Born small for gestational age: consequences for growth

A large number of studies have documented a strong correlation between size at birth and subsequent height, although the reported incidence of catch-up growth and consequently the impact on final height has varied with time and between countries. These variations may be real, but could also be related to a number of methodological problems. The aim of this study was to explore two important aspects related to postnatal growth after disturbed fetal growth: first, the definition of small for gestational age (SGA), including the selection of cut-off points in defining shortness; and, secondly, the importance of the general socio-economic status of the population with regard to the incidence of growth faltering in early life. Data were analysed from two longitudinal population-based studies, one from Sweden and one from Hong Kong. Of the Swedish cohort, 3.8% had a birth length below –2 SD scores; in the Hong Kong population the corresponding value was 11.9% (Swedish reference values were used in both studies). The following conclusions were made. Size at birth is important for postnatal growth, and the difference in length at birth of 9–10 cm between the two extreme birth length subgroups remains, on average, until maturity. This seems to be true for the two study populations with different degrees of socio-economic development. However, the rate of catch-up growth is highly dependent on the definition of SGA, on the rate of catch-up growth in early life and on the incidence of growth faltering between 6 and 18 months of age.     

Long-term metabolic consequences of being born small for gestational age

This review highlights the evidence of linking small for gestational age (SGA) with metabolic/cardiovascular disturbances (dysmetabolic syndrome) in later life. The metabolic and cardiovascular complications associated with in utero undernutrition have been identified during the past 10 yr. Reduced fetal growth is independently associated with an increased risk of the development of cardiovascular diseases, the insulin-resistance syndrome, or one of its components: hypertension, dyslipidemia, impaired glucose tolerance, or type 2 diabetes. All of them appear to result from the initial development of insulin-resistance which appears as a key component underlying the metabolic complications. Although the mechanism remains unclear, there is some evidence that argues in favor of an active contribution of the adipose tissue in the emergence of insulin-resistance associated with in utero undernutrition, but this hypothesis remains to be further documented. From a broader point of view, several hypotheses have been proposed over the past 10 yr to understand this unexpected association. Each of them points to either a detrimental fetal environment or genetic susceptibilities or interactions between these two components as playing a critical role in this context. Although not confirmed, the hypothesis suggesting that this association could be the consequence of genetic/environmental interactions remains at the moment the most attractive.     

Catch-down growth during infancy of children born small (SGA) or appropriate (AGA) for gestational age with short-statured parents

OBJECTIVE: We analyzed postnatal growth in children with familial short stature (FSS) with regard to small (SGA) or appropriate (AGA) for gestational age status at birth. STUDY DESIGN: We studied 96 otherwise healthy short-statured children (58 males; SGA: n = 41, AGA: n = 55). At least one of the parents was short-statured. Cross-sectional data for length/height and weight for the first 4 years of age were collected retrospectively. RESULTS: AGA children had a mean length of 0.09 +/- 1.02 standard deviation score (SDS) at birth, -1.57 +/- 1.16 SDS after 1 year of age, and -2.36 +/- 0.72 SDS after 4 years. SGA children had a mean length of -2.04 +/- 1.06 SDS at birth, -2.70 +/- 1.12 SDS at 1 year of age, and -3.05+/-0.86 SDS at 4 years. The loss of length SDS within the first 2 years of life was greater in AGA than in SGA children. SGA children were significantly shorter than AGA children at all of the study points (p <.001). CONCLUSIONS: Children with an FSS background born AGA show catch-down growth to their lower familial range during the first 2 years of life. SGA children did not catch up to their AGA peers at any time.     

High risk appropriate for gestational age (AGA) and small for gestational age (SGA) preterm infants. Neurological handicap and developmental abnormalities at five years of age

Outcome at five years of age of 110 high risk AGA, 71 high risk SGA preterm infants with similar birth weight and 102 term control infants was studied. Mean IQ in the 3 groups was not statistically different. Major handicaps were found in 16.3% of the AGA and in 8.5% of the SGA preterms. There was no major handicap among the controls. Minor neurodevelopmental abnormalities were present in 25.6% of AGA, 28.2% of SGA and 19.6% of controls. The types of neurodevelopmental handicaps were different in the 3 groups and generally more severe in the AGA group. All the major handicaps among AGA preterms were found in children with severe neonatal complications. In the SGA preterm group, only 1/3 of the major handicaps can be related to perinatal complications. Affective and behavior disorders were probably related in some way to neurodevelopmental achievement. This study showed that preterm infants with GA less than or equal to 32 weeks are more at risk than more mature SGA preterms with similar birth weight.     

Growth and metabolic consequences of growth hormone treatment in prepubertal short normal children

Growth and the metabolic effects of growth hormone were monitored in a randomised, controlled group of 41 short, normal, prepubertal children. The treated group received daily injections of growth hormone as Genotropin (Kabi Pharmacia) 30 IU/m2/week. Fifteen children in the treated group (21 children) have completed three years of treatment, have grown significantly more than 14 (of 20) untreated children, and have a significantly greater adult height prediction. They do, however, remain leaner (body fat 13.5% in the treated group, 18% in the untreated group) and relatively hyperinsulinaemic (insulin 66.7 pmol/l in the treated group, 44.5 in the untreated group) after three years compared with untreated children. Although growth hormone appears to improve the height potential of prepubertal short normal children, the long term outcome is still uncertain.     

生长激素治疗宫内生长迟缓生后持续矮小儿的临床研究

目的 用生长激素治疗宫内生长迟缓（IUGR）生后持续矮小和生长激素缺乏症（GHD）儿，并进行疗效评估。方法 分泌型重组人生长激素，剂量0.1U(kg.d) ,每日1次，于晚上睡觉前30min皮下注射，结果 IUGR组及GHD组经6个月治疗后身高增长率分别为1.03cm/月及1.12cm/月，两组间差异不显著，血清胰岛素样生长因子I（IGF-I）两组均有升高，GHD组升高程度大于IUGR组。结论 生长激素对策 后持续矮小及GHD儿均有良好治疗效果。     

Growth and growth hormone in children born small for gestational age

Although most children born small for gestational age catch up in growth by age 2 y, up to 14% remain more than 2 standard deviations below the mean for height. Recombinant growth hormone is approved by the US Food and Drug Administration and by the European Agency for Evaluation of Medicinal Products for the treatment of children born small for gestational age who fail to manifest catch-up growth by 2 y or 4 y, respectively.

Conclusion: We conclude from clinical studies that growth hormone therapy can induce catch-up growth in these children.     

Efficacy and safety of growth hormone treatment in children born small for gestational age in Japan

Growth-promoting effects and safety of growth hormone (GH) treatment in prepubertal short-statured children born small for gestational age (SGA) were evaluated in a multicenter, open-label, randomized parallel-group comparison study. Patients were randomized to two dose groups; 34 and 33 patients received GH at 0.033 and 0.067 mg/kg/day for one year, respectively. The increase of the mean height velocity standard deviation score (SDS) was significantly (p <0.0001) higher in the 0.067-mg group (from -1.4 to 4.7) than that in the 0.033-mg group (-1.9 to 2.6). A significant (p <0.0001) increase in the mean height SDS was established in the 0.067-mg group; increases of -3.1 to -2.5 vs -3.1 to -2.2 in the 0.033- and 0.067-mg groups, respectively. The trial was non-eventful. Oral glucose tolerance tests indicated a mostly normal pattern of plasma glucose before and after 12-month GH treatment. The growth-promoting effect was significantly higher with GH treatment at 0.067 mg/kg/day.     

小于胎龄儿生后生长发育和激素水平研究

小于胎龄儿 (smallforgestationalage ,SGA)是指出生体重在同胎龄平均体重的第 10百分位以下或低于平均体重 2s的新生儿。国外报道其发生率为 5 % ,在我国发病率约为5 %～ 15 % ,生后常有体格发育落后。一般认为SGA生后发生身材矮小的风险为出生身材正常儿的 5～ 7倍。SGA的本质是宫内生长迟缓 ,内分泌轴形成过程受到影响。有关SGA在胎儿期和新生儿期相关激素的研究已有报道 ,但对SGA生后生长落后与生长激素、胰岛素生长因子 1、胰岛素生长因子结合蛋白 3和瘦素等关系的研究相对较少。本文就此作一简要综述。一、SGA生后生长发育根…     

Growth and metabolic consequences of growth hormone treatment in prepubertal short normal children.

Growth and the metabolic effects of growth hormone were monitored in a randomised, controlled group of 41 short, normal, prepubertal children. The treated group received daily injections of growth hormone as Genotropin (Kabi Pharmacia) 30 IU/m2/week. Fifteen children in the treated group (21 children) have completed three years of treatment, have grown significantly more than 14 (of 20) untreated children, and have a significantly greater adult height prediction. They do, however, remain leaner (body fat 13.5% in the treated group, 18% in the untreated group) and relatively hyperinsulinaemic (insulin 66.7 pmol/l in the treated group, 44.5 in the untreated group) after three years compared with untreated children. Although growth hormone appears to improve the height potential of prepubertal short normal children, the long term outcome is still uncertain.     

Small for gestational age babies: Indian scene

Intrauterine growth retardation (IUGR) is an important determinant of neonatal mortality, morbidity and poor neurologic outcome. The study was aimed to evaluate the magnitude of perinatal risk factors in causation and the neonatal outcome of small for gestational age (SGA) babies. One hundred and three SGA babies born over a period of one year were retrospectively analysed during their hospital stay. 3.53 per cent of the babies were SGA with mean birth weight of 1657±SD 354 gm (range 600–2200 gm). 68.9 per cent were term babies and 51.5 per cent were females. Toxemia of pregnancy (30.09%), hypertensive diseases of pregnancy (HDP) excluding toxemia (5.8%), diabetes mellitus (1.94%), medical disorders including renal and cardiac (3.88%), anemia (Hb<8 gm%) and IU infection (0.97%) were the main conditions responsible for SGA. In 56.3% pregnancies, no cause could be ascertained. The common perinatal problems were infections in 27 (26.2%), birth asphyxia in 22 (21.36%), polycythemia in 25 (24.3%), jaundice in 22 (21.36%) and hypoglycemia in 7 (6.8%). Congenital malformations in 2 (1.94%) and Hyaline membrane disease in 1 (0.97%) were uncommon problems. 5.8 per cent babies died due to various perinatal problems. Based on these findings it was concluded that idiopathic (? Constitutional) intrauterine growth retardation was the commonest cause of SGA in Indian babies. 58.3 per cent babies had neonatal problems and they had a better survival compared to their western counterparts.     

Abnormal fetal growth: intrauterine growth retardation, small for gestational age, large for gestational age

The two extremes of abnormal fetal growth are restricted growth and excessive growth, both of which originate from alterations in the uterine metabolic milieu. The fetus must adapt to these conditions to survive. In both instances, however, the inciting insult and the subsequent adaptation of the fetus carry long-term health consequences. In some instances, these changes may have generational implications. Counseling and care by pediatricians should be directed at the continuum of age ranges, including the expectant mother, the newborn, the child and adolescent, and future generations.