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1概念与流行病学宫内生长迟缓(IUGR)是指胎儿的生长发育因各种原因未能达到其基因所决定的生长发育程度[1]。但这一概念在临床实践中无法应用,其命名与概念通常与小于胎龄儿(SGA)互用。后者是一个统计学概念,是指一组出生体重低于相应胎龄第10百分位数的新生儿。不同作者有不同的观点,如有人认为更合理的是将出生身长减低也考虑在内。由于概念和采用标准(受种族、地域海拔高度、经济水平等因素影响)的不统一,IUGR的流行病学资料也各不相同。美国第三次全国健康与营养调查(采用出生体重低于相应胎龄第10百分位数)报告其发生率为8·6%[2]…     

Intrauterine growth retardation

Two cases of severe intrauterine growth retardation, a boy and a girl studied for 7 and 10 years respectively, are reported. Both patients showed peculiar cranio-facial abnormalities as observed in the socalled Seckel's syndrome, an appearance of premature aging, peripheral GH resistance which was probably due to deficiency in Somatomedin A production, sella areas and volumes consistently at the upper limits of normal when related to the patients' height, and dysharmonic skeletal maturation and ivory cone-shaped epiphyses of the tubular bones of the hands.     

Intrauterine growth retardation: study of placental apoptosis

We studied the rate of apoptosis in the placental tissue of pregnancies complicated with intrauterine growth retardation (IUGR) and compared it with the results obtained in normal placentas. Our results clearly demonstrate a strongly increased rate of apoptosis in placentas of children born with IUGR, suggesting severe placental dysfunction. The significance of these findings needs further study.     

Intrauterine growth retardation and long-term effects on growth.

The authors present intrauterine growth retardation (IUGR) as an entity with significant prevalence, morbidity, and mortality. They discuss short-term and long-term sequelae, and particularly emphasize long-term growth disabilities. The authors review the most important trials with human growth hormone that have been carried out recently to maximize the growth and final height potential of children affected with IUGR. They also highlight the most recent advances in the field of fetal growth, with special attention to genetic and endocrine factors. Finally, the authors discuss in detail epidemiological and clinical evidence of the causes of IUGR in relation to several adult onset disorders.     

Intrauterine growth retardation and early adolescent growth spurt in two sisters

Two sisters who presented with a similar growth pattern are described. They delivered with idiopathic intrauterine growth retardation and had an early adolescent growth spurt. The physical and endocrine findings suggested a potential relationship between intrauterine growth retardation and early puberty.     

宫内发育迟缓引起胰岛素抵抗的遗传与营养学机制

过去十几年的研究证据表明,胎儿宫内发育迟缓(in鄄trauterine growth retardation,IUGR)与胰岛素抵抗的发生发展存在联系。但有关这种联系的具体机制尚未明确,未来十年的挑战将是发现这种联系的细胞学和分子生物学机制,这将有可能提出一些干预方法以降低糖尿病所带来的影响。现从基因水平和营养学角度对这种联系可能的细胞学和分子生物学机制作一综述。1基因因素胎儿发育和胰岛素抵抗之间的联系可能存在基因基础。众所周知,胰岛素在胎儿发育中起主要的作用,它可以保证胎儿在营养供应良好的条件下有相应的生长率,胰岛素抵抗将影响胎儿的正…     

Intrauterine growth retardation and brainstem auditory-evoked response in preterm infants

Intrauterine growth retardation is frequently associated with intrauterine undernutrition, and can deleteriously affect brain function. Twenty-eight premature small for gestational age infants were compared with 28 premature appropriate for gestational age infants to determine whether intrauterine growth retardation was associated with abnormalities in the auditory pathway in the early neonatal period. The auditory pathway was studied between 4-18 wk of life by analysis of brainstem auditory-evoked potentials elicited by a 10/s 75 decibel above normal adult hearing level (dB nHL) click stimulus presented at the infants' ears. Peak latencies of components I, III and V, and interpeak latencies I-III, III-V and I-V, yielded no statistically significant differences between groups. The present study indicates that intrauterine growth-retarded premature infants may not have abnormalities of brainstem auditory-evoked response in the early neonatal period.     

Intrauterine growth retardation: altered hepatic energy and redox states in the fetal rat

We determined the extent to which ligating both maternal uterine arteries affects fetal hepatic energy and redox states in the fetal rat. Bilateral maternal uterine artery ligation on d 18 of the rat's 21.5-d gestation significantly inhibits fetal growth; sham surgery limits growth to a lesser extent. Within 12 h of surgery and persisting to d 19, small-for-gestational age (SGA) fetuses had significantly diminished ATP/ADP and adenylate charge ratios, whereas sham fetuses had values intermediate between SGA and normal. Hepatic mitochondrial redox state demonstrated similar changes. Cytosolic redox state in SGA fetuses at 12 and 24 h after surgery was significantly elevated. SGA fetuses had significantly diminished plasma insulin and elevated glucagon concentrations. On d 19 and 20, hepatic ATP/ADP and cytosolic NAD+/NADH correlated directly for sham and normal but not SGA fetuses. Alterations in glucose, insulin, and glucagon availability and hypoxia were responsible for the changes in energy and redox states. They may also have disassociated hepatic cytosolic from mitochondrial redox states and altered the equilibrium between adenine and nicotinamide nucleotides. These altered cellular functions retarded fetal growth. Newborn SGA, sham, and normal rat pups had similar hepatic ATP/ADP, cytosolic, and mitochondrial redox states at 10 and 240 min after delivery suggesting that the hypoglycemia which developed in SGA pups was not attributable to alterations in these variables.     

Intrauterine growth retardation and its impact on the neurological status of the newborn

The neurological study of 40 “small-for-date” newborn infants by quantitative and qualitative methods revealed a significant incidence of poor muscle tone and diminished reflex activity in term infants compared to the control group. Significantly reduced head circumference was noticed in term small-for-date infants. The neurological score correlated with the head circumference. This score showed a greater reduction in the complicated group of small-for-date infants compared to the uncomplicated group. Maternal smoking was the chief factor related to dysmaturity in this study. The importance of prevention of dysmaturity, prompt treatment of metabolic complications at birth and nutritional rehabilitation is stressed. Careful followup study of these infants for an early detection of neurologic deficit is suggested.     

Renal tubular acidosis: diagnostic work-up,treatment and mechanisms of growth retardation

Astute clinical observations, careful evaluation of laboratory results, together with research aimed at understanding the mechanisms of growth failure in children with the various types of renal tubular acidosis, have led to a more cogent approach to the management of children with renal tubular acidosis. This review examines the different clinical presentations of renal tubular acidosis, the diagnostic workup, the recent advances in our understanding of the mechanisms of growth failure and current therapeutic modalities.