DYNAMICS OF HEMOSTATIC MARKERS THROUGHOUT SYSTEMIC TREATMENT IN PATIENTS WITH BREAST CANCER
DYNAMICS OF HEMOSTATIC MARKERS THROUGHOUT SYSTEMIC TREATMENT IN PATIENTS WITH BREAST CANCER

Summary/Abstract: Breast cancer is the most commonly diagnosed cancer among women globally and is increasingly managed with complex multimodal systemic therapy. Despite advances in oncologic treatment, venous thromboembolism (VTE) is still a major health problem and the second leading cause for cancer-related mortality. Patients with breast cancer have roughly a fourfold higher risk of developing VTE compared with age- and sex-matched healthy controls, and this risk is further amplified by systemic chemotherapy and other adjuvant treatments. The prothrombotic tendency in breast cancer arises from a complex interaction between tumor biology, host response, and anticancer therapy. Tumor cells can directly activate coagulation by expressing tissue factor (TF) and releasing TF-bearing extracellular vesicles, thereby initiating thrombin generation and fibrin formation. Prothrombin fragment 1+2 (F1+2) and thrombin-antithrombin complexes (TAT) are clinical-laboratory parameters, which provide a direct measure of in vivo thrombin formation. D-dimer is widely used in clinical practice as an indicator of ongoing coagulation and fibrinolysis. In cancer patients, the coagulation system is often chronically activated and AT III, a natural anticoagulant, may be consumed through ongoing inhibition of thrombin and factor Xa or down-regulated. Objective: To investigate longitudinal changes in hemostatic markers – F1+2, TAT, D-dimer, TF, fibrinogen and Antithrombin III in patients with breast cancer undergoing systemic treatment. Materials and methods: We investigated 38 women with breast cancer. A control group of 34 age-matched healthy women was also studied. TAT, F1+2, TF, D-dimer, AT III and fibrinogen levels were determined prior to therapy initiation – Visit 1; Visit 2 – monitoring of therapeutic response; Visit 3 – after completing treatment. ELISAs were used to quantify F1+2, TF and TAT. Fibrinogen levels were determined by the Claus clotting method, AT III activity by chromogenic assay, and plasma D-dimer concentration by immunoturbidimetry. Results: Levels of F1+2, TAT, TF and D-dimer declined throughout systemic therapy, with baseline values being significantly higher than those at visits 2 and 3 (P<0.05). ATIII activity showed a statistically significant increase at visit 3 compared to visit 2 (P=0.023). Conclusion: Systemic treatment in breast cancer patients significantly influenced the dynamics of hemostatic markers. A hypercoagulable state persists during the applied therapy, despite the tendency for lower levels of TAT, F1+2, TF, D-dimer and increased AT III activity. This highlights the importance of an individualized anticoagulation strategy aimed at preventing thrombotic events and effectively managing cancer-related venous thromboembolism.

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