Original Title:
Ενδοκρινολογική,αιματολογική, βιοχημική και μεταβολική εικόνα του εμβρύου σε ενδομήτρια καθυστέρηση της ανάπτυξης
Summary:
SUMMARY
Introduction: Intrauterine growth restriction is an important problem in
perinatal
medicine and it is associated with increased perinatal mortality and morbidity.
Several
causes can influence fetal growth and that, is a clinical quandary for medicine.
Diagnosis of IUGR is mainly based in sonographic monitoring in order to have the
best perinatal result for the pregnancy and the fetus.
Aims and Scope: The aim of this retrospective study is to investigate
analytically the
causes, the pathogenesis and the way of diagnosing an IUGR fetus as well as the
way
of treatment and the postnatal management. The importance of customized fetal
growth charts, the distinction of symmetric vs. asymmetric IUGR and the
distinguish
from the SGA fetus are highlighted. The references are mainly from electronic
databases such as Pubmed and Google scholar. The articles are basically foreign.
Results: The reduced penetration of trophoblast in the spiral arteries in
intrauterine
growth restriction leads to placental ischemia. Moreover, the placenta growth
factor
VEGF is reduced in contrast to the PLGF that it increases. The concentration of
Ang-
2 is also reduced. Previous studies have shown that leptin, adiponectin and
ghrelin
are reduced as well as the insulin-like growth factors IGF-I and IGF-2. In
intrauterine
malnutrition or placental insufficiency the transfer of placental nutrients is
influenced
negatively. Most of IUGR fetuses are hypoglycemic, hypo insulinemic and in
serious
IUGR are hypoxic. The mother/fetal aminoacid profile is disturbed and the
activity
of System A for the essential aminoacids transfer is reduced. The ions transfer
Na/K is
also reduced. Many studies after the use of cordocentesis have shown that IUGR
fetuses are hypertriglyceridemic because of the reduced use of triglyceridia or
the
impaired lipids oxidation. Serious IUGR fetuses are thrombocytopenic and
leukopenic
because of the fetal hypoxia or the nutrients insufficiency. There are also
observed
coagulopathies. Recent studies have shown, that the hepatic enzymes such as GT
and
LDH are increased in intrauterine growth restriction and the IUGR fetuses
endocrine
profile as far as thyroid and adrenals is concerned , is impaired. TSH is
increased and
T3, TT4 and FT4 are reduced. CRH and cortisol are increased because of the
hypoglycemia. Final, there are many subsequent neonate complications such as
type
2 diabetes and obesity.
Conclusions: The placental functional capacity in high risk pregnancies depends
on
the dynamic balance between the response of trophoblast in hypoxia, the grade of
hypertension and the gravity of other pathological conditions. Uteroplacental
insufficiency influences the nutrients transfer and the metabolic, endocrine and
hematologic fetal profile is impaired. The most important in intrauterine growth
restriction is the timely diagnosis of the IUGR fetus and the distinguish
between the
IUGR and SGA fetus. All these will reduce the perinatal mortality and
morbidity.
Keywords:
Ιntrauterine growth restriction, Placental insufficiency, Placental nutrients, Fetal metabolic changes, Fetal changes
