Arginine and аrginase levels in the blood serum of pregnant women with intrauterine growth retardation

2016 ◽  
pp. 97-99
Author(s):  
A.V. Basystyi ◽  

The objective: to determine arginine and arginase levels in the blood serum of pregnant women with intrauterine growth retardation of different severity. Patients and methods. The study included 100 pregnant women (from 23 to 40 weeks of gestation). The main group consisted of 80 pregnant women with intrauterine growth retardation. The control group consisted of 20 women with physiological course of pregnancy. The patients of the main group were divided into three clinical groups regarding intrauterine growth retardation staging. Group I included 38 pregnant women with stage I IUGR, 22 pregnant women with stage II IUGR were in group II and 20 pregnant women with stage III IUGR – in group III. L-arginine concentration was determined in the blood serum by the method of T.L. Aleinikova et al [1], arginase activity – by the method of J.W. Geyer, D. Dabich [4]. The statistical analysis was performed by using standard computer programs: STATISTICA 6.0, Microsoft Excel, ANOVA. Statistically significant difference was considered at p<0.05. Results. In the study the reduced level of free arginine in the main group of pregnant women with intrauterine growth retardation of different severity was determined if compared with the control group. Fetomaternal gradient of arginine is reduced significantly due to increasing activity of the enzyme arginase, which competitively uses amino acid. Conclusions. The level of reduced free arginine in the blood serum of pregnant women with intrauterine growth retardation is directly proportional to the severity of fetal growth retardation: the more severe fetal growth retardation, the more marked arginine deficiency. For correcting metabolic disorders in pregnant women with intrauterine growth retardation it is recommended to administer L-arginine containing drugs. Key words: L-arginin, arginase, blood serum, pregnant women with intrauterine growth retardation.

PEDIATRICS ◽  
1976 ◽  
Vol 58 (5) ◽  
pp. 681-685
Author(s):  
Stephen R. Kandall ◽  
Susan Albin ◽  
Joyce Lowinson ◽  
Beatrice Berle ◽  
Arthur I. Eidelman ◽  
...  

An analysis of birthweights of 337 neonates in relation to history of maternal narcotic usage was undertaken Mean birthweight of infants born to mothers abusing heroin during the pregnancy was 2,490 gm, an effect primarily of intrauterine growth retardation. Low mean birthweight (2,615 gm) was also seen in infants born to mothers who had abused heroin only prior to this pregnancy, and mothers who had used both heroin and methadone during the pregnancy (2,535 gm). Infants born to mothers on methadone maintenance during the pregnancy had significantly higher mean birthweights (2,961 gm), but lower than the control group (3,176 gm). A highly significant relationship was observed between maternal methadone dosage in the first trimester and birthweight, i.e., the higher the dosage, the larger the infant. Heroin causes fetal growth retardation, an effect which may persist beyond the period of addiction. Methadone may promote fetal growth in a dose-related fashion after maternal use of heroin.


2016 ◽  
pp. 55-58
Author(s):  
O.V. Basystyi ◽  

The objective: to reveal morphofunctional changes in the placenta of pregnant with intrauterine growth retardation of different severity. Patients and Methods. The study included 100 pregnant (from 23 to 40 weeks of gestation). The main group consisted of 80 pregnant women with intrauterine growth retardation of different severity. The control group consisted of 20 women with physiological course of pregnancy. The patients of the main group were divided into three clinical groups regarding intrauterine growth retardation staging. Group I included 38 pregnant with stage 1 IUGR, 22 pregnant women with stage II IUGR were in group 2 and 20 pregnant with stage 3 IUGR – in group III. Revealing intrauterine growth retardation in pregnant women, the form and the stage, as well as violations of the uteroplacental and fetal blood flow was based on the results of ultrasound Doppler studies. The comparison of fetometry results and normative indices of the definite duration of gestation was made to diagnose intrauterine growth retardation. For morphological studies full-thickness placenta tissue sections were cut from a central, paracentral and areas after the separation of the placenta. From the marginal areas there were cut tissue sections with membranes. From umbilical cord there were cut two sections at 2 cm distance from the insertion of the umbilical cord to the placenta and on the opposite side. The tissue samples were fixed with 10% neutral formalin and embedded in paraffin; histologic sections were stained by hematoxylin-eosin. We paid attention to the severity of compensatory adaptive and involutory destructive reactions in the placenta. The maturity of villous tree was evaluated using the criteria for Voloshchuk’s classification of villous tree maldevelopment. The variational methods were used to make the statistical analysis of outcomes by standard licensed computer programs: STATISTICA 6.0, Microsoft Excel, ANOVA «Statistica». Differences among values were considered statistically significant if p<0.05. Results. The morphology of the placenta in case of intrauterine growth retardation is characterized by a high incidence of uteroplacental blood flow violations. The changes are mainly caused by insufficient maternal blood in intervillous space. The most common morphological manifestations of the violated blood flow in intervillous space were heart attacks, afunctional areas, successive narrowing and thrombosis of intervillous space. The incidence of blood flow violations in intervillous space is growing with increased severity of fetal growth retardation. Conclusions. Placental insufficiency due to morphological and functional changes in the placenta is the leading cause of intrauterine growth retardation and fetal hypoxia. It develops as a result of fetal and placenta combined reaction to various disorders in the mother’s body. The incidence of blood flow violations in intervillous space is growing with increased severity of fetal growth retardation. Key words: intrauterine growth retardation, pregnant, placenta, placental insufficiency, morphofunctional changes.


2021 ◽  
Vol 8 (3) ◽  
pp. 182-187
Author(s):  
V.V. Lazurenko ◽  
I.B. Borzenko ◽  
O.A. Lyashchenko ◽  
O.B. Ovcharenko ◽  
D.Yu. Tertyshnyk

The aim of the study was to improve the modern diagnosis of placental dysfunction and its complications. Materials and methods. The study involved a prospective survey of 70 pregnant women divided into the main group (pregnant women with placental dysfunction) (n = 50) and the control group (n = 20). The main group was divided into subgroups of pregnant women with placental dysfunction and fetal growth retardation (n = 30) and pregnant women with placental dysfunction without fetal growth retardation (n = 20). The control group comprised 20 pregnant women with physiological gestation. Apart from history taking, the study comprised obstetric and general clinical examination, evaluation of endothelium- dependent vasodilation, serum concentrations of soluble forms of vascular and platelet- endothelial molecules of cell adhesion 1, indicators of athrombogenicity of the vascular growth wall, uterine-placental-fetal blood circulation, pathomorphological and histometric examination of the placenta. Results. Based on the obtained clinical-morphological and endotheliotropic criteria, a personalized clinical algorithm for managing pregnant women with placental dysfunction was developed and implemented. Conclusions. Assessment of pregnancy results in a prospective clinical study showed that the proposed algorithm for personalization of the risk of perinatal abnormalities not only helped to avoid antenatal mortality, but also to prevent intranatal and early neonatal losses in patients with placental dysfunction and fetal growth retardation.


2022 ◽  
Vol 15 (6) ◽  
pp. 695-704
Author(s):  
E. A. Orudzhova

Aim: to study the role of antiphospholipid antibodies (AРA) and genetic thrombophilia as a potential cause of the development or a component in the pathogenesis of early and late fetal growth retardation (FGR).Materials and Methods. There was conducted a prospective randomized controlled trial with 118 women enrolled. The main group consisted of 83 patients, whose pregnancy was complicated by FGR degrees II and III, stratified into two groups: group 1 – 36 pregnant women with early FGR, group 2 – 47 pregnant women with late FGR. Women were subdivided into subgroups according to the FGR severity. The control group consisted of 35 pregnant women with a physiological course of pregnancy. АРА were determined according to the Sydney antiphospholipid syndrome criteria by enzyme immunoassay (ELISA): against cardiolipin, β2 -glycoprotein 1, annexin V, prothrombin, etc. (IgG/IgM isotypes); lupus anticoagulant – by the three-stage method with Russell's viper venom; antithrombin III and protein C levels – by chromogenic method; prothrombin gene polymorphisms G20210A and factor V Leiden – by polymerase chain reaction; homocysteine level – by ELISA.Results. AРA circulation (medium and high titers), genetic thrombophilic defects and/or hyperhomocysteinemia were detected in 40 (48.2 %) patients with FGR, which was significantly higher than that in the control group (p < 0.05): in group 1 (41.7 % of women) AРA (30.6 %) and AРA with genetic thrombophilia or hyperhomocysteinemia (11.1 %) were revealed; in group 2 (51.1 % of women) AРA (21.3 %), AРA with hyperhomocysteinemia (4.3 %), genetic thrombophilia (25.5 %), and due to hyperhomocysteinemia (2.1 %) were found. No differences in prevalence of thrombophilia rate in patients were observed related to FGR severity, but a correlation between the FGR severity and AРA titers was found.Conclusion. Testing for the presence of AРA, genetic thrombophilia and hyperhomocysteinemia should be recommended for patients with FGR (including those with FGR in medical history), especially in the case of its early onset. It is recommended to determine the full AРA spectrum.


1992 ◽  
Vol 8 (S1) ◽  
pp. 176-181 ◽  
Author(s):  
Ingemar Leijon

AbstractIntrauterine growth retardation is associated with high risk of perinatal asphyxia. The neonatal mortality rate of small-for-gestational-age (SGA) infants (birthweight ≤ 2 SD) in Sweden decreased from 5.6% in 1973 to 2.0% in 1987. During the same period, the number SGA infants with postnatal asphyxia (5 min Apgar score <7) decreased from 10% to 5%. Based on antenatal diagnosis of fetal growth retardation, an optimal time of delivery reduces the risk of major neurological and developmental sequelae of the individual infant.


PEDIATRICS ◽  
1972 ◽  
Vol 50 (4) ◽  
pp. 547-558
Author(s):  
J. Urrusti ◽  
P. Yoshida ◽  
L. Velasco ◽  
S. Frenk ◽  
A. Rosado ◽  
...  

Intrauterine growth was assessed in a series of 128 cases. Thirty-six infants were small for gestational age, and showed the usual signs of intrauterine growth retardation (IUM). The head circumference of these infants was small, with reference to normal term babies (FT) and comparable to premature infants, appropriately sized for a gestational age (ACA) five weeks less than that of the IUM's. There were 12 neonatal deaths, three among IUM infants within 24 hours and nine in the low birth weight AGA group within 72 hours. The mothers of these three groups of infants were similar with respect to age, weight, height, nutritional patterns, and prior pregnancy histories.


Author(s):  
H. P. Robinson ◽  
W. R. Chatfield ◽  
R. W. Logan ◽  
Frances Hall

Forty-two ‘at risk’ pregnancies were serially monitored by sonar biparietal cephalometry, 24 h urinary oestriol assays and determination of serum human placental lactogen. The results were assessed by a scoring system, and it was found that a combination of sonar cephalometry and 24 h urinary oestriol assays gave the most reliable prediction of intrauterine growth retardation.


Author(s):  
Н.К. Вереина ◽  
В.Ф. Долгушина ◽  
Ю.В. Фартунина ◽  
Е.В. Коляда

Введение: Задержка роста плода (ЗРП) занимает второе место в структуре причин перинатальной смертности, а ее наличие имеет длительное неблагоприятное влияние на здоровье ребенка. Оценка степени активации системы гемостаза при ЗРП в сопоставлении с клиническими исходами имеет важное значение в понимании патогенеза, улучшении прогнозирования и профилактики этого патологического состояния. Цель исследования: оценить состояние гемостаза у беременных с ЗРП в сравнении с женщинами с физиологическим течением беременности. Материалы и методы: Тип исследования: поперечный срез на базе когортного. В исследование включено 52 беременных. Основная группа — 32 пациентки с ЗРП, выявленной при ультразвуковой фетометрии; контрольная группа — 20 практически здоровых женщин без отягощенного акушерско-гинекологического анамнеза, с физиологически протекавшей беременностью, завершившейся неосложненными родами. Оценку состояния системы гемостаза проводили на сроке 24-32 нед гестации. Результаты: Среди факторов тромботического риска у беременных с ЗРП чаще выявлялось табакокурение во время беременности. Наличие ЗРП было значимо связано с маловодием, генитальной и внутриматочной инфекцией, преэклампсией, нарушениями маточно-плацентарно-плодового кровотока. У женщин с ЗРП обнаружен более высокий уровень фибриногена, а также повышение скорости роста сгустка, больший размер сгустка, более частое формирование спонтанных сгустков в сравнении с контрольной группой. Заключение: У беременных с ЗРП имеется протромботическая готовность плазмы, что может служить основанием для дальнейшей разработки антитромботической коррекции с целью улучшения перинатальных исходов. Background: Fetal growth retardation (FGR) is the second leading cause of perinatal mortality, has a long-term adverse effect on child health. Assessment of hemostasis activation in FGR in comparison with clinical outcomes is important for understanding pathogenesis, improving the prognosis and prevention of this pathological state. Objectives: to assess hemostasis state in pregnant women with FGR compared to women with physiological pregnancy. Patients/Methods: Type of study: crosssectional based on cohort. The study included 52 pregnant women. The main group consisted of 32 patients with FGR diagnosed by ultrasound fetometry; the control group consisted of 20 practically healthy women without burdened obstetric-gynecological history, with physiological pregnancy that ended in uncomplicated childbirth. Hemostasis assessment was carried out at 24-32 weeks of gestation. Results: Smoking during pregnancy as a factor of thrombotic risk was more common in pregnant women with FGR. FGR was significantly associated with oligohydramnios, genital and intrauterine infection, preeclampsia, and placental insufficiency. Women with FGR showed a higher level of fibrinogen, as well as an increased rate of clot growth, clot larger size, and more frequent formation of spontaneous clots in comparison with the control group. Conclusions: Pregnant women with FGR are characterized by prothrombotic state that may be the basis for further development of antithrombotic correction for improving perinatal outcomes.


1996 ◽  
Vol 270 (3) ◽  
pp. E491-E503 ◽  
Author(s):  
J. C. Ross, ◽  
P. V. Fennessey ◽  
R. B. Wilkening ◽  
F. C. Battaglia ◽  
G. Meschia

Placental transport and fetal utilization of leucine were studied at 130 days of gestation in six control ewes and in seven ewes in which intrauterine growth retardation (IUGR) had been induced by exposure to heat stress. Leucine fluxes were measured during simultaneous intravenous infusion of L-[1-13C]leucine into the mother and L-[1-14C] leucine into the fetus. In the IUGR group, the following leucine fluxes, expressed as micromol/min/kg fetus, were reduced compared with control: net uterine uptake (3.44 vs. 8.56, P<0.01), uteroplacental utilization (0.0 vs. 4.7, P<0.01), fetal disposal rate (6.4 vs. 8.9, P<0.001), flux from placenta to fetus (5.0 vs. 7.1, P<0.01), direct transport from mother to fetus (1.6 vs. 3.4, P<0.01), flux from fetus to placenta (1.5 vs. 3.2, P<0.001), and oxidation of fetal leucine by fetus plus placenta (2.1 vs. 3.2, P<0.02). Uterine uptake, uteroplacental utilization, and direct transport were also significantly reduced per gram placenta. We conclude that maternal leucine flux into the IUGR placenta is markedly reduced. Most of the reduced flux is routed into fetal metabolism via a decrease in placental leucine utilization and a decrease in the leucine flux from fetus to placenta.


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