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      Низкорослость, обусловленная задержкой внутриутробного развития. Клинические и гормонально-метаболические особенности, возможности ростостимулирующей терапии Translated title: Short stature due to intrauterine growth retardation. Clinical and hormonal-metabolic features, possibilities of growth-stimulating therapy

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          Abstract

          В статье представлены данные о низкорослости, обусловленной задержкой внутриутробного развития. Данный вид низкорослости, выделенный в отдельную нозологию, объединяет детей, родившихся с малыми относительно срока беременности параметрами длины и массы тела. У подавляющего большинства из них в первые годы жизни наблюдаются ускоренные темпы роста, позволяющие ребенку нормализовать свои весоростовые показатели и догнать в развитии сверстников. В случае отсутствия постнатального ростового скачка дети имеют высокий риск на протяжении всего детства отставать в физическом развитии, достигнуть низкого конечного роста и стать низкорослыми взрослыми. Помимо этого, факт рождения с малыми размерами тела ассоциирован с рядом гормонально-метаболических особенностей, отдаленным риском развития метаболического синдрома во взрослые годы.

          Предполагается, что отсутствие постнатального ростового ускорения обусловлено различными повреждениями оси соматотропный гормон/инсулиноподобный фактор роста 1-го типа (СТГ-ИФР1) — парциальным дефицитом СТГ, парциальной резистентностью к СТГ, парциальной резистентностью к ИФР1. Ростостимулирующая терапия гормоном роста, начатая в раннем возрасте, способна нормализовать его темпы в детстве и в конечном итоге значительно улучшить или нормализовать конечный рост низкорослых детей, имевших задержку внутриутробного развития в анамнезе.

          Translated abstract

          The article presents data about short stature due to intrauterine development delay. This type of short stature — separate nosology, unites children born small for gestation age. The majority of them in the first years of life have accelerated growth rates, allowing the child to normalize their weight-growth indicators and catch up in the development of peers. In the absence of an accelerated growth rates, children have a high risk of lagging behind in physical development throughout childhood, achieving low final growth and becoming short adults. In addition, the fact of birth with small body sizes is associated with a number of hormonal and metabolic features, a risk of metabolic syndrome in adult years.

          It is assumed that the absence of postnatal growth acceleration is due to various damages to the GH-IGF1 axis (partial GH deficiency, partial resistance to GH, partial resistance to IGF1). Growth hormone therapy, initiated early in life, is able to normalize growth rates in childhood and ultimately significantly improve or normalize the final growth of short stature children born small for gestational age.

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          Most cited references79

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          International standards for newborn weight, length, and head circumference by gestational age and sex: the Newborn Cross-Sectional Study of the INTERGROWTH-21st Project.

          In 2006, WHO published international growth standards for children younger than 5 years, which are now accepted worldwide. In the INTERGROWTH-21(st) Project, our aim was to complement them by developing international standards for fetuses, newborn infants, and the postnatal growth period of preterm infants. INTERGROWTH-21(st) is a population-based project that assessed fetal growth and newborn size in eight geographically defined urban populations. These groups were selected because most of the health and nutrition needs of mothers were met, adequate antenatal care was provided, and there were no major environmental constraints on growth. As part of the Newborn Cross-Sectional Study (NCSS), a component of INTERGROWTH-21(st) Project, we measured weight, length, and head circumference in all newborn infants, in addition to collecting data prospectively for pregnancy and the perinatal period. To construct the newborn standards, we selected all pregnancies in women meeting (in addition to the underlying population characteristics) strict individual eligibility criteria for a population at low risk of impaired fetal growth (labelled the NCSS prescriptive subpopulation). Women had a reliable ultrasound estimate of gestational age using crown-rump length before 14 weeks of gestation or biparietal diameter if antenatal care started between 14 weeks and 24 weeks or less of gestation. Newborn anthropometric measures were obtained within 12 h of birth by identically trained anthropometric teams using the same equipment at all sites. Fractional polynomials assuming a skewed t distribution were used to estimate the fitted centiles. We identified 20,486 (35%) eligible women from the 59,137 pregnant women enrolled in NCSS between May 14, 2009, and Aug 2, 2013. We calculated sex-specific observed and smoothed centiles for weight, length, and head circumference for gestational age at birth. The observed and smoothed centiles were almost identical. We present the 3rd, 10th, 50th, 90th, and 97th centile curves according to gestational age and sex. We have developed, for routine clinical practice, international anthropometric standards to assess newborn size that are intended to complement the WHO Child Growth Standards and allow comparisons across multiethnic populations. Bill & Melinda Gates Foundation. Copyright © 2014 Elsevier Ltd. All rights reserved.
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            Pathophysiology of placental-derived fetal growth restriction.

            Placental-related fetal growth restriction arises primarily due to deficient remodeling of the uterine spiral arteries supplying the placenta during early pregnancy. The resultant malperfusion induces cell stress within the placental tissues, leading to selective suppression of protein synthesis and reduced cell proliferation. These effects are compounded in more severe cases by increased infarction and fibrin deposition. Consequently, there is a reduction in villous volume and surface area for maternal-fetal exchange. Extensive dysregulation of imprinted and nonimprinted gene expression occurs, affecting placental transport, endocrine, metabolic, and immune functions. Secondary changes involving dedifferentiation of smooth muscle cells surrounding the fetal arteries within placental stem villi correlate with absent or reversed end-diastolic umbilical artery blood flow, and with a reduction in birthweight. Many of the morphological changes, principally the intraplacental vascular lesions, can be imaged using ultrasound or magnetic resonance imaging scanning, enabling their development and progression to be followed in vivo. The changes are more severe in cases of growth restriction associated with preeclampsia compared to those with growth restriction alone, consistent with the greater degree of maternal vasculopathy reported in the former and more extensive macroscopic placental damage including infarcts, extensive fibrin deposition and microscopic villous developmental defects, atherosis of the spiral arteries, and noninfectious villitis. The higher level of stress may activate proinflammatory and apoptotic pathways within the syncytiotrophoblast, releasing factors that cause the maternal endothelial cell activation that distinguishes between the 2 conditions. Congenital anomalies of the umbilical cord and placental shape are the only placental-related conditions that are not associated with maldevelopment of the uteroplacental circulation, and their impact on fetal growth is limited.
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              Birth weight and subsequent risk of type 2 diabetes: a meta-analysis.

              The "small baby syndrome hypothesis" suggests that an inverse linear relation exists between birth weight and risk of type 2 diabetes. The authors conducted a meta-analysis to examine this association. They included studies that reported odds ratios and 95% confidence intervals (or data with which to calculate them) for the association of type 2 diabetes with birth weight. Fourteen studies involving a total of 132,180 persons were identified. Low birth weight ( /=2,500 g, was associated with increased risk of type 2 diabetes (odds ratio (OR) = 1.32, 95% confidence interval (CI): 1.06, 1.64). High birth weight (>4,000 g), as compared with a birth weight of
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                Author and article information

                Contributors
                Journal
                Probl Endokrinol (Mosk)
                Probl Endokrinol (Mosk)
                problendo
                Problems of Endocrinology
                Endocrinology Research Centre
                0375-9660
                2308-1430
                2022
                23 October 2022
                : 68
                : 5
                : 4-13
                Affiliations
                [-1]Национальный медицинский исследовательский центр эндокринологии
                Article
                10.14341/probl13178
                9762449
                36337013
                2409c3d7-fc33-4336-a6a4-8572b62604b5
                Copyright © Endocrinology Research Centre, 2022

                This work is licensed under a Creative Commons Attribution 4.0 License.

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                Research Article

                низкорослость,дети,задержка внутриутробного развития,рост,гормон роста,инсулиноподобный фактор роста,метаболический синдром,соматропин,терапия гормоном роста

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