Full Text
Abstract
Introduction. Thrombophilic mutations and polymorphisms are ethiopathological triggers of reproductive losses and pregnancy complications: intrauterine fetal growth restriction, preeclampsia, premature abruption of normally located placenta. Implantation, trophoblast invasion and further placental functioning are objectively impaired in the presence of genetic coagulation defects.
Aim: to assess the prevalence and role of congenital thrombogenic mutations and polymorphisms and their combinations in the genesis of fetal loss syndrome in women of Kursk region for 2012–2017.
Materials and methods. We studied clinical and anamnestic characteristic, placental morphology, prevalence of genetic polymorphisms in folate cycle and hemostasis in women with fetal loss syndrome (one or more spontaneous miscarriages or undeveloped pregnancies for 10 or more weeks; stillbirth; neonatal death; 3 or more spontaneous miscarriages up to 8 weeks of embryonic development) in Kursk region.
Results. Our study showed that 3 and more thrombophilic polymorphisms (mainly genes of the folate cycle) were revealed in 60% women with early pregnancy losses in this region (р=0,001). The presence of 2 polymorphisms (mainly genes of the folate cycle and plasminogen activator inhibitor-1) were characteristic of patients with reproductive losses in the second half of pregnancy (р=0,001).
Conclusion. It is necessary to develop individual approaches to the management of women with fetal loss syndrome in Kursk region.
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