ASSOCIATION OF PLACENTA PREVIA WITH A HISTORY
OF PREVIOUS CESARIAN DELIVERIES AND INDICATIONS
FOR A POSSIBLE ROLE OF A GENETIC COMPONENT
Matalliotakis M1,*, Velegrakis A1, Goulielmos GN2, Niraki E1, Patelarou AE3, Matalliotakis I1
*Corresponding Author: Dr. Michail Matalliotakis, Venizeleio & Pananio General Hospital of Heraklion,
Knossos Avenue, 71409 Heraklion, Greece. Tel: +30-281-036-8304. Mobile: +30-694-386-1582. Fax: +30-281-036-8305.
E-mail: mihalismat@hotmail.com
page: 5
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DISCUSSION
In the current study, we investigated pregnancies associated
with a placental dysfunction, placenta previa, in
the genetically and environmentally homogeneous population
of Crete, Greece. Placenta previa represents the
placenta that partially or wholly covers the internal cervical
os. Our data indicate that the frequency of observed placenta
previa is slightly higher than the one reported so far,
which ranges between 0.3 and 0.5% [6,7].Thus, 76 cases
out of 5200 live births had placenta previa (1.46%). As a
possible explanation, this inconsistency may be considered
to be due to the very low number of specialized tertiary
centers that are available for a large population.
Placenta previa is subdivided into three main types
that can be confirmed by a transvaginal scan. Complete
form means that the placenta totally covers the cervical
os, partial that the edge of the placenta partially covers
the birth canal and marginal indicates that the placenta
lies close to the cervical os [8].
Several studies suggested that a previous history of
C-section is the primary risk factor for developing placenta
previa. Data show up to 37.5% increased risk due to
previous history [9,10]. In the present study, 50 out of 76
women (66.0%) had a history of previous C-sections, a situation
that can be explained by the fact that the endometrial
cells located close to the scar are unable to differentiate
properly resulting in a defective implantation mechanism.
Interestingly, it has been reported that the rate of placenta
previa increases proportionally with the history of previous
C-sections, which is also consistent in our case [11].
Placenta percreta is a potentially lethal complication.
It is a result of failure of decidua basalis after a repair of a
previous uterine scar, and as a consequence, the chorionic
villi invade the myometrium. Hudon et al. [12] stated
that women who have both placenta previa and previous
uterine scarring are susceptible to develop placenta acreta.
In a total of 76 patients with placenta previa, six of them developed placenta percreta. In this group, all women were older than 36 and had a history of more than one previous
C-section. According to the literature, placenta previa is
more common among increased age group (>30 years
old), which is in line with the data of the present study.
Although, there is not any statistically difference between
ultrasound and magnetic resonance imaging (MRI) for
diagnosing placenta percreta, high risk cases should be
carefully evaluated by MRI in order to determine the degree
of the invasion to adjacent organs. It was suggested
in the literature to use MRI imaging when the placenta is
located in the posterior wall of the uterus [13,14]. In the
evaluation of the related complications in our series, we
reported that seven cases were transferred to the ICU, 14
cases needed blood transfusions and eight underwent hysterectomy
due to placenta invasion into the bladder, which
was confirmed by MRI. As far as the time of delivery is
concerned, each case should be individualized depending
on the patient’s preferences and risks. A planned preterm
hysterectomy after 34 weeks where fetal lungs have matured
is recommended, with the placenta being left in situ,
to avoid massive bleeding in cases where invasion of the
chorionic villi is prominent. However, if the mother has a
desire for future fertilization, surgical management should
be individualized [15].
Upon now, a few studies have linked the male gender
with placenta previa formation. The gender at birth seems
to be influenced by variable factors such as parental age,
race, psychological status, exposure to hormonal treatment
for subfertility and the time of the insemination within
the menstrual cycle. The quality of these series is limited
because of the incompleteness of the information presented
in the reports and the small number of cases [16]. Notably,
Jakobovits and Zubek [17] reported an association
between male gender and placenta previa at the extreme
ends of maternal age. Moreover, it has been proposed that
early and late insemination during the menstrual cycle may
contribute to male conceptions and also leads to a change
in the site of implantation [4].
It is postulated that a male fetus is more likely to
develop from late fertilization during the cycle, as a result
in a delay in the creation and implantation of blastocyst
in the lower uterine segment. Our results suggest that, our
results suggest that male gender dominance has become
obvious. Out of 76 cases, we reported 49 (65.0%) male
newborns. In a population based study in Canada, 433,031
pregnancy outcomes were collected. The male-to-female
ratio was higher in cases complicated by a placenta previa
than in those without [18]. It has been suggested that the
male embryo is a possible risk factor that we should take
into consideration, especially in cases with a history of
previous C-sections that may be associated with invasion
of the placenta further to other organs.
Although the risk factors for placenta previa are well
defined, much less is known about its etiology and the
possible enrolment of genetic factors in the development
of this condition. In the present study, a woman gave birth
to three children and placenta previa was observed in all
cases. Moreover, three out of six women with placenta
percreta were related to each other. Altogether, these observations
indicate that both conditions could be genetically
influenced, although no clear genetic contributions to
susceptibility have thus far been defined. Placenta previa
has an overall prevalence in North America of 2.9/1000
pregnancies, compared with a global prevalence of 5.2/
1000 pregnancies [19], while the highest prevalence internationally
was found in Asian women, appearing an overall
prevalence is 12.2/1000 pregnancies. These regional differences
in these rates have not been explained in depth,
although Iyasu et al. [20] reported that in the United States,
women of Asian ethnicity had twice the risk of placenta
previa compared with women of other ethnicities. This
latter finding strengthens the role of genetics rather than
the effect of environmental factors as regards the development
of placenta previa in Asian women.
Interestingly, the role of genetics in placenta previa
has now been demonstrated. Studies aiming to identify
differentially expressed genes, which may impair placentation
resulting in placenta previa increta/percreta (I/P), have
shown that the metastasis associated lung adenocarcinoma
transcript 1 (MALAT-1) (also known as HCN, NEAT2
and PRO2853) gene expression in placenta previa I/P is
increased and its down-regulation inhibits trophoblast-like
cell invasion in vitro. Placenta previa increta/percreta, a
severe form of invasive placentation (a collective term
for placenta accreta, increta and percreta), is associated
with potentially life-threatening hemorrhage, which often
requires a Cesarean hysterectomy. Therefore, it has been
assumed that MALAT-1 might be involved in regulating
trophoblast invasion during the development of advanced
invasive placentation [21]. Additionally, the role of epigenetics
in pregnancies associated with placental dysfunction
including placenta previa has been also pointed out,
indicating that the contribution of epigenetic alterations
can be detected in susceptible subjects before the onset of
clinical disease. In particular, the involvement of “hypermethylation”
has also been reported in placenta previa.
Thus, it has been demonstrated that an increased concentration
of fetal-derived hypermethylated sequences of
RASSF1A (Ras association domain-containing protein 1)
tumor suppressor gene according to advancing gestation and before the onset of placenta previa [22]. Additionally,
and contrarily to placenta previa, a remarkable genetic
predisposition has been reported for other placentationassociated
obstetric complications such as placental abruption
and postpartum hemorrhage [6,23].
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