The thrombogenic potential of thrombophilia in malignant tumors of the reproductive system

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Objective. To study the significance of genetic and acquired thrombophilia factors in the development of thromboembolic complications (TEC) in patients with pelvic malignancies. Materials and methods. A retrospective-prospective cohort study with a control group was conducted. It included 546 patients with malignant neoplasms of the pelvic organs, as well as a control group of 137 patients with benign tumors. The patients were divided into three groups: I (n=155) – patients with TEC; II (n=391) – patients without TEC; control group (n=137). Laboratory studies were performed to detect antiphospholipid antibodies (anti-β2-glycoprotein (β2GPI), anti-annexin V, and anti-prothrombin), and genetic tests using PCR were performed to detect FV Leiden, MTHFR C677T, prothrombin G20210A mutations, PAI-1 4G/5G and platelet glycoprotein polymorphisms (GPIIb/IIIa, GPIa/IIa, GPIb, and GP ADP). Results. Group I was found to have a significantly higher frequency of antiphospholipid antibodies (aPL) circulation (55.8%) and genetic markers of thrombophilia: FV Leiden mutation (20,6%), homozygous MTHFR C677T (41,3%), PAI-1 gene polymorphism (28,4%) and platelet glycoprotein (44,5%). In group II, a moderate frequency of aPL circulation was observed: to β2GPI (13,1%), prothrombin (7,8%) and annexin V (2,6%). The FV Leiden mutation was detected in 9,7% of patients, the homozygous form of the MTHFR C677T in 6,1%, the PAI-1 gene polymorphism in 9,7%, and platelet glycoprotein in 10,2%. In the control group: aPL to β2GPI and annexin V were present in 2,6% of patients, the FV Leiden mutation – in 10,2%, the homozygous form of the MTHFR C677T – in 7,3%, the PAI-1 gene polymorphism – in 10.9% and platelet glycoprotein – in 8,8%. Conclusion. The study confirmed the significant contribution of genetic and acquired thrombophilia to the development of thrombotic complications in patients with gynaecological cancer. The highest risk was observed in cases involving a combination of genetic mutations and aPL.

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