Polycystic ovarian syndrome: current understanding of pathogenesis, diagnosis and treatment

Review article is devoted to one of the most common polygenic endocrinopathies in women of reproductive age, polycystic ovarian syndrome (PCOS). We review the current criteria used to make a correct diagnosis based on four phenotypes of PCOS: Frank (phenotype A) – biochemical and/or clinical hyperandrogenism, oligo-/anovulation, polycystic ovarian morphology according to ultrasound; anovulatory (phenotype B) – oligo-/anovulation, biochemical and/or clinical hyperandrogenism; ovulatory (phenotype C) – biochemical and/or clinical hyperandrogenism, polycystic ovarian morphology according to ultrasound; non-androgenic (phenotype D) – oligo-/anovulation, polycystic ovarian morphology according to ultrasound. This article presents the main theories of PCOS pathogenesis: peripheral, central, insulin, genetic, and also considers epigenetic factors. PCOS is a multifactorial disease in which genes are responsible for the mechanisms of the process, and environmental factors through epigenetics affect the genetic material. PCOS phenotypes play an important role in clinical practice, as they allow an individualised approach to the selection of therapy in each case, taking into account the pathogenesis of the disease and predicting its course in the future. The main therapeutic options for treating patients with PCOS, taking into account the multifactorial nature of the disease and the patient's interest in pregnancy, are reviewed. The article presents modern methods for the correction of hyperandrogenism and anovulation, with special emphasis on the need for progesterone therapy

The use of combined hormonal contraception in the context of the COVID-19 pandemic

Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV2) was declared the cause of a global pandemic in early 2020. Patients with COVID-19 are at high risk for thrombotic occlusions of the arteries and veins. There are many ways that explain the high risk of thrombosis in COVID-19, they are conditionally divided into two main categories: mechanisms in which the renin-angiotensinaldosterone system is involved and mechanisms that affect the regulation of the immune response. It is assumed that the uncomplicated course of the disease is characterized by endothelial dysfunction, but if the process progresses with a pronounced immune response, plasma coagulation factors may also be involved, which significantly increases the risks of thromboembolic complications. The use of combined hormonal contraception (CHC) in the current conditions raises a number of concerns. According to some researchers, disorders of the hemostasis system observed in patients with COVID-19 may worsen while taking CHC and increase the risk of thromboembolic complications, which is especially important in severe disease with prolonged immobilization. However, with the use of CHC, the increase in thrombotic risks is explained primarily by changes in the plasma component of the hemostasis sys tem. At first glance, the recommendations to stop hormone therapy with confirmed COVID-19 seem logical, but they are based only on the procoagulant activity of estrogens, and not on real evidence. In patients with COVID-19, the increase in coagulation is associ ated with massive damage to the vascular endothelium (the so-called «external» coagulation pathway) and the immune response, and not with a primary increase in the level of coagulation factors per se. At the same time, stopping the intake of estrogens deprives the patient of their important protective effect. Thus, it became necessary to develop clinical guidelines for the management of women using contraception in the context of the COVID-19 pandemic