Objective. To evaluate the efficiency of antithrombotic therapy to prevent repeated preeclampsia in patients with thrombophilia. Subject and methods. A prospective clinical study was conducted 66 patients with thrombophilia (genetic, acquired or concomitant) and with history of preeclampsia: 35 patients addressed and were followed since fertile cycle (subgroup Ia) and 31 patients addressed during pregnancy and were followed since 6-13 weeks of gestation – IIa subgroup. Control group – 50 patients without both obstetrics and gynecology and thrombotic complications in history. Therapy included LMWG (klexan), B vitamins, antioxidants and micronized progesterone. Results. The all period of pregnancy, obstetric and perinatal outcomes were better in patients receiving therapy since fertile cycle compared with group of patients whose therapy was initiated during pregnancy.Conclusion. To prevent re-PE at a subsequent pregnancy, the therapy should be start since fertile cycle, continuing during pregnancy, childbirth and the postpartum period. Therapy should include LMWH, B vitamins, antioxidants and micronized progesterone.

In spite of existing standards of hemorrhages prophylaxis maternal death from massive obstetric bleeding remains the main cause of maternal mortality in developing countries and even occurs in developed countries. The main risk factors of obstetrical bleedings are well known: placental abruption, placenta previa, uterus hypotonia, uterine rupture, amniotic fluid embolism, preeclampsia. However, these are only the tip of the iceberg. What is really assumed as a basis of majority of massive obstetric hemorrhages? From our view genetic thrombophilia, APS and hyperhomocysteinemia may be the etiopathogenetic risk factors of placental abruption, preeclampsia and respectively can be the cause of not only thromboembolic but hemorrhagic complications as well.

Pathogenesis of thrombotic complication caused by hormone replacement therapy and influence of HRT on risk of venous and arterial thrombosis are reviewed. Questionable points of prophylaxis of thrombotic complication of hormone replacement therapy are discussed.

Not only thrombotic, but also “non-thrombotic” mechanisms of antiphospholipid antibodies are being actively studied in regard to their impact on the structure of reproductive losses and other complications of pregnancy. Non-thrombotic effects of APA include the damage of cells, the induction of apoptosis, the inhibition of proliferation, the suppression of human chorionic gonadotropin, the interference to the invasion of the trophoblast, and defects
of differentiation of the endometrium. Thrombotic effects are: widespread thrombosis, placental infarction, disruption of the annexin barrier, and anti-b2GPI and APC resistance.

The pathophysiology of HELLP syndrome is not well defined. Nowadays endothelial dysfunction if considered the key moment of the development of HELLP-syndrome. Endothelial cell dysfunction results in hypertension, proteinuria, and increased platelet activation and aggregation. Furthermore, activation of the coagulation cascade causes consumption of platelets due to adhesion onto a damaged and activated endothelium, in addition to microangiopathic hemolysis caused by shearing of erythrocytes as they traverse through capillaries laden with platelet-fibrin deposits. Multiorgan microvascular injury and hepatic necrosis causing liver dysfunction contribute to the development of HELLP.

Significant biochemical role of magnesium in the body is well-known, as well as good proven clinical efficacy of magnesium in obstetrics and gynecology. Magnesium preparations, in particular magnesium sulfate, are recommended as the treatment of choice for premature birth, pre-eclampsia and eclampsia. There is evidence and its neuroprotective effects on the fetus. Restricts the use of magnesium sulfate possibility of overdose with serious side effects. Reduce the risk of overdose can be minimized using standard protocols, independent double-check, monitoring the patient’s
condition. Magnesium sulfate therapy, as a means of emergency, cannot compensate for a deficiency of magnesium, which is associated with the development of obstetric pathologies such as threatened miscarriage, premature birth, placental insufficiency, preeclampsia, thrombophilia, premenstrual syndrome (PMS), the appointment of combined oral contraceptives (COCs) and hormone replacement therapy (HRT), climacteric syndrome. Justified use of organic salts of magnesium orally – along with better bioavailability they do not lead to serious side effects in overdose. Using organic
magnesium salts to control magnesium deficiency and related symptoms is also shown at the ICP, and the appointment of COCs HRT during menopause. The use of magnesium citrate is the most preferred because citrate anion causes high bioavailability of magnesium, it is also required in the Krebs cycle and recycled into carbon dioxide and water. This
makes it an ideal transporter of magnesium into cells.

Progesterone is a natural female hormone. Called “the pregnancy hormone,” it is essential before and during pregnancy. After ovulation occurs, the ovaries start to produce progesterone needed by the uterus. Progesterone causes the uterine lining or endometrium to thicken. This helps prepare a supportive environment in your uterus for a fertilized egg.A supply of progesterone to the endometrium continues to be important during pregnancy. Following a successful implantation, progesterone helps maintain a supportive environment for the developing fetus.

Thromboembolism represents the most serious, potentially fatal complication of assisted reproductive technologies and in most cases is associated with ovarian hyperstimulation syndrome. This article describes the modern aspects of the pathogenesis of ovarian hyperstimulation syndrome, the pathogenesis of thromboembolic complications
and importance of genetic and acquired thrombophilia for their development, methods of risk assessment of thrombotic complications before using assisted reproductive technology and recommendations for prevention of thromboembolic complications in women enrolled in an IVF program.

Thrombosis of unusual sites (hepatic vein thrombosis, splenic vein thrombosis, mesenteric vein thrombosis, ovarian vein thrombosis, retinal vein thrombosis, cerebral vein thrombosis, portal vein thrombosis, axillary and subclavian vein thrombosis) are life-threatening disorders that often goes unrecognized. Most often thrombosis of
atypical locations develops in patients with inherited hemostasis defects - genetic thrombophilia. Thrombosis of unusual sites often accompany acquired abnormalities of hemostasis, which include antiphospholipid syndrome, hypercoagulability associated with pregnancy, oral contraceptives use, malignant tumors, in conditions of ovarian
hyperstimulation in IVF programs. In case of thrombosis of unusual sites screening for hereditary forms of thrombophilia and antiphospholipid syndrome should be performed and timely administration of anticoagulant therapy is critical. Analysis of genetic and acquired abnormalities of hemostasis allows you to select a group of patients requiring longterm anticoagulation therapy and mandatory anticoagulant prophylaxis in situations with a high risk of thromboembolic complications (pregnancy, surgery).

Pathogenesis, differential diagnostics and treatment strategies of different types of thrombocytopenias are reviewed. Two major mechanisms responsible for development thrombocytopenia might be distinguished – decreased production and increased consumption of platelets. Decline of platelet production due to the depression of megakaryocytes (productive thrombocytopenia) is usually associated with aplastic anemia, different forms of leukemia and myelodysplasia, or cytostatic therapy. Increased consumption might be induced by auto- and/or alloantibodies which bind to platelets and stimulate their rapid removal by the reticuloendothelial system of spleen and liver (idiopathic thrombocytopeniс purpura, drug-induced thrombocytopenia, neonatal alloimmune thrombocytopenic purpura and other forms of immune
thrombocytopenia). Enhanced consumption of platelets due to the intravascular thrombosis leads to the thrombocytopenia (consumptive nonimmune thrombocytopenia) in disseminated intravascular coagulation syndrome, thrombotic thrombocytopenic purpura and haemolytic uremic syndrome. Hereditary forms of thrombocytopenia are caused by congenital defects of platelet production and/or maturation and anomalies of von Willebrand factor. Many of them are also associated with the impaired platelet morphology and function. Defective platelet production is considered as a cause of low platelet count in the majority of hereditary thrombocytopenias (pure familial thrombocytopenia. TAR syndrome, and others) but in some of them the increased consumption has been detected or proposed (Wiscott-Aldrich syndrome, platelet type and type IIb von Willebrand disease, Bernard-Soulier syndrome). Laboratory methods used for the differential diagnostics of thrombocytopenias include: determination of platelet count by automatic counting and microscopy, analysis of megakaryocytes in the bone marrow, investigation of platelet morphology and function, detection of platelet autoantibodies and analysis of target antigens, determination of platelet life span and turnover. Different strategies (among them platelet transfusion, immunosuppressive and cytostatic therapy, antithrombotic therapy, splenectomy and others) are  recommended for the treatment of productive, consumptive (immune and nonimmune
forms) and hereditary thrombocytopenias.

Pregnancy and childbirth in women with genetic or acquired thrombophilia is usually associated with a high risk to both thrombotic and obstetric complications and fruit. Unambiguous answer to the question of routine screening for thrombophilia in women with a history of obstetric history does not exist until now. It should be noted that the physiological hypercoagulable inherent pregnant, often for the first time reveals the background congenital and / or acquired disorders of hemostasis, which previously could be asymptomatic. A history of fetal loss syndrome, severe obstetric complications (severe preeclampsia, severe  twin-platsentranoy failure, fetal death, premature detachment of the placenta), thromboembolism is an indication for the study of genetic thrombophilia and antiphospholipid syndrome.

The article considers the historical aspects of life, medical and scientific activities of the Austrian gynecologist Ernst Wertheim. Describes his invaluable contribution to the operational cancers.

The article describes the concept of monochorionic multiple pregnancies, the relevance and epidemiology of the topic, as well as complications in pregnancy and delivery in monochorionic twins.

A clinical lecture presents the current management of multiple pregnancies, modern diagnostics and treatment of complications in this high risk group of patients. A different approaches to management of multiple pregnancies according to chorionicity, early diagnosis of specific complications is necessary for improving neonatal outcomes.

The clinical lection describes current views about pathogenesis of thrombotic complications in cancer patients. At the same time the risk of iatrogenic thrombophilia under the conditions of radio-, chemotherapy and hormone replacement therapy is considered. Issues concerning scientific explanation of antithrombotic prophylaxis with LMWH are given.