The severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) caused a new coronavirus disease (COVID-19), which is highly contagious and its pathogenesis has not been fully elucidated. In COVID-19, the inflammation and blood coagulation systems are excessively activated. SARS-CoV- 2 damages endothelial cells and pneumocytes, which leads to disruption of hemostasis in SARS. Thromboembolism is the main cause of mortality in patients with COVID-19. Clots, including pulmonary embolism (PE) and deep vein thrombosis (DVT), ranging from minor to fatal complications of the SARS-CoV-2 infection are known. Individuals with pre-existing diseases are more susceptible to the development of blood clots and poor outcomes. High levels of circulating cytokines and D-dimer (DD) are influential biomarkers of poor outcomes in COVID-19. The latter occurs as a result of hyperfibrinolysis and hypercoagulation. Plasmin is a key player in fibrinolysis and is involved in the cleavage of many viral envelope proteins, including SARS-CoV. Due to this function penetration of viruses into the host cell occurs. In addition, plasmin is involved in the pathophysiology of acute respiratory distress syndrome (ARDS) in SARS and promotes the secretion of cytokines, such as IL-6 and TNF, from activated macrophages. The focus of existing treatment to alleviate fibrinolysis in patients with COVID-19 is the use of systemic fibrinolytic therapy given thrombotic pathology in severe forms of COVID-19 which may lead to death. However, fibrinolytic therapy may be harmful in the advanced stages of COVID-19, when the status of disseminated intravascular coagulation (DIC) changes from suppressed fibrinolysis to its enhancement during the progression of the disease. This narrative review aims to elucidate the pathogenesis of COVID-19, which will further help in precise diagnosis and treatment.

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Еритропоетична протопорфірія (ЕПП) є рідкісним спадковим захворюванням, зареєстрованим в усьому світі, проте існують регіональні відмінності у його епідеміології. Хвороба спричиняється частковим дефіцитом ферохелатази, яка є останнім ферментом шляху біосинтезу гему. При типовій ЕПП світлочутливість з'являється вже після першого перебування в ранньому дитинстві на сонці. У 20-60% пацієнтів з ЕПП спостерігається мікроцитарна анемія, яку помилково первинно діагностують як залізодефіцитну анемію, a тому призначають залізовмісні ліки.

An increase in the hypogalactia frequency diagnosis in breastfeeding mothers is one of the world-spread medical and social problems and is especially high in women with risk factors of lactation disorders. Early estimation of risk factors creates opportunities for physicians to diagnose the lactation problem that mothers face and solve it.