الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
The neonatal period is a highly vulnerable time for an infant,
who is completing many of the physiologic adjustments required for
extrauterine existence. The high neonatal morbidity and mortality
rates attest to the fragility of life during this period
Very low-birthweight preterm infants are at risk of unique
immaturity-related neonatal diseases. One common factor in the
pathogenesis of such diseases, including bronchopulmonary
dysplasia (BPD), retinopathy of prematurity (ROP), necrotizing
enterocolitis (NEC), intraventricular hemorrhage (IVH), and
periventricular leukomalacia (PVL), is free radical tissue aggression
resulting from oxidative stress.
In a broad sense, oxidative stress may be considered as an
imbalance between pro- and antioxidant forces or between the
amount of reactive oxygen species (ROS) and antioxidant defenses.
The term oxygen radical disease of neonatology has been suggested to
designate diseases whose pathogenesis includes tissue aggression
from free radicals and ROS.
The transition from an intrauterine hypoxic environment to an
extrauterine normoxic environment leads to an acute increase in
oxygenation, which induces the production of R0S. Moreover, 5% to
10% of newly born infants require active resuscitation with
supplementary oxygen at birth, and the ideal oxygen concentration
for neonatal resuscitation is uncertain, which is of major concern.
This study was aimed to evaluate the extent of oxidative stress
in some neonatal disorders and to evaluate the effect of treatment of
these disorders on oxidative stress .
Free radicals are considered the main product of oxidative stress
and its level can be used as a direct parameter of oxidative stress
extent. These free radicals are highly reactive and unstable
intermediate products, it is difficult to measure them directly in vivo.
0xidative effects are assessed indirectly by determining total
antioxidant capacity through measuring individual antioxidant
enzymes or by determining the stable end products of oxidative
stress on lipids, proteins, and DNA
This study included 50 neonates consisted of 35 patients and 15
controls of matched age and sex.
The patient group was subdivided into 3 groups
1- Preterm group included 20 preterm infants ( were
born before completing 37 weeks of G.A.).
2- Neonatal hyperbiliribinemia group included 10
neonates with total and indirect bilirubin level are
indicated for phototherapy
3- Perinatal asphyxia group included 5 neonates
exposed to perinatal asphyxia which wass
confirmed clinically Each of members of both main groups and subgroups are
subjected to the following :
History taking with Special Emphasis on:
History of consanguinity, maternal history of previous pregnancy,
labor or abortion,
History of present pregnancy, labor and resuscitation, history of
perinatal and/or postnatal events
Thorough Clinical Examination and
anthropometric measurements:
Investigations: in the form of :
1- Routine Laboratory investigations as, Complete blood
picture , Indirect and total billirubin, CRP and blood grouping.
2-Antioxidants profile
Antioxidant enzymes :
Glutathione peroxidase in haemolysate., Catalase in haemolysate., and
Superoxide dismutase in haemolysate
Oxidation reaction products:
Isoprostane metabolite (F-8 isoprostane)in plasma , and
Melanodialdehyde(MDA) in plasma.
These clinical and laboratory procedures were performed twice
1-at the postnatal age of 2 days or at admission (in neonatal
hyperbiliurubinemia group)
2- after recovery and just before discharge ( to detect the effect
of treatment of different neonatal conditions on oxidant/antioxidant
profile) .
Then the results of these 2 steps were statistically analyzed and
showed the following
The capacity of antioxidant enzymes were reduced in preterm
infants when compared to healthy full term infants.
Oxygen therapy of preterm respiratory disorders( which
constitute the main cause of admission in most preterm cases)caused a
rise in products of oxidation reactions.
Neonatal jaundice and phototherapy did not affect products of
oxidation reactions.
Perinatal asphyxia and its treatment caused a detectable
depression in antioxidant enzyme levels and a significant rise in
products of oxidation reactions
from this study it can be concluded that : preterm capacity of
dealing with oxidative stress is reduced in comparison with healthy
full term, though most of these preterm infants are exposed to major
oxidative stress because of intense oxygen therapy.
Neonatal jaundice nor its phototherapy had caused any
additional oxidative stress.
Perinatal asphyxia is a major cause of oxidative stress in
neonatal period, and resuscitation and treatment of such neonates had
been a main source of oxidative stress.
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Summary
So it is recommended that, the main strategy of competing
oxidative stress is its prevention
Prevention of oxidative stress mainly depends on judicial use of
oxygen in different neonatal situations monitored by infant oxygen
saturation.