Open AccessThrombophilia identified as a risk factor for thrombogenesis in cancer patients
Author(s) -
А. В. Воробьев,
Alexander Makatsariya,
В. О. Бицадзе,
А. Г. Солопова,
D. A. Ponomarev
Publication year - 2021
Publication title -
akušerstvo, ginekologiâ i reprodukciâ
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.124
H-Index - 4
eISSN - 2500-3194
pISSN - 2313-7347
DOI - 10.17749/2313-7347/ob.gyn.rep.2021.232
Subject(s) - medicine , thrombophilia , methylenetetrahydrofolate reductase , gynecology , gastroenterology , cancer , ovarian cancer , oncology , thrombosis , gene , genetics , biology , genotype
Aim: to assess a rate and range of genetic and acquired thrombophilia in onco-gynecologic patients with ovarian cancer, uterine corpus cancer and cervical cancer. Materials and Мethods. A prospective controlled cohort non-randomized interventional study was conducted: within the years 2014 to 2020, there were examined 546 women with genital malignancies, divided into 2 groups: group I – 155 cancer patients with former thrombosis, group II – 391 women with female genital cancer without former thrombotic complications. Control group consisted of 137 patients with benign female genital tumors. The spectrum of circulating APA was studied: antibodies to â 2 -glycoprotein I (â 2 -GPI), annexin V and prothrombin as well as genetic thrombophilia due to mutations genes encoding factor V Leiden, methylenetetrahydrofolate reductase (MTHFR) including polymorphism in genes for prothrombin, platelet glycoproteins and plasminogen activator inhibitor-1 (PAI-1). Results. It was found that frequency of circulating APA as well as incidence rate of genetic thrombophilia between cancer patients from group I vs. group II significantly differed: APA in group I vs. group II was 86 (55.5 %; p < 0.01) vs. 92 (23.5 %) compared to 7 (5.1 %) in control group. Genetic thrombophilia was dominated in group I by mutated MTHFR (92.9 %), polymorphismin PAI-1 (28.4 %) and platelet glycoprotein (44.5 %) that were significantly higher (p < 0.05) compared to group II and control group. Hence, it allows to suggest that such identified thrombophilia markers are largely associated with a risk of developing thrombotic complications. Conclusion. Detected high percentage of patients with circulating APA and genetic thrombophilia among cancer patients with former thromboembolic complications corroborate a role for genetic and acquired thrombophilia in developing pre-thrombotic condition. Detecting a range of circulating APA and genetic thrombophilia allows to identify patients who might be referred to a high risk of thrombogenesis and require to preventive application of anticoagulant therapy.