External genital endometriosis is one of the most common gynecological proliferative diseases. The disease development is based on molecular and genetic disorders that occur in women and are the result of the cell response to oxidative stress. In endometriosis the polymorphism of genes of detoxification systems, depletion of antioxidant defense mechanisms due to hormonal imbalance and activity of pro−inflammatory processes are called the causes of oxidative stress. Currently, much attention is paid to aspects of the immune system and local peritoneal factors. To develop diagnostic criteria for the stages of external genital endometriosis by determining the activity of enzymes of the antioxidant system and catalase in serum and peritoneal fluid, a study was performed in 86 patients. The research results showed that in external genital endometriosis of stages I−II in the serum of women the catalase activity increased, and that of superoxide dismutase remained at the physiological level. Determination of the studied enzymes in peritoneal fluid indicates that their parameters correspond to the control values in women without endometriosis. Thus, the study showed that the patients experience multidirectional changes in antioxidant system, which are manifested in increased catalase activity at the systemic level at the disease stages I−II and local one at stages III−IV. At the same time, the activity of superoxide dismutases at all stages of the disease in both serum and peritoneal fluid is normal. The state of the antioxidant system is concluded to depend on the peculiarities of micronutrient metabolism. Further study and correction of its possible disorders may positively affect in preventing and treatment of external genital endometriosis in women. Key words: external genital endometriosis, antioxidant system, diagnostics.
Excessive activation of blood coagulation, imbalance in coagulation potential, presence of endotheliopathies, local hemorrhages and microthrombi in the area of blastocyst invasion may be common in the mechanism of implantation losses in thrombophilia. One of the ways to optimize the results of extracorporeal fertilization is the prevention of thrombotic complications. Despite the achievements of modern morphology, some issues concerning the pathogenesis of infertility and habitual miscarriage remain poorly understood. To assess the system of hemostasis in women with thrombophilia as one of the causative factors of unsuccessful attempts in extracorporeal fertilization, a study of 63 patients was conducted, which included hormonal, genetic studies, HLA−typing, ultrasonography, hysterosalpingography, determination of infectious profile and was performed depending on clinical situation. The study of the hemostasis system included the determination of total coagulation potential, analysis of primary hemostasis, fibrinolytic system, the state of intravascular hemocoagulation and antiplasmin potential of blood. The state of intravascular hemocoagulation was assessed by the concentration in blood plasma of pathological hemocoagulants, i.e. soluble complexes of fibrin monomers and fibrinogen−fibrin degradation products. The results of the study showed that in women with a thrombophilia history and unsuccessful attempts in extracorporeal fertilization, there is a pathological activation of the hemostasis system, which plays a significant role in the pathogenesis of unsuccessful fertilization attempts. In thrombophilia, a subclinical form of chronic disseminated intravascular coagulation develops, the leading link in the development of which is the activation of platelet−vascular hemostasis with subsequent involvement into the process of coagulation potential due to a decrease in the anticoagulant blood system. Key words: thrombophilia, hemostasis system, extracorporeal fertilization, infertility.
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