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Aim: to evaluate the effectiveness of using low molecular weight heparin (LMWH) and low-dose acetylsalicylic acid (ASA) in preventing recurrence of early and late fetal growth retardation (FGR) in patients with antiphospholipid syndrome (APS) and/or genetic thrombophilia.Materials and Methods. A prospective randomized controlled study was conducted by examining 32 patients aged 23 to 43 years with a history of early and late II and III FGR as well as thrombophilia. Prevention protocol using LMWH and ASA was carried out from the pregravid period or early pregnancy. The control group included 35 women with uncomplicated pregnancy. Antiphospholipid antibodies (APA) were measured according to the Sydney antiphospholipid syndrome (APS) criteria by using enzyme immunoassay (ELISA): cardiolipin, β2-glycoprotein 1 and additionally antibodies to annexin V, prothrombin, etc. (IgG/IgM isotypes); lupus anticoagulant – by a three-stage method with Russell's viper venom; antithrombin III and protein C levels – by chromogenic method; prothrombin gene polymorphisms G20210A as well as factor V Leiden polymorphism – by chain reaction; homocysteine – by ELISA.Results. It was found that prevention protocol was effective in 78.1 % cases. FGR re-developed in 7 (21.9 %) pregnant women: in 2 (6.3 %) at 20 and 22 weeks, in 3 (9.4 %) at 30–32 weeks, in 2 (6.3 %) after 34 weeks of pregnancy. All these patients were found to have APA exceeding 40 U/ml with low dynamics of decline, 3 (9.4 %) were older than 35 years, 2 (6.3 %) had chronic kidney pathology and 1 (3.1 %) had a hypertension in the anamnesis.Conclusion. The use of LMWH and low-dose ASA starting from the pre-pregnancy period and early pregnancy as a part of complex therapy allows to effectively prevent re-development of FGR in patients with thrombophilia. In case of high APA titers, the use of LMWH and low-dose ASA may be ineffective, and alternative treatment methods in addition to anticoagulant therapy should be used to improve obstetric results.

Aim: to study the role of antiphospholipid antibodies (AРA) and genetic thrombophilia as a potential cause of the development or a component in the pathogenesis of early and late fetal growth retardation (FGR).Materials and Methods. There was conducted a prospective randomized controlled trial with 118 women enrolled. The main group consisted of 83 patients, whose pregnancy was complicated by FGR degrees II and III, stratified into two groups: group 1 – 36 pregnant women with early FGR, group 2 – 47 pregnant women with late FGR. Women were subdivided into subgroups according to the FGR severity. The control group consisted of 35 pregnant women with a physiological course of pregnancy. АРА were determined according to the Sydney antiphospholipid syndrome criteria by enzyme immunoassay (ELISA): against cardiolipin, β2 -glycoprotein 1, annexin V, prothrombin, etc. (IgG/IgM isotypes); lupus anticoagulant – by the three-stage method with Russell's viper venom; antithrombin III and protein C levels – by chromogenic method; prothrombin gene polymorphisms G20210A and factor V Leiden – by polymerase chain reaction; homocysteine level – by ELISA.Results. AРA circulation (medium and high titers), genetic thrombophilic defects and/or hyperhomocysteinemia were detected in 40 (48.2 %) patients with FGR, which was significantly higher than that in the control group (p < 0.05): in group 1 (41.7 % of women) AРA (30.6 %) and AРA with genetic thrombophilia or hyperhomocysteinemia (11.1 %) were revealed; in group 2 (51.1 % of women) AРA (21.3 %), AРA with hyperhomocysteinemia (4.3 %), genetic thrombophilia (25.5 %), and due to hyperhomocysteinemia (2.1 %) were found. No differences in prevalence of thrombophilia rate in patients were observed related to FGR severity, but a correlation between the FGR severity and AРA titers was found.Conclusion. Testing for the presence of AРA, genetic thrombophilia and hyperhomocysteinemia should be recommended for patients with FGR (including those with FGR in medical history), especially in the case of its early onset. It is recommended to determine the full AРA spectrum.

Aim: to analyze current literature sources on endometriosis-associated cancer (ЕАС) in gynecology.Materials and Methods. We searched for publications in the international scientific databases: eLibrary, Google Scholar, ScienceDirect, Cochrane Library, PubMed/MEDLINE and clinical research registries. For this systematic analysis, only full-text publications were used. We evaluated the reliability of evidence and the methodological quality of the studies. The data on the modern approach to the therapy and rehabilitation of women with external genital endometriosis (EGE) are presented. Search terms for publications in Russian and English were used: «endometriosis», «endometriosis-associated ovarian neoplasia», «oncology», «rehabilitation».Results. Despite the fact that EGE is considered a benign disease, there is a risk for its malignant transformation. However, the pathogenesis and pathomorphological mechanisms of ЕАС are not yet fully understood.Conclusion. Active management of the rehabilitation period for women with EGE provides an opportunity for early diagnosing recurrences that will provide early diagnostics ovarian ЕАС and improve the main indicators of the quality of life for such patients.

The novel coronavirus epidemic is characterized by high rates of morbidity and relatively high mortality. Laboratory test results in patients include leukopenia, an increase in liver function tests and ferritin levels reaching hundreds, and sometimes thousands of units. These data remind us about the macrophage activation syndrome (MAC). Secondary hemophagocytic lymphohistiocytosis syndrome, MAC, which pathogenesis is based on a defect in the mechanisms of T-cell cytotoxicity and decreased level of natural killer cells associated with the defect in the perforin-encoding gene as well as hyperproduction of a number of cytokines – interleukin (IL)-1â, tumor necrosis factor-á, etc. by T-lymphocytes and histiocytes, indirectly leading to the activation of macrophages and production of proinflammatory cytokines, in particular IL-6 hyperproduction. MAC is one of "hyperferritinemic syndromes". These disorders have similar clinical and laboratory manifestations, and they also respond to similar treatments, suggesting that hyperferritinemia may be involved in the overall pathogenesis and is characterized by elevated ferritin level and cytokine storm. Despite the fact that data on the immune and inflammatory status in patients with COVID-19 have only started to appear, it is already clear that hyperinflammation and coagulopathy affect the disease severity and increase the risk of death in patients infected with SARS-CoV-2. Hence, understanding the pathogenesis of the novel coronavirus infection can help in its early diagnostics and treatment.

Fetal growth retardation (FGR) is a complication of pregnancy that determines perinatal morbidity and mortality. It is a complex and multifaceted medical problem that does not lose its relevance. Impaired fetal development and delayed growth result from various etiopathogenesis of pathological processes occurring in the "mother–placenta–fetus" interface. Thrombophilia is one of the factors that can initiate disturbed placental function and the utero-placental blood flow. Here we describe the clinical FGR variants and etiopathogenetic factors of developing this complication of pregnancy (placental, maternal, and fetal). Special attention is paid to genetic and acquired thrombophilia (due to the circulation of antiphospholipid antibodies) and their role in development of such complication of pregnancy.

Thrombophilia might be the essential pathogenetic mechanism of thromboembolism associated with pregnancy. Venous thromboembolism during or after assisted reproductive technologies is predicted to emerge due to increased number of women undergoing this technique. Low molecular weight heparins was effective for preventing recurrent thromboembolism and severe obstetric complications. Women with personal or family history of thromboembolism or with history of obstetric complications should be screened for thrombophilia.

Combined thrombophilia is known as a probable cause of recurrent in vitro fertilization (IVF) failures. The present clinical case demonstrates the importance of considering the possibility of inherited or acquired thrombophilia in patients under the preparation for IVF. Thromboses of rare locations (hepatic vein, splenic vein, mesenteric vein, ovarian vein, retinal vein, cerebral vein, portal vein, axillary and subclavian vein) are life-threatening conditions. Most often thrombosis of atypical location develops in patients with inherited hemostatic defects, e.g. genetic thrombophilia. Such thromboses can also result from acquired abnormalities of hemostasis, which include antiphospholipid syndrome, pregnancy-associated hypercoagulability, IVF, oral contraception, or ovarian hyper-stimulation within IVF procedures.