increase in plasma fibrinogen level and positive D-dimer in cancer patients compared to the control group reflecting subclinical thrombophilia and higher risk of VTE in patients with solid tumors due to activation of prothrombotic and fibrinolytic pathways by malignant cells which is vital for the use of primary prophylaxis by anticoagulants.