الفهرس 
Subject and methodsOnly 14 pages are availabe for public view
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Abstract
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Summary
The period of perinatal growth is vitally important to the
child’s future well-being. So, study of the nature of human life
in utero, especially the growth process, has been and will
continue to be among the most fascinating and rewarding in all
of biological researches.
Fetal growth is a multifactorial phenomenon. It is basically
the result of the relationship between the genetic drive to
growth, environmental factors and the supply of substrata to the
fetus. The genetic control is the dominant factor in early
gestation.
General factors as age of the mother, parity, the maternal
size, endurance exercise during pregnancy, smoking and social
class are important factors influencing fetal growth. The
endocrinological control of fetal growth is very important late in
gestation. Insulin and insulin-like growth factors are the most
important hormones in fetal growth. Insulin has been implicated
as the primary growth hormone for intra-uterine growth and
development. For example, when fetal insulin is absent, marked
IUGR occurs. On the other hand, when fetal hyperinsulinism is
present as a result of maternal and fetal hyperglycaemia, marked
anabolic actions of insulin become manifest. There ensues an
accelerated protein synthesis together with a deposition of
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excessive glycogen and fat stores and the typical macrosmic
infant results. Similarly, insulin-like growth factors are believed
also to be growth hormone dependent and have insulin-like
metabollic effects. They can promote fetal growth and cellular
differentiation. Insulin-like growth factors (somatomedins) have
been implicated as regulators of fetal growth and their
circulating levels increase with gestational age and in normal
intra-uterine growth and decrease in retarded fetal growth. Other
hormones are pituitary growth hormones, human placental
lactogen and fetal renal factor, which mediates normal fetal
growth .
There are abnormal forms of fetal growth as intra-uterine
growth retardation and macrosomia. The IUGR simply is
defined as a birth weight below the IOth percentile for
gestational age and sex. Most fetal growth retardation occur
after the 28th week of gestation with increasing frequency
toward term leading to asymmetrical or head sparing growth
retardation, but if it occurs early before the 28th week of
gestation, symmetrical growth retardation with both somatic
and brain lag results.
Macrosomia is another form of abnormal fetal growth. Fetal
macrosomia is defmed as a birth weight greater than the 90th
percentile for gestational age. Hyperinsulinaemia is the main
cause of fetal macrosomia.
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The present work aimed to determine the correlation
between birth weight and the growth factors believed to be
involved in fetal growth namely insulin (which is reflected by
C-peptide level) and IGF-1 .
Thirty selected pregnant women and their neonates who .
were admitted in labour to the Galaa Maternity Hospital and the
obstetrics department of Benha University Hospitals were the
subjects of this study. They were divided into 3 equal groups:
The first group included 10 normally pregnant women
who delivered AGA neonates (between the 10th and 90th
percentile).
The second group included 10 normally pregnant women
who delivered SGA neonates (below the 1Othpercentile) .
The third group included 10 normally pregnant women
who delivered LGA neonates (above the 90th percentile)
according to Lubchenco et al., (1972) ..
from each subject maternal blood from cubital vein and
fetal blood from umbilical cord were collected and the resulting
sera were separated after centrifugation and were stored at
-200C till they were assayed for IGF-1 and C-peptide by
radioirnmunoessay .
Our results have yeilded the following findings:
1- There was an increase in both maternal and fetal IGF-1 and
C-peptide levels among the (LGA) group in comparison
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with the (AGA) group. Meanwhile, there was a decrease in
both mean maternal and fetal IGF-l and C-peptide levels
among the (SGA) group in comparison with the (AGA)
group.
2- The differences in the maternal serum mean values of IGF-l
showed a statistically significant increase between the
(LGA) and (SGA) groups (p<0.05) .
3- The differences in the fetal serum mean values ofIGF-l,
showed a statistically significant increase between the
(LGA) and (AGA) groups (p<0.05) and between (LGA) and
(SGA) groups (p<0.01) respectively.
4- The differences in the maternal serum C-peptide mean values .
showed a statistically significant increase between the
(LGA) and (AGA) groups (p<0.01), between the (LGA) and
(SGA) groups (p<0.001), and between the (AGA) and
(SGA) groups (P<0.05) respectively.
5- The differences in the fetal serum C-peptide mean values
showed a statistically significant increase only between
(LGA) and (SGA) groups (P<0.05) .
6- There was no significant correlation between serum maternal
IGF-l and serum fetal IGF-l levels among the 3 studied
groups. Also, there was no significant correlation, between
the serum maternal IGF-l levels and birth weight in the 3
studied groups. However, there was a highly significant
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correlation between serum fetal IGF-l levels and birth
weight in the (LGA) and (AGA) groups but not in the
(SGA) group.
7- As regards C-peptide, there was a significant correlation
between serum maternal and fetal C-peptide levels in the
(LGA) group (p<O.05), and in the SGA (p<O.Ol) .
There was no significant correlation between serum
maternal C-peptide levels and birth weight in the 3 studied
groups. The serum fetal C-peptide levels correlated significantly
(p<O.Ol)with birth weight only in the (LGA) group.
from results 0/ this study we can conclude that:
1- Insulin (as reflected by C-peptide level) and IGF-l play
an important role in the regulation of fetal weight gain.
2- Fetal serum IGF-l and C-peptide concentrations are
positively correlated with birth weight, among LGA
newborns indicating that IGF-l and insulin have a
defmite role in the pathogenesis of macrosomic fetuses.
3- Maternal serum levels oflGF-l and C-peptide have no
correlation with birth weight in normal pregnancy .