Intrauterine Growth Retardation Children Research Articles

Self-Concept before and after Two Years of Growth Hormone Treatment in Intrauterine Growth-Retarded Children

Self-Concept before and after Two Years of Growth Hormone Treatment in Intrauterine Growth-Retarded Children

121 INTELLIGENCE AND ACADEMIC ACHIEVEMENT IN SMALL CHILDREN: INTRAUTERINE GROWTH RETARDATION (IUGR) VERSUS CONTROLS

64 children, born after intrauterine growth retardation (IUGR) and all with short stature (height SDS <-1.88), have been psychologically examined before starting growth hormone therapy (at T0). 32 matched control children (height below P10) have been tested as well. The tests concerned intelligence (WISC-RN) and school achievement (Groninger School Examination). Total Intelligence Quotients (TIQ), Verbal IQ and Performance IQ of the experimental group proved to be significantly lower (p<0.01, p<0.05, p<0.01 respectively). No specific area of intellectual dysfunctioning could be detected in the IUGR-group; they achieved less in all areas. Regarding general school achievement, results showed no significant differences. However, IUGR-children proved to have more specific difficulties with arithmetic problem solving. Intelligence and school functioning correlated highly in the IUGR-group (r=0.70, p<0.001), but not in the control group. Auxological data, like duration of pregnancy and birthweight, differed significantly between both groups. Significant correlations were found between height SDS at T0 and intelligence (IUGR: r=0.34, p<0.01; control: r = 0.41, p<0.05).Summarizing, IUGR children obtain lower results on the WISC-RN, while they do not clearly achieve less at school. Being small is correlated with intellectual functioning. Birthlength and birthweight, surprisingly, are not.

Dose-dependent catch-up growth after 2 years of growth hormone treatment in intrauterine growth-retarded children. Belgian and French Pediatric Clinics and Sanofi-Choay (France).

This study reports the results of a 2-yr clinical trial with GH in 95 short prepubertal children with non-GH-deficient intrauterine growth retardation. This randomized, double blind, controlled study compared the effects of placebo (restricted to the first 6 months) and two doses of GH (0.4 and 1.2 IU/kg.week) given sc 6 days/week for 2 yr. A significant GH dose-dependent growth acceleration was observed. Mean height gain (SDS/CA) was 0.66 +/- 0.07 in group I (low dose, 0.4 IU/kg.week) compared to 1.25 +/- 0.07 in group II (high dose, 1.2 IU/kg.week). Mean bone maturation progression (expressed in months) was 26.2 +/- 1.7 and 30.2 +/- 1.5 over 24 months in groups I and II, respectively. Onset of puberty was observed in some patients of both groups. Whether chronic use of a high GH dose will advance the onset of puberty remains to be established. A great variability of growth acceleration was seen among GH dose groups, suggesting that factors in addition to GH dose might modulate individual responses to treatment. In conclusion, it is suggested that in these patients, dose-dependent catch-up growth could be induced by GH treatment.

Dose-dependent catch-up growth after 2 years of growth hormone treatment in intrauterine growth-retarded children. Belgian and French Pediatric Clinics and Sanofi-Choay (France)

Dose-dependent catch-up growth after 2 years of growth hormone treatment in intrauterine growth-retarded children. Belgian and French Pediatric Clinics and Sanofi-Choay (France)

The Health Consequences of Intrauterine Growth Retardation in Southwestern Ethiopia

Although over 90% of low birth weight deliveries occur in the developing world, knowledge of its occurrence and consequences are largely based on studies in developed populations. The aim of this investigation was to determine the health consequences of intrauterine growth retardation (IUGR) among an historical cohort of children delivered in a regional hospital located in southwestern Ethiopia. Following a census of all births over a three year period 116 full-term, IUGR and normal birth weight (NBW) matched pairs between 3 and 40 months of age were identified. IUGR children were found to be at elevated risk for moderate to severe malnutrition [relative risk (RR) = 2.26 (1.15,4.43)], frequent illnesses (RR = 1.29 (1.13, 1.46)), and current illness (RR 1.52 (1.10, 2.09)). Catch-up growth among IUGR children did not occur. A steady decline in the growth of NBW children resulted in similar anthropometric outcomes by 2 years of age between the two groups.

Comparison of the Causes and Consequences of Prematurity and Intrauterine Growth Retardation: A Longitudinal Study in Southern Brazil

A cohort of 5914 liveborns (99% of the city births) was followed up to the age of 4 years in Pelotas, southern Brazil. Besides the perinatal evaluation, the cohort children were examined again at mean ages of 11, 23, and 47 months. During each visit the children were weighed and measured and information on morbidity was collected. Also, multiple sources of information were used for monitoring mortality throughout the study. Of the babies with known gestational age, 9.0% were classified as intrauterine growth-retarded and 6.3% as preterm. Excluding those of unknown gestational age, 62% of low birth weight babies were intrauterine growth-retarded and 36% were preterm. Intrauterine growth retardation was statistically associated with maternal height, prepregnancy weight, birth interval, and smoking, whereas preterm births were associated with maternal prepregnancy weight and maternal age. Preterm babies had a perinatal mortality rate 13 times higher than that of babies of appropriate birth weight and gestational age and 2 times higher than that of intrauterine growth-retarded babies. Infant mortality rates presented a similar pattern, with the differentials being more pronounced during the neonatal than in the postneonatal period. In the first 2 years of life intrauterine growth-retarded children were at almost twice the risk of being hospitalized for diarrhea compared with appropriate birth weight, term children, while preterm children experienced only a slightly greater risk. For pneumonia, however, both groups of children were hospitalized significantly more than appropriate birth weight, term children. In terms of growth, despite their earlier disadvantage, preterm children gradually caught up with their appropriate birth weight, term counterparts.(ABSTRACT TRUNCATED AT 250 WORDS)

7 Intrauterine growth retardation and familial short stature

Intrauterine growth retardation (IUGR) is an important cause of small stature in children presenting to paediatric endocrinologists. IUGR has to be differentiated from familial ('constitutional') short stature, where the growth deficit is genetically determined and/or induced by smallness of the mother (maternal constraint). Intrinsic fetal anomalies such as chromosomal abnormalities, primary growth failure syndromes, congenital infections and congenital anomalies are of equal importance with maternal disorders, in particular chronic use of alcohol, tobacco and narcotics, and pregnancy complications like hypertension and pre-eclampsia, in causing fetal growth retardation. The relative importance of placental abnormalities and environmental factors (with the exception of malnutrition) appears to be small. Some catch-up growth of children with IUGR has been observed in about 70% of all cases during the first year of life. Many IUGR children show major or minor birth defects which may be predisposing factors or may also coexist because of common underlying factors producing both small stature and structural anomalies. Since in most children with IUGR adult heights to be expected are below the population range, growth hormone treatment has been tried for many years, but the data available from the literature are not encouraging to date and need to be re-evaluated in controlled long-term trials.

Growth Hormone Response to a Bolus Injection of 1-44 Growth-Hormone-Releasing Hormone in Very Short Children with Intrauterine Onset of Growth Failure

The release of growth hormone (GH) during the 120 min following a bolus venous injection of 1-44 GH-releasing hormone (GHRH) 2 micrograms/kg was studied in 52 prepubertal children aged 8.4 +/- 2.1 years, having a nonfamilial growth deficiency of prenatal onset (-3.26 +/- 1.13 SDS at birth, -3.22 +/- 0.88 SDS at the time of study) and a normal response to conventional GH stimulation tests. GH release reached a peak level of 96.1 +/- 60.2 microU/ml, being significantly higher than that found in 68 non-GH-deficient very short children whose growth failure had a postnatal onset, and not significantly correlated with the response to conventional tests. 26 of the 52 intrauterine growth retardation (IUGR) patients were re-tested with GHRH in similar conditions after 6-12 months of daily subcutaneous injections of GH and 2 days without. They reached at the second test a peak plasma GH level of 91.7 +/- 56.1 microU/ml, not different from their response to the first test. These data could be taken into consideration for long-term studies of the clinical effects of GH in IUGR children with persisting severe growth deficiency.

Indices of fetal growth-retardation, perinatal hypoxia-related factors and childhood neurological morbidity

Data from seven-year-old children ( N = 4535) who were enrolled prenatally during the 1960s and born at term in the Boston sector of the National Collaborative Perinatal Project (NCPP) have been used to study the association of 7-year neurological morbidity with symmetric and asymmetric intrauterine growth-retardation (IUGR), head circumference at birth, and perinatal hypoxia-related factors (PHRF). In the absence of hypoxia-related factors, symmetric and asymmetric IUGR children were not at higher risk for neurological morbidity compared to nonIUGR children. In the presence of perinatal hypoxia-related factors, IUGR children were more likely to be neurologically abnormal compared to non-IUGR children, and the more severe form of IUGR (symmetric) appeared to be associated with a slightly higher risk than was the asymmetric form. Small head circumference was associated with increased risk of neurological abnormality regardless of the presence of PHRF. Potential metabolic and neurodevelopmental explanations for these findings are discussed.