The role of genetic thrombophilias in the development of fetal loss syndrome in women of Kursk region for 2012–2017

2019 ◽  
Author(s):  
Е.С. Коростелева ◽  
О.Ю. Иванова ◽  
М.В. Хруслов ◽  
Н.А. Пономарева
Keyword(s):  
Fetal Loss ◽  
Plasminogen Activator Inhibitor ◽  
Trophoblast Invasion ◽  
Plasminogen Activator Inhibitor 1 ◽  
Reproductive Losses ◽  
Coagulation Defects ◽  
Folate Cycle ◽  
Kursk Region ◽  
Activator Inhibitor

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.

Inhibitory Role of Plasminogen Activator Inhibitor-1 in Arterial Wound Healing and Neointima Formation

Circulation ◽  
1997 ◽  
Vol 96 (9) ◽  
pp. 3180-3191 ◽  
Author(s):  
Peter Carmeliet ◽  
Lieve Moons ◽  
Roger Lijnen ◽  
Stefaan Janssens ◽  
Florea Lupu ◽  
...  
Keyword(s):  
Wound Healing ◽  
Plasminogen Activator ◽  
Plasminogen Activator Inhibitor ◽  
Neointima Formation ◽  
Plasminogen Activator Inhibitor 1 ◽  
Inhibitory Role ◽  
Activator Inhibitor

scholarly journals Emerging Role of Endothelial and Inflammatory Markers in Preeclampsia

2009 ◽  
Vol 26 (3) ◽  
pp. 127-133 ◽  
Author(s):  
Menha Swellam ◽  
Nervana Samy ◽  
Susan Abdl Wahab ◽  
Mohamed Saeed Ibrahim
Keyword(s):  
Inflammatory Markers ◽  
Linear Regression Analysis ◽  
Plasminogen Activator Inhibitor ◽  
Plasminogen Activator Inhibitor 1 ◽  
New Approach ◽  
Reactive Protein ◽  
Diagnostic Role ◽  
Activator Inhibitor ◽  
Pai 1

Objectives:Endothelial disturbance and excess inflammatory response are pathogenic mechanisms in pre-eclampsia (PE). Authors determine the clinical diagnostic role for thrombomodulin (TM), plasminogen activator inhibitor-1 (PAI-1) as endothelial markers and C-reactive protein (CRP), and interlukin-6 (IL-6) as inflammatory markers when tested independently or in combinations.Materials and methods:We conducted a retrospective study in a cohort of 185 women grouped as 80 women with PE, 55 normotensive pregnant and 50 healthy non-pregnant. Plasma levels of TM, PAI-1, CRP and IL-6 were examined using enzyme linked immunosorbent assays.Results:Median levels and the positivity rates for the investigated markers were higher in PE as compared to the other groups (P< 0.0001). Using linear regression analysis, the investigated markers were significantly correlated regarding healthy nonpregnantvsPE or normotensive pregnantvsPE. The sensitivity of PAI-1 was the highest (98%) among the tested biomarkers. Combination between the investigated markers revealed absolute sensitivity (100%) and reliable specificity especially when PAI-1 was combined with CRP at 83% specificity.Conclusions:Investigated endothelial and inflammatory markers revealed sensitive diagnostic test for PE. However, coupled combination between PAI-1 with CRP showed superior both sensitivity and specificity which represent a promising new approach for detection of PE.

scholarly journals Role of plasminogen activator inhibitor-1 gene polymorphisms in osteoporosis: A study in Chinese post-menopausal women

2018 ◽  
Vol 16 ◽  
pp. 205873921876729
Author(s):  
An Wan ◽  
Daodong Liu
Keyword(s):  
Gene Polymorphisms ◽  
Chinese Women ◽  
Plasminogen Activator Inhibitor ◽  
Plasminogen Activator Inhibitor 1 ◽  
Chain Reaction ◽  
Polymerase Chain ◽  
Post Menopausal ◽  
Activator Inhibitor ◽  
Pai 1

Osteoporosis is a chronic multifactorial disease characterized by deterioration of bone mass and is vulnerable to bone fracture. Plasminogen activator inhibitor-1 (PAI-1) is an important molecule for maintenance of optimum bone mass. Several single-nucleotide polymorphisms (SNPs) in PAI-1 have been reported to alter PAI-1 expression and/or the translational level. In this report, we explored the possible role of common PAI-1 gene polymorphisms on predisposition to osteoporosis in a Chinese cohort. A total of 364 post-menopausal Chinese women diagnosed of having osteoporosis and 350 healthy females hailing from similar areas were enrolled in this study. Five common SNPs (−844G > A, −6754G/5G, +43G > A, +9785G > A and +11053T > G) were genotyped by polymerase chain reaction (PCR) followed by restriction fragment length polymorphism (RFLP). Relative expression of PAI-1 mRNA and plasma PAI-1 levels were quantified by reverse transcription polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA), respectively. Prevalence of homozygous mutant (5G/5G) and minor allele (5G) of PAI-1 (−675 4G/5G) polymorphism was significantly more frequent in patients than in healthy controls (5G/5G: P < 0.0001, odds ratio (OR) = 3.18; 5G: P < 0.0001, OR = 1.65). Both plasma PAI-1 and relative mRNA expression levels were significantly lower in patients compared to healthy controls. Interestingly, the quantity of plasma PAI-1 and mRNA expression was correlated with PAI-1 (−675 4G/5G) polymorphism: subjects with 4G/4G genotype had elevated PAI-1 in comparison to homozygous mutant, and displayed lower quantity of PAI-1 protein and mRNA values. PAI-1 (−675 4G/5G) mutant is associated with susceptibility to development of osteoporosis in post-menopausal Chinese women. Furthermore, this variant in the promoter region alters plasma protein levels and relative expression of PAI-1.

Role of plasminogen activator inhibitor-1 in coronary pathophysiology

2018 ◽  
Vol 164 ◽  
pp. 54-62 ◽  
Author(s):  
Richard G. Jung ◽  
Trevor Simard ◽  
Alisha Labinaz ◽  
F. Daniel Ramirez ◽  
Pietro Di Santo ◽  
...  
Keyword(s):  
Plasminogen Activator ◽  
Plasminogen Activator Inhibitor ◽  
Plasminogen Activator Inhibitor 1 ◽  
Activator Inhibitor

scholarly journals Measurement of plasminogen activator inhibitor 1 in biologic fluids with a murine monoclonal antibody-based enzyme-linked immunosorbent assay

Blood ◽  
1988 ◽  
Vol 71 (1) ◽  
pp. 220-225 ◽  
Author(s):  
PJ Declerck ◽  
MC Alessi ◽  
M Verstreken ◽  
EK Kruithof ◽  
I Juhan-Vague ◽  
...  
Keyword(s):  
Plasminogen Activator ◽  
Immunosorbent Assay ◽  
Healthy Subjects ◽  
Plasminogen Activator Inhibitor ◽  
Enzyme Linked Immunosorbent Assay ◽  
Plasminogen Activator Inhibitor 1 ◽  
Platelet Poor Plasma ◽  
Activator Inhibitor ◽  
Pai 1

An enzyme-linked immunosorbent assay for plasminogen activator inhibitor-1 (PAI-1) in biologic fluids was developed on the basis of two murine monoclonal antibodies raised against PAI-1 purified from HT- 1080 fibrosarcoma cells. The lower limit of sensitivity of the assay in plasma is 2 ng/mL. The assay is 12 times less sensitive toward the PAI- 1/human tissue-type plasminogen activator (t-PA) complex as compared with free PAI-1. The intraassay, interassay, and interdilution coefficients of variation are 5.2%, 8.0%, and 7.1%, respectively. The level of PAI-1 in platelet-poor plasma of healthy subjects is 18 +/- 10 ng/mL (mean +/- SD, n = 45). In platelet-rich plasma after freezing and thawing, 92% of PAI-1 antigen is released from platelets, whereas only 8% is found in the corresponding platelet-poor plasma. In platelet-poor plasma from healthy subjects, a linear correlation (r = 0.80) was found between PAI activity and PAI-1 antigen. In plasma approximately two thirds of the PAI-1 antigen was functionally active, whereas only 5% of the PAI-1 antigen released from platelets was active. During pregnancy a progressive increase of PAI-1 antigen levels up to three- to sixfold the control value was observed. In plasma of patients with recurrent deep vein thrombosis, PAI-1 levels were 44 +/- 20 ng/mL (mean +/- SD, n = 7), during a clinically silent phase. Four of these patients had a level above 38 ng/mL (mean +/- 2 SD of normal). The present assay, based on stable and reproducible reagents, allows the specific determination of PAI-1 antigen in biologic fluids. It may facilitate interlaboratory comparisons and be useful for further investigations of the role of PAI-1 in clinical conditions associated with impaired fibrinolysis and/or a tendency to thrombosis and investigations of the role of PAI-1 in platelets.

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