scholarly journals ПОРІВНЯЛЬНІ ВІДМІННОСТІ ПРОСТОРОВОЇ РЕОРГАНІЗАЦІЇ ПЛАЦЕНТ У ЖІНОК ІЗ СИНДРОМОМ ВТРАТИ ПЛОДА БЕЗ КОРЕКЦІЇ ТА НА ФОНІ МЕДИКАМЕНТОЗНОГО ЛІКУВАННЯ

Author(s):  
L. M. Malanchuk ◽  
G. O. Krivitska ◽  
S. L. Malanchuk ◽  
V. М. Martinyuk

Fetal loss syndrome is a polyethyologic syndrome. In the genesis of reproductive losses, great importance is given to the inferior transformation of the endometrium and to the disturbance of trophoblast invasion processes. Study of changes in the placenta inherent in the fetal loss syndrome will allow to understand the pathogenesis of syndrome formation, to reveal the role of the vascular factor in the development of degenerative changes and to choose pathogenetically valid correction of the revealed disorders.The aim of the study – to compare the macro and microscopic structure of the placenta of women with fetal loss syndrome without additional correction and against the background of the proposed medical treatment.Materials and Methods. 100 placenta examination (group I formed 50 placenta of women who received medical therapy were performed, provided by the provisions of the clinical protocols of the Ministry of Health of Ukraine, group II – placenta mothers, who during the pregnancy additionally appointed a donor of nitric oxide and the drug of vitamin B9).Results and Discussion. In the visual assessment and investigation of the histological structure of the placenta of the I group, we have been detected various pathological changes that are characteristic of the dystrophic-degenerative processes. In the second group placenta is noted reduction of pathological manifestations and activation of adaptive-compensatory processes.Conclusions. Integrated therapy using a nitric oxide dopant and vitamin B9 helps to improve metabolic processes in the fetoplacental system.

2010 ◽  
Vol 76 (17) ◽  
pp. 5736-5744 ◽  
Author(s):  
Heidi M. Luter ◽  
Steve Whalan ◽  
Nicole S. Webster

ABSTRACT A disease-like syndrome is currently affecting a large percentage of the Ianthella basta populations from the Great Barrier Reef and central Torres Strait. Symptoms of the syndrome include discolored, necrotic spots leading to tissue degradation, exposure of the skeletal fibers, and disruption of the choanocyte chambers. To ascertain the role of microbes in the disease process, a comprehensive comparison of bacteria, viruses, fungi, and other eukaryotes was performed in healthy and diseased sponges using multiple techniques. A low diversity of microbes was observed in both healthy and diseased sponge communities, with all sponges dominated by an Alphaproteobacteria, a Gammaproteobacteria, and a group I crenarchaeota. Bacterial cultivation, community analysis by denaturing gradient gel electrophoresis (Bacteria and Eukarya), sequencing of 16S rRNA clone libraries (Bacteria and Archaea), and direct visual assessment by electron microscopy failed to reveal any putative pathogens. In addition, infection assays could not establish the syndrome in healthy sponges even after direct physical contact with affected tissue. These results suggest that microbes are not responsible for the formation of brown spot lesions and necrosis in I. basta.


2020 ◽  
pp. 247-249
Author(s):  
V.O. Potapov

Background. At the menstrual cycle beginning there is a proliferation of endometrial cells under the influence of oestrogen, and in the second half, after ovulation there is a differentiation and hypertrophy of cells under the influence of corpus luteum progesterone. Lutein phase deficiency (LPD) can be divided into 3 types: lack of progesterone production (corpus luteum is absent), low progesterone level (corpus luteum hypofunction), and reduction of progesterone production period (short period of corpus luteum existence, luteal phase duration <11 days). Objective. To describe the role of nitric oxide (NO) donors in women with LPD. Materials and methods. Analysis of literature data on this issue. Results and discussion. The main adverse outcome of LPD is the absence or defective transformation and reception of the endometrium required for successful fertilization of the egg. In case of progesterone deficiency, the depth of trophoblast invasion decreases, resulting in abnormal placental development and inadequate uteroplacental blood flow. The latter can further lead to antenatal foetal death and miscarriage, preeclampsia and eclampsia, placental dysfunction. LPD should be suspected in patients with infertility, abnormal uterine bleeding, severe premenstrual syndrome, endometrial hyperplasia, and habitual miscarriage. Ultrasound signs of LPD include the absence of a dominant follicle, absence of ovulation in the presence of a mature follicle (persistence), absence of corpus luteum in the 2nd phase of the cycle, endometrial thickness in the secretion phase <9 mm, increased echogenicity only in the peripheral parts of the endometrium or three-layered endometrium. Functional tests for the detection of LPD include the basal temperature measurement and examination of smears (hypolutein type of smear, preservation of the symptom of cervical mucus crystallization in the 2nd phase of the cycle). A key element of pregravid preparation for women with LPD is the progesterone donation (in oil solution, in etiloleate or micronized). The therapeutic efficacy of different commercial progesterone drugs is the same. Progesterone helps to prepare the endometrium for trophoblast invasion and promotes uterine hypotension. Incomplete secretory transformation of the endometrium during the treatment with progesterone drugs occurs in case of inadequate blood supply to the endometrium due to low density of functional vessels or insufficient content of NO in the endometrium. Back in the late 90’s of last century, it was shown that NO acts as a powerful uterine relaxant, and reduction of its concentration leads to miscarriage. In humans, NO is produced from L-arginine, however, obtaining the required dose of the latter with food is not always possible. When L-arginine (Tivortin aspartate, “Yuria-Pharm”) is used as a NO donor, peripheral vascular dilatation and neoangiogenesis occur, which improves blood supply and endometrial trophic processes; stimulation of gene transcription and cell cycle, which increases the cell population and physiological thickness of the endometrium; regulation of sex hormone synthesis and expression of their receptors, which increases the receptivity of the endometrium. The regimen of Tivortin aspartate administration is the following: 5 ml (1 g) 6 times per day during the menstrual cycle. According to the results of our own study, L-arginine increases the biological effect of progesterone on the endometrium, promotes a more successful restoration of its physiological structure and thickness in women with LPD. The inclusion of L-arginine in the pregravid preparation of women with LPD showed a 1.9-fold decrease in the infertility incidence, a 3.3-fold increase in the number of pregnancies and births, and a 3.4-fold decrease in the number of miscarriages. Conclusions. 1. The main adverse outcome of LPD is the absence or defective transformation and reception of the endometrium required for successful fertilization of the egg. 2. Usage of L-arginine (Tivortin aspartate) as a donor of NO promotes dilatation of peripheral vessels and neoangiogenesis, stimulation of the cell cycle, regulation of the synthesis of sex hormones. 3. Inclusion of L-arginine in the pregravid preparation of women with LPD leads to the decrease in infertility, to the increase in the number of pregnancies and births and to the decrease in the number of miscarriages.


2018 ◽  
Vol 46 (8) ◽  
pp. 893-899 ◽  
Author(s):  
Svetlana Akinshina ◽  
Alexander Makatsariya ◽  
Victoria Bitsadze ◽  
Jamilya Khizroeva ◽  
Nadine Khamani

Abstract Background Despite intensive research, thromboembolism still accounts for significant maternal morbidity and mortality. We examined thrombophilia in patients with thromboembolism during pregnancy and evaluated the efficiency of antithrombotic prophylaxis in patients with thrombophilia for the prevention of recurrent thromboembolism. Materials and methods Sixty-eight women with a history of thromboembolism were managed during pregnancy, in light of their thrombotic history and the result of thrombophilia assessment. Group I (n=50) received prophylaxis with low molecular weight heparin (LMWH)±aspirin (50–100 mg/day) in preconception period or from the 1st trimester, during pregnancy and at least 6 weeks postpartum. Group II (n=18) received LMWH±aspirin from the II to III trimester. Results Thromboses were associated with pregnancy in 27 patients (39.7%), with systemic diseases – in nine (13.2%), oral contraceptives use – 22 (32.3%), immobilization due to surgery and/or trauma, long flight – six (8.9%), septic complications – two (2.9%). Nevertheless, 24.5% of patients had no apparent provoking factor for the development of thrombotic complications. Thirty-seven (54%) patients with venous thromboembolism (VTE) had familial history of VTE, and 25 (36.7%) had personal history of pregnancy complications (fetal loss syndrome, preeclampsia and placental abruption) (P<0.05 vs. control). Thrombophilia was detected in 58 (85.3%). Usual thrombogenic polymorphisms [factor V (FV) Leiden and prothrombin G20210A, heterozygous forms] were revealed in 16 (23.5%) and eight (11.7%) patients, respectively. Antiphospholipid antibodies (aPL) circulation was found in 34 (50%) patients. Non-usual thrombogenic polymorphisms were identified in 44 (64.7%) of the women and hyperhomocysteinemia – in 30 (44.2%). In group I no one had severe obstetric complications. All the patients were delivered at term and all the babies were alive. In group II moderate-to-severe obstetric complications were noted: preeclampsia – in 11 (16.2%), severe preeclampsia – seven (10.3%), preterm delivery – in 18 (26.4%) patients from subgroup II (P<0.05). Conclusions Women with a personal or a family history of thromboembolism and obstetric complications should be screened for thrombophilia. Beginning anticoagulant therapy early in such patients is effective not only for preventing recurring thrombosis but also preventing obstetric complications. Late prophylaxis after the completion of the trophoblast invasion therapy is much less effective.


Author(s):  
Е.С. Коростелева ◽  
О.Ю. Иванова ◽  
М.В. Хруслов ◽  
Н.А. Пономарева

Введение. Тромбогенные мутации и полиморфизмы являются этиопатогенетическим триггером репродуктивных потерь и осложнений беременности: синдрома задержки внутриутробного роста плода, преэклампсии, преждевременной отслойки нормально расположенной плаценты. Имплантация, инвазия трофобласта и дальнейшее функционирование плаценты объективно нарушаются в случае генетических дефектов свертывания. Цель исследования: оценка распространенности, роли врожденных тромбогенных мутаций и полиморфизмов и их сочетаний в генезе синдрома потери плода у женщин Курской области за 20122017 гг. Материалы и методы. Изучена клиникоанамнестическая характеристика, морфология плаценты, распространенность полиморфизма генов фолатного цикла и системы гемостаза у женщин, проживающих на территории Курской области, с синдромом потери плода: один или более самопроизвольных выкидышей или неразвивающихся беременностей на сроке 10 и более недель мертворождение неонатальная смерть 3 и более самопроизвольных выкидыша до 8 нед эмбрионального развития. Результаты. Наше исследование показало, что у женщин данного региона с ранними потерями беременности практически в 60 наблюдений выявлено 3 и более тромбогенных полиморфизмов, преимущественно генов фолатного цикла (р 0,001). Для пациенток с репродуктивными потерями во второй половине беременности характерно наличие 2 полиморфизмов, в основном, генов фолатного цикла и ингибитора активатора плазминогена 1 (р 0,001). Заключение. Необходима разработка индивидуальных подходов к тактике ведения женщин с синдромом потери плода в Курской области. Introduction. Thrombophilic mutations and polymorphisms are ethiopathological triggers of reproductive losses and pregnancy complications: intrauterine 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 20122017. 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.


1998 ◽  
Vol 5 (1) ◽  
pp. 115A-115A
Author(s):  
K CHWALISZ ◽  
E WINTERHAGER ◽  
T THIENEL ◽  
R GARFIELD
Keyword(s):  

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