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Intrauterine growth retardation and familial short stature
Insights
Intrauterine growth retardation (IUGR) causes short stature in children and requires differentiation from familial short stature. Causes include fetal anomalies and maternal disorders, with limited catch-up growth observed.
Area of Science:
- Pediatric Endocrinology
- Genetics
- Obstetrics
Background:
- Intrauterine growth retardation (IUGR) is a significant cause of pediatric short stature.
- Differentiating IUGR from familial short stature is crucial for appropriate management.
- Multiple intrinsic fetal and maternal factors contribute to fetal growth retardation.
Purpose of the Study:
- To review the causes and characteristics of intrauterine growth retardation (IUGR).
- To discuss the challenges in managing short stature associated with IUGR.
- To evaluate the current evidence for growth hormone treatment in IUGR.
Main Methods:
- Literature review of studies on intrauterine growth retardation (IUGR).
- Analysis of factors contributing to fetal growth failure.
- Evaluation of growth patterns and treatment outcomes in IUGR children.
Main Results:
- IUGR is caused by fetal anomalies (chromosomal, infections, syndromes) and maternal disorders (substance use, hypertension).
- Placental abnormalities and environmental factors have a minor role, except for malnutrition.
- About 70% of IUGR children experience some catch-up growth in the first year.
- Many IUGR children have birth defects, potentially linked to common underlying causes.
- Growth hormone treatment data for IUGR is currently not encouraging.
Conclusions:
- Intrauterine growth retardation (IUGR) has diverse etiologies, necessitating careful diagnosis.
- While catch-up growth occurs in many, adult height is often below average.
- Further controlled, long-term trials are needed to re-evaluate growth hormone efficacy in IUGR.
Abstract:
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.